Medical Management of The Surgical Patient, 3rd Edition
Medical Management of The Surgical Patient, 3rd Edition
Medical Management of The Surgical Patient, 3rd Edition
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Knowledge and best practice in this field are constantly changing. As new research
and experience broaden our knowledge, changes in practice, treatment and drug
therapy may become necessary or appropriate. Readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manu-
facturer of each product to be administered, to verify the recommended dose or
formula, the method and duration of administration, and contraindications. It is
the responsibility of practitioners, relying on their own experience and knowledge
of the patient, to make diagnoses, to determine dosages and the best treatment for
each individual patient, and to take all appropriate safety precautions. To the fullest
extent of the law, neither the Publisher nor the editors assume any liability for any
injury and/or damage to persons or property arising out of or related to any use of
the material contained in this book.
RD49.M43 2008
617'.9192--dc22 2007041425
ROBERT F. ATKINS, MD
Anesthesiologist, Department of Anesthesiology, Abington
Memorial Hospital, Abington, Pennsylvania
Selected Medical Challenges of Anesthesia
RODNEY D. BELL, MD
Professor of Neurology and Vice-Chairman for Hospital
Affairs, Department of Neurology, Jefferson Medical College
of Thomas Jefferson University, Philadelphia, Pennsylvania
Perioperative Assessment and Management of the Surgical Patient
with Neurologic Problems
BARTOLOME R. CELLI, MD
Professor of Medicine, Tufts University School of Medicine;
Chief, Pulmonary/Critical Care Medicine, St. Elizabeth’s
Medical Center, Boston, Massachusetts
Perioperative Assessment with Management of Patients with
Pulmonary Diseases
GRETCHEN DIEMER, MD
Clinical Instructor of Medicine, Jefferson Medical College
of Thomas Jefferson University; Assistant Residency
Program Director, Department of Internal Medicine,
Thomas Jefferson University Hospital, Philadelphia,
Pennsylvania
Managing Medication in the Perioperative Period
vii
JOHN A. EVANS, MD
Assistant Professor of Medicine, Duke University School of
Medicine, Durham, North Carolina
Gastrointestinal Complications in the Postoperative Period
FREDERICK M. FELLIN, MD
Assistant Professor of Medicine, Jefferson Medical College of
Thomas Jefferson University, Philadelphia, Pennsylvania
Perioperative Evaluation of Patients with Hematologic Disorders
JAMES FINK, MD
Instructor of Medicine, Jefferson Medical College of Thomas
Jefferson University; Director, Jefferson Hospital Medicine
Program, Thomas Jefferson University Hospital, Philadelphia,
Pennsylvania
Bariatric Surgery: Preoperative Evaluation and Postoperative Care
DAVID G. FORCIONE, MD
Instructor in Medicine, Harvard Medical School, Boston,
Massachusetts
Gastrointestinal Complications in the Postoperative Period
LAWRENCE S. FRIEDMAN, MD
Professor of Medicine, Harvard Medical School, Boston;
Professor of Medicine, Tufts University School of Medicine,
Boston; Chair, Department of Medicine, Newton-Wellesley
Hospital, Newton; Assistant Chief of Medicine,
Massachusetts General Hospital, Boston, Massachusetts
Gastrointestinal Complications in the Postoperative Period;
Management of the Surgical Patient with Liver Disease
KEVIN FURLONG, DO
Clinical Assistant Professor of Medicine, Jefferson Medical
College of Thomas Jefferson University, Philadelphia,
Pennsylvania
Perioperative Management of Endocrine Disorders
DEBORAH T. GLASSMAN, MD
Clinical Assistant Professor of Urology, Jefferson Medical
College of Thomas Jefferson University,
Philadelphia, Pennsylvania
Appendix D: Urologic Surgery
MARVIN E. GOZUM, MD
Clinical Assistant Professor of Medicine, Jefferson Medical
College of Thomas Jefferson University; Director of Jefferson
Hospital for the Neurosciences Preoperative Assessment
Center, Division of Internal Medicine, Jefferson Hospital
for the Neurosciences, Philadelphia, Pennsylvania
Perioperative Management of the Ophthalmologic Patient;
Appendix F: Ophthalmologic Surgery
MARK G. GRAHAM, MD
Associate Professor of Medicine, Jefferson Medical College
of Thomas Jefferson University; Director, Jefferson
Hospital Ambulatory Practice, and Associate Director,
Internal Medicine Residency, Thomas Jefferson University
Hospital, Philadelphia, Pennsylvania
Appendix A: Thoracoscopy and Video-Assisted Thorascopic
Surgery; Appendix B: Laparoscopic Surgeries; Appendix E:
Otolaryngologic Surgery
BRENDA HOFFMAN, MD
Associate Professor of Clinical Medicine, University
of Pennsylvania School of Medicine, Philadelphia,
Pennsylvania
Surgery in the Patient with Kidney Disease
DANIEL K. HOLLERAN, MD
Assistant Professor, Jefferson Medical College of Thomas
Jefferson University, Philadelphia, Pennsylvania
Perioperative Care of the Patient with Psychiatric Illness
SERGE JABBOUR, MD
Clinical Associate Professor of Medicine, Jefferson Medical
College of Thomas Jefferson University, Philadelphia,
Pennsylvania
Perioperative Management of Endocrine Disorders
GREGORY C. KANE, MD
Professor of Medicine, and Director, Residency Program,
Jefferson Medical College of Thomas Jefferson University,
Philadelphia, Pennsylvania
Perioperative Assessment and Management of Patients with
Pulmonary Diseases
BARBARA KNIGHT, MD
Instructor, Jefferson Medical College of Thomas Jefferson
University, Philadelphia, Pennsylvania
Nonobstetric Surgery in the Pregnant Patient
JANINE V. KYRILLOS, MD
Instructor, Division of Internal Medicine, Jefferson Medical
College of Thomas Jefferson University; Director, Preventive
Health Care Program, Jefferson Internal Medicine
Associates, Philadelphia, Pennsylvania
Nonobstetric Surgery in the Pregnant Patient; Appendix E:
Otolaryngologic Surgery
KENNETH LIEBMAN, MD
Assistant Professor of Neurosurgery, Jefferson Medical
College of Thomas Jefferson University, Philadelphia,
Pennsylvania
Appendix H: Neurosurgery
MICHAEL F. LUBIN, MD
Professor of Medicine, Emory University School of
Medicine; Director, Preadmission Clinic, Grady
Memorial Hospital, Atlanta, Georgia
Perioperative Care of the Elderly Patient
TRACY McGOWAN, MD
Associate Medical Director, Clinical Affairs, Ortho Biotech,
Bridgewater, New Jersey
Surgery in the Patient with Kidney Disease
GREGORY MOKRYNSKI, MD
Instructor of Medicine, Jefferson Medical College of Thomas
Jefferson University, Philadelphia, Pennsylvania
Appendix A: Thoracoscopy and Video-Assisted Thorascopic Surgery
JOSEPH M. MONTELLA, MD
Clinical Assistant Professor of Obstetrics and Gynecology,
Jefferson Medical College of Thomas Jefferson University,
Philadelphia, Pennsylvania
Appendix C: Obstetric and Gynecologic Surgery
JAVAD PARVIZI, MD
Associate Professor, Jefferson Medical College of Thomas
Jefferson University, Philadelphia, Pennsylvania
Appendix G: Orthopedic Surgery
JEFFREY M. RIGGIO, MD
Instructor of Medicine and Associate Medical Director of
Informatics, Jefferson Medical College of Thomas Jefferson
University, Philadelphia, Pennsylvania
Appendix B: Laparoscopic Surgeries
ELIZABETH TEPEROV, MD
Clinical Instructor of Medicine, Jefferson Medical College
of Thomas Jefferson University; Director, Hospital Medicine,
Jefferson Hospital for Neurosciences, Philadelphia,
Pennsylvania
The Patient with Substance Abuse Going to Surgery
GEORGE L. TZANIS, MD
Instructor of Medicine, Jefferson Medical College of Thomas
Jefferson University; Associate Director, Jefferson Center for
Vascular Diseases, Philadelphia, Pennsylvania
Prophylaxis for Deep Vein Thrombosis and Pulmonary Embolism
in the Surgical Patient
JENNY Y. WANG, MD
Assistant Professor, Jefferson Medical College of Thomas
Jefferson University; Associate Director, Jefferson Hospital
Medicine Program, Thomas Jefferson University Hospital,
Philadelphia, Pennsylvania
Perioperative Care of the Patient with Psychiatric Illness
SUSAN E. WEST, MD
Assistant Clinical Professor of Medicine, Division of Internal
Medicine, Jefferson Medical College of Thomas Jefferson
University, Philadelphia, Pennsylvania
Appendix C: Obstetric and Gynecologic Surgery; Appendix D:
Urologic Surgery
1.
Determine the question and address that question.
2.
Perform the consultation in a timely manner.
3.
Perform a thorough evaluation.
4.
Write as concise a consultation report as appropriate.
5.
Make recommendations clear and concise.
6.
Provide prompt communication.
7.
Do not “clear for OR.” Identify risks and attempt to
reverse them. Optimize the patient for surgery.
8. Provide appropriate follow-up.
9. Know your role: pure consultant versus co-manager.
10. Provide options and alternative approaches and teach
with tact.
PERIOPERATIVE MEDICATIONS
The number of new pharmacologic agents for the treatment
of disease continues to grow exponentially. On average, four
or more drugs are available to treat a disease process, and
each agent has some special action or effect. These differ-
ences and the numbers of drugs make it challenging for
physicians to maintain a working familiarity with all these
agents.
The medical consultant is often faced with preparing pati-
ents for surgery for whom he or she has not been the primary
physician. In such cases, a variety of medications may be
encountered with which the consultant may not be familiar,
or the consultant may not agree with their indications. The
consultant’s responsibility is to decide which of the patient’s
outpatient medications should be continued in the periop-
erative period and to develop a strategy for parenteral drug
administration for patients who will be unable to resume oral
medications immediately following surgery. In some cases,
this will be particularly challenging. For patients whose out-
patient medication is not available in parenteral form, a sub-
stitution will have to be made until oral medications can
be resumed. Some medications have specific perioperative
recommendations, such as insulin, agents for DVT-PE pro-
phylaxis, and antihypertensive medications. Several medica-
tions (e.g., -blockers) are initiated preoperatively in an
effort to decrease the risk of perioperative complications. The
POSTOPERATIVE COMPLICATIONS
As the information base for medical consultation has ex-
panded, the area of postoperative complications has also
grown. This focus has been largely on the effects of anes-
thesia and surgery on the patient.
The role of the consultant is not to select or recommend
the anesthetic agent, but rather to understand the effect of
the agent on the patient. This is important in patients with
concomitant diseases that may be exacerbated by the effects
of general, spinal, or local anesthesia. The consultant should
also be familiar with the patient’s anesthesia record. This
document provides important information concerning vital
signs, type and amount of fluid administered, and additional
intraoperative medications. A postoperative change in men-
tal status, for example, may result from intraoperative hypo-
tension or from a decrease in hemoglobin secondary to the
dilutional effect of increased fluid volume.
Our surgical colleagues have long focused on the postop-
erative complications of procedures. More recently, medical
consultation texts have included descriptions of surgical pro-
cedures and their complications. It is important that a
knowledge of the description, indications, and complications
of surgical procedures become part of both the medical
consultant’s preparation of the patient for surgery and post-
operative management. This familiarity with surgical proce-
dures and their postoperative complications allows a better
working relationship with the consulting surgeon and fre-
quently a better outcome for the patient.
MEDICAL INSURANCE
Third-party payers were the first to provide definitions,
coding, and reimbursement for the responsibilities of the
medical consultant. This area will continue to evolve as
third-party payers determine compensation for the service
provided. The following are descriptions of the responsibili-
ties of the consultant as they pertain to the complexity of the
service provided.
A consultation includes services rendered by a physician
whose opinion or advice is requested by a physician or other
appropriate source for the further evaluation or management
(or both) of the patient. When the consulting physician assumes
responsibility for the continuing care of the patient, any subse-
quent service rendered by him or her ceases to be a consulta-
tion. Five levels of consultation are recognized: limited, interme-
diate, extended, comprehensive, and complex.
In a limited consultation, the physician confines his or her
service to the examination or evaluation of a single organ
system. This procedure includes documentation of the com-
plaints, evaluation of the present illness, pertinent examina-
tion, review of medical data, and establishment of a plan of
management relating to the specific problem. An intermediate
consultation involves examination or evaluation of an organ
system, a partial review of the general history, recommenda-
tions, and preparation of a report. An extended consultation
involves the evaluation of problems that do not require a
comprehensive evaluation of the patient as a whole. This
procedure includes the following: documentation of a history
of the chief complaint, past medical history, and pertinent
physical examination; review and evaluation of the past
medical data; establishment of a plan of investigative or
therapeutic management, or both; and the preparation of an
appropriate report. A comprehensive consultation involves the
following: (1) an in-depth evaluation of a patient with a
problem requiring the development and documentation of
MEDICAL-LEGAL LIABILITY
The medical consultant must practice in accordance with the
basic principles of medical liability. These principles are quite
broad in most jurisdictions. It is our interpretation of the law
that a consultant performing a preoperative evaluation must
possess and employ the same skill and knowledge possessed
by other consultants practicing in this field, giving regard to
the state of preoperative evaluation and perioperative care at
the time of service. We believe that a consultant will be held
liable if his or her actions are inconsistent with the standard
of care at the time of the patient encounter if that inconsis-
tency results in injury to the patient. A “poor result” or a
“mistake in judgment” alone is not a sufficient basis for liabil-
ity. Physicians are neither guarantors nor warrantors of the
result of a treatment or procedure result. Finally, if more than
one diagnostic or treatment plan is recognized as proper, a
consultant should not be held responsible if he or she follows
one of the recognized plans as opposed to another. We be-
lieve that the consultant is responsible for patient care in his
or her area of expertise until the problem or question under
study has been resolved or the consultant has transferred
responsibility to another physician. Finally, if the circum-
stances surrounding a case raise the issue of medical-legal
CONCLUSION
With the preceding issues in mind, it is obvious that the role
and responsibilities of the medical consultant have changed
and will continue to evolve as new studies are performed to
improve the field. We stress the importance of an orderly and
in-depth approach to patient evaluation, accurate documen-
tation, and precise recommendations as well as ongoing
communication with the surgical team (Box 1-3). Following
these principles will result in effective medical consultation
for the surgical patient with medical problems.
• Timely response
• Precise recommendations
• Follow-up care
• Communication with the requesting physician
Selected Readings
Arozullah AM, Khuri SF, Henderson WG, et al: Development and validation
of a multifactorial risk index for predicting postoperative pneumonia
after major non-cardiac surgery. Ann Intern Med 135:847-857, 2001.
Boucher C, Brewster D, Darling R, et al: Determination of cardiac risk by
dipyridamole-thallium imaging before peripheral vascular surgery.
N Engl J Med 312:389-394, 1985.
Detsky A, Abrams H, Forbath N, et al: Cardiac assessment for patients
undergoing noncardiac surgery: A multifactorial clinical risk index.
Arch Intern Med 146:2131-2134, 1986.
Eagle K, Berger P, Calkins H, et al: ACC/AHA guideline update for periop-
erative cardiovascular evaluation for non-cardiac surgery: Executive
summary. A report of the ACC/AHA Task Force on Practice Guidelines.
J Am Coll Cardiol 39:542-553, 2002.
Eagle K, Coley C, Newell J, et al: Combining clinical and thallium data op-
timizes preoperative assessment of cardiac risk before major vascular
surgery. Ann Intern Med 110:859-866, 1989.
Geerts W, Pineo G, Heit J, et al: Prevention of venous thromboembolism.
Chest 126(Suppl):338S-400S, 2004.
Goldman D, Brown F, Guarnieri D: Perioperative Medicine: The Medical
Care of the Surgical Patient, 2nd ed. New York, McGraw-Hill, 1994.
Goldman L, Caldera D, Nussbaum S, et al: Multifactorial index of cardiac risk
in noncardiac surgical procedures. N Engl J Med 297:845-850, 1977.
Goldman L, Lee T, Rudd P: Ten Commandments for effective consultation.
Arch Intern Med 143:1753-1755, 1983.
Greenfield L: Complications of Surgery and Trauma, 2nd ed. Philadelphia,
JB Lippincott, 1990.
Gross R, Caputo G: Medical Consultation: The Internist on Surgical, Obstetric,
and Psychiatric Services, 2nd ed. Baltimore, Williams & Wilkins, 1998.
Hertzer N: Fatal myocardial infarction following lower extremity revascular-
ization. Ann Surg 193:492-498, 1981.
Huddleston J, Long K, Naessens J, et al: A randomized controlled trial of
medical and surgical co-management following elective hip and knee
arthroplasty. Ann Intern Med 141:28-38, 2004.
Lubin H, Walker H, Smith R: Medical Management of the Surgical Patient,
4th ed. Philadelphia, JB Lippincott, 2006.
Mangano D, Browner W, Hollenberg M, et al: Association of perioperative
myocardial ischemia with cardiac morbidity and mortality in men un-
dergoing noncardiac surgery. N Engl J Med 323:1781-1788, 1990.
Mercado D, Betty B: Perioperative medication management. Med Clin North
Am 87:41-57, 2003.
Merli G: The hospitalist joins the surgical team. Ann Intern Med 141:67-69,
2004.
THE HISTORY
• A complete medication history including nonprescription
and herbal medications.
• A review of allergies with particular attention to latex and
iodine allergies as well as anesthetic agents.
• A review of surgical history with attention to bleeding
complications or coagulation disorders.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized clinical trials,
systematic reviews of studies other than RCTs, cross-sectional studies, retrospective
studies. C —Consensus statements, expert guidelines, usual practice, opinion.
15
FUNCTIONAL STATUS
Multiple cardiac risk assessment tools have been published.
Several of these studies identified poor functional capacity as
a clinical predictor of risk. Activity scales such as the Duke
Activity Status Index can assess functional capacity (Fig. 2-1).
The American College of Cardiology/American Heart Associa-
tion (ACC/AHA) guidelines for perioperative cardiovascular
risk evaluation state that an inability to perform four or more
metabolic equivalents (METs) activities, even if the factor
limiting the activity is noncardiac (e.g., severe arthritis) is a
risk factor for cardiac complications in noncardiac surgery.
12/19/07 6:15:45 PM
18 2 • Preoperative Assessment for the Healthy Patient
CONSIDERATIONS IN PREOPERATIVE
Box 2-1
CHEST RADIOGRAPHY
CONSIDERATIONS IN PREOPERATIVE
Box 2-2
ELECTROCARDIOGRAPHY
CONSIDERATIONS IN PREOPERATIVE
Box 2-3
HEMOGLOBIN DETERMINATIONS
CONSIDERATIONS IN PREOPERATIVE
Box 2-4 BLEEDING AND COAGULATION
EVALUATIONS
CONSIDERATIONS IN PREOPERATIVE
Box 2-5
SERUM BIOCHEMISTRY EVALUATIONS
Recommendations
1. Biochemical profiles are not routinely indicated before
elective admission to the hospital.
2. In selected institutions, biochemical profiles may be less
expensive than tests of individual components.
Special Considerations
1. Patients with known liver disease should have at least al-
bumin and bilirubin concentrations determined for as-
sessment using the Child risk classification.
2. Patients with a remote history of hepatitis should have
testing of serum aminotransferase, alkaline phosphatase,
bilirubin, and albumin levels.
3. Patients with known malignancy may benefit from bio-
chemical testing of the liver as a screen for metastatic
disease.
Urinalysis
Multiple studies have shown that abnormalities are commonly
found in routine urinalysis. However, abnormalities in protein,
ketones, or glucose are also frequently discovered and quanti-
tated in blood chemistry panels. Because blood chemistry
panels are more reliable and are ordered in the same popula-
tion, a urinalysis provides no additional benefit.
A possible exception to this is the finding of asympto-
matic bacteriuria. Studies have estimated the frequency of
asymptomatic bacteriuria in women at 3.3%. In men, the
frequency increases with age. For this reason, urinalysis con-
tinues to be used as a preoperative test before the insertion
of a prosthetic joint or heart valve. However, at least one
study has questioned whether an abnormal preoperative
urinalysis predicts wound infection.
Recommendations
1. Urinalysis is not routinely indicated preoperatively.
2. Urinalysis may be useful before any surgical procedure
in which urinary tract instrumentation is anticipated,
SUMMARY
Historically, preoperative tests have been used to find occult
disease in low-risk populations. For almost all tests, this ap-
proach has been shown to yield a small number of true ab-
normalities. It also results in many false-positive findings,
which can lead to surgical delay and patient anxiety. This
approach is not cost effective.
Unfortunately, dissemination of this information some-
times results in minimizing the use of tests when they would
be helpful. The current approach is to use the history and
physical examination to identify groups at risk for abnor-
malities and then to order tests to identify and quantitate
abnormalities. Based on the likelihood of the disease, the
tests shown in Table 2-1 should routinely be ordered for
surgery in which low blood loss is anticipated. In addition to
aPTT, partial thromboplastin time; CBC, complete blood count; ECG, elec-
trocardiogram; PT, prothrombin time; SMA-7, seven-factor sequential multiple
analysis; SMA-12, 12-factor sequential multiple analysis; TSH, thyroid-stimulat-
ing hormone.
Selected Readings
Archer C, Levy EB, Staten M: Value of routine preoperative chest x-rays: A
meta-analysis. Can J Anaesth 40:1022-1027, 1993.
Bryson GL, Wyand A, Bragg PR: Preoperative testing is inconsistent with
published guidelines and rarely changes management. Can J Anaesth
53:236-241, 2006.
Cebul RD, Beck RJ: Biochemical profiles: Applications in ambulatory screening
and preadmission testing of adults. Ann Intern Med 106:403-413, 1987.
Dzankic S, Pastor D, Gonzalez C, Leung J: The prevalence and predictive
value of abnormal preoperative laboratory tests in elderly surgical pa-
tients. Anesth Analg 93:301-308, 2001. B
Eagle KA, Berger PB, Calkins H, et al: ACC/AHA guideline update for peri-
operative cardiovascular evaluation for noncardiac surgery: A report of
the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (Committee to Update the 1996 Guidelines
on Perioperative Cardiovascular Evaluation for Noncardiac Surgery).
American College of Cardiology, 2002. Available at http://www.acc.org.
Eisenberg J, Goldfarb S: Clinical usefulness of measuring prothrombin time
as a routine admission test. Clin Chem 22:1644-1647, 1976.
Gibbs J, Cull W, Henderson W, et al: Preoperative serum albumin level as a
predictor of operative mortality and morbidity results from the National
VA Surgical Risk Study. Arch Surg 134:36-42, 1999.
Goldberger AL, O’Konski M: Utility of the routine electrocardiogram before
surgery and on general hospital admission. Ann Intern Med 105:552-
557, 1986.
Goldman L, Caldera DL, Nussbaum SR, et al: Multifactorial index of cardiac
risk in noncardiac surgical procedures. N Engl J Med 297:845-850,
1977.
Hlatky MA, Boineau RE, Higginbotham MB, et al: A brief self-administered
questionnaire to determine functional capacity (the Duke Activity Status
Index). Am J Cardiol 64:651-654, 1989.
Kannel WB, Abbott RD: Incidence and prognosis of unrecognized myocar-
dial infarction: An update on the Framingham study. N Engl J Med
311:1144-1147, 1984.
Kaplan EB, Sheiner LB, Boeckmann AJ, et al: The usefulness of preoperative
laboratory screening. JAMA 253:3576-3581, 1985.
Kolwalsyn TJ, Prageer D, Young J: A review of the present status of preop-
erative hemoglobin requirements. Anesth Analg 51:75, 1972.
Lawrence VA, Kroenke K: The unproven utility of preoperative urinalysis:
Clinical use. Arch Intern Med 148:1370-1373, 1988.
Macpherson DS, Snow R, Lofgren RP: Preoperative screening: Value of previ-
ous tests. Ann Intern Med 113:969-973,1990. B
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized controlled
trials, systematic reviews of studies other than RCTs, cross-sectional studies, retro-
spective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
35
NONANTIMICROBIAL INTERVENTIONS
Box 3-2 OF BENEFIT IN DECREASING THE RISK
OF SURGICAL WOUND INFECTIONS
PREOPERATIVELY
Minimize preoperative hospitalization.
Treat remote sites of infection.
Avoid shaving or delay it until time of surgery.
Avoid preoperative antibiotic use.
Resolve malnutrition and obesity.
Maximize diabetes control.
INTRAOPERATIVELY/POSTOPERATIVELY
Use careful skin preparation.
Use rigorous aseptic technique.
Use high-flow filtered air or laminar flow.
Minimize dead space.
Minimize the use of catheters and intravenous lines postopera-
tively.
Maintain adequate hydration, oxygenation, and nutrition post-
operatively.
PERIOPERATIVE ANTIBIOTICS
General Principles of Antibiotic Selection and Use
Antibiotic Choice
Cefazolin is the most commonly used antibiotic for prophy-
laxis. It offers the advantages of a moderately long half-life,
activity against most staphylococci and streptococci (in addi-
tion to some gram-negative aerobic organisms), and low cost.
Cefazolin has had extensive clinical use and has proven ef-
fectiveness. For intra-abdominal and pelvic procedures that
may involve bowel anaerobes, cefoxitin (Mefoxin) is used in-
stead because of its enhanced activity against these organisms.
Recently, ertapenem (Invanz) was also approved for prophy-
laxis in patients undergoing colorectal surgeries after a trial
Adult Dose
Nature Common Recommended before
of Operation Pathogens Drugs Surgery1
Vascular
Arterial surgery in- S. aureus, Cefazolin OR 1–2 g IV
volving a pros- S. epidermidis, en- vancomycin3 1 g IV
thesis, abdomi- teric gram-negative
nal aorta, or bacilli
groin incision
Lower extremity S. aureus, Cefazolin OR 1–2 g IV
amputation for S. epidermidis, vancomycin3 1 g IV
ischemia enteric gram-
negative bacilli
1
Give as single dose within 60 minutes before operation. For prolonged op-
erations, additional doses may be necessary. If vancomycin or a fluoroquinolone
is used, give 60 to 120 minutes before incision.
2
An additional dose is often given when patients are removed from bypass
machine.
3
For patients previously colonized with methicillin-resistant S. aureus
(MRSA) or who are allergic to penicillins or cephalosporins. Watch for hypoten-
sion, and give at a slow infusion rate over 60 minutes or more. Additional gram-
negative coverage should be given for procedures in which gram-negative bacilli
are likely pathogens, such as vascular surgery through a groin incision; ciproflox-
acin, levofloxacin, gentamicin, and aztreonam are acceptable.
4
Morbid obesity, esophageal obstruction, use of H2-blockers/proton pump
inhibitors, decreased gastric motility.
5
For cephalosporin allergy, clindamycin plus either gentamicin, ciprofloxa-
cin, levofloxacin (750 mg), or aztreonam is acceptable.
6
Age older than 70 years, acute cholecystitis, nonfunctioning gallbladder,
obstructive jaundice, or common duct stones.
7
Continue for 3 to 5 days. Need to expand coverage for nosocomial patho-
gens in postoperative dehiscence.
8
Preoperative catheter, urine culture positive or unavailable, transrectal prostatic
biopsy, placement of prosthetic material (some would add vancomycin or cefazolin).
9
Previous pelvic inflammatory disease, gonorrhea, or multiple sex partners.
10
If tourniquet is used, infuse entire dose before inflation.
IV, intravenously; PO, orally.
From The Medical Letter Treatment Guidelines, April 2004. This material has
been reproduced with special permission from The Medical Letter.
Gastrointestinal Surgery
ESOPHAGEAL SURGERY
The esophagus is generally a sterile viscus as a result of peri-
stalsis. However, diseases that lead to obstruction, decreased
peristalsis, or stasis prompt proliferation of oral aerobes and
anaerobes. In turn, the risk of mediastinal infection is in-
creased, and prophylaxis is generally recommended. One
prospective, randomized study in endoscopic sclerotherapy
of esophageal varices showed no benefit of prophylactic an-
tibiotics in reducing the risk of bacteremias or SSIs.
GASTRODUODENAL SURGERY
The incidence of postoperative infection in gastroduodenal
surgery is proportionate to the number of bacteria within
the stomach; consequently, the risk of infection is highest
when gastric acidity and gastrointestinal motility are dimin-
ished by defects in the gastric mucous membrane or by
prolonged therapy with histamine (H2)-blockers or proton
pump inhibitors. Cessation of H2-blockers or proton-pump
inhibitors and preoperative use of a cephalosporin can de-
crease the incidence of postoperative infection in patients
with carcinoma, gastric ulcer, bleeding, obstruction, or per-
foration. Prophylaxis is also recommended in patients who
are morbidly obese. Prophylactic antibiotics are not indi-
cated for routine gastroesophageal endoscopy, but they are
indicated before placement of percutaneous gastrostomy
tubes.
BILIARY PROCEDURES
The biliary tract is normally sterile, and patients less than
70 years of age who are undergoing elective surgery with-
out preoperative infections are generally not at risk for
postoperative infectious complications. Thus, prophylactic
antibiotics are generally not indicated in routine elective
laparoscopic cholecystectomy. However, prophylaxis is rec-
ommended before biliary tract surgery in patients who are
at increased risk of infection. This group includes patients
more than 70 years of age and those with common bile duct
stones, bile duct stricture or obstruction, recent acute cho-
lecystitis, or prior biliary surgery. This recommendation
also applies to patients who undergo endoscopic retrograde
cholangiopancreatography.
COLORECTAL SURGERY
The risk of significant perioperative infections in patients
undergoing colorectal operations may be as high as 40% if
prophylactic antibiotics are not used. An oral regimen of lu-
minal catharsis and antibiotics can reduce the postoperative
infection rate to less than 7% and appears to be as effective
as the use of parenteral antimicrobials. Whether a combina-
tion of oral and parenteral agents is better than either regi-
men alone is unclear, but such a combination is widely em-
ployed in the United States. The prophylactic regimen
should include an oral lavage solution (e.g., polyethylene
glycol) and antimicrobials effective against both aerobic
gram-negative bacilli and anaerobes—usually neomycin in
combination with either erythromycin or metronidazole.
APPENDECTOMY
Prophylactic antibiotics decrease the incidence of infection af-
ter appendectomy. If the appendix has perforated, the patient
should be treated as though an infection were present. In that
instance, antibiotics should be used therapeutically (i.e., for
5 to 7 days). Regimens with activity against both aerobic gram-
negative bacilli and anaerobes are recommended.
PENETRATING ABDOMINAL TRAUMA
Escape of endogenous bacteria as a result of hollow lumen
visceral damage is a major risk factor for postoperative infec-
tion following penetrating abdominal trauma. Before surgical
treatment of penetrating abdominal trauma, a single dose of
prophylactic antibiotic is indicated. If at exploratory laparot-
omy gastrointestinal leakage is observed, antibiotics should be
continued on a therapeutic basis. Studies have suggested that
shorter courses of antibiotics (e.g., 12 to 24 hours) may be just
Selected Readings
Andersen BR, Kallegave FL, Andersen HK: Antibiotics versus placebo for
prevention of postoperative infection after appendicectomy. Cochrane
Database Syst Rev 2:CD001439, 2003.
Barker FG 2nd: Efficacy of prophylactic antibiotic therapy in spinal surgery:
A meta-analysis. Neurosurgery 53:243, 2002. B
Bratzler DW, Houck PM, for the Surgical Infection Prevention Guideline
Writers Workgroup: Antimicrobial prophylaxis for surgery: An advisory
statement from the National Surgical Infection Prevention Project. Clin
Infect Dis 38:1706-1715, 2004.
Bratzler DW, Houck PM, Richards C, et al: Use of antimicrobial prophylaxis
for major surgery: Baseline results from the national surgical infection
prevention project. Arch Surg 140:174-182, 2005.
Burke JF: The effective period of preventive antibiotic action in experimental
incisions and dermal lesions. Surgery 50:161-168, 1961.
Chong AJ, Dellinger EP: Infectious complications of surgery in morbidly
obese patients. Curr Treat Options Infect Dis 5:387, 2003.
Classen DC, Evans RS, Pestotnik SL, et al: The timing of prophylactic
administration of antibiotics and the risk of surgical wound infection.
N Engl J Med 326:281-286, 1992. B
Cornwell EE, Dougherty WR, Berne TV, et al: Duration of antibiotic pro-
phylaxis in high-risk patients with penetrating abdominal trauma:
A prospective randomized trial. J Gastrointest Surg 3:648-653, 1999.
Dimick JB, Lipsett PA, Kostuik JP: Spine update: Antimicrobial prophylaxis
in spine surgery. Basic principles and recent advances. Spine 25:
2544-2548, 2000.
Furnary AP, Zerr KJ, Grunkemeier GL, Starr A: Continuous intravenous in-
sulin infusion reduces the incidence of deep sternal wound infection in
diabetic patients after cardiac surgical procedures. Ann Thorac Surg
67:352-360, 1999. A
Grief R, Akca O, Horn E-P, et al: Supplemental perioperative oxygen to re-
duce the incidence of surgical wound infection. N Engl J Med 342:
161-167, 2000.
Itani KMF, Wilson SE, Awad SS, et al: Ertapenem versus cefotetam prophy-
laxis in elective colorectal surgery. N Engl J Med 355:2640-2651, 2006.
Kurz A, Sessler DI, Lenhardt RA: Perioperative normothermia to reduce the
incidence of surgical-wound infection and shorten hospitalization.
N Engl J Med 334:1209-1215, 1996.
Langley JM, LeBlanc JC, Drake J, Milner R: Efficacy of antimicrobial pro-
phylaxis in placement of cerebrospinal fluid shunts: Meta-analysis. Clin
Infect Dis 17:98-103, 1993. B
Maki DG, Bohn MJ, Stolz SM, et al: Comparative study of cefazolin, cefa-
mandole, and vancomycin for surgical prophylaxis in cardiac and vascu-
lar operations: A double-blind randomized trial. J Thorac Cardiovasc
Surg 104:1423-1434, 1992.
Sessler DI, Akca O: Nonpharmacologic prevention of surgical wound infec-
tions. Clin Infect Dis 35:1397-1404, 2002.
Strom BL, Abrutyn E, Berlin JA, et al: Dental and cardiac risk factors for
infective endocarditis: A population-based, case-control study. Ann In-
tern Med 129:761-769, 1998.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized con-
trolled trials, systematic reviews of studies other than RCTs, cross-sectional
studies, retrospective studies. C —Consensus statements, expert guidelines, usual
practice, opinion.
51
SPINAL HEADACHE
Spinal anesthesia (SA) is an extremely popular anesthetic
technique that, along with its close relative epidural anes-
thesia, makes up a significant majority of all regional anes-
thetics given in the United States. A regional anesthetic,
which anesthetizes a region of the body (e.g., one or more
extremities, entire lower half of the body), is distinguished
from local anesthesia, which focuses on the area surrounding
the surgical incision, and from general anesthesia. In contrast
to general anesthesia, deep unconsciousness is not induced
during surgery with regional anesthesia, although intrave-
nous sedation, which produces a mild depression of con-
sciousness in conjunction with anxiolysis, is frequently
employed simultaneously to improve the subjective experi-
ence for the patient.
Although generally well tolerated, SA can have various
sequelae, which are not usually serious. Spinal headache,
technically known as postdural puncture headache (PDPH), is
among the concerns about SA most frequently expressed by
patients, especially those with no previous experience with
SA or those with a history of PDPH. Moreover, patients suf-
fering from PDPH can be severely incapacitated, often unable
to perform basic activities of daily living as a result of pain
and associated symptoms.
Epidemiology
Given the ubiquitous loss of CSF that follows dural puncture,
the incidence of PDPH after SA is surprisingly low, ranging
from 1% to 25% in most contemporary studies. It is unknown
why, in similar clinical circumstances, one patient acquires
PDPH and another does not. Nonetheless, considerable inves-
tigation has been done to elucidate the factors that do affect
the incidence of PDPH among various patient groups.
Most of the research on PDPH performed over the past
several decades has consistently identified the importance
of age, gender, and needle size. PDPH is significantly more
frequent with decreasing age, female gender (especially when
SA is used for obstetric procedures), and increasing needle
diameter (Fig. 4-1). The frequency of PDPH following diag-
nostic lumbar puncture exceeds that following SA, because
larger needles are used in lumbar puncture, and CSF is inten-
tionally withdrawn.
Significantly modifying the effect of needle diameter,
however, is the position of the needle tip. First, the direction
of the needle bevel with respect to the patient at the time
20
15
10
0
Male
Female
Female (OB)
16
19
20
22
24
10–19
20–29
30–39
40–49
50–59
60–69
70–79
80–89
and less CSF loss. This explanation has recently been ques-
tioned by the results of electron microscopic studies showing
that dural fibers are actually arranged randomly, rather than in
a precise pattern. Thus, the precise cause of the significant
benefit realized with parallel bevel insertion remains unclear.
By far, the most important innovation in spinal needle
design has been the replacement of the traditional beveled
tip in favor of “pencil point” (e.g., Whitacre, Sprotte) con-
struction (Fig. 4-2). This newer design further reduces dural
trauma during lumbar puncture, with an additional reduc-
tion in CSF leakage. Numerous clinical and in vitro studies
with these needles have yielded overwhelmingly favorable
results. Indeed, many anesthesiologists have, with occasional
A B C D
Figure 4-2 • Array of needles used for neuraxial anesthesia (A–C are used
for spinal anesthesia). A, Traditional beveled (Quincke) needle, with orifice
within the diagonal cutting tip. B and C, Newer “pencil point” designs (Sprotte
and Whitacre, respectively). These end in a rounded, noncutting tip and have
orifices arranged distally on the side. D, Standard epidural (Tuohy) needle. This
is larger in diameter and has a curved tip containing the orifice oriented perpen-
dicular to its long axis that allows passage of an epidural catheter up the epidural
space within the vertebral canal.
OBESITY
In 2002, an estimated 30.6% of adults in the United States
were obese, more than double the prevalence 20 years earlier.
Obesity is thus the most common nutritional-metabolic disor-
der among patients undergoing surgery. The disorder is both
defined and graded by comparison of actual weight with an
accepted index of ideal body weight. The currently accepted
standard for making this comparison is the calculation of body
mass index (Table 4-2). Patients with a body mass index
greater than 30 are considered clinically obese; a body mass
index greater than 40 defines the state of morbid obesity.
Providing a safe anesthesia experience to a morbidly obese
patient undergoing major surgery is among the most difficult
tasks anesthesiologists face. The anesthetic challenges that
obese patients present, and their perioperative risks, vary in
proportion to the severity of the disorder. The anesthetic
risks of obesity are caused by technical difficulties imposed
Technical Difficulties
Even mildly obese patients pose challenges to the anesthesi-
ologist. Standard procedures that are often taken for granted in
slender patients can be more difficult in mildly to moderately
obese patients. These include placement of peripheral intrave-
nous infusion lines, noninvasive blood pressure monitoring,
moving and positioning patients on the operating table, laryn-
goscopy and tracheal intubation, and use of regional anesthetic
techniques, all of which can be sufficiently problematic to re-
quire advance planning and the use of alternative techniques
(e.g., venous cutdown or central venous access, intra-arterial
catheters, awake fiberoptic laryngoscopy).
Cardiovascular Derangements
Compared with patients of normal weight, obese patients are
at increased risk of coronary artery and peripheral vascular
disease, and anesthesiologists must be prepared to manage
these problems perioperatively. Moreover, chronic obesity
produces a characteristic series of hemodynamic abnormali-
ties. Termed the cardiomyopathy of obesity, the syndrome in-
cludes a high–cardiac output state, systemic and pulmonary
hypertension, and cardiac hypertrophy that can lead to bi-
ventricular dilation and cardiac failure.
The pathophysiology of this syndrome relates to the pres-
ence of the large, metabolically active adipose mass. Al-
though adipose tissue is less vascular on a per weight basis
than lean tissue (blood flow, 2 to 3 mL/100 g/minute), a
morbidly obese patient weighing 50 kg more than ideal body
weight has a cardiac output 1.5 to 2 L/minute greater than
normal, with an accompanying increase in total circulating
volume (preload). In addition, the metabolic demands cause
chronically elevated sympathetic tone (afterload) and in-
creased global oxygen demand. This is often not met by an
increase in oxygen supply because of concurrent pulmonary
dysfunction, and the chronic hypoxemia that is highly preva-
lent in obesity increases pulmonary vascular resistance. The
ultimate result is biventricular heart failure.
Evidence indicates that the same factors that combine to
produce the cardiomyopathy of obesity also predispose
obese individuals to a 50% higher risk of new-onset atrial
fibrillation, compared with their nonobese counterparts.
When this arrhythmia occurs during anesthesia, manage-
ment of the hemodynamic derangements of obese patients
becomes that much more complicated.
Pulmonary Derangements
Abnormalities involving the respiratory system can be severe in
obesity and often represent the most difficult aspect of anes-
thetic care. Four main categories of pulmonary dysfunction
Hypoxemia
Chronic hypoxemia is ubiquitous in obesity. As with the other
types of pulmonary dysfunction that characterize the syn-
drome, two features are typical. First, the degree of hypoxemia
correlates with the degree of obesity and is significantly worse
in patients with obstructive sleep apnea syndrome. Second,
the hypoxemia that exists preoperatively as a baseline state in
obesity is exaggerated by recumbency, exposure to anesthetics
and sedatives, and the effects of surgery.
The pathophysiology of the hypoxemia of obesity can be
considered an exaggeration of the “normal pathophysiology” of
the respiratory system. This statement is meant to imply that
even in physiologically normal individuals, the lungs are imper-
fect gas exchangers (although they function quite well). During
anesthesia and surgery, particularly thoracic or abdominal sur-
gery, these imperfections become magnified and functionally
more significant. In obesity, this pattern becomes extreme.
The abnormalities of respiratory gas exchange relate to the
fundamental relationship between the functional residual
capacity (FRC) of the lungs and their closing capacity
(CC) and the way in which this relationship changes during
anesthesia and surgery. The FRC is the volume of the lungs at
end-expiration, when there is equilibrium of forces favoring
expansion and contraction of lung tissue. The CC is that
volume, ordinarily less than FRC, at which the forces of con-
traction gain priority and small airways begin to close. Any
circumstances that tend to decrease the difference between FRC
and CC favor atelectasis and consequently cause hypoxemia.
In physiologically normal individuals, the FRC is known to
be progressively reduced by the following: (1) supine posture,
as a result of redistribution of abdominal contents and pres-
sure on the inferior surface of the diaphragm; (2) anesthetic
agents and muscle relaxants, which cause a further cephalic
Initial upright
position of
diaphragm
Pab
↓ FRC
Supine
position
Surgical position
and displacement Induction of
anesthesia
Paralysis
Figure 4-3 • Progressive reduction in functional residual capacity (FRC)
resulting from displacement of the diaphragm during anesthesia and surgery. Pab,
pressure of abdominal contents. (From Benumof JL: Respiratory physiology and res-
piratory function during anesthesia. In Miller RD [ed]: Anesthesia, 3rd ed. New York,
Churchill Livingstone, 1990, p 535.)
Regional Anesthesia
Regional anesthetic techniques are often advocated as a
means of circumventing the perioperative cardiopulmonary
sequelae seen in obesity. Unfortunately, in obese patients re-
gional anesthesia has its own unique problems that can
greatly limit its benefit.
First, several inches of subcutaneous tissue may overlie
normal landmarks (e.g., spinous processes) and may thus
make it completely impossible to perform regional anesthesia,
regardless of its apparent advantage. Second, with spinal or
epidural anesthesia, the normal dose-response relationships
that enable the prediction of a given level of sensory blockade
are distorted in obesity, and patients can experience an abnor-
mally high sensory and motor block. The resulting intercostal,
and occasionally even diaphragmatic, weakness can pro-
foundly exacerbate the underlying pulmonary dysfunction
present in these patients. Third, because the sensory supply of
the abdominal and thoracic viscera is through the autonomic
nervous system, it is nondiscrete and nonsegmental; this dis-
tinctly contrasts with the sensory innervation of the extremi-
ties and body wall. An accepted tenet in anesthetic manage-
ment is that the more rostral the site of surgery within the
abdomen, the less adequate will be the sensory block obtained
with regional anesthesia. Consequently, the surgical procedure
itself may invalidate the use of regional techniques, regardless
of the presence of obesity.
Finally, it is extremely difficult for any patient to lie mo-
tionless, often in an awkward position, on an operating table
for several hours with the knowledge that surgery is ongoing.
Added to this is the physical and emotional discomfort of feel-
ing “deafferented” from the waist or chest down, accompa-
nied by pharmacologically induced paraplegia. Thus, the
need to provide intravenous sedation to patients during
regional anesthesia cannot be overemphasized. Although this
Summary
The evaluation and perioperative management of obese pa-
tients undergoing surgery can be complex. From the forego-
ing discussion, certain guidelines are suggested (Table 4-4).
Postoperative Immobility
Not all patients who exhibit a profound lack of movement dur-
ing postanesthetic recovery have CNS depression. In the ab-
sence of exposure to anesthesia, findings such as no purposeful
or reflex movements and absent or significantly diminished
spontaneous ventilation raise the likelihood of stupor or coma.
By contrast, in the recovery room the possibility exists that a
patient with these symptoms may be suffering from profound
residual muscle weakness related to unexpectedly prolonged
neuromuscular blockade. Resembling myasthenic crisis, the
sensorium may be relatively intact.
This assessment is readily made by use of a peripheral
nerve stimulator, one of the standard monitoring devices
commonly employed during general anesthesia. This device
delivers a series of supramaximal stimuli to motor nerves
(typically the ulnar nerve at the wrist), and an elicited twitch
response is evaluated. Standard patterns of stimulation in-
clude the train-of-four, in which four such stimuli are deliv-
ered at a frequency of two per second, and a tetanic stimulus
at 50 Hz. In both cases, patients should exhibit a normal
response that is sustained without loss of amplitude (“fade”).
Peripheral nerve stimulators should be readily available in
any recovery area, and their use is mandatory in the assess-
ment of such patients.
Reexamination of Risk
Concomitant with the reduction in the frequency of pulmo-
nary aspiration has been an evolution in an understanding
of the relationship between the composition of gastric con-
tents and the risk of acid aspiration syndrome. The rarity of
pulmonary aspiration during anesthesia, the large sample
size needed to make statistically significant observations,
and ethical concerns have hampered research into the risk
of anesthesia-related aspiration. Designing a statistically
valid study of the various risk factors for this complication
Clinical Data
The debate about the validity of an 8-hour preoperative fast
is accompanied by the recognition that this duration is fre-
quently uncomfortable for patients and frustrating for those
Contemporary Guidelines
In summary, the reappraisal of historical precepts relating to
preoperative fasting and the abundance of contemporary
clinical data have failed to support the validity of a pro-
longed, all-inclusive preoperative fast (i.e., for solids and
clear liquids). A growing awareness of this fact has inspired
a gradual alteration in anesthetic practice nationwide.
In recognition of the need for an evidence-based analysis
to address the evolution in clinical practice regarding preop-
erative fasting, the ASA organized a Task Force on Preopera-
tive Fasting and the Use of Pharmacologic Agents to Reduce
the Risk of Pulmonary Aspiration. The task force’s guidelines,
published in 1999, are summarized in Table 4-10. Although
efforts have been made to determine the extent to which the
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of pharmacologic agents to reduce the risk of pulmonary aspiration: Ap-
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Biring MS, Lewis MI, Liu JT, et al: Pulmonary physiologic changes of morbid
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Candido KD, Stevens RA: Post-dural puncture headache: Pathophysiology,
prevention and treatment. Best Pract Res Clin Anaesthesiol 17:451-469,
2003.
Cheney FW, Domino KB, Caplan RA, et al: Nerve injury associated with
anesthesia: A closed claims analysis. Anesthesiology 90:1062-1069,
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Ogunnaike BO, Jones SB, Jones DB, et al: Anesthetic considerations for
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Parikh SS, Chung F: Postoperative delirium in the elderly. Anesth Analg
80:1223-1232, 1995.
Peyton PJ, Myles PS, Silbert BS, et al: Perioperative epidural analgesia and
outcome after major abdominal surgery in high-risk patients. Anesth Analg
96:548-554, 2003. A
Phillips S, Hutchinson S, Davidson T: Preoperative drinking does not affect
gastric contents. Br J Anaesth 70:6-9, 1993.
Rasmussen LS, Johnson T, Kuipers HM, et al: Does anaesthesia cause post-
operative cognitive dysfunction? A randomised study of regional versus
general anaesthesia in 438 elderly patients. Acta Anaesthesiol Scand
47:260-266, 2003.
Ray CS, Sue DY, Bray G, et al: Effects of obesity on respiratory function.
Am Rev Respir Dis 128:501-506, 1983.
Read MS, Vaughan RS: Allowing pre-operative patients to drink: Effects on
patients’ safety and comfort of unlimited oral water until 2 hours before
anaesthesia. Acta Anaesthesiol Scand 35:591-595, 1991.
Rigg JRA, Jamrozik K, Myles PS, et al: Epidural anaesthesia and analgesia and
outcome of major surgery: A randomised trial. Lancet 359:1276-1282,
2002. A
Rosenberg H, Clofine R, Bialik O: Neurologic changes during awakening from
anesthesia. Anesthesiology 54:125-130, 1981.
Roth S, Thisted RA, Erickson JP, et al: Eye injuries after nonocular surgery:
A study of 60,965 anesthetics from 1988 to 1992. Anesthesiology
85:1020-1027, 1996.
Sarr MG, Felty CL, Hilmer DM, et al: Technical and practical considerations
involved in operations on patients weighing more than 270 kg. Arch
Surg 130:102-105, 1995.
Tuman KJ, McCarthy RJ, March RJ, et al: Effects of epidural anesthesia and
analgesia on coagulation and outcome after major vascular surgery.
Anesth Analg 73:696-704, 1991.
Warner MA, Warner DO, Matsumoto JY, et al: Ulnar neuropathy in surgical
patients. Anesthesiology 90:54-59, 1999.
Warner MA, Warner ME, Weber JG: Clinical significance of pulmonary as-
piration during the perioperative period. Anesthesiology 78:56-62,
1993.
Williams-Russo P, Sharrock NE, Mattis S, et al: Cognitive effects after epi-
dural vs general anesthesia in older adults. A randomized trial. JAMA
274:44-50, 1995.
Yeager MP, Glass DD, Neff RK, et al: Epidural anesthesia and analgesia in
high-risk surgical patients. Anesthesiology 66:729-736, 1987.
ETIOLOGY
The triad of stasis, intimal injury, and hypercoagulability
contributes to thrombosis, DVT, and PE. This section dis-
cusses the secondary risk factors that enhance this triad.
The first component of the triad, stasis, results from supine
positioning and the effects of anesthesia. Stasis causes venous
91
1. Surgery
2. Trauma (major or lower extremity)
3. Immobility, paresis
4. Malignant disease
5. Cancer therapy (hormonal therapy, chemotherapy, or
radiotherapy)
6. Previous deep vein thrombosis or pulmonary embolism
7. Increasing age
8. Pregnancy and the postpartum period
9. Estrogen-containing oral contraceptives or hormone
replacement therapy
10. Selective estrogen-receptor modulators
11. Acute medical illness
12. Heart or respiratory failure
13. Inflammatory bowel disease
14. Nephrotic syndrome
15. Myeloproliferative disorders
16. Paroxysmal nocturnal hemoglobinuria
17. Obesity
18. Smoking
19. Varicose veins
20. Central venous catheters
21. Inherited or acquired thrombophilia
Modified from Geerts WH, Pineo GF, Heit JA, et al: Prevention of venous thrombo-
embolism. Chest 126:338S-400S, 2004. Copyright 2004 by the American College of
Chest Physicians. Reproduced with permission of the American College of Chest Physi-
cians in the format Textbook via Copyright Clearance Center.
PROPHYLAXIS MODALITIES
At present, there are seven recognized modalities for DVT
and PE prophylaxis. In this section, each modality is re-
viewed with respect to dose, administration, length of ther-
apy, and adverse reactions.
Heparin (Unfractionated Heparin)
Fixed-Dose Heparin
Heparin is administered subcutaneously at 5000 U 2 hours
before surgery. This is followed postoperatively by adminis-
tration of 5000 U subcutaneously every 8 to 12 hours until
the patient is discharged (Box 5-2). In double-blind trials, the
incidence of major hemorrhagic events was 1.8% versus 0.8%
METHOD 1
• 10 mg by mouth the evening before surgery
• 5 mg by mouth the evening of surgery
• Adjust dose daily based on an INR of 2 to 3
• Maintain warfarin until discharge
METHOD 2
• 10 mg by mouth the evening of surgery
• No warfarin on postoperative day 1
• On postoperative day 2, begin warfarin to adjust INR to
2 to 3
• Maintain warfarin until discharge
General Surgery
The incidence of DVT in general surgery has been docu-
mented to be 20% to 30%. These studies evaluated a wide
age group of patients undergoing a variety of procedures.
The recommended prophylactic agents, in order of prefer-
ence, are heparin, LMWH, and external pneumatic com-
pression stockings. In high-risk general surgery, low-dose
subcutaneous heparin or LMWH should be used. In very
high-risk general surgery, low-dose unfractionated or LMWH
should be combined with external pneumatic compression
sleeves (Table 5-6).
SC, subcutaneously.
Heparin-Induced Thrombocytopenia
Heparin-induced thrombocytopenia is the most frequent and
important hematologic drug reaction that occurs secondary
to an immunologic mechanism. In 12 prospective studies of
more than 1500 patients receiving heparin, pooled data re-
vealed a frequency of thrombocytopenia of 6% and an inci-
dence of thrombocytopenia with arterial thrombosis of less
than 1%. This latter form is the most severe clinically. Porcine
heparin is associated with a lower incidence of thrombocyto-
penia than is bovine heparin. The development of thrombo-
cytopenia is independent of the route of administration and
occurs between 6 and 12 days after initiation of therapy. In
patients with a previously documented episode of thrombo-
cytopenia or thrombocytopenia with arterial thrombosis, re-
exposure to heparin results in a faster onset of the process.
Because heparin-induced thrombocytopenia and its recur-
rence cannot be predicted, the surgical patient with a history
of this disorder, with or without thrombosis, should have an
alternative form of prophylaxis for DVT and PE, as discussed
previously for different types of surgical procedures. Although
heparin antibodies may be absent 90 days after cessation of
heparin, I avoid the repeat use of unfractionated heparin or
LMWH in the patient with a prior history of heparin-induced
thrombocytopenia. Currently, studies are being conducted
with fondaparinux as an agent for VTE prophylaxis in patients
with heparin-induced thrombocytopenia because of the low
affinity of this agent for binding to platelet factor IV and the
theoretically lower risk of precipitating an antibody response.
Selected Readings
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(enoxaparin) as prophylaxis against venous thromboembolism after total
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Caprini J, Scurr J, Hasty J: Role of compression modalities in a prophylactic
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Clagett G, Reisch J: Prevention of venous thromboembolism in general sur-
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Cohen AT, Bailey CS, Alikhan R, et al: Extended thromboprophylaxis with
low molecular weight heparin reduces symptomatic venous thromboem-
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Douketis JD, Eikelboom JW, Quinlan DJ, et al: Short duration prophylaxis
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meta-analysis of prospective studies investigating symptomatic out-
comes. Arch Intern Med 162:1465-1471, 2002.
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lism. Chest 126:338S-400S, 2004.
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Hirsh J, Levine M: Low molecular weight heparin. Blood 79:1-17, 1992.
Hull R, Raskob G, McLoughlin D, et al: Effectiveness of intermittent pneu-
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Kelton J, Levine M: Heparin induced thrombocytopenia. Semin Thromb
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Much J, Herbst K, Rapaport S: Thrombosis in patients with lupus antico-
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Nicolaides A, Fareed J, Kakkar A, et al: Prevention and treatment of venous
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Virchow R: Neuer fall von todlichen: Emboli der Lungenarterie. Arch Pathol
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Wilson N, Das S, Kakkar V, et al: Thromboembolic prophylaxis in total knee
replacement: Evaluation of the A-V impulse system. J Bone Joint Surg Br
74:50-52, 1992.
ANEMIA
Anemia is the most commonly encountered hematologic prob-
lem in the perioperative period. Because the major function of
red blood cells is to facilitate oxygen transport to tissues, a suf-
ficient number of red blood cells is crucial to provide adequate
oxygenation. Given that additional factors such as cardiac
output, pulmonary gas exchange, vessel compliance, blood
volume, blood viscosity, and oxygen affinity for hemoglobin
contribute to oxygen delivery, the level of hemoglobin itself
serves only as a rough guide to the adequacy of oxygenation.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed syste-
matic reviews of RCTs. B —Case-control or cohort studies, nonrandomized
controlled trials, systematic reviews of studies other than RCTs, cross-sectional
studies, retrospective studies. C —Consensus statements, expert guidelines, usual
practice, opinion.
117
High Low
Therapeutic Considerations
The physiologic needs of the patient must be carefully as-
sessed. The clinician must consider all the previous determi-
nants of tissue oxygenation, as well as the consequences of the
planned operative procedure, before making a decision to
administer red blood cells. When the procedure is elective, it
seems prudent to delay surgery, complete the evaluation, and
treat the underlying problem (if indicated) to avoid the poten-
tial hazards of transfusion. Because reversal of “correctable”
anemia (deficiency of vitamin B12, folate, or iron; transient
bone marrow suppression; uremia; and immune hemolysis)
may take days to weeks, blood transfusion may be the only
recourse if surgery is urgently needed. Similarly, “uncorrect-
able” anemia (myelodysplasia, chronic disease, or thalassemia)
requires blood transfusion.
Patients who do need blood transfusion are often con-
cerned about the potential risks associated with blood prod-
ucts. The following list contains recent estimates of the fre-
quency of various transfusion-related complications that
indicate the safety of the modern blood supply.
Alloimmunization 1:100
Fever, chill, allergic reactions 1:30 to 1:200
Acute hemolysis 1:12,000 to
1:25,000
Delayed hemolysis 1:5,000 to
1:11,000
Immunosuppression Unknown
Bacterial infection 1:200,000
Hepatitis B infection 1:137,000
Hepatitis C infection 1:1,000,000
Human immunodeficiency virus infection 1:1,900,000
Management of patients who refuse blood transfusion
poses significant issues. Generally, primary blood components
are declined, but the use of blood “fractions” such as immune
globulin or albumin or the use of intraoperative blood salvage
or normovolemic hemodilution may be acceptable to some
patients who would otherwise refuse blood transfusion. Gen-
eral guidelines for management of these patients include the
following: maintenance of blood volume; limitation of phle-
botomy as much as possible; use of folate, iron, and epoetin to
enhance erythropoiesis; use of pharmacologic agents to reduce
blood loss (antifibrinolytics, recombinant factor VIIa); and
consideration of intraoperative blood salvage.
Preoperative donation of autologous blood for elective
procedures has become common practice. If more than 1 U
of red cells is required, use of epoetin alfa and iron supple-
ments can allow for the collection of as much as 3 to 4 U in
a month. Epoetin doses of 50 U/kg to 150 U/kg three times
per week have been used.
ERYTHROCYTOSIS
Preoperative Considerations
As with anemia, the major physiologic consequence of eryth-
rocytosis is tissue hypoxemia. The mechanism by which
this occurs is through a marked increase in blood viscosity,
leading to slowing of capillary blood flow. Although the vis-
cosity of blood is directly proportional to the hematocrit, the
Preoperative Evaluation
In the presence of elevated leukocyte and platelet counts and
splenomegaly, the diagnosis of polycythemia vera is virtually
ensured if the red blood cell mass is increased and the patient
has no severe cardiopulmonary disease (Fig. 6-2). If only
erythrocytosis is present, the diagnosis centers on the careful
evaluation of cardiopulmonary function. In the absence of
cardiopulmonary disease or obvious plasma volume deple-
tion, determination of red blood cell mass may be helpful but
certainly is not necessary to make a diagnosis, particularly if
the hematocrit is markedly elevated (⬎55%). The recent dis-
covery of a mutation in the JAK-2 gene in virtually all patients
with polycythemia vera may aid in diagnosis as well.
Therapeutic Considerations
In addition to the indications for phlebotomy given in Box 6-1,
considerations in the treatment of erythrocytosis are as
follows:
1. In the case of relative erythrocytosis resulting from sig-
nificant volume depletion, replacement of plasma volume
is all that may be necessary to minimize risk.
2. No intervention is necessary in patients with stress
erythrocytosis.
Low Normal
"Relative"
dehydration Red cell mass
"Third spacing"
Normal High
"Stress"
Cardiopulmonary
assessment
Normal Abnormal
"Appropriate"
Primary Secondary
Polycythemia vera Renal cyst
Tumors
High-affinity hemoglobin
Figure 6-2 • Evaluation of erythrocytosis.
LEUKOPENIA
Preoperative Considerations
Leukopenia is occasionally encountered in patients in the
perioperative period. It can occur as a manifestation of a pri-
mary hematologic disorder but is more often secondary to
nonhematologic causes. The most important consideration is
the increased risk of infection in these patients. Neutrophil
counts greater than 1000/L are rarely associated with a
Preoperative Evaluation
The diagnostic evaluation should begin with the identification
of the type of leukocyte that is low (Table 6-3). Although most
commonly this is the neutrophil, less frequently monocyte or
lymphocyte levels can be depressed. The most clinically signifi-
cant type of leukopenia is related to depressed numbers of
neutrophils. Neutropenia has many causes; however, most
cases are related to exposure to drugs or radiation. Neutropenia
related to radiation or cytotoxic antineoplastic agents is the
result of predictable and dose-dependent toxicity to stem cells
and granulocytic precursors. Other classes of drugs associated
with neutropenia are phenothiazines, anti-inflammatory agents
(particularly phenylbutazone), sulfonamides, semisynthetic
penicillins, chloramphenicol, and antithyroid drugs. In general,
the most common mechanism is idiosyncratic bone marrow
suppression. Some drugs may also have an immune compo-
nent. Other common causes of neutropenia are congenital
neutropenia, myelodysplasia, sepsis, viral or rickettsial infec-
tion, Felty’s syndrome, and systemic lupus erythematosus.
Therapeutic Considerations
If the cytopenia is related to predictable bone marrow suppres-
sion from antineoplastic agents or radiation, recovery usually
begins 14 to 21 days after exposure. When the cytopenia
LEUKOCYTOSIS
Preoperative Considerations
Leukocytosis is usually an indicator of an underlying inflam-
matory, infectious, or neoplastic process. Although lymphocy-
tosis is most often associated with chronic lymphatic leuke-
mia, neutrophilia or monocytosis of modest degree is most
frequently associated with inflammation or infection. Marked
elevation in the neutrophil and monocyte count raises the
possibility of chronic leukemia. Moderate leukocytosis, in-
volving mature white cells, carries no significant increase in
perioperative risk. In most situations, leukocytosis requires
no specific therapy except that of the underlying disorder. If
THROMBOCYTOSIS
Thrombocytosis is present when the platelet count is higher
than 500,000/L. The major complications associated with
an elevated platelet count are thrombosis and, to a lesser
degree, hemorrhage. The magnitude of the risk varies con-
siderably with the underlying disorder.
Preoperative Considerations
For the purpose of assessing risk, thrombocytosis can be
divided into two broad categories (Box 6-2). Primary throm-
bocytosis is generally regarded as a manifestation of one of
the myeloproliferative disorders (polycythemia vera, essential
thrombocythemia, chronic myeloid leukemia, or myeloid
metaplasia). Within the myeloproliferative disorders, risk var-
ies widely. Thrombocytosis associated with chronic myeloid
leukemia carries a low risk of thrombosis or hemorrhage.
THROMBOHEMORRHAGIC RISK
Box 6-2
ASSOCIATED WITH THROMBOCYTOSIS
PRIMARY
Polycythemia vera: Thrombosis common, hemorrhage less
common
Essential thrombocythemia and myeloid metaplasia: Hemor-
rhage common, thrombosis less common
Chronic myelogenous leukemia: Bleeding and thrombosis un-
common
SECONDARY
Nonmalignant: No risk
Malignant: Increased risk but not clearly related to platelets
Preoperative Evaluation
The diagnostic evaluation should focus on symptoms and
signs of thrombosis, mucosal hemorrhage, acute or chronic
bleeding, anemia, infection, and inflammatory disorders or
neoplasms. Additional laboratory studies may be helpful in
the evaluation. Erythrocytosis and leukocytosis associated
with splenomegaly are signs of polycythemia vera. The char-
acteristic leukocytosis with a leftward shift and splenomegaly
indicate a probable diagnosis of chronic myeloid leukemia.
Iron deficiency should prompt an evaluation for gastrointes-
tinal or genitourinary abnormalities. Appropriate studies to
exclude infection are indicated if the situation suggests an
infectious cause. If no obvious underlying disorder is found,
essential thrombocythemia, which is usually a diagnosis of
exclusion, is often the problem, especially in patients who
have a history of unexplained thrombosis or hemorrhage.
Therapeutic Considerations
In general, patients with secondary or reactive thrombocyto-
sis require no specific therapy to lower the platelet count.
Successful treatment of the underlying disorder often results
in normalization of the platelet count. Even if the platelet
count remains high, there is no substantial increase in throm-
bohemorrhagic risk.
Thrombocytosis associated with chronic myeloid leuke-
mia usually does not require specific therapy, although stan-
dard therapy with busulfan, hydroxyurea, interferon alfa, or
imatinib usually lowers the platelet count. Uncontrolled
polycythemia vera is associated with significant perioperative
risk. It is not completely clear to what degree this risk
depends on the erythrocytosis or the thrombocytosis. Efforts
should be made to normalize the platelet count in patients
with polycythemia vera who have a hematocrit less than
45%, thrombocytosis, and a history of thrombohemorrhagic
events. In addition, older patients or those with significant
vascular disease may be more prone to problems and are
likely to benefit from lowering the platelet count.
The principles of therapy for essential thrombocythemia
include lowering the platelet count in older and sicker pa-
tients who have had prior vascular events. The most effective
method of lowering the platelet count is with the use of
anagrelide or cytotoxic chemotherapy such as hydroxyurea,
although it may take days or weeks for a platelet response to
occur. If immediate platelet reduction is required, platelet-
pheresis, along with the use of cytotoxic agents, is effective in
reducing the count to normal levels. Aspirin is rarely indi-
cated in the perioperative therapy of average patients with
thrombocytosis because it can lead to an increase in hemor-
rhagic phenomena. Patients younger than 60 years old, who
are nonsmokers, who have no cardiac risk factors, and
who have no history of thrombosis typically do not require
platelet-lowering therapy before minor surgical procedures if
their platelet counts are less than 1,500,000/L.
HEMOSTASIS
Hemostasis is crucial to both the patient and the surgeon
during surgical procedures. Without adequate function of
the hemostatic system, even the most trivial procedure can
quickly result in life-threatening hemorrhage. Because the
hemostatic system plays an important role in the ability to
perform surgery safely, a basic understanding of the physiol-
ogy of blood clotting is essential to assess potential abnor-
malities and to select appropriate therapy.
Preoperative Considerations
Hemostasis is a complex ongoing process involving precise
interactions among connective tissue, blood vessels, endothe-
lial cells, platelets and other formed elements of the blood, the
soluble coagulation factors, the natural anticoagulant and
fibrinolytic substances, and exogenous drugs. Figure 6-3
shows the coagulation scheme with anticoagulant mecha-
nisms. The process of coagulation can be arbitrarily divided
into several stages (Box 6-3). The initial stage is damage to the
vessel wall. The second stage involves primary vasoconstric-
tion. The third stage involves binding of von Willebrand factor
to the subendothelium to facilitate platelet adhesion. Platelet
XII
Intrinsic Extrinsic
(PTT) (PT)
XI
VIII
IX VII
Common
X
Protein S V
Protein C Thrombin
Antithrombin III XIII tPA
Anticoagulant Fibrin
Plasmin
FSP
Fibrinolytic
Preoperative Evaluation
Abnormalities anywhere in the coagulation pathway can re-
sult in abnormal hemostasis. Various laboratory studies help
to identify defects in particular stages of the process. The
platelet count is a straightforward measure of an important
component of the system. The bleeding time is most sensitive
to abnormalities in the subendothelial matrix, von Wille-
brand protein, and qualitative and quantitative disorders of
platelets. The partial thromboplastin time (PTT) and the
prothrombin time (PT) test the intrinsic and extrinsic path-
ways, respectively, whereas the thrombin time assesses the
clotting ability of fibrinogen. Fibrin split products are an in-
direct indication of fibrinolytic activation.
The most important component of the evaluation of he-
mostatic function is a careful history [} A Houry et al, 1995].
Nearly all potential hemostatic problems can be uncovered
through careful questioning, although definition of the prob-
lem may require extensive laboratory evaluation. Several areas
should be stressed in all patients, including unusual bleeding
with prior trauma or surgery, episodes of spontaneous bleeding
or thrombosis, a family history of bleeding or thrombosis,
nutritional habits, drug ingestion, and other medical problems,
particularly hepatic or renal disease. Tooth extraction, an
“operation” most individuals have undergone, poses the same
hemostatic challenge as a major abdominal procedure. Occa-
sionally, unsuspected findings on the physical examination will
alert the consultant to the presence of potential bleeding prob-
lems. The findings include jaundice, petechiae, ecchymoses,
adenopathy, hepatomegaly, and splenomegaly.
HISTORY
BT, bleeding time; PLT, platelet count; PT, prothrombin time; PTT, partial
thromboplastin time.
Therapeutic Considerations
Thrombocytopenia
Thrombocytopenia is defined as a platelet count less than
150,000/L. The risk of bleeding varies inversely with the
platelet count, assuming that no functional platelet defect is
present. A platelet count greater than 100,000/L should be
adequate for all surgical procedures. There should be no signi-
ficant increase in bleeding for most low- or moderate-risk
Hemophilia B
The management of hemophilia B, or factor IX deficiency, is
similar to the treatment of hemophilia A. Several distinctions
are worth noting, however. The volume of distribution of
Liver Disease
Patients with liver disease have multiple coagulation disor-
ders, including thrombocytopenia, platelet function abnor-
malities, malabsorption of the fat-soluble vitamin K, and
hepatocellular dysfunction leading to abnormal synthesis of
clotting factors, decreased clearance of activated clotting fac-
tors, and dysfibrinogenemia. Most patients with liver disease
should have preoperative screening tests, including PT, PTT,
fibrinogen levels, and thrombin time. Although the most
common hematologic complication of severe liver disease is
bleeding, these patients may be at increased risk for throm-
bosis or DIC because of abnormal hepatic clearance of acti-
vated clotting factors.
Management of these patients is frequently difficult. It is
reasonable to administer 10 mg of vitamin K parenterally to
any patient with a prolonged PT, although only patients with
biliary obstruction or malnutrition are likely to respond. For
patients with predominantly hepatocellular disease, the pre-
ferred therapy is fresh frozen plasma, which should be given
at a dose of 10 to 20 mL/kg to bring the PT to within 2 to
3 seconds of the control value. Because of rapid consumption
of clotting factors, it may be necessary to administer additional
plasma every few hours, with serial PTs used as a guide.
Platelet transfusion can be useful, particularly in patients
with bone marrow suppression. The treatment is somewhat
less effective in patients with hypersplenism and may be of
some value in patients with prolonged bleeding times.
Postoperative Bleeding
Bleeding in the postoperative period may have numerous
causes. Unmasking of a previously unsuspected bleeding dis-
order such as von Willebrand disease or thrombocytopenia
can occur. Drug-related thrombocytopenia, acquired platelet
function defects, and abnormal clotting factors resulting from
malabsorption or starvation are occasionally noted. Other fac-
tors to consider are DIC resulting from sepsis, transfusion
reactions, or tissue damage. Dilutional coagulopathies may be
caused by inadequate perioperative blood component re-
placement, particularly in the massively transfused patient.
Bleeding may also be related to the use of anticoagulant drugs
or inadequate surgical hemostasis in the wound.
A low platelet count is most often seen acutely in associa-
tion with inadequate replacement during operations in which
there is massive blood loss, in DIC resulting from transfusion
reaction, or in association with drug toxicity. In a less acute
setting, hours to days postoperatively, sepsis and drug-
related causes are most common.
Prolonged bleeding time in the postoperative period is
most often caused by thrombocytopenia, uremia, or platelet
dysfunction after cardiopulmonary bypass. A prolonged PT
is typically seen in association with nutritional deficiency of
vitamin K, prolonged administration of antibiotics, DIC, or
liver disease. A prolonged PTT is usually the result of nutri-
tional deficiency, DIC, or occult von Willebrand disease. Fi-
brinogen levels are rarely low in any disorder other than se-
vere DIC. Fibrin split products may be elevated postoperatively
for various reasons, including DIC, heparin administration,
the usual postoperative lysis of hematomas, and significant
venous thrombosis.
Postoperative bleeding must be evaluated quickly and ef-
ficiently (Box 6-5). A thorough history and physical exami-
nation are crucial, with attention paid to all factors described
in the preoperative evaluation of hemostatic function. In
addition, the clinical characteristic of bleeding may suggest a
BT, bleeding time; PLT, platelet count; PT, prothrombin time; PTT, partial throm-
boplastin time.
Selected Readings
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nent therapy: A report by the American Society of Anesthesiologists Task
Force on Blood Component Therapy. Anesthesiology 84:732-747, 1996.
Armas-Loughran B, Kalra R, Carson JL: Evaluation and management of
anemia and bleeding disorders in surgical patients. Med Clin North Am
87:229-242, 2003.
Carson JL: Morbidity risk assessment in the surgically anemic patient.
Am J Surg 170(Suppl 6A):32S-36S, 1995.
Charache S: Treatment of sickle cell anemia. Annu Rev Med 32:195-206,
1981.
Eschbach JW, Abdulhadi MH, Browne JK, et al: Recombinant human erythro-
poietin in anemic patients with end stage renal disease: Results of a phase
III multicenter clinical trial. Ann Intern Med 111:992-1000, 1989.
Grounds M: Recombinant factor VIIa (rFVIIa) and its use in severe bleeding
in surgery and trauma: A review. Blood Rev 17:S11-S21, 2003.
Hardy J, De Moerloose P, Samama M, et al: Massive transfusion and coagu-
lopathy: Pathophysiology and implications for clinical management. Can
J Anaesth 51:293-310, 2004.
Houry S, Georgeac C, Hay JM, et al: A prospective multicenter evaluation
of preoperative hemostatic screening tests. Am J Surg 170:19-23,
1995. A
Martlew VJ: Perioperative management of patients with coagulation disor-
ders. Br J Anaesth 84:446-455, 2000.
McKenna R: Abnormal coagulation in the postoperative period contributing
to excessive bleeding. Med Clin North Am 85:1277-1310, 2001.
Nash MJ, Cohen H: Management of Jehovah’s Witness patients with haema-
tological problems. Blood Rev 18:211-217, 2004.
National Institutes of Health: Consensus conference: Perioperative red blood
cell transfusion. JAMA 260:2700-2703, 1988.
Patel T: Surgery in the patient with liver disease. Mayo Clin Proc 74:
593-599, 1999.
Rauck R: The anticoagulated patient. Reg Anesth 21(Suppl):51-56, 1996.
Rodgers RP, Levin J: A critical appraisal of the bleeding time. Semin Thromb
Hemost 16:1-20, 1990.
Rosse WF: Clinical management of adult ITP prior to splenectomy: A per-
spective. Blood Rev 16:47-49, 2002.
Samama CM, Bastien O, Forestier F, et al: Antiplatelet agents in the periope-
rative period: Expert recommendations of the French Society of Anesthesi-
ology and Intensive Care (SFAR) 2001—summary statement. Can J
Anaesth 49:S26-S35, 2002.
Smetana GW, Macpherson DS: The case against routine preoperative labora-
tory testing. Med Clin North Am 87:7-40, 2003.
Spahn D: Perioperative transfusion triggers for red blood cells. Vox Sang
78(Suppl 2):163, 2000.
Spence RK: Surgical red blood cell transfusion practice policies: Blood Man-
agement Practice Guidelines Conference. Am J Surg 170(Suppl 6A):
3S-15S, 1995.
Tefferi A, Murphy S: Current opinion in essential thrombocythemia: Patho-
genesis, diagnosis, and management. Blood Rev 15:121, 2001.
Vichinsky EP, Haberkern CM, Neumayr L, et al: A comparison of conserva-
tive and aggressive transfusion regimens in the perioperative manage-
ment of sickle cell disease: The Preoperative Transfusion in Sickle Cell
Disease Study Group. N Engl J Med 333:206-213, 1995.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized clinical
trials, systematic reviews of studies other than RCTs, cross-sectional studies, ret-
rospective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
157
157
Ch07-X2385_157_248.indd 162
1 MET Can you take care of yourself? 4 METs Climb a flight of stairs or walk up a hill?
Eat, dress, or use the toilet? Walk on level ground at 4 mph or 6.4 km per h?
Walk indoors around the house? Run a short distance?
Walk a block or two on level ground
at 2 to 3 mph or 3.2 to 4.8 km per h? Do heavy work around the house like
scrubbing floors or lifting or moving heavy
Do light work around the house like furniture?
4 METs dusting or washing dishes?
Participate in moderate recreational activities
like golf, bowling, dancing, doubles tennis, or
throwing a baseball or football?
Figure 7-1 • Duke activity scale. MET, metabolic equivalent. (From Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA guidelines on periop-
erative cardiovascular evaluation and care for noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force
on Practice Guidelines [Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery]. J Am Coll
Cardiol 50:e159-241, 2007.)
7 • Noncardiac Surgery in the Patient with Cardiovascular Disease
12/20/07 7:42:09 PM
7 • Noncardiac Surgery in the Patient with Cardiovascular Disease 163
No
Yes
Good functional
(class I, LOE B)
capacity (MET level Proceed with
Step 4 greater than or equal planned surgery
to 4) without symptoms†
Step 5 No or unknown
Class IIa,
LOE B
Figure 7-2 • Cardiac evaluation and care algorithm for noncardiac surgery
based on active clinical conditions, known cardiovascular disease, or cardiac risk
factors for patients 50 years of age or older. *See Table 7-1 for active clinical
conditions. †See Figure 7-1 for estimated MET level equivalent. ‡Clinical risk fac-
tors include ischemic heart disease, compensated or prior heart failure, diabetes
mellitus, renal insufficiency, and cerebrovascular disease. §Consider perioperative
beta blockade for populations in which this has been shown to reduce cardiac
morbidity/mortality. ACC/AHA, American College of Cardiology/American Heart
Association; HR, heart rate; LOE, level of evidence; MET, metabolic equivalent.
(From Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA guidelines on perioperative
cardiovascular evaluation and care for noncardiac surgery: A report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines
[Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular
Evaluation for Noncardiac Surgery]. J Am Coll Cardiol 50:e159-241, 2007.)
*Noninvasive stress testing is not useful for patients who have no clinical
risk factors and are undergoing intermediate-risk noncardiac surgery and for pa-
tients who are undergoing low-risk noncardiac surgery.
†
Clinical risk factors: history of ischemic heart disease, history of compen-
sated or prior heart failure, history of cerebrovascular disease, diabetes mellitus,
renal insufficiency (serum creatinine ⬎2.0).
METs, metabolic equivalents.
From Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA guidelines on
perioperative cardiovascular evaluation and care for noncardiac surgery: A report
of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Periop-
erative Cardiovascular Evaluation for Noncardiac Surgery). J Am Coll Cardiol 50:
e159-241, 2007.
ANESTHESIA CONSIDERATIONS
Physiologic Response to Anesthesia and Surgery
Anesthesia and surgery are accompanied by physiologic re-
sponses to preserve homeostasis. In the patient with compen-
sated heart disease, these normal responses may precipitate
decompensation. Catecholamine production increases in re-
sponse to the stress of surgery, and it leads to increases in myo-
cardial oxygen demand as well as increased afterload that may
provoke myocardial ischemia in the patient with coronary ar-
tery disease. In addition, several perioperative factors may lead
to decreased myocardial oxygen delivery. Hypoventilation and
atelectasis may reduce arterial oxygen saturation. Anemia de-
creases myocardial oxygen delivery. Volume depletion or peri-
operative hypotension may result in coronary artery hypoper-
fusion. Sodium and water retention are increased in response
RECOMMENDED
1. Patient already receiving -blocker therapy
2. Vascular surgery: Myocardial ischemia identified on preop-
erative testing
PROBABLY RECOMMENDED
1. Vascular surgery: Patient with known coronary artery disease
2. Vascular surgery: Patient with multiple clinical risk factors
3. Intermediate-risk or high-risk surgery: Patient with multiple
clinical risk factors
MAY BE CONSIDERED
1. Intermediate-risk or high-risk surgery (including vascular
surgery): Single clinical risk factor
2. Vascular surgery: No cardiac risk factors
Adapted from Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA 2006 guide-
line update on perioperative cardiovascular evaluation for noncardiac surgery: Fo-
cused update on perioperative beta-blocker therapy. A report of the American College
of Cardiology/American Heart Association Task Force on Practice Guidelines (Writ-
ing Committee to Update the 2002 Guidelines on Perioperative Cardiovascular
Evaluation for Noncardiac Surgery). J Am Coll Cardiol 47:2343-2355, 2006.
HYPERTENSION
Perioperative Hypertension
Despite the extent of preoperative blood pressure control,
perioperative hypertension or hypotension each occurs in up
to 25% of hypertensive patients who undergo surgery. Two
preoperative predictors of perioperative hypertension are
previous hypertension, especially a diastolic b1ood pressure
greater than 110 mm Hg, and the type of surgical procedure.
Hypertensive events occur most commonly with carotid sur-
gery, abdominal aortic surgery, peripheral vascular proce-
dures, and intraperitoneal or intrathoracic surgery.
PERIOPERATIVE HYPOTENSION
Perioperative hypotension may result in myocardial ischemia
and is a predictor of postoperative cardiac morbidity. A peri-
operative decrease of mean arterial blood pressure of more
than 20 mm Hg has been shown to increase postoperative
cardiac complications. The most common causes of periop-
erative hypotension are intravascular volume depletion and
excessive vasodilation. Hypotension may be induced by
anesthetic agents. Spinal anesthesia may result in hypoten-
sion related to vasodilation. Several of the inhalational anes-
thetic agents (e.g., isoflurane, desflurane, and sevoflurane)
may cause hypotension by peripheral vasodilation as well
as by myocardial depression. Other causes of perioperative
hypotension include MI, pulmonary embolus, and sepsis.
Hypotension caused by volume depletion or vasodilation is
best treated by volume expansion. When clinically signifi-
cant vasodilation-induced hypotension does not respond to
this approach, a peripheral vasoconstrictor (phenylephrine)
should be considered. Hypotension resulting from direct
myocardial depression may be treated with inotropic agents
such as dopamine, dobutamine, and milrinone.
Mitral Regurgitation
Mitral regurgitation may be caused by one or more abnor-
malities of the structures that compose the mitral valve appa-
ratus: anterior and posterior valve leaflets, chordae tendineae,
papillary muscles, and mitral valve annulus. It may also result
from poor alignment of a structurally normal valve apparatus
or from mitral annular dilation, both of which are caused by
left ventricular dysfunction or dilation. Common causes of
mitral apparatus dysfunction are myxomatous degeneration of
the mitral valve leaflets or chordae, infective endocarditis that
may involve the valve leaflets, coronary artery disease with
myocardial ischemia resulting in papillary muscle dysfunction,
and rheumatic valve disease. Less common but clinically sig-
nificant causes of mitral regurgitation include mitral annular
calcification (usually limited to elderly persons) and distortion
of the mitral valve apparatus as a result of systolic anterior mo-
tion of the mitral valve in the setting of hypertrophic cardio-
myopathy. Degeneration of the mitral valve may be seen in
patients receiving long-term hemodialysis, as well as those
with the antiphospholipid antibody syndrome.
Aortic Regurgitation
Aortic regurgitation may be caused by processes that affect the
aortic valve leaflets (e.g., rheumatic fever, infective endocardi-
tis, congenital bicuspid aortic valve) or the aortic root and
valve-supporting structures (aortic dissection, systemic hyper-
tension, cystic medial necrosis, Marfan’s syndrome). Eighty
percent of cases that come to medical attention are chronic.
Aortic Stenosis
In adults, clinically significant aortic stenosis is usually the re-
sult of degenerative calcification of otherwise normal tricuspid
aortic valves. When aortic stenosis manifests in adults less than
50 years old, it is usually a result of calcification and
fusion of a congenital bicuspid aortic valve. Even when it is
severe, aortic stenosis remains clinically silent for many years.
The onset of symptoms indicates that patients are at risk
for sudden cardiac death. In the patient with untreated
falls to less than 1.5, and restarted within 24 hours after the
procedure. For patients at high risk of thrombosis without an-
ticoagulation (e.g., mechanical valve in the mitral position,
mechanical aortic valve with one or more of the foregoing risk
factors), therapeutic unfractionated heparin should be started
when the INR falls to less than 2.0. The heparin should be
stopped 4 to 6 hours preoperatively and restarted after the
surgical procedure as soon as hemostasis allows. Heparin is
continued until the INR becomes therapeutic. The guidelines
do support the consideration of low-molecular-weight heparin
to prevent valve thrombosis during the period of subtherapeu-
tic INR. For patients at low risk of intraoperative bleeding while
they are anticoagulated (e.g., cataract surgery, superficial proce-
dures), my approach has been to reduce the INR briefly to the
low or subtherapeutic range preoperatively and to resume the
patient’s maintenance dose of warfarin after the procedure.
Dental extractions can be safely performed on patients at a
therapeutic level of anticoagulation.
*Except for the conditions listed above, antibiotic prophylaxis is no longer rec-
ommended for any other form of CHD.
†Prophylaxis is recommended because endothelialization of prosthetic material
occurs within 6 months after the procedure.
From Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis.
Guidelines from the American Heart Association. Circulation 116:1736-1754, 2007.
HYPERTROPHIC CARDIOMYOPATHY
Patients with hypertrophic cardiomyopathy with left ventricu-
lar outflow tract obstruction are at risk for worsening of left
ventricular outflow tract obstruction in the perioperative pe-
riod. Factors that may lead to worsening of the left ventricular
outflow tract gradient include excessive reductions in preload
and afterload, as may occur with volume depletion or vasodi-
lator therapy. Perioperative catecholamine release may directly
act on the left ventricular outflow tract to increase myocardial
contractility and increase the outflow tract gradient.
Ventricular Arrhythmias
Patients are commonly found to have asymptomatic ventricular
ectopy at the time of preoperative evaluation. When significant
ventricular ectopy (e.g., frequent ventricular premature con-
tractions, nonsustained ventricular tachycardia) is identified,
I search for a metabolic cause such as hypoxia or hypokalemia.
If none is identified, I then search for the presence of underly-
ing structural cardiac disease and perform an echocardiogram
to evaluate left ventricular function. I frequently perform an
Sinus Tachycardia
Sinus tachycardia is the most common perioperative rhythm
abnormality and is almost always benign. It is characterized
by a heart rate between 100 and 160 beats/minute. The ECG
demonstrates a regular rhythm with a normal P wave before
each QRS complex. The QRS complex is normal unless pa-
tients have myocardial ischemia, aberrant ventricular con-
duction, or conduction abnormalities. The most common
causes of sinus tachycardia are pain, hypovolemia, anemia,
hypoxia, fever, and hypercarbia. Treatment is directed at the
inciting factor. Patients with coronary artery disease may
develop myocardial ischemia as a result of increased heart
rate and increased myocardial oxygen demand. -Adrenergic
blockers may be beneficial in this instance to decrease the
Long QT Syndrome
The long QT syndrome is a heterogeneous group of disorders
characterized by a prolonged QT interval when corrected for
heart rate, malignant ventricular arrhythmias (classically the
SELECTED INDICATIONS
Box 7-4 FOR IMPLANTATION
OF CARDIAC PACEMAKERS
AV, atrioventricular.
Adapted from Gregoratus G, Abrams J, Epstein A, et al: ACC/AHA/NASPE 2002
guideline update for implantation of cardiac pacemakers and antiarrhythmia devices.
Available at www.acc.org/clinical/guidelines/pacemaker/pacemaker.pdf.
ANTIARRHYTHMIC DRUGS
Type IA agents (e.g., quinidine, procainamide, disopyramide)
Type III agents (amiodarone, sotalol)
NONCARDIAC DRUGS
Phenothiazines
Tricyclic antidepressants
Haloperidol
Selective serotonin reuptake inhibitors
Antibiotics (e.g., erythromycin, azithromycin, clarithromycin,
ampicillin, trimethoprim-sulfamethoxazole, ketoconazole,
itraconazole)
METABOLIC AND ELECTROLYTE DISORDERS
Hypokalemia
Hypomagnesemia
Nutritional disorders (starvation, liquid protein diets)
CENTRAL NERVOUS SYSTEM DISORDERS
Subarachnoid hemorrhage
Intracerebral hemorrhage
Head trauma
Encephalitis
Pathophysiology
Once valvular lesions, pericardial disease, and noncardiac
conditions that increase the demand for cardiac output are
ruled out, a primary myocardial abnormality is usually the
cause of CHF. Approximately 70% of cases are related to left
and then give the oral agents again as soon as possible in the
postoperative period. Patients’ left ventricular function, degree
of compensation, dependence on ACE inhibitors or ARBs, and
risk for perioperative CHF determine the need for parenteral
ACE inhibitors postoperatively until oral intake can be re-
sumed. Patients with moderate to severe ventricular dysfunc-
tion who are at high risk for perioperative CHF are given intra-
venous ACE inhibitors (enalapril, at 0.625 to 1.25 mg every
6 hours) until oral ACE inhibitors can be resumed. No paren-
teral ARBs are available.
Many patients, particularly those who cannot tolerate
ACE inhibitors or ARBs, take the combination of nitrates and
hydralazine as vasodilator therapy for CHF. During the time
that patients are unable to take oral medications, topical or
intravenous nitrates are given. Because of the short duration
of action and risk for hypotension, I do not use parenteral
hydralazine as a substitute for oral hydralazine. If CHF
decompensates while patients maintained on nitrates and
hydralazine are unable to take oral medications, I may dis-
continue the nitrates and use intravenous nitroprusside for
its preload- and afterload-reducing properties. In some cases,
if the contraindication to ACE inhibitors or ARBs is not well
defined, I attempt to administer intravenous enalaprilat. In
patients who are unable to receive ACE inhibitors or ARBs,
perioperative CHF therapy is centered on diuretics, preload
reduction with nitrates, preload and afterload reduction with
nitroprusside, digoxin if indicated, and intravenous inotropic
agents such as dopamine, dobutamine, and milrinone.
-Blockers decrease symptoms and mortality in patients
with NYHA class II and III heart failure as a result of left ven-
tricular systolic dysfunction and have become standard therapy
in this patient group. These drugs are initiated when the patient
has been clinically compensated for at least 2 to 4 weeks. Their
use in the patient whose CHF is not compensated can provoke
further decompensation. Although there are no established
guidelines regarding the use of these drugs in the perioperative
Selected Readings
2005 American Heart Association Guidelines for Cardiopulmonary Resusci-
tation and Emergency Cardiovascular Care: Part 7.3: Management of
symptomatic bradycardia and tachycardia. Circulation 112(24 Suppl):
IV1-203, 2005. Epub 2005 Nov 28. Available at http://circ.ahajournals.
org/cgi/content/full/112/24_suppl/IV-67
Auerbach A, Goldman L: Assessing and reducing the cardiac risk of noncar-
diac surgery. Circulation 113:1361-1376, 2006.
Ballantyne JC, Kupelnick B, McPeek B, Lau J: Does the evidence support the
use of spinal and epidural anesthesia for surgery? J Clin Anesth 17:
382-391, 2005. A
Bonow RO, Carabello BA, Chatterjee K, et al: ACC/AHA 2006 guidelines for
the management of patients with valvular heart disease: A report of the
American College of Cardiology/American Heart Association Task Force
on Practice Guidelines (Writing Committee to Develop Guidelines for the
Management of Patients with Valvular Heart Disease). Available at http://
www.acc.org/clinical/guidelines/valvular/index.pdf. C
Charlson ME, MacKenzie CR, Gold JP, et al: Risk for postoperative conges-
tive heart failure. Surg Gynecol Obstet 172:95-104, 1991.
Cooperman LH, Price HL: Pulmonary edema in the operative and postop-
erative period. Am Surg 172:883-891, 1970
Dajani AS, Taubert KA, Wilson W, et al: Prevention of bacterial endocarditis:
Recommendations by the American Heart Association. Circulation
96:358-366, 1997.
Eagle K, Berger PB, Calkins H, et al: ACC/AHA guideline update for periop-
erative cardiovascular evaluation for noncardiac surgery: A report of the
American College of Cardiology/American Heart Association Task Force
on Practice Guidelines (Committee to Update the 1996 Guidelines on
Perioperative Cardiovascular Evaluation for Noncardiac Surgery). 2002.
American College of Cardiology Web site. Available at http:/www.acc.
org/qualityandscience/clinical/guidelines/perio/update/periupdate_
index.htm. C
Eagle KA, Guyton RA, Davidoff R, et al: ACC/AHA 2004 guideline update
for coronary artery bypass graft surgery: A report of the American Col-
lege of Cardiology/American Heart Association Task Force on Practice
Guidelines (Committee to Update the 1999 Guidelines for Coronary
L’Italien GJ, Cambria RP, Cutler BS, et al: Comparative early and late cardiac
morbidity among patients requiring different vascular surgery proce-
dures. J Vasc Surg 21:935-944, 1995. B
Lee TH, Marcantonio ER, Mangione CM, et al: Derivation and prospective
validation of a simple index for prediction of cardiac risk of major non-
cardiac surgery. Circulation 100:1043-1049, 1999.
Mangano DT, Browner WS, Hollenberg M, et al: The Study of Perioperative
Ischemia Research Group: Association of perioperative myocardial ischemia
with cardiac morbidity and mortality in men undergoing noncardiac sur-
gery. N Engl J Med 323:1781-1788, 1990.
McFalls EO, Ward HB, Moritz TE, et al: Reduction of postoperative mortal-
ity and morbidity with epidural or spinal anesthesia: Results from over-
view of randomised trials. BMJ 321:1493, 2000.
McFalls EO, Ward HB, Moritz TE, et al: Coronary-artery revascularization
before elective major vascular surgery. N Engl J Med 351:2795-2804,
2004. A
Paul SD, Eagle KA, Kuntz K, et al: Concordance of preoperative clinical risk
with angiographic severity of coronary artery disease in patients under-
going vascular surgery. Circulation 94:1561-1566, 1996. B
Polanczyk CA, Goldman L, Marcantonio E, et al: Supraventricular arrhyth-
mia in patients having noncardiac surgery: Clinical correlates and effect
on length of stay. Ann Intern Med 129:279-285, 1998.
Rodgers A, Walker N, Schug S, et al: Reduction of postoperative mortality
and morbidity with epidural or spinal anaesthesia: Results from over-
view of randomised trials. BMJ 321:1493, 2000.
Sandham JD, Hull RD, Brant RF, et al: A randomized, controlled trial of the
use of pulmonary-artery catheters in high-risk surgical patients. N Engl
J Med 348:5-14, 2004. A
Uretsky BF, Young JB, Shahidi F, et al: Randomized study assessing the effect of
digoxin withdrawal in patients with mild to moderate chronic congestive
heart failure: Results of the PROVED trial. J Am Coll Cardiol 22:955-962,
1993.
Warner M, Lunn R, O’Leary P, Schroeder D: Outcomes of noncardiac surgi-
cal procedures in children and adults with congenital heart disease.
Mayo Clin Proc 73:728-734, 1998. C
Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis:
Guidelines from the American Heart Association: A guideline from the
American Heart Association Rheumatic Fever, Endocarditis and Kawasaki
Disease Committee, Council on Cardiovascular Disease in the Young, and
the Council on Clinical Cardiology, Council on Cardiovascular Surgery
and Anesthesia, and the Quality of Care and Outcomes Research Interdis-
ciplinary Working Group. J Am Dent Assoc 138:739-745, 747-760, 2007.
Published online April 19, 2007. Available at http://circ.ahajournals.org.
EFFECTS OF SURGERY
The function of the respiratory system is invariably affected
during and after surgical procedures [ B Tisi, 1979; B Breslin,
1981; B Jackson, 1988]. Despite a better understanding of the
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized controlled
trials, systematic reviews of studies other than RCTs, cross-sectional studies, retrospec-
tive studies. C —Consensus statements, expert guidelines, usual practice, opinion.
249
Atelectasis
Respiratory failure
Figure 8-1 • Pathophysiology of the events leading to postoperative pulmo-
nary complications. V/Q, ventilation/perfusion.
Smoking
Investigators have shown an association between the amount
of cigarette smoking and related bronchial epithelial abnor-
malities and the incidence of postoperative pulmonary com-
plications in asymptomatic smokers [ B Chalon et al, 1975;
B McAlister et al, 2003; B Warner et al, 1984]. Cigarette smok-
Asthma
It is accepted that patients with poorly controlled asthma are
at increased risk for postoperative pulmonary complications
[ B Gold and Helrich, 1963]. Nevertheless, even patients with
severe, steroid-dependent asthma may undergo needed surgi-
cal procedures if an adequate plan is prepared and followed.
The known risks for asthmatic patients who are undergoing
anesthesia and abdominal surgery are bronchospasm, atelec-
tasis, and cough. Cough may become an important factor in
incisional pain and possible wound dehiscence. Although
investigators have argued about avoidance of endotracheal
intubation through the use of spinal anesthesia, “high” spinal
anesthesia (above T6) may result in enhanced bronchospasm
through blockade of sympathetic efferents that leave the vagal
innervation of the bronchi unopposed. The risk in patients
Preoperative History–Predicted
TABLE 8-2
Postoperative Pneumonia Point System
Category Risk Factor Point Value
Type of surgical procedure Abdominal aortic aneurysm 15
Thoracic 14
Upper abdominal 10
Neck/neurosurgical 8
Vascular other than AAA/ 3
emergency
GET/transfusion ⬎4 U 4/3
Age ⬎80 yr/⬎70 yr/⬎60 yr/⬎50 yr 17/13/9/4
General health Dependent/partially dependent 10/6
Weight loss ⬎10% 7
Current smoker/drinker (⬎2/day) 3/2
History Chronic obstructive pulmonary 5/4
disease/stroke/altered MS
Long-term steroid use 3
Preoperative History–Predicted
TABLE 8-3
Postoperative Pneumonia Rate Correlation
Rate of Pneumonia: Rate of Pneumonia:
Risk Class (Points) Development Cohort Validation Cohort
1 (0–15) 0.24 0.24
2 (15–25) 1.19 1.18
3 (26–40) 4.0 4.6
4 (41–55) 9.4 10.8
5 (⬎55) 15.8 15.9
From Arozullah A, Khuri SF, Henderson WG, Daley J: Development and vali-
dation of a multifactorial risk index. Ann Intern Med 135:847-857, 2001.
POSTOPERATIVE CARE
Once the surgical procedure is completed, the patient enters
a critical period in which he or she should be observed
closely. During this time, good suctioning and lateral turning
of the head help to prevent any possible aspiration. The
Selected Readings
Arozullah A, Khuri SF, Henderson WG, Daley J: Development and validation of
a multifactorial risk index. Ann Intern Med 135:847-857, 2001. B
Aubier M, DeTroyer A, Sampson M, et al: Aminophylline improves dia-
phragmatic contractility. N Engl J Med 305:249–252, 1981. B
Bartlett RH, Brennan ML, Gazzaniga AB, Hanson EL: Studies on the patho-
genesis and prevention of postoperative pulmonary complications. Surg
Gynecol Obstet 1367:925–933, 1973. B
Bermudez M, Rodriguez K, Celli B: Is weight an independent risk factor in
the development of postoperative pulmonary complications after ab-
dominal surgery? Am Rev Respir Dis 135:A211, 1987.
Breslin EH: Prevention and treatment of pulmonary complications in patients
after surgery of the upper abdomen. Heart Lung 10:511–519, 1981. B
Buchwald H, Avidor Y, Braunwald E, et al: Bariatric surgery: A systematic
review and meta-analysis. JAMA 292:1724-1737, 2004.
Cain HD, Stevens PM, Adanija R: Preoperative pulmonary function and
complications after cardiovascular surgery. Chest 76:130–135, 1979. B
Celli BR, Rodriguez K, Snider GL: A controlled trial of intermittent positive
pressure breathing, incentive spirometry, and deep breathing exercise
in preventing pulmonary complications after abdominal surgery.
Am Rev Respir Dis 130:12-15, 1984. A
Chalon J, Tayae MA, Ramanathan S: Cytology of respiratory epithelium as a
predictor of respiratory complications after operation. Chest 67:32–35,
1975. B
Dureuil B, Viires N, Contineau JP, et al: Diaphragmatic contractility after
upper abdominal surgery. J Appl Physiol 61:1775–1780, 1986. B
Epstein SK, Faling LJ, Daly BD, Celli BR: Predicting complications after
pulmonary resection: Preoperative exercise testing vs. a multifactorial
cardiopulmonary risk index. Chest 104:694-700, 1993. B
Ford GT, Whitelaw W, Rosenal TW, et al: Diaphragmatic function after up-
per abdominal surgery in humans. Am Rev Respir Dis 127:431–436,
1983. B
Ford GT, Guenter CA: Toward prevention of postoperative pulmonary com-
plications. Am Rev Respir Dis 130:4–5, 1984. B
PERIOPERATIVE MANAGEMENT
OF GASTROINTESTINAL DISEASES
Gastroesophageal Reflux Disease
Gastroesophageal reflux is common in the general population
and is a frequent cause of esophagitis in the perioperative
period. The pathogenesis involves an increased frequency of
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized clinical tri-
als, systematic reviews of studies other than RCTs, cross-sectional studies, retro-
spective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
275
275
bid, twice a day; qd, every day; qhs, at bedtime; qid, four times a day; PO,
by mouth; tid, three times a day.
Treatment
With available drug therapy for ulcer disease, rigid dietary
guidelines are no longer considered necessary. The single
controllable nondrug determinant of ulcer healing is ciga-
rette smoking, which should be restricted. Most available
ulcer drugs result in 6- to 8-week healing rates of 80% to
90%. The main differences in the drugs relate to cost and
side effect profiles (see Table 9-1).
Because of the role of H. pylori in the pathogenesis of pep-
tic ulcer disease and ulcer recurrence, therapy to eradicate
H. pylori from the stomach should be employed routinely
when the organism is detected in a patient with an ulcer.
Currently, the most commonly used triple-drug therapy for
H. pylori consists of a proton pump inhibitor twice daily,
amoxicillin 1000 mg twice daily, and clarithromycin 500 mg
twice daily. Eradication rates in excess of 90% can be achieved
with a 10- to 14-day course of therapy. Seven-day courses of
antibiotics also appear to be cost effective but do not lead to
eradication rates as high as with 10-day or 14-day regimens.
For patients with persistent H. pylori infection after treatment,
a quadruple-drug regimen consisting of bismuth subsalicylate
two tablets four times daily, metronidazole 250 mg three
times daily, tetracycline 500 mg four times daily, and a proton
pump inhibitor twice daily is recommended. Recent data
suggest that a 10-day course of levofloxacin 500 mg daily
with a proton pump inhibitor twice daily and amoxicillin or
clarithromycin also may be effective. Potential drawbacks to
the use of multiple drugs to cure H. pylori infection and to
heal ulcers include poor compliance, adverse reactions, and
resistance to metronidazole and clarithromycin. In addition,
patients must be cautioned not to take metronidazole
with alcohol because of a disulfiram-like reaction. Never-
theless, in practice, side effects have not been a frequent
problem.
Ulcers caused by NSAIDs are treated by discontinuation
of the NSAID and use of a proton pump inhibitor for 4 to
Perioperative Management
It is important for the medical consultant to confirm a diag-
nosis of ulcerative colitis or Crohn’s disease and to determine
the extent and severity of the disease at the time surgical
treatment is planned. If necessary, diagnostic studies may
include upper and lower barium radiographs and colonos-
copy with biopsy. In about 10% of cases of chronic colitis, a
distinction between ulcerative colitis and Crohn’s colitis may
not be possible, and the designation indeterminate colitis may
apply. Serologic tests (antineutrophil cytoplasmic antibodies
in ulcerative colitis and anti-Saccharomyces cerevisiae antibod-
ies in Crohn’s disease) may help to classify some such pa-
tients. In a patient with a recent flare in disease activity, stool
cultures and examination for ova and parasites and Clostrid-
ium difficile toxin may be indicated to exclude superimposed
infectious colitis. It is important to ask about systemic symp-
toms, including fever, arthritis, rash, ocular symptoms, jaun-
dice, and weight loss, which may require further evaluation
and treatment. Objective indicators of disease activity such as
the hemoglobin level, hematocrit value, erythrocyte sedi-
mentation rate, C-reactive protein, and serum albumin level
should be obtained. In general, unless a surgical procedure is
being performed for medically intractable inflammatory
bowel disease, every effort should be made to control disease
activity before elective surgery is undertaken. It is important
to consider the potential for perioperative NSAIDs to
exacerbate disease activity in patients with inflammatory
bowel disease [ B Bonner et al, 2004].
Corticosteroid Use
Concern is often raised about an adverse effect of intravenous
corticosteroids on wound healing and predisposition to post-
operative infection, although the magnitude of the latter risk
is uncertain. In addition, the clinician needs to be alert to
other effects of corticosteroid use, including hyperglycemia,
hypokalemia, fluid retention, and hypertension. The patient
who has received long-term corticosteroid therapy is also at
risk of osteoporosis, glaucoma, and cataracts.
Acute and Chronic Pancreatitis
Acute Pancreatitis
Acute pancreatitis is associated with a mortality rate as high
as 10% and should lead to postponement of all but emer-
gency surgery. The more common causes of acute pancreatitis
include gallstones, alcohol, certain drugs, hyperlipidemia,
and trauma (Box 9-1). (Postoperative pancreatitis is discussed
later.)
The clinical presentation of acute pancreatitis is with bor-
ing epigastric abdominal pain, localized abdominal tender-
ness with signs of peritoneal irritation, nausea and vomiting,
fever, hyperamylasemia, and, occasionally, hypotension or
shock. Severe acute pancreatitis, which occurs in only a mi-
nority of patients, may affect multiple organs and may lead
Ethanol
Gallstones
Abdominal surgery
Toxins (e.g., organophosphorus)
Trauma
Idiopathic
Hypertriglyceridemia
Hypercalcemia
Drugs: Furosemide, hydrochlorothiazide, sulfonamides, tetra-
cyclines, valproic acid, azathioprine/6-mercaptopurine,
L-asparaginase, estrogens
Pancreas divisum
Ischemic (hypoperfusion, vasculitis)
Viral infections
Endoscopic retrograde cholangiopancreatography
Pancreatic or ampullary neoplasm
Hereditary pancreatitis
Penetrating peptic ulcer disease
Obesity
End-stage renal disease
Sphincter of Oddi dysfunction
Postoperative status
AT ADMISSION
Age ⬎55 yr
White blood cells ⬎16,000/mm3
Glucose ⬎200 mg/dL
Lactate dehydrogenase ⬎350 U/L
Aspartate aminotransferase ⬎250 U/L
DURING INITIAL 48 HR
Hematocrit decrease of ⬎10 mg/dL
Blood urea nitrogen increase of ⬎5 mg/dL
Calcium ⬍8 mg/dL
Partial pressure of arterial oxygen ⬍60 mm Hg
Base deficit ⬎4 mEq/L
Fluid sequestration ⬎6 L
GASTROINTESTINAL COMPLICATIONS
IN THE POSTOPERATIVE PERIOD
Constipation
Causes
Constipation is common in bedridden postoperative pa-
tients; it is usually mild and self-limited and often multifacto-
rial in origin. Many drugs used in the perioperative period
may contribute to constipation (Box 9-3). Several common
metabolic disorders that may occur postoperatively may con-
tribute to constipation, including hypokalemia, hypercalce-
mia, acidosis, and uremia. Diabetes mellitus and hypothy-
roidism are additional metabolic causes of constipation. In
some cases, mechanical disorders that may lead to constipa-
tion should be considered, including fecal impaction, intes-
tinal tumors, volvulus, hernias, and strictures from ischemia,
radiation, diverticulitis, or surgical procedures. Anorectal
disorders that may lead to constipation include painful
hemorrhoids, fissures, perirectal abscess, ulcerative proctitis,
and rectal prolapse. Intestinal ileus and colonic pseudo-
obstruction are common following gastrointestinal surgery
(see later) and may account for constipation. Occasionally,
extraperitoneal causes such as acute pancreatitis and retro-
peritoneal hemorrhage must be considered.
ANALGESICS
Opiates (e.g., morphine, codeine)
Opioids (e.g., fentanyl, pethidine, tramadol)
Nonsteroidal anti-inflammatory drugs (e.g., diclofenac,
naproxen)
PSYCHIATRIC DRUGS
Antidepressants
Tricyclic antidepressants (e.g., amitriptyline, doxepin)
Monoamine oxidase inhibitors (e.g., phenelzine)
Selective serotonin reuptake inhibitors (e.g., fluoxetine, parox-
etine)
Anxiolytics (e.g., trazodone, diazepam, chlordiazepoxide)
Antipsychotics (e.g., thioridazine, prochlorperazine, thiothixene)
ENDOCRINE AGENTS
Calcium supplements
Pamidronate, alendronate
Bromocriptine
GASTROINTESTINAL AGENTS
Proton pump inhibitors
Cholestyramine
Sucralfate
Others (5-acetylsalicylate agents, octreotide)
CARDIOVASCULAR DRUGS
Amiodarone
Disopyramide
Encainide
Flecainide
Clonidine
Guanfacine
Calcium antagonists (e.g., nifedipine)
Postoperative Management
The management of constipation in the postoperative patient
begins with discontinuation of predisposing medications
when possible, especially opiate analgesics, and correction of
any metabolic abnormalities that may be present. Resump-
tion of normal physical activity and dietary intake, including
adequate fluids and bulk, often helps. Various laxatives are
available for the short-term treatment of constipation, as long
as mechanical obstruction has been excluded. Bulk agents
such as psyllium (e.g., Metamucil, 1 tbsp orally twice a day)
and cellulose derivatives are generally the first line of ther-
apy; it is important that they be accompanied by adequate
fluid intake. Emollient agents such as docusate sodium (e.g.,
docusate, 100 mg twice a day) and lubricants such as mineral
oil (15 to 45 mL orally twice a day) can be used to soften
hard stool in the colon. Occasionally, saline cathartics such as
magnesium citrate (200 mL orally every day), stimulant laxa-
tives such as senna derivatives, osmotic agents such as lactu-
lose (30 mL orally twice a day) or polyethylene glycol (Mira-
Lax, 1 tsp/8 ounces of fluid/day), or a secretory agent such as
lubiprostone (24 g orally twice daily) may be needed.
Age
Alcoholism
Drugs
Narcotics
Antidepressants
Anticholinergics
Clonidine
Phenothiazines
Metabolic causes
Electrolyte imbalance
Acid-base disturbances
Hypothyroidism
Diabetes mellitus
Uremia
Sepsis
Surgery
Inflammatory processes (e.g., pancreatitis and cholecystitis)
Malignancy
Infection
Nonoperative trauma
Radiation therapy
Respiratory failure
Cardiovascular disease
Respiratory disease
Length of anesthesia
Type of surgery (abdominal, gynecologic, urologic, ophthal-
mologic, middle ear)
Female gender
History of motion sickness
Postoperative ileus or pain
Gastroparesis
Refeeding after prolonged disuse of gastrointestinal tract
Metabolic factors
Uremia
Hyperglycemia/hypoglycemia
Electrolyte disturbances
Dehydration
Drugs
General anesthetics
Opiate analgesics
Digitalis
Mechanical causes
Intestinal obstruction
Gastric outlet obstruction (e.g., pyloric channel ulcer)
Inflammatory processes
Peritonitis
Acute pancreatitis
Acute cholecystitis
Perioperative Management
The cornerstone of treatment for postoperative nausea and
vomiting is the elimination of precipitating causes, including
contributing drugs. Intestinal obstruction and infection
should be sought and treated. Intravenous hydration is criti-
cal, and nasogastric suction may be useful. Antiemetic drugs
and proton pump inhibitors may be of benefit, but gastric
prokinetic agents must be avoided if intestinal obstruction is
present. The prokinetic agent metoclopramide (5 to 20 mg
intravenously or orally four times a day 30 minutes before
meals and at bedtime if the patient is eating) promotes gastro-
intestinal motility. The patient receiving metoclopramide
must be monitored closely for side effects, including dystonic
reactions, tremor, and mental confusion. When administered
toward the end of a surgical procedure, ondansetron (4 mg
intravenously), droperidol (1.25 mg intravenously), and
dexamethasone (4 mg intravenously) have each been shown
to decrease the frequency of postoperative nausea and vomit-
ing. Combination therapy may be required in some patients.
The 5-hydroxytryptamine receptor antagonists (5-HT3) with
activity similar to that of ondansetron include granisetron,
tropisetron, and dolasetron. A newer class of antiemetics,
neurokinin-1 receptor antagonists such as aprepitant, show
promise for the treatment of postoperative nausea and vomit-
ing. Droperidol has been associated with cardiac arrhythmias.
Phenothiazines such as prochlorperazine are no longer rou-
tinely recommended.
Diarrhea
Diarrhea is common in the postoperative period and may be
caused by numerous factors.
Drugs
Drugs are a frequent cause of postoperative diarrhea
(Table 9-2). Common pharmacologic causes of diarrhea in
the postoperative period include magnesium-containing ant-
acids, antibiotics, digitalis, quinidine, theophylline, and laxa-
tives. Frequently, diarrhea can result from nutritional addi-
tives such as sorbitol. Oral caloric supplements may also
cause diarrhea. Diarrhea can be expected to resolve when the
offending drug is discontinued or when a caloric supplement
is diluted or administered at a slower rate.
ANTIBIOTIC-ASSOCIATED DIARRHEA
Antibiotic-associated diarrhea is a major cause of diarrhea in
postsurgical patients. The mild diarrhea that frequently oc-
curs in postsurgical patients receiving antibiotics is thought to
be caused by alteration of colonic bacterial flora and usually
resolves promptly with discontinuation of the antibiotic. Of
all patients with antibiotic-associated diarrhea, 15% to 25%
have a positive stool assay for C. difficile toxin, which may
Mallory-Weiss Tears
Factors that predispose to Mallory-Weiss tears in the postop-
erative period include retching, vomiting, and coughing,
with resulting high intra-abdominal pressures and large pres-
sure gradients across the gastroesophageal junction. Mallory-
Weiss tears account for fewer than 5% of cases of postop-
erative bleeding, are generally self-limited, and respond to
control of nausea and vomiting with the use of nasogastric
suction, antiemetics, and gastric acid suppression. Endo-
scopic intervention may occasionally be required.
Esophagitis
Esophagitis resulting from gastroesophageal reflux disease is
discussed earlier in the section on gastroesophageal reflux
disease. Postoperative patients are also at risk for the develop-
ment of infectious esophagitis caused by Candida albicans,
herpesvirus, and cytomegalovirus, which may cause bleed-
ing. Predisposing factors include antibiotics, immunosup-
pression (including acquired immunodeficiency syndrome),
diabetes, debility, and malnutrition. Symptoms of esophagitis
such as substernal burning, dysphagia, and odynophagia
may be minimal or absent. Moreover, oral thrush is absent in
half of all persons with Candida esophagitis. The diagnosis of
infectious esophagitis may be confirmed by endoscopy with
brush cytologic studies, potassium hydroxide stain, biopsy,
and culture. Treatment of Candida esophagitis consists of oral
nystatin (500,000 U orally four times daily) or fluconazole
(100 to 200 mg orally daily), which is preferred over itracon-
azole or ketoconazole. In refractory cases, low-dose (500 mg
total) intravenous amphotericin can be used. For herpes
esophagitis, intravenous acyclovir (250 mg/m2 intravenously
every 8 hours, then 200 to 400 mg orally five times daily)
should be prescribed. For cytomegalovirus, ganciclovir
(5 mg/kg intravenously every 12 hours) is given; foscarnet is
an alternative. Nystatin and fluconazole are generally well
tolerated; ketoconazole may cause hepatitis, nausea, and
Jaundice
Jaundice is common in the postoperative period. The cause
is usually multifactorial, but the pathophysiologic mecha-
nisms may be grouped into four major categories (Table 9-3):
(1) increased bilirubin load to the liver; (2) intrahepatic dis-
ease; (3) preexisting liver disease; and (4) extrahepatic ob-
structive disease.
In the postoperative period, hemolysis of transfused
blood and resorption of hematomas account for the major
portion of the increased load of bilirubin delivered to the
liver. Similarly, medications administered in the postopera-
tive period may induce hemolysis. Jaundice is particularly
common in patients who have undergone extensive surgical
procedures and have received multiple transfusions; the
hyperbilirubinemia is primarily indirect, occasionally as high
as 20 mg/dL. In patients undergoing cardiac surgical proce-
dures, risk factors for postoperative jaundice include preop-
erative serum bilirubin elevation, elevated right atrial pres-
sure, cardiac valve replacement, and the use of intra-aortic
balloon counterpulsation.
Ischemic liver injury is a common cause of postoperative
jaundice. The origin is multifactorial, likely related to a
Management
Investigation of postoperative jaundice should include the
following: an ultrasonographic examination to exclude evi-
dence of extrahepatic obstruction (a dilated common bile
duct, common hepatic ducts, or intrahepatic ducts); serologic
studies for hepatitis A, B, and C; evaluation for hemolysis
(reticulocyte count and examination of the peripheral blood
smear); a review of the patient’s medications for potential
hepatotoxic agents; and exclusion of sepsis. As noted earlier,
it is often not possible to attribute postoperative jaundice to a
single cause, and several factors may be implicated. Fatty liver
from total parenteral nutrition may be reversed with lecithin
or choline supplementation, and cholestasis may be reversed
with ursodeoxycholic acid or metronidazole.
Cholecystitis
Clinical Features
Acute cholecystitis is an uncommon but often overlooked
complication after nonbiliary surgical procedures. Cholecys-
titis is classified as calculous (associated with stones in the
biliary tree) or acalculous (no evidence of stones). Choleli-
thiasis may be common in patients undergoing renal trans-
plantation, whereas patients who undergo cardiac trans-
plantation and have cholelithiasis are at high risk of
posttransplantation cholecystitis and should undergo pre-
transplant cholecystectomy. More than half the patients with
postoperative cholecystitis have acalculous cholecystitis.
Mortality rates of patients with acalculous cholecystitis range
from 12% to 65%. Acute acalculous cholecystitis may follow
abdominal or nonabdominal surgical procedures (especially
orthopedic procedures), spinal cord injury, or bone marrow
transplantation. Trauma and burns are also important risk
factors.
Presentation
Postoperative acalculous cholecystitis usually manifests
within 2 to 4 weeks of the surgical procedure. Patients are
usually elderly, and in contrast to calculous cholecystitis,
there is a male predominance. The clinical presentation is
with fever, anorexia, epigastric and right upper quadrant
pain and tenderness, nausea, vomiting, and a palpable ab-
dominal mass. Patients may have leukocytosis and slight el-
evations in liver biochemical tests. Not infrequently, however,
symptoms and signs may be masked, especially in comatose
or obtunded patients. The diagnosis should be considered in
any postoperative patient, even children, with unexplained
fever. In postoperative acalculous cholecystitis, bile cultures
are frequently positive for E. coli, Pseudomonas, Klebsiella, and
Staphylococcus aureus. There is a high frequency of gangrene
and perforation of the gallbladder, with mortality rates as
high as 50%.
Pathogenesis
The pathogenesis of postoperative cholecystitis is unknown.
Gallbladder stasis and local ischemia are important precipi-
tating factors. Increased viscosity of bile may result from fe-
ver, fasting, and dehydration and may contribute to biliary
stasis and cystic duct obstruction. Narcotic-induced ampul-
lary contraction may also cause bile stasis, and positive pres-
sure ventilation can increase common bile duct pressure.
Hemolysis from multiple blood transfusions administered in
the perioperative period may alter bile flow. Mucosal is-
chemia and necrosis can result from decreased vascular per-
fusion of the gallbladder as a result of hypotension or heart
failure. Ischemia may also lead to cystic duct stenosis. Finally,
activation of factor XII in the circulation can cause acute
vasculitis of the gallbladder serosa and muscularis. In heart
transplant recipients, a high rate of bile duct stones is
thought to be the result of reduced bile flow and changes in
serum lipids caused by cyclosporine, postoperative gallblad-
der stasis, rapid weight change, and hemolysis.
Management
A high index of suspicion is needed for early diagnosis. In
some patients, typical findings of acute cholecystitis are evi-
dent on physical examination. In others, greater reliance must
be placed on imaging studies. Abdominal ultrasound is usu-
ally the initial diagnostic test and may show a thickened
gallbladder wall, an enlarged tender gallbladder, a perichole-
cystic fluid collection, or evidence of air within the gallblad-
der wall (emphysematous cholecystitis). Computed tomogra-
phy may also show a thickened gallbladder wall with
surrounding fluid. A gallbladder wall thicker than 3.5 mm
is virtually diagnostic of acute cholecystitis. Hepatobiliary
scintigraphy shows nonvisualization of the gallbladder in
more than 90% of cases, although it has a higher rate of false-
positive results than ultrasonography.
Management of postoperative cholecystitis consists of fluid
and electrolyte replacement, administration of broad-spectrum
antibiotics, and urgent cholecystectomy, if possible, once the
diagnosis is confirmed. In patients who are poor surgical risks,
percutaneous cholecystostomy is preferable to cholecystec-
tomy. In patients with ascites or coagulopathy, endoscopic
decompression with a stent placed in the cystic duct may be
feasible.
Acute Pancreatitis
Acute pancreatitis may occur as a complication of both ab-
dominal and nonabdominal surgical procedures. Postopera-
tive pancreatitis has been recognized increasingly after heart
surgery with cardiopulmonary bypass and is thought to result
from ischemic injury to the pancreas secondary to hypoperfu-
sion, which is more common with nonpulsatile bypass sys-
tems than with pulsatile systems. Other possible contributory
factors include hypothermia, atheromatous or cholesterol em-
boli broken off during cannulation and cross-clamping of the
aorta, venous sludging, and angiotensin-mediated selective
blockade of pancreatic perfusion [ B Perez et al, 2005]. Risk
COMPLICATIONS OF GASTROINTESTINAL
SURGERY
Complications of Peptic Ulcer Surgery
Traditionally, the goal of peptic ulcer surgery has been to re-
duce gastric acid production, usually by removing the
gastrin-producing cells of the antrum (antrectomy) and
interrupting cholinergic stimulation to the parietal cells of
the fundus (vagotomy). The gastric remnant is usually anas-
tomosed from end to side to a loop of jejunum, with forma-
tion of a gastrojejunostomy (Billroth II) or, less often, a gas-
troduodenostomy (Billroth I). Because a complete vagotomy
impairs gastric motility, highly selective (proximal) vagotomy
(without antrectomy) was introduced. With the discovery of
H. pylori and the recognition that its eradication cures peptic
ulcer disease, the need for peptic ulcer surgery has decreased
dramatically. Postgastrectomy syndromes may still be seen in
patients who underwent ulcer surgery in the past or in the
occasional patient who undergoes surgical treatment for a
complication of ulcer disease (Table 9-4).
Ulcer Recurrence
Recurrence of peptic ulcer disease postoperatively occurs in
approximately 5% of cases. Recurrence is more likely when
the original operation was performed for duodenal ulcer
(3% to 10%) than for gastric ulcer (2%) and is less likely
after antrectomy and vagotomy (1% to 4%) than after va-
gotomy alone (ⱕ25%). Recurrent (stomal) ulcers occur most
commonly at or just distal to the anastomosis.
Causes of ulcer recurrence include use of ulcerogenic
drugs (e.g., aspirin, NSAIDs), inadequate vagotomy, inade-
quate gastric resection, retained gastric antrum, a long jeju-
nal afferent loop, inadvertent gastroileal or gastrocolic anas-
tomosis, poor gastric emptying, gastric neoplasm (mistaken
preoperatively as a benign ulcer or newly occurring), undiag-
nosed Zollinger-Ellison syndrome, and persistent H. pylori
infection. Most recurrent ulcers are attributable to the use of
aspirin and other NSAIDs.
DIAGNOSIS
It is more common for patients with recurrent ulcers to pre-
sent with hemorrhage than with pain; the bleeding is more
often chronic than acute. A stomal ulcer may also cause
symptoms of obstruction. Because upper gastrointestinal
barium radiographs of the postoperative stomach are difficult
to interpret, the diagnosis of a recurrent ulcer is best made
by endoscopy. Surreptitious use of aspirin may be detected
by a low platelet cyclooxygenase level. Fasting serum gastrin
and calcium levels should be checked before any planned
ulcer operation to screen for evidence of Zollinger-Ellison
syndrome and a multiple endocrine neoplasia syndrome.
MANAGEMENT
Recurrent peptic ulcer disease has traditionally been treated
with proton pump inhibitors, in some cases with continua-
tion of full-dose therapy for life. Ulcerogenic drugs (aspirin
and other NSAIDs) should be withheld. Treatment should
include diagnosis and eradication of H. pylori. Surgical treat-
ment, usually further resection and repeat vagotomy, may be
indicated for complications (e.g., massive bleeding, obstruc-
tion) and should be considered carefully in patients with a
refractory ulcer, because ulcers caused by aspirin and other
NSAIDs tend to recur.
Dumping Syndrome
The dumping syndrome is characterized by postprandial
vasomotor symptoms such as tachycardia, flushing, and
palpitations in association with dyspeptic symptoms. The
dumping syndrome is often divided arbitrarily into early and
late phases.
Early dumping syndrome, occurring within 30 minutes of
eating, is characterized by palpitations, tachycardia, diapho-
resis, flushing, and dizziness with nausea, vomiting, and
bloating. It is thought to result from rapid emptying of hy-
perosmolar gastric contents into the small intestine and con-
sequent large fluid shifts that lead to contraction of plasma
volume, release of vasoactive hormones, and triggering of
autonomic reflexes by jejunal distention. Late dumping syn-
drome, occurring 90 minutes to 3 hours after eating, is char-
acterized by similar symptoms and is thought to result from
the rapid gastric emptying of carbohydrates into the proxi-
mal small intestine, followed by the sudden release of insulin
in response to rapid increases in blood glucose, with subse-
quent hypoglycemia.
The dumping syndrome is generally managed by en-
couraging the patient to eat small, frequent meals and to avoid
drinking liquids with solid food. The diet should be low in
carbohydrates and lactose and high in protein and fat. In some
cases, the somatostatin analogue octreotide, 25 to 100 g sub-
cutaneously three times a day, may be helpful. There are some
case reports describing use of long-acting octreotide (monthly
intramuscular depot injections) for this indication. Rarely, sur-
gical revision to a Roux-en-Y gastrojejunostomy is necessary.
Postvagotomy Diarrhea
Chronic diarrhea may follow any ulcer operation; it is not
clear whether the frequency is actually higher in patients
who have had a vagotomy. The exact mechanism is unclear,
but rapid gastric emptying and decreased intestinal transit
time have been postulated, as have extragastric mechanisms
Selected Readings
Anonymous: NIH state-of-the-science statement on endoscopic retrograde
cholangiopancreatography (ERCP) for diagnosis and therapy. NIH Con-
sens State Sci State 19:1-26, 2002.
Apfel CC, Korttila K, Abdalla M, et al: A factorial trial of six interventions for
the prevention of postoperative nausea and vomiting. N Engl J Med
350:2441-2451, 2004.
Apfel CC, Roewer N: Risk assessment of postoperative nausea and vomiting.
Int Anesthesiol Clin 41:13-32, 2003.
Bardou M, Youbouti Y, Benhaberou-Brun, et al: Meta-analysis: Proton-pump
inhibition in high-risk patients with acute peptic ulcer bleeding. Aliment
Pharmacol Ther 21:677-686, 2005.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed syste-
matic reviews of RCTs. B —Case-control or cohort studies, nonrandomized
controlled trials, systematic reviews of studies other than RCTs, cross-sectional
studies, retrospective studies. C —Consensus statements, expert guidelines, usual
practice, opinion.
349
Hemodynamic Effects
Cirrhosis causes a hyperdynamic circulation with increased
cardiac output, decreased systemic vascular resistance, and,
in some patients, increased extravascular volume, increased
or decreased intravascular volume, arteriovenous shunting,
and decreased renal blood flow. At baseline, hepatic arterial
and venous perfusion of the cirrhotic liver may be decreased:
portal blood flow is reduced in patients with portal hyperten-
sion, and arterial blood flow can be decreased because of
impaired autoregulation. The decreased hepatic perfusion
makes the cirrhotic liver more susceptible to hypoxemia and
hypotension. Decreased oxygen delivery to the liver during
Hypoxemia
Risk factors for intraoperative hypoxemia in patients with cir-
rhosis include ascites, hepatic hydrothorax, hepatopulmonary
syndrome (the triad of liver disease, an increased alveolar-
arterial gradient, and intrapulmonary shunting), hypoalbu-
minemia, and pulmonary hypertension. Hypoxemia also can
be caused by aspiration. Ascites, encephalopathy, and anes-
thetic agents increase the risk of aspiration in patients with
cirrhosis.
Hepatic Metabolism of Anesthetic Agents
Metabolism of anesthetic agents by the liver may result in the
formation of toxic metabolites, especially in the presence of
reduced hepatic blood flow and hypoxia. Occasional episodes
of acute hepatitis associated with the administration of halo-
thane, now rarely used in adults, are thought to be caused by
immune sensitization to trifluoroacetylated liver proteins
formed by oxidative metabolism of halothane by cytochrome
CONTRAINDICATIONS TO ELECTIVE
Box 10-1 SURGERY IN PATIENTS WITH LIVER
DISEASE
*Primary biliary cirrhosis and primary sclerosing cholangitis are in the differ-
ential diagnosis of chronic hepatitis but generally manifest as cholestatic liver
disease.
ANA, antinuclear antibodies; anti-HCV, antibody to hepatitis C virus; anti-HDV, anti-
body to hepatitis D virus; ASMA, anti–smooth muscle antibody; HBsAg, hepatitis B
surface antigen; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis D virus.
Data from Bedossa P, Poynard T: An algorithm for the grading of activity in chronic hepatitis C. Hepatology 24:289-293, 1996.
10 • Management of the Surgical Patient with Liver Disease
359
12/19/07 2:48:08 PM
360 10 • Management of the Surgical Patient with Liver Disease
Hepatitis C
One hundred seventy million people are infected with
HCV worldwide, and in the United States 1.8% of the
population is infected. Acute HCV infection is often asymp-
tomatic, and serum aminotransferase elevations may be
mild (100 to 300 U/L). Following acute HCV infection, up
to 85% of patients progress to chronic infection. Patients
with chronic HCV infection typically have elevated amino-
transferase levels ranging from 1.3 to 3 times the upper
limit of normal, although the serum aminotransferase lev-
els may be within normal limits. The 15% of patients with
acute HCV infection who clear the virus spontaneously
and those with chronic HCV infection who achieve a sus-
tained virologic response following treatment with PEG-
interferon and ribavirin continue to have detectable anti-
body to HCV (anti-HCV) for life. Approximately 20% of
patients with chronic hepatitis C progress to cirrhosis over
20 years; normal serum aminotransferase levels do not
preclude the possibility of advanced fibrosis on a liver bi-
opsy specimen. Of patients with cirrhosis caused by HCV,
decompensated liver disease develops in 30% within
10 years. Host factors that favor progression to cirrhosis
include male gender, alcohol use, age greater than 40 years
at the time of acquisition of HCV infection, and human
immunodeficiency virus (HIV) coinfection; other possible
risk factors include increased hepatic iron concentrations
and steatosis.
Hepatic Resection
Hepatocellular carcinoma (HCC) is a well-established com-
plication of liver disease. Chronic hepatitis B is thought to
lead to HCC as a result of chronic necroinflammatory activity
in the liver as well as integration of HBV DNA into the host
genome. In endemic areas where HBV infection is acquired
at or near birth, the 5-year cumulative frequency of HCC in
cirrhotic patients is as high as 15%. Chronic hepatitis C can
lead to HCC primarily by causing cirrhosis. After cirrhosis
occurs, the risk of HCC is 1.4% to 6.9% per year. Like hepa-
titis C, most other forms of liver disease put patients at in-
creased risk of HCC only after cirrhosis has occurred. Of all
causes of liver disease, patients with hemochromatosis and
cirrhosis have the highest risk of HCC. Screening for
HCC with ultrasound and with serum ␣-fetoprotein testing
every 6 months is recommended for all patients with cirrho-
sis and for noncirrhotic patients with chronic (replicative)
hepatitis B as well as inactive HBV carriers who are more
than 40 years old.
Patients with cirrhosis who undergo hepatic resection for
HCC or other liver tumors are at increased risk of hepatic
decompensation as compared with cirrhotic patients who
undergo other types of surgical procedures. In addition to
NA, not available. Data from Wahlstrom K, Ney AL, Jacobson S, et al: Trauma
in cirrhotics: Survival and hospital sequelae in patients requiring abdominal ex-
ploration. Am Surg 66:1071-1076, 2000; Tachibana M, Kotoh T, Kinugasa S, et al:
Esophageal cancer with cirrhosis of the liver: Results of esophagectomy in 18 con-
secutive patients. Ann Surg Oncol 7:758-763, 2000; Poulsen TL, Thulstrup AM,
Sorensen HT, et al: Appendectomy and perioperative mortality in patients with
liver cirrhosis. Br J Surg 87:1664-1665, 2000; Nielsen SS, Thulstrup AM, Lund L,
et al: Postoperative mortality in patients with liver cirrhosis undergoing transure-
thral resection of the prostate: A Danish nationwide cohort study. BJU Int 87:
183-186, 2001; Milanez de Campos JR, Filho LO, de Campos Werebe E, et al:
Thoracoscopy and talc poudrage in the management of hepatic hydrothorax.
Chest 118:13-17, 2000; Wong R, Rappaport W, Witte C, et al: Risk of nonshunt
abdominal operation in the patient with cirrhosis. J Am Coll Surg 179:412–416,
1994; Lehnert T, Herfarth C: Peptic ulcer surgery in patients with liver cirrhosis.
Ann Surg 217:338–346, 1993; Gervaz P, Pak-art R, Nivatvongs S, et al: Colorectal
adenocarcinoma in cirrhotic patients. J Am Coll Surg 196:874-879, 2003; and
Shih LY, Cheng CY, Chang CH, et al: Total knee arthroplasty in patients with liver
cirrhosis. J Bone Joint Surg Am 86:335-341, 2004.
Preoperative Preparation
The hemostatic stress of surgery requires that the patient un-
dergo careful preoperative preparation as well as intraopera-
tive monitoring of hemostatic parameters. Vitamin K, 10 mg
given intramuscularly, usually corrects hypoprothrombinemia
related to malnutrition or intestinal bile salt deficiency as a
result of obstructive jaundice but not hypoprothrombinemia
related to hepatocellular disease. Although an injection of vi-
tamin K on 3 consecutive days is often recommended, one
dose may be sufficient, and the effect is often evident within
6 to 12 hours.
When vitamin K repletion does not correct the coagu-
lopathy, considerable hepatocellular dysfunction exists. In
such patients, fresh frozen plasma (typically 6 to 8 U for se-
vere coagulopathy) is the cornerstone of therapy. Correction
of the prothrombin time to within 3 seconds of the normal
control value is recommended. Unfortunately, the large
quantities of fresh frozen plasma required to shorten a pro-
longed prothrombin time and the transient nature of the re-
sponse limit the effectiveness of this therapy. A prolonged
bleeding time also can be treated with diamino-8-D-arginine
vasopressin (DDAVP). DDAVP shortens the bleeding time in
patients with cirrhosis by releasing endogenous stores of von
Willebrand multimers. Because cryoprecipitate contains large
quantities of these multimers and is also rich in fibrinogen,
intravenous infusion of 10 U of cryoprecipitate should be
considered when hemorrhage cannot be controlled by other
means. Recombinant activated factor VIIa is another option.
Preoperative platelet transfusions are indicated when the
platelet count is less than 100,000/mm3; 8 to 10 U are given
initially and are repeated postoperatively until the patient
is hemodynamically stable. Hyperfibrinolysis may develop
Paracentesis
Preoperative evaluation in a patient with new or worsening
ascites should include diagnostic paracentesis to exclude in-
fection or malignancy and to differentiate spontaneous from
secondary bacterial peritonitis (Table 10-7). Routine admis-
sion paracentesis should be strongly considered for all
patients with cirrhotic ascites because up to 20% of these
patients are found to have spontaneous bacterial perito-
nitis [ C Gines et al, 2004]. The classic symptoms and signs
of spontaneous bacterial peritonitis are abdominal pain,
Gastrointestinal bleeding
High protein intake
Constipation
Azotemia
Hypokalemic alkalosis
Infection (especially spontaneous bacterial peritonitis)
Hypoxia
Central nervous system depressant drugs (e.g., narcotics and
benzodiazepines)
Portosystemic shunt (TIPS or surgical shunt)
Progressive hepatocellular dysfunction
Nutrition
Many patients with chronic liver disease experience severe
protein-energy malnutrition, which may contribute to the
development of complications and may adversely affect sur-
vival. In malnourished patients unable to tolerate enteral
feeding, a period of preoperative parenteral nutrition may be
beneficial. Parenteral nutrition is not without potentially seri-
ous hazards, such as those related to the central venous cath-
eter itself (i.e., pneumothorax and catheter-related sepsis).
Enteral nutritional supplementation appears to improve im-
munocompetence and short-term prognosis in patients with
cirrhosis. Limited evidence shows that perioperative nutritional
support may reduce short-term operative mortality and morbid-
ity, but the effect of this support on long-term survival is uncer-
tain. Although oral supplementation is preferred, placement of
a small-bore feeding tube may be necessary in patients with
POSTOPERATIVE MONITORING
In the postoperative period, patients with liver disease need
to be observed closely for signs of hepatic decompensation,
including encephalopathy, coagulopathy, ascites, and wors-
ening jaundice. The prothrombin time and serum bilirubin
level are probably the best measures of hepatic function to
follow. However, an elevated serum bilirubin without wors-
ening coagulopathy can be expected in the immediate post-
operative period, especially after complicated surgical proce-
dures, multiple blood transfusions, bleeding, hemodynamic
instability, or infection. Renal function must be monitored as
well because of the risk of hepatorenal syndrome.
Hypoglycemia may occur in patients with end-stage cir-
rhosis or fulminant hepatic failure as a result of depleted he-
patic glycogen stores. Serum glucose levels should be moni-
tored closely when postoperative liver failure is suspected.
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Aranha GV, Sontag SI, Greenlee HB: Cholecystectomy in cirrhotic patients:
A formidable operation. Am J Surg 143:55-60, 1982.
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elective cardiac surgery in patients with cirrhosis. Ann Thorac Surg 67:
1334-1338, 1999.
Brolin RE, Bradley LJ, Taliwal RV: Unsuspected cirrhosis discovered during
elective obesity operations. Arch Surg 133:84-88, 1998. B
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Cheung RC, Hsieh F, Wang Y, et al: The impact of hepatitis C status on
postoperative outcome. Anesth Analg 97:550-554, 2003. B
Dixon JM, Armstrong CP, Duffy SW, et al: Factors affecting morbidity and
mortality after surgery for obstructive jaundice: A review of 373 patients.
Gut 24:845-852, 1983. B
Friedman LS: The risk of surgery in patients with liver disease. Hepatology
29:1617-1623, 1999. C
Garrison RN, Cryer HM, Howard DA, et al: Clarification of risk factors for
abdominal operations in patients with hepatic cirrhosis. Ann Surg
199:648-655, 1984.
Gholson CF, Provenza JM, Bacon BR: Hepatologic considerations in patients
with parenchymal liver disease undergoing surgery. Am J Gastroenterol
85:487-496, 1990. C
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N Engl J Med 350:1646-1654, 2004. C
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hepatocellular carcinoma. Surg Gynecol Obstet 174:245-254, 1992.
Malinchoc M, Kamath PS, Gordon FD, et al: A model to predict poor sur-
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Mansour A, Watson W, Shayani V, et al: Abdominal operations in patients
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1997.
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2004. B
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Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized controlled
trials, systematic reviews of studies other than RCTs, cross-sectional studies, retro-
spective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
393
393
Adapted from Presutti RJ, Gorman RS, Swain JM: Primary care perspective
on bariatric surgery. Mayo Clin Proc 79:1158-1166, 2004.
Diabetes
Coronary artery disease
Hypertension
Osteoarthritis
Obstructive sleep apnea
Gastroesophageal reflux disease
Pulmonary insufficiency
Chronic venous stasis
Dysmenorrhea
Gallbladder disease
Skin infections
NONSURGICAL MANAGEMENT
Dieting, exercise, and medications have been the mainstays
of treatment for obesity; however, there is little evidence in
support of these methods. The 5-year failure rate approaches
100% for persons who diet to control weight. The reason is
that few people can sustain a high dietary adherence level,
and most do not exercise the recommended 150 minutes/
week. Medications such as sibutramine (Meridia) and orlistat
(Xenical) have afforded some weight loss. However, side
Pouch
Figure 11-1 • A band and staples are used to create a small stomach pouch.
To subcutaneous reservoir
Pouch
Figure 11-2 • The stomach opening can be tightened or loosened over time
to change the size of the passage.
Common limb
To colon
Figure 11-3 • Schematic view of Roux-en-Y stomach bypass. (Adapted from
Choban PS: Bariatric surgery for morbid obesity: Why, who, when, how, where, and then
what? Cleve Clin J Med 69:897-903, 2002.)
Stomach
Small Roux-en-Y
intestines stomach bypass:
large portion of
stomach and
duodenum are
bypassed
Duodenum
“Y” connection
Figure 11-4 • Roux-en-Y stomach bypass. Large portions of the stomach
and duodenum are bypassed.
Biliopancreatic
diversion (BPD)
Biliopancreatic
diversion with
duodenal switch
Pyloric
valve
PREOPERATIVE ASSESSMENT
Although preoperative requirements for bariatric surgical
procedures vary, the medical consultant is certainly a
key link in coordinating the preoperative screening and
assessments for patients who are interested in these proce-
dures. The current indications for bariatric surgery are a BMI
of at least 40 or a BMI of 35 or greater in patients with co-
morbid conditions (Box 11-2). In addition to these standard
criteria, the medical consultant and patient will need to ver-
ify attempts at weight loss using diet, exercise, and medica-
tions for approximately 6 months during the last 2 years. The
medical consultant may also have some insight into which
patients would be at risk for maladaptive eating disorders or
would be poor follow-up candidates. Additional assistance
includes counseling and providing medical therapies as
needed for cessation of tobacco use, a requirement for bariat-
ric procedures. Depending on the patient’s medical condi-
tions and comorbidities, evaluation by subspecialists, includ-
ing those in the fields of cardiology, pulmonology, and
endocrinology, may also be requested before proceeding. The
reasons for referral may include stress testing and evaluation
of pulmonary hypertension, pulmonary function testing, and
maximizing control of diabetes. Some surgical candidates are
required to undergo a right upper quadrant ultrasound ex-
amination to identify possible cholelithiasis. Patients who
have evidence of cholelithiasis are generally given a prophy-
lactic cholecystectomy during the bariatric procedure.
A psychiatric assessment is required and is usually performed
PREOPERATIVE ASSESSMENT
Box 11-2
AND REQUIREMENTS FOR PROCEDURES
PERIOPERATIVE MANAGEMENT
Although the selection of anesthetic agents and their admin-
istration is the responsibility of the anesthesiologist, the
medical consultant must know several important concepts.
Anesthesia for these procedures has the potential to be haz-
ardous because of the increased risk of difficult intubation
and the potential for aspiration of gastric contents. Neck
circumference in the obese patient is an excellent predic-
tor of problematic intubation; the reported incidence of
difficult intubation in patients with a 40-cm neck circum-
ference is 5%, and the probability of difficult intubation
POSTOPERATIVE MANAGEMENT
Expected hospital stay following a bariatric surgical proce-
dure is between 2 to 5 days. Two to 3 days following the
procedure, before the initiation of enteral feeding, patients
usually undergo an upper gastrointestinal radiographic series
with contrast to evaluate for any leaks. If no leaks are identi-
fied, patients remain on a pureed diet for 4 weeks. Additional
instructions may vary, but patients are often advised to re-
frain from lifting and from heavy work. They must not drive
for 2 weeks following the procedure and should abstain from
sexual intercourse for the first month postoperatively. Follow-
up occurs at approximate intervals of 2 weeks, 1 month,
6 weeks, 3 months, 12 months, 18 months, and 2 years, with
annual visits thereafter.
SHORT-TERM COMPLICATIONS
Operative mortality rates evaluated in different studies vary
anywhere from 0.1% for restrictive procedures alone, to 0.5%
for gastric bypass procedures, to 1% for biliopancreatic diver-
sion with or without duodenal switch. Immediate postopera-
tive complications include wound problems (infections, dehis-
cence, hernias, and seromas) in approximately 15% of patients.
After upper abdominal operations, obese patients have a 45%
incidence of atelectasis, which may prompt anesthesiologists or
pulmonologists to use continuous positive airway pressure or
bilevel positive airway pressure postoperatively. Laparoscopic
bariatric surgery decreases these wound problems and reduces
atelectasis and postoperative pain. Laparoscopic procedures are
increasingly used more frequently for patients who weigh less
than 350 lb (ⱕ160 kg). DVT and PE affect 1% and 0.2% of
these patients, respectively, despite preventive measures. All
patients should receive prophylaxis for DVT and PE according
to the 2004 American College of Chest Physicians guidelines
LONG-TERM COMPLICATIONS
The dumping syndrome consists of postprandial sweating,
weakness, hypoglycemia, and malaise and occurs in the ma-
jority of patients who have undergone a malabsorptive pro-
cedure. This syndrome most commonly occurs after eating
foods high in sugar or fat and is believed to be related to fluid
shifts from the intravascular space to the intestine. For this
reason, these foods should be avoided by persons who have
undergone gastric bypass. The condition is severe in ap-
proximately 1% of patients, but it generally disappears over
time as the body adjusts to the malabsorption. Most bariatric
surgeons believe that this is a favorable side effect that
teaches patients to avoid maladaptive eating behaviors.
Nutritional deficiencies are a concern with all types of
bariatric surgical procedures because of both decreased in-
take and absorption. Procedures that have a malabsorptive
component and those with a shorter common channel are
much more commonly associated with these deficiencies.
Vitamin and mineral deficiencies are particularly common
because absorption of these substances occurs in the proximal
small intestine, which is bypassed with these procedures. Fat-
soluble (A, D, E, K) vitamin deficiencies are particularly com-
mon after biliopancreatic bypass procedures. Vitamin B12 and
folate deficiencies have been implicated in hyperhomocystein-
emia, seen in approximately 66% of patients who undergo
bariatric surgical procedures. Iron deficiency is most com-
monly seen in menstruating women, with a prevalence rang-
ing from 20% to 50%. The deficiency of iron is caused by two
Postoperative Maintenance
Prevention and treatment of these long-term complications are
accomplished by taking daily multivitamins and minerals. In-
gesting 60 g/day of protein is recommended for malabsorptive
procedures. Laboratory testing should be done every 3 months
CONCLUSION
Bariatric surgery is proving to be a safe, effective, and increas-
ingly popular method for combating obesity and its related
comorbid conditions. The medical consultant will play an
important role preoperatively in deciding which patients
may be appropriate candidates for these procedures, by help-
ing to document weight loss attempts, and in coordinating
surgical clearance. Postoperatively, the medical consultant
should be aware of possible short- and long-term complica-
tions and can provide support and knowledge for patients
who have undergone these procedures.
Selected Readings
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Brodsky JB, Lemmens HJM, Brock-Utne JG, et al: Morbid obesity and tra-
cheal intubation. Anesth Analg 94:732-736, 2002. A
Brolin RE: Bariatric surgery and long-term control of morbid obesity. JAMA
288:2793-2796, 2002.
Buchwald H, Avidor Y, Braunwald E, et al: Bariatric surgery: A systematic
review and meta-analysis. JAMA 292:1724-1737, 2004.
Choban PS: Bariatric surgery for morbid obesity: Why, who when, how,
where, and then what? Cleve Clin J Med 69:897-903, 2002.
Dansinger ML, Gleason JA, Griffith JL, et al: Comparison of the Atkins,
Ornish, Weight Watchers and Zone Diets for weight loss and heart dis-
ease risk reduction: A randomized trial. JAMA 293:43-53, 2005.
Hocking MP, Duerson MC, O’Leary JP, Woodward ER: Jejunoileal bypass
for morbid obesity: Late follow-up in 100 cases. N Engl J Med 308:
995-999, 1983.
MacGregor A: The story of surgery for obesity. American Society of Bariatric
Surgery. Available at http://www.asbs.org
Mokdad AH: The spread of the obesity epidemic in the United States, 1991-
1998. JAMA 282:1519-1522, 1999.
National Heart, Lung and Blood Institute and North American Association
for the Study of Obesity: The Practical Guide to the Identification,
Evaluation and Treatment of Overweight and Obesity in Adults. Bethesda,
MD, National Institutes of Health, 2000.
Ogunnaike BO, Jones SB, Jones DB, et al: Anesthetic considerations for
bariatric surgery. Anesth Analg 95:1793-1805, 2002. C
Presutti RJ, Gorman RS, Swain JM: Primary care perspective on bariatric
surgery. Mayo Clin Proc 79:1158-1166, 2004. C
Scholten DJ, Hoedema RM, Scholten SE: A comparison of two different
prophylactic dose regimens of low molecular weight heparin in bariatric
surgery. Obes Surg 12:19-24, 2002. B
Schumann R, Jones S, Ortiz V, et al: Best practice recommendations for an-
esthetic perioperative care and pain management in weight loss surgery.
Obes Res 13:254-266, 2005.
Shepherd MF, Rosborough TK, Schwartz M: Heparin thromboprophylaxis in
gastric bypass surgery. Obes Surg 13:249-253, 2003. B
Sjöström L: Lifestyle, diabetes and cardiovascular risk factors 10 years after
bariatric surgery. N Engl J Med 351:2683-2693, 2004.
Steinbrook R: Surgery for severe obesity. N Engl J Med 350:1075-1079,
2004.
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2005.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized clinical tri-
als, systematic reviews of studies other than RCTs, cross-sectional studies, retro-
spective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
411
Preoperative Evaluation
Diabetic patients undergoing surgical procedures fall into a
higher risk category than comparable patients without diabe-
tes. Diabetic patients in general have a higher prevalence of
cardiovascular, renal, and neurologic diseases, all of which
can lead to increased perioperative morbidity and mortality.
The prevalence and incidence of and mortality from all forms
of cardiovascular disease are two- to eightfold higher in per-
sons with diabetes than in persons without diabetes. More-
over, patients with diabetes have an increased risk of cardiac
events once the diagnosis of cardiovascular disease has been
established. Therefore, the American College of Cardiology/
American Heart Association guideline for risk stratification
before noncardiac surgery designates diabetes as a coronary
risk equivalent, which means that patients with diabetes
when they are used with insulin or other agents that increase
endogenous insulin secretion. These drugs should be with-
held starting on the day of surgery and resumed when the
patient’s oral intake is reestablished.
5-␣-Glucosidase Inhibitors
␣-Glucosidase inhibitors work by delaying glucose absorp-
tion and therefore lowering postprandial hyperglycemia.
They tend to have minimal effects on glycemic control and
are not well suited to postoperative patients with variable
oral intake. Furthermore, they cause abdominal pain, diar-
rhea, and flatulence in a large percentage of patients. These
agents should be held starting on the day of surgery and
resumed when the patient reestablishes oral intake.
In conclusion, each of these major classes of oral diabetes
agents has significant limitations for use in the hospitalized
surgical patient. These drugs offer little flexibility and may
produce untoward side effects. A summary of these agents is
provided in Table 12-1.
Subcutaneous Insulin
Insulin is the agent of choice to obtain glycemic control in the
hospitalized surgical patient (Table 12-2). The components of
the daily insulin requirement are classified as basal, nutri-
tional or prandial, correction or supplemental, and illness or
stress related. Basal insulin is defined as the amount of exog-
enous insulin per unit of time necessary to prevent hepatic
gluconeogenesis and ketogenesis. Therefore, it is always re-
quired in patients with type 1 diabetes and in patients who
lack endogenous insulin production. It may not be required
in patients with type 2 diabetes or in those with only stress-
induced hyperglycemia because these patients maintain some
endogenous insulin production. In general, basal insulin ac-
counts for approximately 40% to 50% of the total daily insu-
lin requirement, and it can be provided by any one of several
strategies such as continuous subcutaneous insulin infusion
(i.e., insulin pump), once-daily injection of a long-acting
Ch12-X2385_411_452.indd 418
TABLE 12-2 Insulin Formulations Used in the Treatment of Diabetes
Name: Generic
Type of Insulin (Proprietary) Onset Peak Duration
Rapid-acting analogues Lispro (Humalog) 5-15 min 1-2 hr 3-4 hr
Aspart (NovoLog)
Glulisine (Apidra)
Mixed insulin: 70% intermediate-acting insulin aspart Novolog Mix 70/30 5-15 min 1-4 hr 15-18 hr
protamine suspension and 30% rapid-acting aspart insulin
12/19/07 3:00:37 PM
12 • Perioperative Management of Endocrine Disorders 419
cally mixed in a 1:1 ratio with 0.9% saline solution, and the
infusion is given as a piggy back with other intravenous flu-
ids. Frequent blood glucose monitoring is performed, and
adjustments to the insulin infusion rate are made according
to the hospital protocol.
Conversion from intravenous insulin infusion to subcuta-
neous insulin therapy should be attempted only after the
patient’s clinical status has stabilized; more specifically, the
patient is no longer critically ill, is not receiving volume re-
suscitation and pressors, and has stabilized nutritional re-
quirements. The patient’s 24-hour insulin requirement can
be estimated by extrapolating the average hourly rate neces-
sary to achieve the goal serum glucose in the most recent
6- to 8-hour period. Eighty percent of the 24-hour require-
ment is then divided equally into basal and nutritional insu-
lin. For example, suppose a patient has been maintained in
the target glycemic range for the past 6 hours on an average
of 2 U/hour. The total 24-hour requirement for that patient
is 2 U/hour ⫻ 24 hours ⫽ 48 U of insulin. One then multi-
plies this number by 80%, which equals 38 U when round-
ing to the nearest unit. Therefore, 19 U would be given as
basal insulin, and 19 U would be given throughout the day
as nutritional or prandial doses.
When transitioning from continuous intravenous insulin
infusion to subcutaneous insulin therapy, the first dose of
subcutaneous insulin must be given before the intravenous
insulin is stopped. If administering rapid-acting or short-
acting insulin, one should wait 15 to 30 minutes before dis-
continuing the infusion. If intermediate-acting or long-acting
insulin is given, one should wait 2 to 3 hours before discon-
tinuing the insulin infusion.
A minority of patients receiving insulin infusions will not
require standing subcutaneous doses of insulin on discon-
tinuing the infusion. These patients typically have type
2 diabetes or stress-induced hyperglycemia and tend to
require less than 0.5 U/hour of insulin.
Special Situations
Enteral Tube Feeding
Management of glycemic control for the patient requiring
enteral tube feeding is dictated by the manner in which the
tube feeding is administered. Continuous 24-hour tube feed-
ing infusions provide the patient with a steady supply of car-
bohydrate; therefore, insulin needs to be present in a more
continuous fashion to prevent hyperglycemia. Several options
are available, none of which has been studied in large clinical
trials. Basal insulin can be provided by a once-daily injection
of long-acting insulin or twice-daily injections of an interme-
diate-acting insulin. Correction doses of a rapid-acting ana-
logue are used to correct unexpected hyperglycemia. The
major concern with this approach is the high risk of hypogly-
cemia if the tube feeding is interrupted; therefore, the basal
insulin should be kept at no more than 40% of the total daily
insulin requirement, and the blood glucose should be main-
tained at the high end of the target range. We prefer to use
regular insulin every 6 hours with the addition of correction
doses to correct for unexpected hyperglycemia. This offers
flexibility and reduces the risk of hypoglycemia if the tube
feeding is inadvertently discontinued. If the tube feeding is
given during only a portion of the day, an intermediate-acting
insulin should be given approximately 1 to 2 hours before the
tube feeding is started. For example, if the tube feeding is
given from 8 PM to 6 AM the patient would receive a dose of
intermediate-acting insulin such as NPH at 6 or 7 PM.
HYPOTHYROIDISM
The most common cause of hypothyroidism in the United
States is chronic autoimmune thyroiditis (Hashimoto’s thy-
roiditis), which causes destruction of the thyroid gland.
Other causes of primary hypothyroidism include surgical
removal, treatment with radioactive iodine, drugs, or infiltra-
tion and replacement of the gland by tumor. Secondary hy-
pothyroidism can be caused by pituitary and hypothalamic
diseases. Patients classically present with fatigue, weight
gain, constipation, cold intolerance, dyslipidemia, depres-
sion, and dry skin. Laboratory evaluation shows an elevated
thyroid-stimulating hormone (TSH) concentration in pri-
mary hypothyroidism.
Myxedema coma is an extreme expression of hypothy-
roidism. It is characterized by coma, loss of deep tendon re-
flexes, cardiovascular collapse, and even death. This clinical
presentation is frequently accompanied by hypothermia,
hypoxia, hyponatremia, and hypoglycemia. It occurs mostly
during or after the sixth decade, and 80% of the cases occur
in women. More than 90% of cases have been reported to
occur during winter months and are frequently associated
with intercurrent illness or stressors such as burns, trauma,
and nonthyroid surgery. Other common precipitating factors
include pneumonia, other infections, and sedating drugs.
Perioperative Management
Hypothyroid patients undergoing nonthyroid surgery can be
broadly grouped into the following categories, based on their
clinical and biochemical profiles:
1. Most patients with hypothyroidism on replacement ther-
apy are euthyroid (clinically and biochemically) at the
time of surgery. Euthyroidism can be confirmed by a nor-
mal TSH level. In patients with central hypothyroidism
(reduced circulating thyroid hormone as a result of inad-
equate stimulation of a normal thyroid gland by TSH,
which may be secondary to pituitary disease or tertiary
resulting from hypothalamic dysfunction), TSH levels are
not representative of thyroid function, and free thyroxine
(T4) should be obtained. Such euthyroid patients do not
carry an increased risk of perioperative morbidity and do
not require special treatment other than continuation of
their usual thyroid hormone replacement. Most of these
patients can take their replacement dose on the day of the
operation, although it is optional because the half-life of
T4 is 6 to 7 days. During the postoperative period, pa-
tients can be given levothyroxine (LT4) treatment orally or
HYPERTHYROIDISM
Hyperthyroidism has many causes, the most common be-
ing Graves’ disease. This is an autoimmune disorder in
which TSH receptor antibodies abnormally stimulate the
thyroid gland to produce excessive thyroid hormone.
Other causes of hyperthyroidism include toxic multinodu-
lar goiters, toxic nodules, thyroiditis, and exogenous inges-
tion of LT4.
Hyperthyroidism may be clinically overt, and patients
may present with classic symptoms such as tachycardia,
tremor, weight loss, heat intolerance, goiter, and ophthal-
mopathy. However, patients may also present in an atypical
fashion. This presentation is known as apathetic or “masked”
hyperthyroidism and is more common in the geriatric popu-
lation. These patients may be asymptomatic, or they may
complain only of fatigue. Occasionally, they present in atrial
fibrillation without any other symptoms.
Laboratory investigation reveals a suppressed TSH with a
high free T4 or free T3 concentration. Patients may also have
subclinical hyperthyroidism, which is defined by a sup-
pressed TSH but normal free T4 and free T3. Subclinical hy-
perthyroidism can manifest by increased nocturnal pulse
rates, frequent atrial premature beats, or the onset of atrial
fibrillation in elderly patients.
Perioperative Management
1. For an elective surgical procedure, patients with medi-
cally treated and adequately controlled hyperthyroidism
should take their antithyroid medications on the morning
of surgery. It is common for TSH values to remain sup-
pressed as a result of prolonged hyperthyroidism in pa-
tients who have otherwise normalized their free T4 and T3
values on therapy. The TSH level in such cases will even-
tually increase (within few months) and should not be
considered a contraindication to surgery.
2. If possible, patients with uncontrolled hyperthyroidism
should have their surgical procedure postponed until they
receive adequate medical therapy to reduce the risk of
thyroid storm.
PHEOCHROMOCYTOMA
Pheochromocytoma is an uncommon neuroendocrine tumor
of the chromaffin cells that occurs in less than 0.2% of
patients with hypertension. In approximately 10% of pa-
tients, the tumor is discovered incidentally during com-
puted tomography or magnetic resonance imaging of the
abdomen for unrelated symptoms. The classic triad of
symptoms in patients with pheochromocytoma consists of
episodic headache, sweating, and tachycardia, accompa-
nied by paroxysmal hypertension. The presence of this
triad has a sensitivity and specificity of more than 90%,
although not all patients have the three classic symptoms,
and patients with essential hypertension may present with
similar symptoms. The diagnosis is made by detecting sig-
nificantly elevated urinary metanephrines or catechol-
amines (24-hour urine collection). Alternatively, plasma
Perioperative Management
Patients with pheochromocytoma have excessive circulat-
ing catecholamines causing vasoconstriction that leads to
both hypertension and hypovolemia. These patients may
experience severe hypertensive crisis or hypotension.
Removal of a pheochromocytoma can result in acute hypo-
tension as a result of a sudden decrease in catecholamines.
Therefore, the perioperative management of pheochromo-
cytoma requires vital cooperation of multispecialty teams
to avoid any preoperative, intraoperative, or postoperative
complications. The goal of perioperative management is to
minimize the risk of clinically significant hypertension or
hypotension in the perioperative period. ␣-Adrenergic
blockers are initiated 10 to 14 days preoperatively to
inhibit the peripheral vasoconstriction produced by
pheochromocytoma-released catecholamines. Another
approach is to treat the patient preoperatively with
calcium channel antagonists to control hypertension
and to use intraoperative nitroprusside for treatment of
significant hypertension [ C Ulchaker et al, 1999]. Periop-
eratively, intravenous hydration with 0.9% saline is also
essential to prevent hypovolemic shock and hypotension
(mainly after removal of the tumor).
PITUITARY DISEASES
The perioperative management of patients with pituitary
disease is complex and varies depending on the underlying
disease. Therefore, an endocrinologist with expertise in pitu-
itary disorders should be involved in the perioperative man-
agement of these patients. Key management concepts include
the following:
• Patients who have a macroadenoma (⬎1 cm) can suffer
from mass effect by tumor compression of adjacent struc-
tures, such as the optic chiasm; therefore, formal visual
field testing should be performed preoperatively.
• Patients with macroadenomas should be screened for hy-
popituitarism, particularly central hypothyroidism (low
free T4 with low to normal TSH) and central adrenal insuf-
ficiency (low cortisol, either random morning value or af-
ter cosyntropin stimulation testing with low to normal
ACTH). Replacement therapy with glucocorticoids and LT4
should be initiated while waiting for the surgical procedure
to be performed. Glucocorticoids should always be started
before LT4 therapy to prevent the onset of adrenal crisis.
• For pituitary surgery, glucocorticoids should be given peri-
operatively because normal ACTH-secreting cells can be
damaged perioperatively, thus leading to adrenal insuffi-
ciency. Glucocorticoids are then tapered over a few days to a
maintenance dose (e.g., prednisone, 5 mg/day), and the HPA
axis is reassessed in 3 months by performing a cosyntropin
stimulation test. The reason we wait 3 months is that it takes
a few weeks to a few months for the adrenals to atrophy and
therefore to lose their response to cosyntropin.
• Transient or permanent diabetes insipidus may occur peri-
operatively. Moreover, during the second postoperative
week, a transient phase of syndrome of inappropriate
antidiuretic hormone can result from release of stored an-
tidiuretic hormone. This syndrome may cause clinically
CALCIUM DISORDERS
Calcium is essential to homeostasis and the function of mul-
tiple organ systems. It should be strictly maintained in the
normal range before, during, and after surgical procedures.
Abnormalities in calcium metabolism are mostly secondary
to parathyroid disease, but they may be a harbinger of other
underlying conditions, such as neoplasia or granulomatous
diseases. Management strategies depend on the severity of
clinical symptoms and the urgency of the underlying medical
conditions. Patients who require urgent surgery can be taken
to the operating room with careful intraoperative and post-
operative monitoring, and calcium concentrations can be
maintained with medical management. Elective surgery can
be deferred until workup of the calcium derangement is
complete. Rarely, patients require intensive care management
secondary to cardiac arrhythmias.
HYPERCALCEMIA
The most common causes of hypercalcemia are hyperpara-
thyroidism and malignancy. In malignant disease, mecha-
nisms of hypercalcemia include parathyroid hormone (PTH)-
related peptide-secreting neoplasms, 1,25(OH)2D-secreting
Diagnosis
Establishing the correct diagnosis is the essential first step in the
treatment of hypercalcemia. A careful history and physical ex-
amination will often help to identify the underlying cause.
Measurement of calcium and intracellular PTH will differentiate
all causes of hypercalcemia into two main categories, PTH me-
diated and non–PTH mediated (malignancy and other causes).
The presence of elevated calcium and PTH invariably estab-
lishes the diagnosis of primary hyperparathyroidism. Plasma
1,25(OH)2D should be measured when sarcoidosis, other
granulomatous disorders, and 1,25(OH)2D-secreting lympho-
mas are considered in the differential diagnosis.
Perioperative Management
Any management of hypercalcemia should be directed at the
underlying pathophysiologic mechanism. The goal is to lower
the serum calcium to a safe level. An assessment of the severity
of the hypercalcemia is needed to guide therapy. Although
there are no formal guidelines, a serum calcium level of 10.5
to 11.9 mg/dL (2.6 to 2.9 mmol/L) is regarded as mild hyper-
calcemia, a level of 12.0 to 13.9 mg/dL (3.0 to 3.4 mmol/L) is
moderate, and severe hypercalcemia is a level of 14.0 mg/dL
(3.5 mmol/L) or greater [Stewart, 2005].
Intravenous Fluids
Patients with moderate to severe hypercalcemia may be
substantially dehydrated as a result of a renal water-
concentrating defect (nephrogenic diabetes insipidus) in-
duced by hypercalcemia and by decreased oral hydration
resulting from anorexia, nausea, or vomiting. The dehydra-
tion leads to a reduction in the glomerular filtration rate that
further reduces the ability of the kidney to excrete the excess
serum calcium. Therefore, volume expansion should be the
first goal of treatment. Although no randomized clinical trials
have been conducted to guide this therapy, in general prac-
tice normal saline is administered at a rate of 200 to 500 mL/
hour, depending on the baseline level of dehydration and
renal function, the patient’s cardiovascular status, the degree
of mental impairment, and the severity of the hypercalcemia.
Patients should have careful clinical monitoring for physical
findings that are consistent with fluid overload.
Medications
1. Loop diuretics are used to increase the renal excretion of
calcium. They should not be administered until after full
hydration has been achieved because they can cause
or worsen dehydration. Dehydration, in turn, leads to a
decline in the glomerular filtration rate and the filtered
load of calcium.
Dialysis
In patients who have acute or chronic renal failure, aggres-
sive saline infusion is not possible, and other therapies such
as bisphosphonates should be used with caution, if at all. In
these circumstances, dialysis against a dialysate containing
little or no calcium is a reasonable and highly effective option
for selected patients.
Ch12-X2385_411_452.indd 448
TABLE 12-7 Commonly Used Treatments for Hypercalcemia
Intervention Dose Onset of Action Calcium Response Cautions
Intravenous fluids 200–500 mL/hr Hours Decreases by 1–3 mg/dL Watch for fluid overload
Loop diuretics 20–40 mg Hours Decreases by 1–3 mg/dL Give only after patient has been
adequately hydrated.
Zoledronic acid 4 mg IV 1–3 days Normalizes in 90% of patients Can cause renal failure and flulike
symptoms
Pamidronate 60–90 mg IV 1–3 days Normalizes in 70% of patients Can cause renal failure and flulike
symptoms
Calcitonin 4–8 IU SQ or IM q12h 12–24 hr Decreases by 1–2 mg/dL May cause flushing and nausea
12/19/07 3:00:41 PM
12 • Perioperative Management of Endocrine Disorders 449
HYPOCALCEMIA
Hypocalcemia is common in older patients with multiple
chronic illnesses. Common causes include idiopathic or auto-
immune hypoparathyroidism, hypomagnesemia, vitamin D
deficiency, acute pancreatitis, hyperventilation, and hypo-
parathyroidism from previous surgery or radiation to the
neck. Before instituting any treatment for hypocalcemia, the
diagnosis should always be verified, because many cases of
hypocalcemia are the artifact of hypoalbuminemia. Manage-
ment aimed at correcting calcium concentrations depends on
the severity of the patient’s symptoms. If symptoms are mild,
oral calcium supplementation can be given; otherwise, intra-
venous calcium should be administered.
Patients with long-standing hypocalcemia may be asymp-
tomatic. In acute hypocalcemia, the patient may present with
perioral numbness, paresthesias, muscle cramps, and mild
mental status changes such as irritability. As hypocalcemia
becomes more severe, there can be neuromuscular and car-
diac findings, including Chvostek’s sign (elicited by tapping
the facial nerve anterior to the ear, which produces spasm of
the muscles of the face; it has been shown to be positive in
10% to 30% of people with normal calcium concentrations)
and Trousseau’s sign (positive when pressure on the wrist in-
duced by inflation of a blood pressure cuff for 3 to 5 minutes
or tapping on the median nerve induces carpal spasm), as
well as mental status changes, seizures, tetany, hypotension,
and acute heart failure.
Acute hypocalcemia decreases cardiac function by length-
ening phase 2 of the cardiac action potential, which results
in prolongation of the ST segment and the QT interval on the
electrocardiogram. This finding is an independent risk factor
for arrhythmias and cardiac death. Patients who present to
the hospital in cardiac arrest often are severely hypocalcemic.
Hypocalcemia can rarely lead to cardiac failure, and this can
be reversed with administration of calcium.
Perioperative Management
Treatment should be given to every symptomatic patient and
to patients with serum calcium of less than 7.6 mg/dL who
may be at risk of developing complications. In general,
symptomatic patients should be given parenteral calcium,
whereas asymptomatic patients can be managed with oral
calcium supplementation as follows:
1. Intravenous calcium: Calcium gluconate, 10 mL
10% weight/volume (90 mg of calcium) diluted in 50 mL
of 5% dextrose or 0.9% sodium chloride can be given
intravenously by slow injection (5 to 10 minutes) and
can be repeated as necessary until symptoms disappear.
If deemed necessary, a continuous infusion can be started
by diluting 10 ampules of calcium gluconate in 1 L of 5%
dextrose or normal saline at a rate of 50 mL/hour. The
goal is to keep serum calcium in the low normal range.
In the setting of hypocalcemia, one should always antici-
pate simultaneous abnormalities in magnesium concen-
trations because intravenous magnesium administration
may be necessary to achieve normalization of calcium
concentrations.
2. Oral calcium: Different calcium supplements are available
on the market. The patient can be given 400 to 800 mg of
elemental calcium every 8 to 12 hours. The goal is to keep
the patient asymptomatic and to avoid any complications
associated with hypercalciuria, especially in the absence of
PTH or its function.
3. Vitamin D: In the setting of severe 25-hydroxyvitamin D
deficiency, ergocalciferol (vitamin D2) 50,000 U (every
week for 8 weeks) can be given without any risk of toxicity.
Patients with mild or moderate deficiency should receive
800 to 1200 IU/day of cholecalciferol (vitamin D3). Serum
calcium and urine calcium should be initially checked on a
weekly basis and then at least every 6 months to ensure
stabilization.
Selected Readings
American College of Endocrinology: Position statement on inpatient diabe-
tes and metabolic control. Endocr Pract 10:5-9, 2004.
American Diabetes Association: Clinical practice recommendations 2005.
Diabetes Care 28(Suppl 1):S24-S28, 2005.
Axelrod L: Perioperative management of patients treated with glucocorti-
coids. Endocrinol Metab Clin North Am 32:367-383, 2003.
Binstock ML, Mundy GR: Effect of calcitonin and glutocorticoids in combi-
nation on the hypercalcemia of malignancy. Ann Intern Med 93:269-
272, 1980.
Bode BW, Braithwaite SS, Steed RD, et al: Intravenous insulin infusion
therapy: Indications, methods, and transition to subcutaneous insulin
therapy. Endocr Pract 10(Suppl 2):71-80, 2004. A
Clement S, Braithwaite S, Magee MF, et al: Management of diabetes and
hyperglycemia in hospitals. Diabetes Care 27:553-591, 2004. C
Connery LE, Coursin DB: Assessment and therapy of selected endocrine
disorders. Anesthesiol Clin North Am 22:93-123, 2004.
Furnary AP, Wu Y, Bookin SO: Effect of hyperglycemia and continuous in-
travenous insulin infusions on outcomes of cardiac surgical procedures:
The Portland Diabetes Project. Endocr Pract 10(Suppl 2):21-33, 2004.
Glister B, Vigersky R: Perioperative management of type 1 diabetes mellitus.
Endocrinol Metab Clin North Am 32:411-436, 2003.
Jabbour SA: Steroids and surgical patients. Med Clin North Am 85:
1140-1147, 2001.
Krinsley JS: Effect of an intensive glucose management protocol on the mor-
tality of critically ill adult patients. Mayo Clin Proc 79:992-1000, 2004.
Mercado DL: Perioperative medication management. Med Clin North Am
87:41-57, 2003. C
Oelkas W: Adrenal insufficiency. N Engl J Med 335:1206-1212, 1996.
Pacak K, Linehan WM, Eisenhofer G, et al: Recent advances in genetics,
diagnosis, localization, and treatment of pheochromocytoma. Ann In-
tern Med 134:315-329, 2001. C
Salem M, Tainsh RE, Bromberg J, et al: Perioperative glucocorticoid cover-
age: A reassessment 42 years after emergence of a problem. Ann Surg
219:416-425, 1994. C
Schiff RL, Welsh GA: Perioperative evaluation and management of the patient
with endocrine dysfunction. Med Clin North Am 87:175-192, 2003.
Sherman SI, Ladenson PW: Complications of surgery in hypothyroid pa-
tients. Am J Med 90:367-370, 1991.
Stewart AF: Hypercalcemia associated with cancer. N Engl J Med 352:373-
379, 2005.
Ulchaker JC, Goldfarb DA, Bravo EL, et al: Successful outcomes in pheochro-
mocytoma surgery in the modern era. J Urol 161:764-767, 1999. C
Umpierrez GE, Isaacs SD, Bazargan N, et al: Hyperglycemia: An indepen-
dent marker of in-hospital mortality in patients with undiagnosed diabe-
tes. J Clin Endocrinol Metab 87:978-982, 2002.
Van den Berghe G, Wouters P, Weekers F, et al: Intensive insulin therapy in
critically ill patients. N Engl J Med 345:1359-1367, 2001. A
Van den Berghe G: How does blood glucose control with insulin save lives
in intensive care? J Clin Invest 114:1187-1195, 2004.
Vance ML: Perioperative management of patients undergoing pituitary sur-
gery. Endocrinol Metab Clin North Am 32:355-365, 2003.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized clinical
trials, systematic reviews of studies other than RCTs, cross-sectional studies,
retrospective studies. C —Consensus statements, expert guidelines, usual prac-
tice, opinion.
453
PREOPERATIVE EVALUATION
Cardiovascular Risk Stratification
Patients should be evaluated in the same manner as general
surgical patients, and all medical conditions should be opti-
mally controlled. Perioperative cardiovascular risk is esti-
mated by using criteria developed by the American Society of
Anesthesiologists or the American College of Cardiology/
American Heart Association.
Unless specified, ophthalmic procedures are often per-
formed in the outpatient setting, in which advanced medical
services are sparse or unavailable. Patients at moderate car-
diovascular risk should preferably have procedures per-
formed in facilities with advanced medical support, whereas
PERIOPERATIVE ANTICOAGULANTS
Patients undergoing cataract surgery do not need to dis-
continue antiplatelet agents or reverse therapeutic anti-
coagulation [ B Dunn and Turpie, 2003]. In general, antiplate-
let agents and therapeutic anticoagulation need not be
discontinued for most ophthalmic procedures. However,
small amounts of bleeding can reduce surgical outcome con-
siderably. Antiplatelet agents are preferably discontinued if
the patient has no coexisting diseases requiring antiplatelet
therapy, such as in the healthy geriatric patient taking daily
aspirin. Warfarin is safely discontinued only in patients re-
ceiving prophylactic anticoagulation, such as in atrial fibril-
lation with no history of embolic stroke; otherwise, these
patients should be therapeutically anticoagulated preopera-
tively. Surgeons will then make specific requests, on a case-
by-case basis, to hold anticoagulation based on the type of
procedure or a prior history of bleeding [ C Parkin and Man-
ners, 2000]. Patients who require that therapeutic anticoagu-
lation be reversed may need intravenous unfractionated
heparin or subcutaneous low-molecular-weight heparin to
maintain anticoagulation while warfarin is discontinued.
OPHTHALMIC MEDICATIONS
A review of the topical ocular medications received by pa-
tients is part of the differential diagnosis when postoperative
complications are evaluated. Eye drops may enter the naso-
lacrimal duct and may be systemically absorbed through the
nasal mucosa or the gastrointestinal tract. -Blockers can
cause bradycardia (especially in the patient with cardiac con-
duction disease), bronchospasm, or congestive heart failure.
Sympathomimetic agents and atropine cause tachycardia and
aggravate underlying coronary artery disease. Summaries of
the most common ophthalmic medications and their compli-
cations are given in Tables 13-1 and 13-2. The consultant
TYPE OF ANESTHETIC
The final decision regarding the use of general or local anes-
thesia resides with the anesthesiologist and the surgeon. From
a technical standpoint, general anesthesia offers greater im-
mobilization of the patient and better surgical control. Gen-
eral anesthesia may offer benefits to patients who are unduly
anxious, restless, or suffering from specific conditions (e.g.,
osteoarthritis) that prohibit lying comfortably in a supine
position. Although data suggest that local anesthesia is equiv-
alent to general anesthesia in terms of the risk of complica-
tions, the design of this research may have been flawed be-
cause sicker patients may have been selected to receive local
anesthesia. No large-scale series have been repeated. A com-
monly held belief is that local anesthesia is safer for patients
with borderline pulmonary status or those who have heart,
liver, or kidney disease and who are susceptible to problems
related to mechanical ventilation or anesthetics. In addition,
blood pressure shifts are more likely with general anesthesia.
ANTIBIOTIC PROPHYLAXIS
The use of systemic antibiotic prophylaxis for patients at
risk for endocarditis remains undefined. The eye is a sterile
organ, and manipulation is unlikely to cause bacteremia. In
Postoperative Bradycardia
Postoperative bradycardia is a physiologic reflex that produces
a decrease in heart rate secondary to the vagotonic effects of
traction on the extraocular muscles or pressure on the eye.
This arrhythmia is more common in children. The oculocar-
diac reflex can result in asystole or arrhythmias, and this reflex
should be kept in mind if a patient experiences intraoperative
bradycardia. The consultant should evaluate the possibility of
other reversible causes (such as -blocker eye drops) while
observing the patient. The effects of the reflex should resolve
within several hours if the bradycardia has no other cause.
Other arrhythmias may be triggered by perioperative drugs or
undiagnosed coronary artery disease and should be managed
and evaluated similarly to any new-onset arrhythmia.
Metabolic Acidosis
Carbonic anhydrase inhibitors produce non–anion gap aci-
dosis that is usually marked after the first few days of starting
one of these drugs. This condition is often compensated and
of little clinical concern.
Urinary Retention
Male patients who experience symptomatic urinary retention
following ophthalmic surgical procedures often have some
form of prostate disease. In patients with prostate disease,
diuretics of all types should be used with caution.
High-Dose Corticosteroids
Patients who receive high-dose corticosteroids are at risk for
steroid-related complications, most commonly glucose intol-
erance, gastritis, hypertension, and mental status changes.
Patients receiving corticosteroids for more than 3 to 4 weeks
should be considered for preoperative stress doses.
I recommend that patients receiving high-dose cortico-
steroids be evaluated with daily serum finger glucose checks
Selected Readings
Adler AG, Kountz DS: Eye surgery in the elderly. Clin Geriatr Med 6:
659-667, 1990. C
Bass EB, Steinberg EP, Luthra R, et al: Do ophthalmologists, anesthesiologists,
and internists agree about preoperative testing in healthy patients under-
going cataract surgery? Arch Ophthalmol 113:1248-1256, 1995. C
Britman NA: Cardiac effects of topical timolol. N Engl J Med 300:562,
1979. C
Cavallini GM, Saccarola P, D’Amico R, et al: Impact of preoperative testing
on ophthalmologic and systemic outcomes in cataract surgery.
Eur J Ophthalmol 14:369-374, 2004. A
Dunn AS, Turpie AG: Perioperative management of patients receiving oral
anticoagulants: A systematic review. Arch Intern Med 163:901-908,
2003. B
Hall DL, Steen WH, Drummond JW: Anticoagulants and eye surgery.
Ann Ophthalmol 12:759, 1980. C
Katz J, Feldman MA, Bass EB, et al: Study of Medical Testing for Cataract
Surgery Study Team: Adverse intraoperative medical events and their
association with anesthesia management strategies in cataract surgery.
Ophthalmology 108:1721-1726, 2001. B
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized controlled
trials, systematic reviews of studies other than RCTs, cross-sectional studies, ret-
rospective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
465
Cardiovascular Changes
Because the diaphragm is elevated, the heart is displaced to
the left and upward. This change results in apparent enlarge-
ment of the cardiac silhouette on chest radiography and
straightening of the left heart border. Electrocardiographic
changes can also occur with a left axis shift, positional
Q waves in leads III and aVF, and nonspecific ST segment/
T-wave abnormalities.
Cardiac output increases 30% to 50% over nonpregnant
levels as a result of increased stroke volume and heart rate.
Systemic vascular resistance decreases, thus reducing dia-
stolic blood pressure and mean arterial pressure by 5 to
10 mm Hg, and reaches a nadir at 16 to 20 weeks. Cardiac
output is affected by maternal position. In the supine posi-
tion, the enlarged uterus puts pressure on the vena cava and
Pulmonary Changes
As pregnancy progresses and the uterus enlarges, the dia-
phragm is elevated by as much as 4 cm, and the ribs flare
outward. This change causes a slight decrease in total lung
capacity, although vital capacity is unchanged, and a 20%
reduction in functional residual capacity. These anatomic al-
terations increase the risk of postoperative atelectasis, and the
patient should be instructed on deep breathing exercises.
Minute ventilation increases by as much as 50% during
pregnancy as a result of elevated tidal volume. The increase
in minute ventilation leads to the hyperventilation (or dysp-
nea) of pregnancy, which produces mild respiratory alkalosis
with compensatory metabolic acidosis. Normal blood gas
values in pregnancy are a pH of 7.4 to 7.47, a partial pressure
of arterial carbon dioxide (PaCO2) of 30 to 32 mm Hg, and a
normal to slightly elevated partial pressure of arterial
oxygen (PaO2). Serum bicarbonate values remain between
18 and 21 mEq/L. Therefore, a PaCO2 of 40 mm Hg can
represent hypoventilation in the pregnant patient and a risk
Ch14-X2385_465_494.indd 470
loud split 1 88%
M.C. T.C. A2 P2
Diastolic “flow”
murmur 18%
4th
occasional 3rd
loud 84%
14 • Nonobstetric Surgery in the Pregnant Patient
Figure 14-1 • Findings on auscultation of the heart in pregnancy. A2 and P2, aortic and pulmonary elements of
the second heart sound; M.C., mitral closure; T.C., tricuspid closure. (From Gabbe SG, Niebyl JR, Simpson JL [eds]:
Obstetrics: Normal and Problem Pregnancies, 4th ed. New York, Churchill Livingstone, 2001.)
12/20/07 6:46:31 PM
14 • Nonobstetric Surgery in the Pregnant Patient 471
Gastrointestinal Changes
Much of the problem in diagnosing intra-abdominal disor-
ders in pregnant women stems from changes in abdominal
landmarks as the pregnancy progresses, as well as from the
physiologic changes normally seen in pregnancy. By the sec-
ond trimester, the intestines and omentum are displaced su-
periorly and laterally by the expanding uterus, thereby mak-
ing the gastrointestinal tract more vulnerable to penetrating
injuries and the omentum less able to contain areas of peri-
tonitis. The anterior abdominal wall is also elevated so that
underlying inflammation is less likely to manifest with usual
symptoms of peritoneal irritation.
Smooth muscle relaxing effects of elevated levels of pro-
gesterone and decreased levels of motilin cause delayed gas-
tric emptying and decreased intestinal transit times. Delayed
gastric emptying and relaxation of the lower esophageal
sphincter lead to an increased risk of acid reflux and aspira-
tion. Aspiration can be associated with chemical pneumoni-
tis and superimposed bacterial pneumonia; therefore, pa-
tients should be given nonparticulate antacids (e.g., 30 mL
sodium citrate) before induction of general anesthesia. If the
surgical procedure is elective, adequate time should be given
to allow for gastric emptying. Liver function tests remain
normal, with the exception of elevated levels of alkaline
phosphatase to two to four times normal values during the
third trimester.
Renal Changes
The glomerular filtration rate increases during pregnancy by
50%, and the serum concentration of creatinine and blood urea
nitrogen are proportionally decreased. Plasma levels of creati-
nine greater than 0.8 mg/100 mL and blood urea nitrogen
GENERAL CONSIDERATIONS
Timing of Surgery
Timing of nonurgent surgical procedures is an important
consideration in the pregnant patient to minimize the risk of
complications. Common complications of surgery in this
population include bleeding, aortocaval compression syn-
drome, delayed healing, infection, dehiscence, spontaneous
abortion, preterm labor, and fetal morbidity. Because the
most active phase of organogenesis occurs between 6 and
13 weeks’ gestation, the fetus is most susceptible to terato-
genic effects or spontaneous abortion at this time. Anesthesia
is generally avoided during this trimester if at all possible.
Furthermore, although no anesthetic agent has been linked
specifically to premature labor, uterine manipulation,
intra-abdominal infection, and decreased uteroplacental
blood flow and oxygen delivery are predisposing factors to
Imaging
There is always concern about the use of radiologic studies dur-
ing pregnancy, and this is the source of great anxiety to the
pregnant patient. Used properly, diagnostic imaging is usually
harmless to the fetus, and knowledge about the risks of
exposure will help to allay fears and to ensure proper use
(Table 14-3). Most single diagnostic radiologic procedures have
shown no measurable increased risk for fetal harm. However,
cumulative doses or exposure to therapeutic or prolonged fluo-
roscopic examinations may cause significant risk for miscar-
riage, fetal malformation, or mental impairment. Care should
Anesthesia
Anesthesia remains a significant cause of maternal mortality.
Failed intubation and pulmonary aspiration of gastric con-
tents remain the two leading causes of maternal mortality
associated with anesthesia [ C Goodman, 2002]. Pregnant
Ch14-X2385_465_494.indd 475
TIME POST CONCEPTION
Adapted from Centers for Disease Control and Prevention (CDC): Prenatal Radiation Exposure: A Fact Sheet for Physicians by the CDC. Available at http://www
.bt.cdc.gov/radiation/prenatalphysician.asp
12/20/07 6:46:32 PM
476 14 • Nonobstetric Surgery in the Pregnant Patient
Risk of Thromboembolism
It is well established that pregnancy alone increases the risk
of thromboembolic disease (Fig. 14-2 and Table 14-6). This
factor further predisposes the pregnant patient to thrombo-
embolism in addition to the already known perioperative
Suspected DVT
CUS
Positive Negative*
Positive Negative
radiation exposure for the fetus is 0.021 cGy, well within ac-
cepted radiation dose levels of less than 0.05 Gy.
PE is a major cause of maternal death. It may be difficult
to diagnose, given the changes in physiology, which can
cause tachycardia and dyspnea. A careful history and physi-
cal examination are essential to make a decision for further
testing. A lower extremity ultrasound scan may reveal a
thrombus, and no further study is required to begin antico-
agulation. If suspicion remains high, most institutions
now use helical computed tomography (CT) or CT angi-
ography to diagnose PE [ C Schuster et al, 2003].
Investigators have shown that helical CT delivers an
estimated mean fetal dose ranging from 3.3 to 130.8 mGy,
depending on the trimester; the highest exposure occurs late
in pregnancy when the fetus is larger and cannot be shielded
as easily. Radiation exposure during the third trimester, how-
ever, poses the least risk of fetal harm. The dose of exposure
during a ventilation/perfusion scan can be as high as
370 mGy; it exposes the fetus to a higher risk of radiation
effects, and the study may not be adequate for diagnosis.
Patients with acute DVT or PE during pregnancy are treated
with a continuous heparin infusion or low-molecular-weight
heparin. After acute management with heparin, long-term an-
ticoagulation is required. Because of the risk of teratogenesis
with oral warfarin, subcutaneous heparin is the drug of choice
for the continuation of anticoagulation. For patients with a
previous history of DVT or PE, the recommended regimens for
prophylaxis remain controversial because of the lack of con-
trolled trials for this population. The American College of Chest
Physicians conference guidelines recommend the use of subcu-
taneous heparin, 5000 U every 12 hours, as a method of pre-
venting peripartum DVT in patients with a previous history of
thromboembolism. A large, systematic review of the use of
low-molecular-weight heparin in pregnancy confirmed that
this agent is safe and effective for treating and preventing
thrombosis in pregnancy [ B Greer and Nelson-Piercy, 2005].
Analgesia
Pregnancy and lactation present obvious concerns over the ef-
fects of drugs on the developing fetus and newborn. The U.S.
Food and Drug Administration created a classification system
for drugs based on the analysis of risk data (Tables 14-7 and
14-8). Acetaminophen appears to be safe to use during preg-
nancy and lactation in therapeutic doses. Aspirin consumption
during pregnancy may produce adverse effects in the mother,
including anemia, antepartum and postpartum hemorrhage,
prolonged gestation, and prolonged labor. High doses of aspi-
rin may be related to increased perinatal mortality, intrauterine
growth retardation, and teratogenic effects. Regarding the use
of aspirin and other nonsteroidal anti-inflammatory agents,
there is a theoretic risk of premature closure of the ductus
arteriosus in utero that would result in persistent pulmonary
Acute Appendicitis
Acute appendicitis is the most common nonobstetric surgical
problem in the pregnant patient. The incidence of appendi-
citis during pregnancy has been estimated to range from
Cholecystitis
Cholecystectomy for gallbladder disease represents the sec-
ond most common surgical procedure performed in the preg-
nant patient. Its occurrence is estimated to be approximately
0.2 to 0.5 cases per 1000 pregnancies. It is estimated that
between 3.5% and 10% of pregnant patients have asymptom-
atic gallstones. The rate of gallstone formation is increased in
the pregnant patient secondary to decreased gallbladder con-
tractility, higher residual gallbladder bile volume, increased
viscosity of bile, and increased numbers of micelles in which
cholesterol crystals precipitate. The risk of cholelithiasis in-
creases with age and multiparity. Cholelithiasis is the most
common cause of cholecystitis in the pregnant patient.
Presenting signs and symptoms of acute cholecystitis are
similar to those in the nonpregnant patient. Common symp-
toms include nausea, vomiting, anorexia, dyspepsia, intoler-
ance to fatty foods, and colicky right upper quadrant or epi-
gastric pain that may radiate to the flank or the scapula. Biliary
colic attacks are often characterized as acute in onset, triggered
by fatty meals, and episodic. Physical examination may reveal
a low-grade fever, right upper quadrant pain, and Murphy’s
sign (tenderness under the liver with deep inspiration).
Laboratory findings of acute cholecystitis are also similar to
those in the nonpregnant patient. An increased white blood cell
count with a left shift is commonly seen in cholecystitis, as well
as elevated liver enzymes such as aspartate aminotransferase,
alanine aminotransferase, alkaline phosphatase, and bilirubin.
Ultrasound is the diagnostic test of choice for evaluating
biliary disease. It is 95% sensitive in detecting gallstones in
pregnancy and also can show signs of inflammation such
as distention of the gallbladder, pericholecystic fluid, and
Ovarian Disease
Increased use of ultrasonography has led to the increased find-
ing of adnexal masses during pregnancy. Most adnexal masses
are incidental findings on ultrasound and spontaneously
Trauma
The incidence of trauma during pregnancy is approximately
7%. The most common cause of trauma is motor vehicle ac-
cidents, which account for 40% of all traumas in pregnancy.
This is followed by falls (30%), direct assault on maternal
abdomen (20%), and other causes (10%). Domestic violence
is an increasingly recognized cause of trauma to the mother
and fetus. The most common cause of fetal demise is death
of the mother. The second most common cause of fetal death
is abruptio placentae.
Primary treatment in pregnant patients who experience
trauma consists of resuscitation and stabilization of the
Uncommon Disorders
Splenic Artery Aneurysm
Splenic artery aneurysm occurs in approximately 0.1% of
all adults. It is estimated that 6% to 10% of splenic artery
aneurysms will rupture, and 25% to 40% of those ruptures
will occur during pregnancy, especially during the third
trimester. Risk factors for rupture include portal hyperten-
sion and pregnancy. Maternal mortality for ruptured splenic
artery aneurysm is 75%, and fetal mortality is up to 95%.
Patients with a splenic artery aneurysm before rupture are
fairly asymptomatic; vague epigastric pain, left upper
quadrant pain, and left shoulder pain are among the most
common complaints.
Radiologic studies for the diagnosis of splenic artery aneu-
rysm include plain abdominal film, ultrasound, and angiog-
raphy. On plain abdominal film, an oval calcification with a
central lucent area is a very specific sign for aneurysm. In
pregnancy, ultrasound evaluation with Doppler study is pre-
ferred to minimize radiation exposure to the fetus. Angiogra-
phy is the gold standard when the patient is stable, but this
procedure increases radiation exposure to the fetus.
CONCLUSION
In pregnant patients requiring nonobstetric surgical proce-
dures, maternal and fetal morbidity and mortality do increase
with a delay in diagnosis and treatment. In 2003, the American
College of Obstetricians and Gynecologists reissued an opinion
statement that recommended the following: “Although there
are no data to support specific recommendations regarding
nonobstetric surgery and anesthesia in pregnancy, it is impor-
tant for nonobstetric physicians to obtain obstetric consultation
before performing nonobstetric surgery.” The decision to use
fetal monitoring should be individualized, and each case
warrants a team approach for optimal safety of the woman
and her baby. Indeed, close communication among all special-
ists involved in the care of the pregnant patient—the internist,
the obstetrician, the surgeon, and the anesthesiologist—
ensures that both the mother and the fetus will have the best
possible outcome.
Selected Readings
American College of Obstetricians and Gynecologists Committee on Obstet-
ric Practice: ACOG Committee Opinion Number 284: Nonobstetric
Surgery in Pregnancy. Obstet Gynecol 102:431, 2003.
Andersen B, Nielsen TF: Appendicitis in pregnancy: Diagnosis, management
and complications. Acta Obstet Gynecol Scand 78:758-762, 1999.
Angelini DJ: Obstetric triage revisited: Update on non-obstetric surgical condi-
tions in pregnancy. J Midwifery Womens Health 48:111-118, 2003.
Chesnutt AN: Physiology of normal pregnancy. Crit Care Clin 20:609-615,
2004.
Coleman MT, Trianfo VA, Rund DA: Nonobstetric emergencies in pregnancy:
Trauma and surgical conditions. Am J Obstet Gynecol 177:497-502,
1997.
Curet MJ, Allen D, Josloff RK, et al: Laparoscopy during pregnancy. Arch Surg
131:546-551, 1996.
Czeizel AE, Pataki T, Rockenbaue M: Reproductive outcome after exposure
to surgery under anesthesia during pregnancy. Arch Gynecol Obstet
261:193-199, 1998.
Faure EA: Anesthesia for the Pregnant Patient, Department of Anesthesia and
Critical Care, University of Chicago. Available at http://acc-www.uchicago
.edu/manuals/obstetric/obanesthesia.html
Goodman S: Anesthesia for nonobstetric surgery in the pregnant patient.
Semin Perinatol 26:136-145, 2002. C
Graham G, Baxi L, Tharakan T: Laparoscopic cholecystectomy during preg-
nancy: A case series and review of the literature. Obstet Gynecol Surv
53:566-574, 1998.
Greer IA, Nelson-Piercy C: Low-molecular-weight heparins for thrombopro-
phylaxis and treatment of venous thromboembolism in pregnancy: A sys-
tematic review of safety and efficacy. Blood 106:401-407, 2005. B
Holschneider CH: Surgical diseases and disorders in pregnancy. Curr Obstet
Gynecol Diagn Treat 451-465, 2003.
International Commission on Radiological Protection (ICRP): Pregnancy and
medical radiation. Annals of the International Commission on Radiological
Protection. Publication 84. 30/1 December 2000.
Jilma B, Kamath S, Lip G: Antithrombotic therapy in special circumstances.
I. Pregnancy and cancer. BMJ 326:37-40, 2003. C
Mazze RI, Kallen B: Reproductive outcome after anesthesia and operation
during pregnancy: A registry study of 5405 cases. Am J Obstet Gynecol
161:1178-1185, 1989. C
McKellar DP, Anderson CT, Boynton CJ, Peoples JB: Cholecystectomy during
pregnancy without fetal loss. Surg Clin North Am 70:1249-1262, 1990.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized con-
trolled trials, systematic reviews of studies other than RCTs, cross-sectional
studies, retrospective studies. C —Consensus statements, expert guidelines, usual
practice, opinion.
495
DSM-IV TR CRITERIA
Box 15-1
FOR SUBSTANCE ABUSE
PERIOPERATIVE CARE
OF THE ALCOHOL-DEPENDENT PATIENT
Background
Alcohol is a major public health problem in the United
States. Alcohol abuse is usually defined as the consumption of
60 g/day or more of alcohol, although smaller quantities can
certainly be physically and psychologically harmful. Patients
with alcoholism are frequent users of the health care system,
particularly of surgical and trauma services. Alcoholic pa-
tients also have two to three times more postoperative com-
plications than nonalcoholic patients. The most commonly
encountered problems are infections, bleeding, alcohol with-
drawal syndrome, and cardiac and respiratory dysfunction.
Chronic abusers of alcohol are also noted to have diminished
cellular immunity and exaggerated responses to surgical
stress. Some studies suggest that 1 month of abstinence
Symptoms of Withdrawal
One of the most common complications that occurs when
the alcoholic patient enters the hospital is withdrawal. It can
be divided into four stages in ascending severity: autonomic
hyperactivity, hallucinations, seizures, and delirium tremens.
Mild to moderate signs and symptoms related to autonomic
hyperactivity (e.g., tremulousness, irritability and sleep dis-
turbance, nystagmus, hyperreflexia, nausea and vomiting,
tachycardia, diaphoresis, and fever) start within hours, peak
24 to 48 hours after the last drink, and generally resolve
within 24 to 36 hours.
The hallucinations that characterize the second stage are
usually visual, but they may be tactile or auditory as well. They
develop about 12 to 24 hours after cessation of alcohol use and
usually resolve within 24 hours, but may persist up to 6 days.
Approximately 10% of patients progress from the second
to the third stage and develop seizures. The seizures are usu-
ally generalized, tonic-clonic, single, and of short duration.
Although seizures typically do not occur until after 12 to
48 hours of abstinence, they have been reported as early as
2 hours after the last use of alcohol.
Delirium tremens (also known as DTs) is the fourth and
most severe stage of alcohol withdrawal syndrome. It peaks
about 5 days after the last drink and consists of symptoms from
any or all of the preceding categories in addition to delirium. A
typical patient may present with confusion, prominent auto-
nomic symptoms (e.g., temperature ⬎101°F, blood pressure
⬎140/90 mm Hg, pulse ⬎100), and visual and auditory hal-
lucinations. The normal duration is several days, but like the
other complications, delirium tremens has been reported to last
Treatment of Withdrawal
All patients with symptoms of alcohol withdrawal should re-
ceive thiamine, folate, and multivitamins either orally or paren-
terally (Table 15-1). Benzodiazepines, preferably those with
Nausea and vomiting. Ask “Do you feel sick to your stomach?
Have you vomited?”
Observation:
0–No nausea and no vomiting
1–Mild nausea with no vomiting
2–
3–
4–Intermittent nausea with dry heaves
5–
6–
7–Constant nausea, frequent dry heaves, and vomiting
Tremor. Ask patient to extend arms and spread fingers apart.
Observation:
0–No tremor
1–Tremor not visible but can be felt, fingertip to fingertip
2–
3–
4–Moderate tremor with arms extended
5–
6–
7–Severe tremor, even with arms not extended
Paroxysmal sweats
Observation:
0–No sweat visible
1–Barely perceptible sweating; palms moist
2–
3–
4–Beads of sweat obvious on forehead
5–
6–
7–Drenching sweats
Anxiety. Ask “Do you feel nervous?”
Observation:
0–No anxiety (at ease)
1–Mildly anxious
2–
3–
4–Moderately anxious or guarded, so anxiety is inferred
5–
6–
7–Equivalent to acute panic states as occur in severe delirium or acute
schizophrenic reactions
Agitation
Observation:
0–Normal activity
1–Somewhat more than normal activity
2–
3–
4–Moderately fidgety and restless
5–
6–
7–Paces back and forth during most of the interview or constantly
thrashes about
Tactile disturbances. Ask “Do you have any itching, pins-and-needles
sensations, burning, or numbness, or do you feel like bugs are crawling
on or under your skin?”
Seizures
The peak period of risk for an alcohol withdrawal seizure is
between 1 and 2 days after the last drink. Unless a patient
has a known underlying seizure disorder, prophylactic anti-
convulsants are not routinely used. Alcohol withdrawal sei-
zures are typically grand mal, nonfocal, and one or two in
number. When a seizure occurs more than 48 hours after the
last drink or when the patient has a history of head trauma,
Hepatic Complications
It is thought that only approximately 10% to 20% of patients
with chronic alcoholism develop significant liver disease. The
broad spectrum of disease includes fatty liver, alcoholic hepa-
titis, portal hypertension, and cirrhosis (see Chapter 10). An
individual patient may be affected by more than one problem.
Patients who have alcohol-related liver disease have been
shown in multiple studies to have more perioperative compli-
cations. In fact, older studies from the 1970s reported mortal-
ity rates as high as 55% for patients undergoing open liver
biopsy. Patients should be carefully questioned and examined
for suggestive physical findings of advanced hepatic dysfunc-
tion such as jaundice, hepatomegaly or splenomegaly, ascites,
edema, gynecomastia, varices, and abnormalities on laboratory
tests and studies, as previously outlined. Individual patient
risk for perioperative complications is multifactorial and is
generally determined by the number and severity of comorbid
medical conditions, the extent of liver disease, and the risk
of the procedure. Various scoring systems, such as the
MELD (Model for End-Stage Liver Disease) score and the
Child-Turcotte-Pugh classification, have been developed and
validated as preoperative risk assessment tools in patients with
cirrhosis. Anesthesiologists should be notified of suspected
or known alcohol abuse, so they can select less hepatotoxic
anesthetics, sedatives, and analgesics to use in the operating
room. Acute alcoholic hepatitis is a relative contraindication to
surgery, and patients with this condition should have elective
procedures postponed until they can be medically optimized
and, if possible, encouraged to undergo preoperative detoxifi-
cation programs.
Gastrointestinal Complications
Alcoholic patients with advanced liver disease are prone to
developing esophageal and gastric varices and subsequent
life-threatening bleeding (see Chapter 9). Alcohol is also the
most common cause of acute pancreatitis in the United States;
this disease usually occurs only after 4 to 7 years of heavy
ethanol abuse. Twenty to 30% of these patients develop acute
necrotizing pancreatitis, which has been reported to have a
mortality rate as high as 30%. Alcohol also increases gastric
acid secretion, and patients are prone to developing gastritis,
ulceration, and bleeding complications. Perioperative acid
suppression therapy should be initiated for patients with epi-
gastric pain or suspected upper gastrointestinal bleeding. Pa-
tients with chronic alcohol use have also been found to have
increased risk for gastrointestinal malignancies as compared
with the general population.
Hematologic Complications
Anemias of various causes have been found in 10% to 60% of
hospitalized patients with alcoholism (see Chapter 6). Micro-
cytic anemia can be caused by gastritis, peptic ulcer disease,
or malignancy and exacerbated by alcohol-related coagulopa-
thy. Hemolytic anemia is usually the result of alcohol-related
splenomegaly and sequestration. Nutritional folate deficiency
can cause megaloblastic anemia. By an unknown mechanism,
alcohol can also independently cause macrocytosis, with or
without anemia, in the presence of normal folate levels. The
increased risk for infection with chronic alcohol use and fre-
quent comorbid conditions predispose patients with long-
term alcoholism to anemia of chronic disease.
Thrombocytopenia, defined as a platelet count of less than
150,000/µL from direct bone marrow toxicity, is also com-
mon in alcoholic patients. A hospitalized patient with a forced
period of abstinence from alcohol may subsequently develop
rebound thrombocytosis. The platelet count usually rises after
MEDICAL COMPLICATIONS
Box 15-2
OF COCAINE USE
Data from Ghuran A, Nolan J: Recreational drug misuse: Issues for the cardiologist.
Heart 83:627-633, 2000; Hollander J, Henry T: Evaluation and management of the pa-
tient who has cocaine-associated chest pain. Cardiol Clin 24:103-114, 2006; Jones J,
Weir W: Cocaine-associated chest pain. Med Clin North Am 89:1323-1342, 2005;
Stouffer G, Sheahan R, Lenihan D, et al: Cocaine associated chest pain. Am J Med Sci
324:37-44, 2002.
PERIOPERATIVE MANAGEMENT
OF THE OPIOID-DEPENDENT PATIENT
Background
Opioids are synthetic and natural substances derived from
the opium poppy that all have effects similar to those of mor-
phine. Heroin, morphine, codeine, oxycodone, meperidine,
and fentanyl are the most commonly abused drugs in this
class. Opioid dependence, from either illicit or increasingly
prevalent prescription drug abuse, may result in many seri-
ous medical complications (Box 15-4). Up to 2% of opioid-
dependent individuals die annually of complications from
the drug, and 53% of individuals who ever try heroin be-
come addicted to it. In certain areas of the United States,
rates of infection with human immunodeficiency virus have
been reported to be as high as 60% in patients who are
Opioid Toxicity
The major physiologic effects of opioids are on the central ner-
vous system and the cardiovascular system. The characteristic
signs of acute opioid intoxication or overdose may be analgesia,
euphoria, varying degrees of lethargy (including coma), respi-
ratory depression, bradycardia, hypotension, hypothermia, and
miosis. An opioid antagonist such as naloxone should be given
to any patient exhibiting signs of hemodynamic instability such
as respiratory depression, bradycardia, or hypotension. An
initial dose of 0.4 mg of naloxone may be sufficient to reverse
the respiratory depression. This same dose may be repeated
two or three times in the first few minutes if there is no impro-
vement in symptoms, especially if the diagnosis is in doubt.
Because naloxone is a short-acting antagonist, if a clinical res-
ponse is seen, a continuous infusion of two thirds of the initial
bolus dose each hour should be started promptly. The adult
dose is typically 0.25 mg/hr to 6.25 mg/hr. The infusion should
be continued for at least 12 hours and titrated according to the
patient’s medical status. If a patient is hemodynamically stable,
recommended initial doses are 2 g/kg three times per day for
7 to 10 days, then taper over 3 days. The transdermal patch
(Catapres-TTS) may also be used, although it should be over-
lapped with oral clonidine, because it takes several days to be
fully effective. Patients need to be carefully monitored for hy-
potension and bradycardia. For short-acting opioids such as
heroin, clonidine-assisted withdrawal can be completed in 4 to
6 days. In noncompliant patients, clonidine is a poor choice for
continued outpatient therapy in light of its potential life-threat-
ening toxicities as well as a risk of rebound malignant hyper-
tension if the drug is abruptly discontinued. Withdrawal can
also be treated symptomatically with antidiarrheals, antiemet-
ics, antispasmodics, and nonsteroidal anti-inflammatory medi-
cations. Anxiolytics may also be required, but they must be
used with caution because of their high risk of dependence.
PERIOPERATIVE MANAGEMENT
OF THE BENZODIAZEPINE-DEPENDENT PATIENT
Benzodiazepines, one of the most prescribed classes of drugs in
the United States, have a significant abuse potential and may
cause physiologic dependence and withdrawal. Substance
Selected Readings
Agency for Health Care Policy and Research: Smoking cessation clinical
practice guideline. JAMA 275:1270-1280, 1996.
Al-Sanouri I, Dikin M, Soubani A: Critical care aspects of alcohol abuse.
South Med J 98:372-381, 2005.
American Psychiatric Association: Practice Guidelines. Practice Guideline
for the Treatment of Patients with Substance Abuse Disorders, 2nd ed,
part A. Available at http://www.psychiatryonline.com
Busto U, Sellers EM, Naranjo CA, et al: Withdrawal reactions after long-term
therapeutic use of benzodiazepines. N Engl J Med 315:854-859, 1986.
Ewing JA: Detecting alcoholism: The CAGE questionnaire. JAMA 252:
1905-1907, 1984. A
Ferguson JA, Suelzer CJ, Eckert GJ, et al: Risk factors for delirium tremens
development. J Gen Intern Med 11:410-414, 1996.
Ghuran A, Nolan J: Recreational drug misuse: Issues for the cardiologist.
Heart 83:627-633, 2000.
Gordon R, Lowy F: Current concepts: Bacterial infections in drug users.
N Engl J Med 353:1945-1954, 2005.
Hollander JE: The management of cocaine associated myocardial ischemia.
N Engl J Med 333:1267-1272, 1995.
Hollander J, Henry T: Evaluation and management of the patient who has
cocaine-associated chest pain. Cardiol Clin 24:103-114, 2006.
Kitchens JM: Does this patient have an alcohol problem? JAMA 272:
1782-1787, 1994.
Mayo-Smith MF, Beecher LH, Fischer TL, et al: Management of alcohol
withdrawal delirium: An evidence based practice guideline [published
correction appears in Arch Intern Med 164:2068, 2004]. Arch Intern
Med 164:1405-1412, 2004. C
Mendelson JH, Mello NK: Management of cocaine abuse and dependence.
N Engl J Med 334:965-972, 1996.
Mouhaffel AH, Madu EC, Satmary WA, Fraker TD: Cardiovascular compli-
cations of cocaine. Chest 107:1426-1434, 1995.
Sorensen LT, Karlsmark T, Gottrup F: Abstinence from smoking reduces
incisional wound infection: A randomized controlled trial. Ann Surg
238:1-5, 2003. A
Sullivan JT, Sykora K, Schneiderman J, et al: Assessment of alcohol with-
drawal: The revised Clinical Institute Withdrawal Assessment for Alco-
hol Scale (CIWA-Ar). Br J Addict 84:1353-1357, 1989.
Tonnesen H: Alcohol abuse and postoperative morbidity. Dan Med Bull
50:139-160, 2003. B
Tonnesen H, Kehlet H: Preoperative alcoholism and postoperative morbid-
ity. Br J Surg 86:869-874, 1999. B
Tonnesen H, Peterson KR, Hojgaard L: Postoperative morbidity among
symptom-free alcohol misusers. Lancet 340:334-337, 1992. B
Warner D: Preoperative smoking cessation: The role of the primary care
provider. Mayo Clin Proc 80:252-258, 2005. C
Weber JE, Chudnofsky CR, Boczar M, et al: Cocaine-associated chest pain:
How common is myocardial infarction? Acad Emerg Med 7:873-877,
2000.
West LJ, Maxwell DS, Nobel EP, et al: Alcoholism. Ann Intern Med 100:
445-446, 1984.
NEUROMUSCULAR DISEASES
Myasthenia Gravis
Myasthenia gravis is an uncommon disorder; the estimated
prevalence is 0.05 to 5 per 100,000 population, and the in-
cidence is 0.4 per 100,000 population. Women are affected
more frequently than men (2 to 3:1), and there are no racial
or geographic predilections. The average age of onset is
26 years in women and 31 years in men. Two separate groups
of patients are recognized, one with an early onset of disease
and another with a peak incidence at 70 years. Myasthenia
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized clinical tri-
als, systematic reviews of studies other than RCTs, cross-sectional studies, retro-
spective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
535
Treatment
Despite the use of immunotherapy, anticholinesterase medi-
cation is still the mainstay of therapy for many myasthenic
patients. Pyridostigmine (Mestinon) is the most frequently used
anticholinesterase for the management of myasthenia gravis.
This medication is available in oral formulations (60-mg tablet
and syrup, 12 mg/mL). Pyridostigmine is absorbed from the
gut, although inactivation occurs, and the dosage required is
greater than with other agents. The onset of action is 30 to
60 minutes, and the peak effect is at 2 hours. There is little
effect after 4 hours. A sustained-action capsule is available,
but release and absorption are erratic, and this mode of delivery
is generally used only at bedtime. The usual starting dose of
pyridostigmine is 15 to 60 mg every 4 to 6 hours and can be
increased in 15- to 60-mg increments.
*IV dose 1/30 the total oral dose, q4–6h; IM dose 1/60 the total oral dose, q4–6h.
IM, intramuscularly; IV, intravenously; PO, by mouth; q, every.
Perioperative Considerations
Numerous medications affect the myoneural junction and
may exacerbate myasthenia gravis (Table 16-2). Local anes-
thetics of the ester group (cocaine, procaine, amethocaine)
should be avoided because they are hydrolyzed by cholines-
terase. Alternatively, anesthetics of the amide group (ligno-
caine, prilocaine, mepivacaine, bupivacaine) can be used
because they are metabolized in the liver. Aminoglycoside
antibiotics (gentamicin, tobramycin, neomycin, kanamycin,
streptomycin) reduce the amount of acetylcholine released at
the neuromuscular junction and can cause exacerbation of
Muscular Dystrophy
Muscular dystrophy refers to a group of genetically deter-
mined progressive myopathies. Each type of muscular dystro-
phy has specific genetic inheritance, medical problems, and
long-term prognostic factors. The most frequently encoun-
tered myopathies are reviewed in this section.
Duchenne muscular dystrophy is inherited as an X-linked
recessive trait and is the most common and severe of the
myopathies. The onset is in early childhood, and the disease
follows a progressive downhill course, with patients confined
to a wheelchair at a mean age of 9.5 years. Survival after the
age of 25 years is rare. Seventy percent of deaths among pa-
tients with Duchenne muscular dystrophy are from respira-
tory failure alone. Approximately 12% of deaths may be at-
tributable to cardiac causes, but it is often difficult to
distinguish between primary involvement of the cardiac
muscle and cardiac decompensation caused by nocturnal
hypoxemia and pulmonary hypertension.
Becker’s dystrophy is a milder, less common allelic form of
Duchenne muscular dystrophy. The muscle weakness is a
slowly progressive process, with survival into the fourth and
fifth decades of life. Pulmonary insufficiency is the major
long-term problem.
Myotonic dystrophy is manifested as an autosomal domi-
nant trait (chromosome 19) with variable expression, with an
age of onset in the teens or 20s. It is probably the most fre-
quently encountered muscular dystrophy in a general hospi-
tal. This disorder appears most commonly in the second and
third decades of life, but a congenital form has been observed.
The myopathy is slowly progressive, involving proximal and
distal muscle groups; death occurs in the fifth and sixth
decades of life. Myotonia is manifested clinically by an im-
paired ability to relax skeletal muscle. This can be seen by the
Perioperative Considerations
Pulmonary assessment is directed to the degree of restrictive
disease and the oxygenation status of the patient. Pulmonary
function tests, with and without bronchodilators, and arterial
blood gas determinations are performed preoperatively. The
respiratory disability in patients with muscular dystrophy is
a product of reduced muscle strength and decreased pulmo-
nary and chest wall compliance. This is especially apparent
Malignant Hyperthermia
MH is a rare, fatal complication of general anesthesia caused
by an inherited myopathy. After exposure to inhaled anes-
thetics or depolarizing muscle relaxants, susceptible indi-
viduals experience a hypermetabolic state characterized by
tachycardia, hyperpyrexia, fluctuation in blood pressure,
metabolic and respiratory acidosis, cyanosis, and muscle ri-
gidity. Multiple organ failure and death may result if the
entity is not recognized and treated promptly.
The incidence of MH reactions in North America and
Europe is approximately 1 in 15,000 anesthesia procedures
in children and ranges from 1 in 50,000 to 1 in 150,000
anesthesia procedures in middle-aged adults. Clinical mani-
festations can occur with the presence of one autosomal
dominant gene or two autosomal recessive genes.
The detection of susceptible individuals before anesthesia
and surgery is of primary concern. Frequently, nothing in the
clinical history or physical examination suggests that the
patient may acquire MH. However, the following should alert
the clinician to the possibility. Patients with a family history
of unusual reactions or death from anesthesia are at risk for
the development of MH. A history of unexplained muscle
Management
The mainstay of treatment in MH is dantrolene sodium (Dan-
trium). Dantrolene is a phenytoin derivative that attenuates
calcium release from the sarcoplasmic reticulum. An initial
intravenous dose of 2.5 mg/kg is given and repeated every 5 to
10 minutes until a maximal dose of 10 mg/kg is given or until
the episode is controlled. Control of MH is marked by decreas-
ing temperature, decreasing muscle rigidity, and improving
acid-base balance. Dantrolene has a half-life of 5 hours and
should be continued for 24 hours at 1 to 2 mg/kg in four
divided doses following control of the MH episode. Dantrolene
should be reinstituted immediately if signs of increased me-
tabolism or acidosis develop.
Symptomatic treatment of MH includes the administra-
tion of sodium bicarbonate at 1 to 4 mg/kg in accordance
with blood gas pH measurements, maintenance of adequate
urine output with intravenous fluids, and cooling of body
temperature with a cooling blanket. The patient should be
monitored in the intensive care unit with blood gas determi-
nations, complete blood count, electrolyte determinations
(especially potassium), and creatine kinase. Patients thought
to have MH can be pretreated with dantrolene, 2.5 mg/kg
1 hour preoperatively and then 4 to 7 mg/kg/day in
divided intravenous doses [ C Larach et al, 1987].
Ch16-X2385_535_580.indd 548
TABLE 16-5 Medications and Their Relationship to Malignant Hyperthermia
From Kaus SJ, Rocko MA: Malignant hyperthermia. Pediatr Clin North Am 41:233, 1994.
16 • Perioperative Assessment/Management of Neurologic Problems
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16 • Perioperative Assessment/Management of Neurologic Problems 549
Parkinsonism
Parkinson’s disease is one of the most common neurologic
disorders the medical consultant will encounter in preopera-
tive evaluation. This slowly progressive, degenerative disease is
characterized pathophysiologically by a depletion of dopamine
in the striatonigral pathways. Most cases are idiopathic, but
atherosclerosis, infection, trauma, and medications can pro-
duce a parkinsonian syndrome. Tremor, rigidity, bradykinesia,
and impaired postural reflexes are cardinal manifestations of
the syndrome. Another important clinical manifestation is
Parkinsonian Medications
The cardiovascular system is affected by antiparkinsonian
therapy. The metabolite of levodopa and levodopa-
carbidopa therapy, dopamine, acts on three receptors in the
cardiovascular system. Dopamine acts directly on myocardial
Antiparkinsonian Medications
TABLE 16-6
(Dopaminergic Action)*
Drug Dose Schedule
Carbidopa/L-dopa
Carbidopa/levodopa 10 mg/100 mg, 0.5–1 g/day up to 8 g/day
(Parcopa) 25 mg/100 mg,
25 mg/250 mg Tablets/capsules
Carbidopa/levodopa 10/100 mg, 25/100 mg, 1 tablet, tid; titrate up-
(Sinemet)† 25/250 mg ward based on clinical
response
Monoamine Oxidase-B Inhibitors
Selegiline (Eldepryl) 5 mg 5–10 mg bid
Rasagiline (Azilect) 0.5 mg, 1 mg 0.5 mg adjunct therapy
Dopamine Agonists (Nonergot)
Ropinirole 0.25 mg, 0.5 mg, 1 mg, Titrate to maximum dose
(Requip) 2 mg, 3 mg, 4 mg, 3 mg tid
5 mg
Pramipexole 0.125 mg, 0.25 mg, Titrate to maximum dose
(Mirapex) 0.5 mg, 1 mg, 1.5 mg 1.5 mg tid
Catechol-O-Methyltransferase
Entacapone (Comtan) 200 mg 200 mg tid
Entacapone 12.5 mg/50 mg/200 mg tid dosing
carbidopa/ 25 mg/100 mg/200 mg tid dosing
levodopa 37.5 mg/150 mg/200 mg tid dosing
(Stalevo)
Perioperative Considerations
Pulmonary care in the perioperative period is directed
toward the restrictive lung impairment secondary to the
rigidity and bradykinesia of the respiratory muscles. This
problem is exacerbated by the postoperative withdrawal
of antiparkinsonian medication. In addition, kyphosis,
pharyngeal dysfunction, and sialorrhea compound the
restrictive dysfunction [ C Frucht, 2004].
Antiparkinsonian Medications
TABLE 16-7
(Anticholinergic Action)
Drug Dose Schedule
Trihexyphenidyl
(Artane) 2 mg 5 mg tid
Benztropine
(Cogentin) 2 mg; 1-mg ampule 2 mg tid or 0.5–1 mg IM, up
to 1–7 mg/day
Procyclidine 10 mg 10 mg qid
(Kemadrin)
Diphenhydramine 50-mg ampule 10–50 mg IM/IV, up to 150 mg/day
(Benadryl)
IM, intramuscularly; IV, intravenously; qid, four times daily; tid, three times
daily.
EPILEPSY
Epilepsy is one of the most common neurologic disorders
encountered in clinical practice, affecting an estimated 2 to
4 million people in the United States, approximately 1 in
50 children and 1 in 100 adults. Seizures are classified into
(1) partial seizures with elementary symptoms (these may
occur without an alteration in consciousness, e.g., focal mo-
tor seizures), (2) partial seizures with complex symptoms
(temporal lobe or psychomotor seizures), and (3) generalized
seizures (petit mal, grand mal, tonic-clonic seizures). The
complete classification of seizures is complex and is not dis-
cussed here; however, the problem facing the consultant is
not the diagnosis or classification of the seizure disorder but
management of the antiepileptic drugs and prevention of
recurrent seizure activity preoperatively and postoperatively.
Stage I (excitation) and stage II (delirium) of anesthesia are
the periods of risk for seizure activity. Knowledge of the phar-
macokinetics and toxicity of antiepileptic drugs is important
for the prevention of seizures and for understanding the
possible adverse reactions in the patient undergoing surgery.
Categorization of Patients
Preoperative patients with seizure disorders who are to un-
dergo elective or emergency surgical procedures can be clas-
sified as having well-controlled or poorly controlled disor-
ders. Contributing factors are sought for the patient with a
poorly controlled seizure disorder such as noncompliance,
alcohol ingestion, or concurrent illness.
Treatment Modalities
Phenytoin is the most frequently used parenteral antiepileptic
drug. To avoid the risks of hypotension and asystole, this drug
must be administered in saline solution or lactated Ringer’s
solution at a rate no faster than 50 mg/minute. An oral load-
ing schedule of an initial 400 mg, followed by 300 mg every
2 hours for a total of 1 g, will achieve a therapeutic range of
phenytoin. Phenytoin should not be given intramuscularly or
rectally because of erratic absorption. Phenytoin is given in an
intravenous loading dose of 15 to 18 mg/kg and a mainte-
nance dose of 4 to 8 mg/kg/day. When given intravenously,
phenytoin should be given in divided doses.
Fosphenytoin sodium is a water-soluble prodrug of
phenytoin that can be administered intravenously and intra-
muscularly. It has the advantages of being better tolerated at
the injection site, and a loading dose of 15 to 20 mg/kg can be
given at a rate of 150 mg/minute. Fosphenytoin may be given
intramuscularly when intravenous access is not available.
Phenobarbital is the second most frequently used paren-
teral antiepileptic medication. It is given in a loading dose of
2 to 6 mg/kg and a maintenance dose of 1 to 5 mg/kg/day. It
can be given intramuscularly or intravenously if the oral
route is not available. If administered parenterally, phenobar-
bital should be given in divided doses.
Many newer antiepileptic drugs are available (Table 16-8).
These agents are all formulated as oral preparations, except for
valproate sodium and levetiracetam, which are available in
parenteral form. Valproate sodium is given at 10 to 15 mg/kg/
Ch16-X2385_535_580.indd 556
TABLE 16-8 Anticonvulsant Medication (Adult Dosing)
Therapeutic
Drug Route Half Life Range (mg/L) Dose
Phenytoin (Dilantin) PO, IV 2412 10–20 mg/L 200–600 mg/day
Carbamazepine (Tegretol) PO 9–15 8–12 mg/mL 400–2000 mg/day divided dose
Oxcarbazepine PO 9 10–35 mg/mL 300–2400 mg/day divided dose
(Trileptal)
Valproic acid (Depakene) PO 5–20 50–100 mg/L 1000–3000 mg/day divided dose
Valproate sodium IV 5–20 50–100 mg/L 10–15 mg/kg/day
administered over 1 hr (20 mg/min)
Divalproex sodium (Depakote) PO 6–16 hr 50–100 mg/L 750–3000 mg
Phenobarbital (Luminal) PO, IV, IM 24–110 hr 10–40 mg/L 60–240 mg/day
Primidone PO 12–36 hr 6–12 mg/L 500–2000 mg/day
Clonazepam (Klonopin) PO 18–50 hr 20–80 g/mL 0.5–20 mg/kg; divided doses
Diazepam IV, PO, IM, IV, 0.5–4 100–1000 mg/L 0.3 mg/kg, maximum 20 mg
PO 24
Lorazepam IV, PO, IM, IV 1-4 10–30 mg/L 2 mg IV followed by another 2 mg; can repeat up to 6-8 mg
Ethosuximide (Zarontin) PO 30–60 hr 40–80 mg/L 20–40 mg/kg/day divided dose
Topiramate (Topamax) PO 20 hr 15 mg 200–400 mg/day
Levetiracetam (Keppra) PO 6–8 hr N/A 1000–3000 mg/day
Felbamate (Felbatol) PO 14–20 hr N/A 1200–3600 mg/day
Lamotrigine (Lamictal) PO 11–60 hr N/A 300–500 mg/day; 100–150 mg/day with other medications
Zonisamide (Zonegran) PO 60 hr N/A 400–600 mg/day
Gabapentin (Neurontin) PO 5–7 hr N/A 900–1800 mg/day
16 • Perioperative Assessment/Management of Neurologic Problems
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16 • Perioperative Assessment/Management of Neurologic Problems 557
Perioperative Considerations
Seizures can occur following withdrawal from any sedative-
hypnotic medication, but patients in withdrawal from alcohol
or barbiturates are particularly prone to generalized convul-
sions. Acute ingestion of alcohol can also cause alcoholic ke-
toacidosis and hypoglycemia. If the patient has no history of
a previous seizure disorder, a toxicology screen should be
obtained. Seizures associated with enflurane administration
may occur during inhalation induction, on emergence, or
during the postoperative period. Local anesthetic overdose
(excessive dose of local anesthetic, intravascular injection, or
rapid uptake) can cause generalized convulsions. Meperidine
in large doses, or administered to patients receiving MAO
inhibitors, may cause seizures. Seizures may also be seen after
injection of retrobulbar block for ophthalmic surgery.
Most nonepileptic patients with perioperative seizures
have a metabolic derangement. Hyponatremia is common
after subarachnoid hemorrhage, and hypercalcemia may be
seen after thyroid or parathyroid surgical procedures. Patients
with seizures postoperatively should be screened for electrolyte
abnormalities guided by the operative procedure and the
preoperative electrolyte balance. Acute organ failure from any
cause may produce seizures. Sepsis can cause seizures and
should be considered in any trauma patient with an obvious
source of infection or with spillage of bowel contents. Rapidly
developing MH may manifest with seizures. Although alcohol
withdrawal may cause generalized seizures, many alcoholic
patients have a predisposing cause for the development of a
chronic seizure disorder, such as head trauma. If the seizure is
clearly a generalized withdrawal seizure, no chronic anticon-
vulsant medication is generally required. The convulsion can
CEREBROVASCULAR DISEASE
Stroke
Stroke is the third leading cause of death in the United States,
after myocardial infarction and cancer. Stroke also accounts for
half of all patients hospitalized for acute neurologic disease.
The major risk factors for stroke are age, hypertension, coinci-
dent coronary heart disease, diabetes, and smoking. Stroke is
a syndrome and includes hemodynamic obstruction, artery-
to-artery emboli, occlusion of small penetrating arteries pro-
ducing a lacunar infarction, cardiogenic emboli, ruptured in-
tracranial aneurysms, and intracranial hemorrhages.
Large multicenter clinical trials have provided the clini-
cian with information regarding the management of the pa-
tient with cerebrovascular disease:
1. Prevention of Cerebral Ischemic Events in Patients with
Noncardioembolic Transient Ischemic Attack (TIA) or
Stroke: Acceptable options for initial therapy are as follows:
aspirin, at a dose of 50 to 325 mg once daily; or the
combination of aspirin, 25 mg, and extended-release di-
pyridamole, 200 mg, twice daily; or clopidogrel, 75 mg,
once daily.
2. Prevention of Cardioembolic Cerebral Ischemic Events:
Atrial fibrillation is a risk factor for stroke, and that risk can
be reduced by anticoagulation with warfarin with an inter-
national normalized ratio (INR) of 2 to 3. Patients may re-
ceive aspirin for management if warfarin is contraindicated.
3. In patients with recent TIA or ischemic stroke within the last
6 months and ipsilateral severe carotid artery stenosis (70%
to 99%), carotid endarterectomy by a surgeon with a record
of perioperative morbidity and mortality of less than 6% is
recommended. When the degree of stenosis is less than
50%, there is no indication for carotid endarterectomy.
4. Among patients with symptomatic severe stenosis (70%)
in whom the stenosis is difficult to access surgically, who
have medical conditions that greatly increase the risk of
surgery, or when other specific circumstances exist such
as radiation-induced stenosis or restenosis after carotid
endarterectomy, carotid artery stenting is not inferior to
endarterectomy and may be considered.
5. Acute ischemic stroke: For eligible patients, tissue plas-
minogen activator is given within 3 hours of the clearly
defined symptom onset at a dose of 0.9 mg/kg (maximum,
Subarachnoid Hemorrhage
Rupture of an intracranial aneurysm is a catastrophic event.
Approximately 27,000 patients in the United States and
Canada suffer from a ruptured intracranial aneurysm every
year. Subarachnoid hemorrhage is more common in women
than in men (2:1). Of those 27,000 patients, approximately
10,000 die of the initial insult, 3000 die of a massive hemor-
rhage, and 7000 die as a result of misdiagnosis or a delay in
surgery. Of the 17,000 patients who reach neurosurgical care,
approximately 50% of them die or become disabled.
Rebleeding is one of the major causes of death and dis-
ability after subarachnoid hemorrhage. Two to 4% of patients
hemorrhage again within the first 24 hours after the initial
episode, and approximately 15% to 20% bleed a second time
within the first 2 weeks. The recent emphasis has been on
early clipping or coiling of the aneurysm to prevent the
bleeding. Patients who have grade III or greater in the Hunt
modified system (Table 16-10) are generally submitted to
early angiography and immediate surgical clipping or coiling
of the aneurysm. This approach prevents recurrent bleeding
and allows for the treatment of vasospasm.
Angiographic evidence of vasospasm following subarach-
noid hemorrhage occurs in approximately 60% of patients.
The angiographic appearance of vasospasm is correlated with
Perioperative Considerations
Delirium or a confusional state may develop in the immedi-
ate postoperative period as the patient emerges from anesthe-
sia, or it may follow lucid intervals for several days. Although
the typical course runs 1 or 2 days, it may be longer, espe-
cially in patients with underlying structural brain disease,
and occasionally it lasts for weeks. The three possible out-
comes in a delirious patient are recovery, progression to de-
mentia, or progression to death.
This is called neurotmesis and implies that both the axon and
the Schwann cells are interrupted. The prognosis for this type
of injury is poor despite surgical intervention. The patient
may have only a partial return of nerve function.
Specific Nerve Injuries
Optic Nerve
The retina is supplied by the central retinal artery that enters
the optic nerve just distal to the point at which the artery
branches from the ophthalmic artery. If external pressure is
applied to the eye, the intraocular pressure can be increased
to the point at which it exceeds the pressure in the central
retinal artery. Blood flow through the artery then ceases, and
sive flexion of the leg at the hip may compress the nerve.
Sensory loss with paresthesias over the anterolateral portion
of the thigh may result. This condition is also sometimes re-
ferred to as meralgia paresthetica. It has been reported with
groin flap procedures.
Special Considerations
Total hip arthroplasty can result in injury to the sciatic femo-
ral nerve or obturator nerve. This can occur with direct sur-
gical trauma, bleeding, or stretching of the nerve itself.
The femoral nerve may be damaged during renal trans-
plantation. This injury is frequently caused by a hematoma.
This nerve may also be injured during delivery of a baby and
may be unilateral or bilateral. A good outcome is generally
expected. Meralgia paresthetica can also occur from injury to
the lateral femoral cutaneous nerve during bone procure-
ment from the iliac crest for purposes of grafting.
Lower abdominal surgery for hernia repair or gynecologic
surgery may cause damage to local nerves traversing the ab-
dominal wall. The ilioinguinal nerve may be damaged during
surgical hernia repair. This nerve originates from T12 to L1
nerve roots, crosses retroperineally, and becomes extraperito-
neal just after passing the medial to the anterior iliac crest. It
then runs along the inguinal canal with its spermatic cord.
When this nerve is damaged during surgery, the patient com-
plains of pain and may have sensory loss in a strip of skin
extending along the inguinal canal to the base of the penis
and scrotum or to the labia. The iliohypogastric nerve is
slightly caudal to the ilioinguinal nerve. Damage to this nerve
causes sensory loss to the region of the skin over the greater
trochanter into the lower abdominal wall just above the
pubis. The genital femoral nerve supplies the femoral triangle
and a small area of skin on the medial thigh with most of the
scrotum, penis, or labia. Damage to this nerve in the retro-
peritoneal area can produce loss of sensation in those areas.
Selected Readings
Albers GW, Amarenco P, Easton JD, et al: Antithrombotic and thrombolytic
therapy for ischemic stroke. Chest 126:483S-512S, 2004.
Aldrieh TK, Uhrlass RM: Weaning from mechanical ventilation: Successful
use of modified inspiratory resistive training in muscular dystrophy.
Crit Care Med 15:247-249, 1987.
Alvine FG, Schurrer ME: Postoperative ulnar nerve palsy: Are there predis-
posing factors? J Bone Joint Surg Am 69:255-259, 1987.
Albin RL: Parkinson’s disease: Background, diagnosis, and initial manage-
ment. Clin Geriatr Med 22:735-751, 2006.
Bell RD: Perioperative seizures in decision making. In Bready LL, Smith RB
(eds): Anesthesiology. Toronto, BC Decker, 1987, pp 224-225.
Bell RD, Lastimosa AC: Metabolic encephalopathies. In Rosenberg RN (ed):
Neurology. New York, Grune & Stratton, 1980, pp 115-164.
Bernstein RA: Risks of stroke from general surgical procedures in stroke
patients. Neurol Clin 24:777-782, 2006.
Bertorini TE: Perisurgical management of patients with neuromuscular dis-
orders. Neurol Clin 22:293-313, 2004. C
Blacker DJ, Flemming KD, Wijdicks EF: Risk of ischemic stroke in patients
with symptomatic vertebrobasilar stenosis undergoing surgical proce-
dures. Stroke 34:2659-2663, 2003.
Brisman JL, Song JK, Newell DW: Medical progress: Cerebral aneurysms.
N Engl J Med 355:928-939, 2006.
Cooper DE, Jenkins RS, Bready L, Rockwood CA: The prevention of injuries
of the brachial plexus secondary to malposition of the patient during
surgery. Clin Orthop 228:33-41, 1988.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized controlled tri-
als, systematic reviews of studies other than RCTs, cross-sectional studies, retrospec-
tive studies. C —Consensus statements, expert guidelines, usual practice, opinion.
581
581
Cardiovascular Effects
Cardiac output at rest may not decrease with age, but the
maximal heart rate and maximal cardiac output decline. The
ventricular filling rate decreases, ventricular compliance de-
creases, and atrial contraction becomes more important in
maintaining cardiac output. Peripheral resistance increases as
aortic stiffness increases, and the vascular bed cross-sectional
area decreases. Responsiveness to catecholamine stimulation
decreases. The net result is that the elderly heart is likely to
be less able to withstand severe stress such as volume over-
load or hypotension.
In addition to changes related to aging, underlying car-
diovascular disease becomes more prevalent; up to 50% of
patients who are more than 65 years old have some sort of
heart disease. Up to 50% of patients more than 70 years
old have hypertension, and up to 20% have coronary ar-
tery disease. More than half of elderly patients have sys-
tolic murmurs, which usually represent valvular sclerosis
rather than stenosis. The identification of aortic stenosis is
important, however, because this condition increases the
surgical risk.
Pulmonary Effects
Physiologic changes in lung function begin at the age of
30 years and accelerate with advancing age. Lung elasticity
decreases, the chest wall becomes stiffer, and the respiratory
muscles weaken. The consequences of these changes are de-
creased vital capacity and increased residual volume. Expira-
tory flow rates and maximal minute ventilation decrease, as
does closing volume. In elderly persons, closing capacity may
exceed residual functional capacity. Thus, closure of small air-
ways occurs during normal breathing. This predisposes the
individual to lower lobe atelectasis postoperatively. Ventilation/
perfusion mismatches occur with resultant decreases in oxygen
tension. Many of these changes are exacerbated by smoking, a
history of which is quite common in older patients.
Renal Effects
Renal mass decreases by 25% to 30% between the ages of
30 and 90 years. Creatinine clearance and renal blood flow
diminish with age in most individuals. By 80 years of age, the
glomerular filtration rate is only one half to two thirds of
what it was at 30 years of age. However, serum creatinine
levels may remain normal, because lean body mass also de-
creases. Thus, a normal serum creatinine level may mask
significant renal dysfunction. Creatinine clearance in men
may be estimated by the Cockroft-Gault equation:
Creatinine clearance (140 age) weight (kg) /
(72 serum creatinine)
For an estimate in women, 0.85 of this value is used.
Tubular function is also affected by age. Changes include
an impaired ability to concentrate and dilute urine maxi-
mally. Because thirst in response to volume depletion is
decreased, elderly persons are more prone to dehydration.
Elderly persons also show decreased excretion of sodium,
potassium, and acid loads.
Drug Metabolism
An understanding of how drug metabolism differs in the el-
derly is important, because these patients frequently have
adverse drug reactions. Some of these reactions may be pre-
vented with a good understanding of the changes that com-
monly occur in aging (Box 17-1 and Table 17-1).
Drug Distribution
Lean body mass and total body water decrease with age,
whereas total body fat increases. Thus, drugs that are water
soluble may have higher concentrations in elderly patients
than in young patients. Drugs that are fat soluble may have
prolonged half-lives.
Renal Excretion
Creatinine clearance declines with age, and drugs excreted
by the kidney must be given in decreased doses based on
measured drug levels or measured or estimated creatinine
clearance.
IMPORTANT CONSIDERATIONS
Box 17-1
IN GERIATRIC DRUG THERAPY
Hepatic Excretion
Although some decrease in oxidative metabolism occurs,
overall hepatic metabolism and excretion are less affected by
age than is renal excretion. These changes vary considerably
among elderly persons.
Absorption
Drug absorption changes little with age.
Other Considerations
Elderly persons, especially those with dementia, often suffer
further cognitive decline as a result of drugs. Sedatives, anti-
hypertensive agents, and analgesic agents can all lead directly
or indirectly to cognitive decline. This age group is also more
subject to drug-induced delirium.
PREOPERATIVE ASSESSMENT
General Principles
There is a modest increase in surgical risk associated with age,
but age alone should not be a reason to forgo necessary surgery
if the benefit outweighs the risk. The life expectancy of the
average 75-year-old man is approximately 9 years; for a
woman, it is 11 years. Population studies of patients under-
going surgical procedures in their 90s demonstrated that
History
The history should address all medical problems, especially
those concerning the heart and lungs. Most elderly patients
undergoing surgical procedures have underlying medical prob-
lems in addition to the surgical indication. For example, Vaz
and Seymour found that only 20% of general surgical patients
who were more than 65 years old had no preoperative medical
problems [ C Vaz and Seymour, 1989]. Each of those underlying
medical problems must be identified so that its impact on sur-
gical risk can be assessed and managed perioperatively.
History taking may be difficult in this population. Elderly
patients often have poor recollection of their medical history
and may have impaired memory, factors that often make the
information they give inaccurate. These patients frequently
minimize symptoms because they believe the symptoms to
be part of the aging process.
A careful cardiac history is necessary. As in all patients, a
history of recent myocardial infarction or angina should be
sought. The degree of exercise tolerance is exceedingly impor-
tant; many studies have shown a clear correlation between an
ability to exercise and a decrease in mortality. If a patient has a
history of ischemic heart disease and no recent chest pain, this
may indicate either a good prognosis (i.e., no angina) or lack
of enough exertion to induce angina. The clinician should ask
specifically about the patient’s activity level. Can the patient
climb stairs without stopping? Can he or she go to the grocery
store and carry groceries home? In a younger individual, one
may take these things for granted, but many elderly patients
have significant limitations in their exercise tolerance.
The elderly patient with ischemic heart disease and poor
exercise tolerance of noncardiac origin (e.g., arthritis) poses
a problem for the consultant, because the degree of angina is
not ascertainable. Poor functional capacity, even if it does not
have a cardiac cause, is a risk factor for cardiac complication
associated with noncardiac surgical procedures. Gerson and
associates demonstrated that these patients are at higher risk
overall [ B Gerson et al, 1990]. The physician should ask about
exertional shortness of breath, because this sign may be an
anginal equivalent or may represent underlying lung disease.
Elderly patients are somewhat less likely to have typical
anginal chest pain, so exertional dyspnea may be the only
clue to underlying coronary artery disease. A history of
smoking, chronic cough, and dyspnea are all important in
identifying the patient with lung disease.
A formal evaluation for dementia should be performed,
especially in patients more than 75 years of age. Dementia
increases surgical risk, affects the ability of the patient to
cooperate postoperatively, and lowers the likelihood that the
Laboratory Studies
Currently, no uniform standardized approach to preoperative
laboratory testing in the elderly patient exists. A complete
blood count, serum electrolytes, and creatinine determina-
tions are usually performed. Age alone does not cause anemia,
but significant numbers of older patients are found to have
anemia, the cause of which should be investigated (although
this may not be necessary in all cases before important surgi-
cal procedures). As noted previously, a normal creatinine level
in an elderly person is often not indicative of normal creati-
nine clearance. Lean body mass decreases with age, and body
fat increases. The Cockcroft-Gault equation mentioned earlier
should be used to estimate clearance so that this can be taken
into account for drug dosing and other uses. Even if only
minimally elevated, a raised creatinine level indicates signifi-
cant renal impairment in the geriatric age group. An electro-
cardiogram and chest radiograph should be obtained as
baseline studies; many older people have abnormalities on
their electrocardiographic tracings and chest films that would
not be expected from the history. The presence of abnormali-
ties on these tests may be needed postoperatively for accurate
evaluation of complications or symptoms.
Beyond these basic tests, the necessity of routinely ordering
more involved and invasive tests is controversial. Pulmonary
function tests have been recommended by some authors for all
elderly patients. No good evidence indicates that these tests are
useful for surgical decision making for most patients. This pa-
tient population undergoes few minor elective surgical proce-
dures; thus, most surgery is necessary and important. As in
younger patients, pulmonary function tests should generally be
limited to patients who are having lung resection procedures.
ANESTHESIA
Local anesthesia is associated with low risk in elderly pa-
tients. If local anesthesia is not feasible, the choice between
spinal and general anesthesia is the surgeon’s and anesthesi-
ologist’s, based on the patient’s medical condition and prefer-
ence. There is no significant difference in mortality between
the two routes. Although general anesthesia is often followed
by a short-term cognitive decline, in some studies spinal
anesthesia had a similar effect.
POSTOPERATIVE COMPLICATIONS
General Complications
Older patients face the same postoperative complications as
younger patients. However, older patients have less physio-
logic reserve. There are significant decreases in function of
important physiologic systems, as discussed earlier; the older
patient is less able to compensate for these changes, and
complications are more likely to ensue. The older patient is
also more likely to have underlying chronic disease that pre-
disposes to complications. The most serious complications in
elderly patients, as in younger patients, are cardiac and pul-
monary problems; in addition, neurologic complications
such as delirium are more likely to occur in this patient
population.
Cardiac Complications
Congestive heart failure may manifest postoperatively even
in patients who never had a history of heart disease. This
finding was noted in Goldman’s initial study in which many
of the cases of congestive heart failure were found in patients
older than 60 years and without a history of heart disease. It
is important to ask about shortness of breath, orthopnea, and
paroxysmal dyspnea. Physical findings of elevated neck veins
or S3 gallop are useful, whereas rales are a nonspecific finding
Pulmonary Complications
Pulmonary complications are probably the most common
postoperative problems. As many as 40% of elderly patients
suffer postoperative pulmonary problems, which often con-
tribute to the cause of death. Atelectasis is extremely com-
mon and, if allowed to go unchecked, may lead to collapse
of major lung segments or pneumonia.
The prevention of these complications is possible with
good preoperative planning. Ideally, patients should stop
smoking at least 6 weeks preoperatively. Inspiratory maneu-
vers such as inspiratory incentive spirometry appear to be
effective deterrents to atelectasis and pneumonia, and these
techniques should be taught preoperatively. In patients with
known chronic obstructive pulmonary disease or asthma,
maximization of preoperative pulmonary status with bron-
chodilators should be considered. The use of chest physio-
therapy has not been well studied, but it should probably be
used in patients at high risk of pulmonary complications.
Delirium
Delirium, also known as acute confusional state, is often seen
postoperatively in elderly patients. It is associated with in-
creased hospital morbidity, mortality, and a longer length of
From Lipowski ZJ: Delirium in the elderly patient. N Engl J Med 320:578-582,
1989.
Hypothermia
Another important but lesser known problem is postopera-
tive hypothermia. Most operating rooms and recovery suites
are kept at low ambient temperatures, and many patients
have been found to have temperatures lower than 36ºC. Al-
though this temperature does not cause problems for most
patients, in some it may contribute to hypoxia, hypotension,
and altered mental status.
Different Presentations
Certain surgical diseases may manifest differently in elderly
patients. Appendicitis, although more common in younger
age groups, has a higher mortality in elderly patients
(6% to 10%). Two reasons are generally cited for this phe-
nomenon: (1) delay in diagnosis and (2) increased rate of
perforation.
The delay in diagnosis is attributed to both a delay on the
part of the elderly person in seeking medical attention and a
failure by the physician to make the correct diagnosis preop-
eratively. Symptoms in elderly patients may be less severe, be-
cause fever is less common and abdominal pain is usually
milder. Right lower quadrant tenderness is present in 80% to
90% of patients, however. Rebound tenderness is less common
in elderly patients. Abscess formation may result in a right
lower quadrant mass that may be mistakenly diagnosed as cecal
carcinoma. Perforation is common, occurring in up to 70% in
elderly individuals versus 20% in young patients, probably
because the appendix atrophies with age and the blood supply
Cancer
General Considerations
Because the risk of most cancers increases with age, elderly
patients have a disproportionate number of malignant tu-
mors, and surgery is the primary treatment for many of
them. The decision to perform cancer surgery in the elderly
patient, however, rests on certain factors. The first is the
combination of the life expectancy of the patient without
surgical intervention and the natural history of the underly-
ing cancer. Radical surgery for prostate cancer in an ill
90-year-old man is not indicated, whereas resection of
bowel carcinoma in a vigorous 70-year-old patient certainly
Key Points
Selected Readings
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116:1-8, 2003.
Beck LH: Perioperative renal fluid, and electrolyte management. Clin Geriatr
Med 6:557-569, 1990.
Berggren D, Gustafson Y, Eriksson B, et al: Postoperative confusion after
anesthesia in elderly patients with femoral neck fractures. Anesth Analg
66:497-504, 1987.
Bridget P, Bellows W, Leung JM: The prevalence of preoperative diastolic
filling abnormalities in geriatric surgical patients. Anesth Analg 97:
1214-1221, 2003.
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recovery of function one year after coronary artery bypass surgery. J Am
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Dimick JB, Cowan KA, Upchurch GR, et al: Hospital volume and surgical
outcomes for elderly patients with colorectal cancer in the United States.
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prognosis in coronary artery disease. Isr Med Assoc J 5:713-716, 2003.
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nary complications related to elective abdominal and noncardiac thoracic
surgery in geriatric patients. Ann Intern Med 88:101-107, 1990. B
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Does the choice affect patient outcome? J Am Geriatr Soc 50:191-194,
2002.
Lipowski ZJ: Delirium in the elderly patient. N Engl J Med 320:578-582,
1989.
Marcantonio ER, Flacker JM, Wright RJ, et al: Reducing delirium after hip
fracture: A randomized trial. J Am Geriatr Soc 49:516-522, 2001. C
McCallion J, Canning GP, Knight PV, et al: Acute appendicitis in the elderly:
A 5-year retrospective study. Age Ageing 16:256-260, 1987.
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surgical emergency. Arch Surg 113:1149-1152, 1978.
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endovascular surgical repair of abdominal aortic aneurysms in octoge-
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octogenarian. Chest 126:733-738, 2004.
Pruner G, Castellano R, Jannello AM, et al: Carotid endarterectomy in the
octogenarian: Outcomes of 345 procedures performed from 1995-2000.
Cardiovasc Surg 11:105-112, 2003.
Ropper AH, Wechsler LR, Wilson LS: Carotid bruit and the risk of stroke in
elective surgery. N Engl J Med 307:1388-1390, 1982. C
Saidi RF, Bell JL, Cucrick PS: Surgical resection for gastric cancer in elderly
patients: Is there a difference in outcome? J Surg Res 118:15-20, 2004.
Seymour DG, Vaz FG: Prospective study of elderly general surgical patients.
II. Postoperative complications. Age Ageing 18:316-326, 1989.
Sherman S, Guidot CE: The feasibility of thoracotomy for lung cancer in the
elderly. JAMA 258:927-930, 1987.
Thomas P, Sielezneff I, Ragni J, et al: Is lung cancer resection justified in
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Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized
controlled trials, systematic reviews of studies other than RCTs, cross-sectional
studies, retrospective studies. C —Consensus statements, expert guidelines, usual
practice, opinion.
605
Hyperkalemia
Hyperkalemia is common as the GFR falls and is secondary to
impaired renal excretion of hydrogen and potassium. Ordi-
narily, hyperkalemia in patients with CKD but with some
residual renal function is managed by dietary potassium re-
striction and diuretics. However, even in these patients, dialy-
sis may be necessary in catabolic states, during which potas-
sium release can be immense. Blood in the gastrointestinal
tract or the administration of units of packed red blood cells,
especially cells with an older shelf life, can also result in a
heavy potassium load caused by the lysis of red blood cells.
Hyperkalemia in CKD can be treated in several ways, de-
pending on its severity. As a general rule, potassium levels less
than 6 mEq/L rarely result in changes in the ECG and do not
require emergency therapy. Potassium levels greater than
6 mEq/L require an ECG to interpret the effects of hyperkale-
mia on the cardiac conduction system. Tall, peaked T waves
are an early sign of hyperkalemia. As potassium levels
Acidemia
Patients with renal failure can have either normal anion gap
or elevated anion gap acidosis. The former occurs when renal
failure is mild to moderate (ClCr 20 mL/minute), and the
latter occurs in more severe renal dysfunction. When a pa-
tient with CKD is acidemic and dialysis is not feasible or in-
dicated, correction to a minimum pH of 7.25 is indicated
preoperatively. Bicarbonate deficit can be calculated by the
following formula:
(Desired HCO3 observed HCO3)
50% body weight (kg)
where HCO3 is bicarbonate.
The patient with CKD may have acidemia for reasons
other than CKD alone, especially when it is high anion gap
metabolic acidosis. High anion gap can be caused by ketoac-
ids, lactic acid, and poisoning with ethylene glycol, aspirin,
or methanol.
Hematologic Considerations
Progressive anemia is common as the GFR falls to less than
60 mL/minute. Moreover, as renal function declines, the degree
of anemia worsens. Anemia of CKD is normochromic and nor-
mocytic. The principal cause of the anemia relates to relative
underproduction of erythropoietin, although the uremic milieu
causes suppression of erythroid progenitor cells. Recombinant
human erythropoietin is the mainstay of treatment for ure-
mic anemia in all stages of CKD [ A Eschbach et al, 1987]. In
dialysis for ESRD, the removal of uremic toxins may also
help to stimulate erythropoiesis. However, both dialysis and
erythropoietin therapy are slow to correct anemia and thus
Intraoperative Considerations
Anesthesia
CKD can affect the disposition of commonly used anesthetic
drugs by changes in the renal excretion of drug and active
metabolites and by changes in protein binding. The benzodi-
azepines diazepam, lorazepam, and midazolam are highly
protein bound agents. In renal failure, displacement of ben-
zodiazepines from protein by other molecules results in
an increased free fraction of these agents. This process, in
Vascular Access
During surgical procedures, the anesthesia team must take
special measures to protect the dialyzed patient’s vascular ac-
cess. The limb should be properly positioned without re-
straints to prevent prolonged occlusive pressure and possible
thrombosis of the access site. Needle sticks and blood pres-
sure measurements should also be avoided in the access-
related limb. Central lines should be avoided on the same side
as the vascular access if at all possible. Internal jugular lines
are preferred over subclavian lines to prevent venous stenosis
and loss of potential access sites. Intraoperative hypotension
can also lead to thrombosis of the access. The anesthesiologist
should auscultate the access frequently during the surgical
procedure to verify patency. In the event of thrombosis,
prompt thrombectomy should be arranged. Special care must
be taken in patients with CKD who are not yet receiving di-
alysis to protect potential vascular access sites. The forearm
and upper arm veins of the nondominant arm should be pro-
tected from needle sticks. Displaying a sign at the patient’s
bedside to save the designated arm may be helpful.
In kidney transplant recipients, femoral access, such as
arterial or venous catheters or intra-aortic balloon pumps,
should generally be avoided on the side ipsilateral to the re-
nal allograft. In the event of cross-clamping of the abdominal
aorta, a temporary bypass, usually from the ipsilateral axil-
lary artery to the femoral artery, must be performed to main-
tain the arterial blood supply to the transplanted kidney.
Postoperative Management
Pharmacotherapy
Care must be taken to administer all postoperative medica-
tions at doses appropriate to the patient’s level of renal func-
tion. The use of prewritten postoperative order templates can
create increased potential for inappropriate dosing of medi-
cations in patients with CKD and should be avoided. ClCr
should be calculated or estimated for all patients, and doses
of medications should be adjusted accordingly. Special care
must be taken with those drugs that are excreted primarily
by the kidney and that have narrow toxic-therapeutic win-
dows such as digoxin and aminoglycoside antibiotics. In
these situations, drug levels must be monitored frequently.
The use of magnesium- or phosphate-containing antacids
and cathartics in the postoperative setting can lead to danger-
ous hypermagnesemia and hyperphosphatemia in patients
with advanced CKD and should generally be avoided.
Options for postoperative analgesia include acetamino-
phen, fentanyl, and oxycodone. As mentioned earlier, me-
peridine should not be used in patients with CKD because of
the accumulation of its neurotoxic metabolite, and morphine
should be used cautiously because of prolongation of its
sedative effects. Other drugs that should be used with cau-
tion include angiotensin-converting enzyme inhibitors, an-
giotensin II receptor blockers, and nonsteroidal anti-
inflammatory agents (NSAIDs). These agents can decrease
renal blood flow and GFR and can lead to further decrement
in kidney function, especially during periods of effective
circulating volume depletion that can occur postoperatively.
The low-molecular-weight heparin enoxaparin is eliminated
primarily by the kidney, and administration at fixed doses
without monitoring has an unpredictable anticoagulant effect
in patients with CKD. If this agent is used, doses should be
reduced and anti–factor Xa activity frequently monitored. To
date, enoxaparin has not been approved by the U.S. Food
and Drug Administration for use in dialyzed patients.
Drug dosing in the renal transplant recipient can create
unique challenges in the perioperative setting. Immunosup-
pressant medications must be continued in renal transplant
recipients perioperatively to prevent organ rejection. The use
of stress-dose steroids is not indicated for routine, elective
surgical procedures unless the patient has documented adre-
nal insufficiency. The CNIs cyclosporine and tacrolimus can
be given intravenously at one third the usual dose for those
patients who cannot yet take oral medications. Trough drug
levels must be monitored very closely to verify appropriate
perioperative dosing. Moreover, CNIs are metabolized by the
cytochrome P-450 system, and numerous drug interactions
can occur. Some of the more frequently prescribed drugs
metabolized by this system include diltiazem, verapamil,
fluconazole, ketoconazole, and erythromycin, which increase
CNI levels, as well as rifampin, barbiturates, phenytoin, and
carbamazepine, which decrease CNI levels. The immunosup-
pressant agent sirolimus may have a negative effect on
fibrosis, and some evidence suggests a higher incidence of
surgical wound complications, such as infection and hernia,
with this agent.
Nutrition
Careful attention must be paid to the postoperative nutri-
tional needs of patients with CKD. There is an overall high
prevalence of protein-calorie malnutrition in these patients
Fluid-Electrolyte Management
Patients with renal failure are prone to electrolyte abnor-
malities in the postoperative period. Hyperkalemia should be
treated as outlined earlier. Enemas containing the cation-
exchange resin Kayexalate and sorbitol should be used with
extreme caution to treat hyperkalemia in patients after
surgical procedures because of the increased incidence of
intestinal necrosis. This usually occurs in the setting of
decreased colonic motility and may be precipitated by hyper-
osmotic sorbitol-induced tissue damage. Dialysis should
be performed in patients with CKD who have persistent
hyperkalemia despite medical therapy. Dialysis treatments
performed in the first 24 to 48 postoperative hours should
be done without the use of heparin to prevent bleeding.
Care must be taken not to administer large amounts of
hypotonic fluids to patients with advanced renal failure be-
cause this may lead to severe hyponatremia. Fluid repla-
cement should generally be given with isotonic saline. Hy-
potonic saline should be reserved for those patients
who have increased free water losses, such as patients with
osmotic diarrhea or diuresis or patients who are already
hypernatremic.
Differential Diagnosis
Although the surgical setting creates unique conditions that can
lead to ARF, the general approach to the patient and the gen-
eration of the differential diagnosis are the same in all patients
Diagnosis
Most cases of postoperative ARF are the result of prerenal
failure or ATN usually related to prolonged renal ischemia.
Differentiating between these two disorders can sometimes
be difficult, because they often exist on a continuum. Proper
diagnosis is important, however, in that management of the
patient differs depending on the cause.
A thorough history should focus on episodes of volume loss
such as vomiting, diarrhea, hemorrhage, and aggressive diure-
sis. Third spacing of fluid can be tremendous in pancreatitis,
and insensible losses of fluid can be high with fever, mechani-
cal ventilation, and severe burns. The intraoperative flow
sheets must be reviewed for episodes of hypotension. The
medical record must be thoroughly reviewed to ascertain any
exposure of the patient to nephrotoxins such as intravenous
contrast agents, aminoglycosides, NSAIDs, or myoglobin.
The physical examination should focus on accurate as-
sessment of volume status and cardiac function and the pres-
ence of rash, livedo reticularis, or embolic stigmata. Diagnos-
tic studies that can assist in making the proper diagnosis
include urine electrolytes and urinalysis with examination of
spun urinary sediment. Low urine sodium (10 mEq/L)
with a fractional excretion of sodium less than 1% and a
bland urinary sediment suggests a diagnosis of prerenal
failure. In an oliguric patient, high urine sodium
(20 mEq/L) with fractional excretion of sodium greater
than 1% and the presence of renal tubular epithelial cells
and granular casts in the urine is indicative of ATN
[ A Miller et al, 1978]. A renal ultrasound scan should always
be performed in postoperative ARF to rule out hydrone-
phrosis and urinary obstruction quickly. Urine eosinophils
may be present in interstitial nephritis and atheroemboli
Management
The management of postoperative ARF is mainly supportive
and initially involves the treatment of intravascular volume
depletion with isotonic fluids or blood products. Renal blood
flow should be maximized by optimizing cardiac output. This
may require controlling rhythm disturbances if present, reduc-
ing afterload, and possibly using inotropic agents. The use of
diuretic therapy may be necessary for oliguria that persists de-
spite the repletion of intravascular volume and the optimization
of hemodynamic status. Emphasis and energy are often placed
on the conversion of oliguric to nonoliguric renal failure. Al-
though the ability of a patient to respond to diuretics does
generally imply less severe disease and can facilitate manage-
ment, the successful ability to convert a patient from oliguric to
nonoliguric renal failure has not been shown to improve the
clinical outcome. In fact, some evidence suggests that the use
of diuretics in ARF may be associated with poorer renal
functional outcome [ C Mehta et al, 2002]. High doses of loop
diuretics are needed to induce natriuresis in patients with renal
failure. Continuous infusion of loop diuretics may produce a
greater percentage of increase in sodium excretion compared
with large-bolus dosing. RRT is indicated for patients with
hypervolemia resistant to diuretics, hyperkalemia or metabolic
acidosis that does not respond to medical therapy, and uremic
manifestations such as pericarditis, increased bleeding, or de-
creased mental status.
The use of agents to reverse renal failure or potentially to
hasten the recovery of renal function has generated much
interest. Dopamine, at “renal doses,” has been one such agent
that continues to be used frequently in the surgical setting.
The theoretical benefit of lower-dose dopamine is based on
the ability of this agent to increase renal blood flow, increase
Prevention
Given the lack of current therapy to treat postoperative renal
failure, emphasis should focus on its prevention. Strategies to
prevent postoperative renal failure include the early identifi-
cation of at-risk surgical patients, the maintenance of effec-
tive intravascular volume status and the optimization of
cardiovascular performance, the avoidance of nephrotoxins,
and the proper spacing of procedures. Many pharmacologic
agents have been investigated for benefit in preventing ARF.
Agents that have been studied but so far have not shown to
be of benefit include renal-dose dopamine, loop diuretics,
calcium channel blockers, atrial natriuretic peptide, and
various growth factors such as insulin-like growth factor and
fibroblast growth factor.
Two agents that have shown some promise in the preven-
tion of ARF resulting from intravenous contrast agents are
N-acetylcysteine and the dopamine analogue fenoldopam.
Whether there is some benefit in the use of these agents for the
prevention of postoperative renal failure remains to be eluci-
dated. One review of evidence-based strategies to lower the
risk of contrast-induced nephropathy suggested that pa-
tients at increased risk for contrast-induced nephropathy
be considered to receive N-acetylcysteine, 600 to 1200 mg
orally twice daily for two doses before the contrast-related
procedure and two doses after the procedure, OR ascorbic
acid, 3 g orally 2 hours before the procedure and 2 g orally
twice daily after the procedure. These patients should also
receive intravenous hydration before the procedure (intra-
venous normal saline, 1 mL/kg/hour for 6 to 12 before the
procedure, OR intravenous 5% dextrose and water AND
sodium bicarbonate, 3 mL/kg for 1 hour before the proce-
dure, with monitoring for metabolic alkalosis) and intrave-
nous hydration following the procedure (intravenous
normal saline, 1 mL/kg/hour for 6 to 12 hours, OR intrave-
nous 5% dextrose and water AND sodium bicarbonate,
154 mEq/L, 1 mL/kg for 6 hours, with monitoring for
metabolic alkalosis). Because these preprocedure and
postprocedure hydration regimens use a significant vol-
ume load, it is essential to monitor the patient carefully for
volume overload. It is also recommended that the mini-
mum possible volume of iso-osmolar or low-osmolar con-
trast agent be used [ C Pannu et al, 2006].
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Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized con-
trolled trials, systematic reviews of studies other than RCTs, cross-sectional studies,
retrospective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
633
Methotrexate
Methotrexate (MTX) is usually prescribed once weekly, along
with daily folic acid (1 mg) to reduce side effects. MTX is
normally cleared very rapidly from the circulation following
each administration; but because the kidney excretes metho-
trexate, the drug should not be given immediately before any
procedure likely to be associated with significant renal insuf-
ficiency. No data have strongly shown that the use of metho-
trexate within the week before surgery adversely affects sur-
gical outcome. Several small, controlled studies demonstrated
the safety of providing the drug a week before a surgical
procedure. Preoperative withdrawal of the drug has been
Postoperative Complications
Postoperative flares of disease are usually the result of with-
holding medications. Anti-inflammatory medications should
be reinstituted as soon as possible. Low-dose corticosteroids
(ⱕ7.5 mg prednisone daily) may be helpful, as may NSAIDs.
Postoperative fever is not likely the result of a flare in RA or
spondylitis. A monoarticular “flare” should be assumed to be
an infection until proven otherwise by arthrocentesis, even in
the absence of leukocytosis or fever. Postoperative neurologic
complications can be caused by myelopathy, but they are
more commonly the result of compressive neuropathies.
CRYSTALLINE ARTHRITIS
Disease Characteristics
It is useful to try to document the validity of the prior diag-
nosis of gout or pseudogout. Frequently, the diagnosis
of gout has been unreliably based solely on the presence of
hyperuricemia or an episode of foot pain. The frequency of
attacks and the need for aggressive prophylaxis should be
ascertained from the patient and prior medical records.
Previous episodes of postoperative attacks of arthritis are
noteworthy. Hyperuricemia is strongly associated with
coronary artery disease and the metabolic syndrome; thus,
an especially careful cardiac risk assessment should be
obtained.
Medications
Postoperative flares are particularly common and may prolong
hospitalization. It is therefore important to consider periopera-
tive prophylaxis. For the patient who takes allopurinol or
colchicine on a long-term basis, we recommend that these
medications be continued up to the time of surgery and re-
started immediately thereafter. Given orally, colchicine can
cause dose-related diarrhea or nausea, but it is not ulcerogenic.
We generally avoid low-dose intravenous prophylaxis or treat-
ment with intravenous colchicine because of the reported fatal
complications with the intravenous form of this medication.
For the patient who has a history of frequent or recent attacks
of gout but who comes to surgery not taking allopurinol or
colchicine, prophylactic oral low-dose (0.6 mg once to twice
daily) colchicine can be considered if renal function and bili-
ary function are normal. However, the possibility of diarrhea
exists, even with low doses. NSAIDs or corticosteroids can be
used as prophylactic therapy, but because of their myriad of
side effects in this setting, these drugs are generally used as
therapy if an attack should occur.
Postoperative Flares
Flares (attacks) of gout are common and are frequently associ-
ated with fever. Patients have usually experienced previous gout
attacks, although that history may not have been elicited at the
time of surgical admission. Acute arthritis in the postoperative
setting warrants arthrocentesis not only to diagnose crystalline
arthritis definitively, but also to exclude infection. Indirect
evaluation (presence or absence of fever, leukocytosis, or eryth-
rocyte sedimentation rate elevation) is inadequate to distinguish
infection from crystalline arthritis. There is no diagnostic value
in obtaining radiographs or nuclear imaging studies to distin-
guish between acute septic and crystalline arthritis. Unrecog-
nized crystal-induced arthritis is a cause of unexplained fever,
particularly in intubated or uncommunicative patients.
Medications
Treatment of myositis usually requires a prolonged course of
high-dose corticosteroids. Methotrexate, calcineurin antago-
nists, and azathioprine are also frequently utilized in relatively
Postoperative Complications
Weaning from the ventilator may be difficult in patients with
respiratory muscle involvement, and having the patient in a
seated position may provide significant advantage. There is also
an increased risk for aspiration because of dysphagia as well as
ineffective cough resulting from muscle weakness. The diagno-
sis of myocardial infarction may be difficult as a result of in-
flammatory muscle disease that causes an elevation in serum
enzymes traditionally linked to acute myocardial infarction.
Although CPK-MB is classically a marker of myocardial injury
Medications
Drugs, other than corticosteroids, used to maintain remission
may be held during the immediate perioperative period as
noted earlier and in Table 19-2. Corticosteroids taken on a
long-term basis should be continued during the perioperative
period, given intravenously until enteral absorption is en-
sured. Some clinicians recommend a slight elevation in corti-
costeroid dose to prevent a flare induced by the stress of
surgery. Data are inadequate to support or refute this practice.
The need for aggressive antithrombotic prophylaxis should be
considered at the time of preoperative assessment in patients
who have APLAs and especially lupus anticoagulant.
Postoperative Complications
Flares in disease may occur in the perioperative setting and
may be difficult to distinguish from infection, corticosteroid
withdrawal syndromes, drug reactions, or a surgical compli-
cation. Fever may be a manifestation of disease activity,
thrombosis, infection, or drug reaction. Acute leukopenia or
thrombocytopenia favors the diagnosis of lupus flare instead
of infection. The presence of rigors favors infection. Acute-
phase reactants may be elevated in the postoperative period
in the absence of an SLE flare. They are of minimal clinical
utility during that period.
SCLERODERMA
Disease Characteristics
Severe disease may produce facial tightening with decreased
ability to open the mouth wide enough to permit easy intu-
bation. Dental health may be poor. Vascular and soft tissue
Medications
Medications that the patient takes on a long-term basis for
Raynaud’s phenomenon, pulmonary hypertension, and gas-
troesophageal reflux should be continued in the periop-
erative period.
Postoperative Complications
Fever is not expected from a disease flare, so alternative
causes of fever must be sought. Scleroderma involvement of
the gut may make oral drug absorption slow and unreliable.
Bacterial overgrowth is common. Postoperative ileus may be
particularly problematic. Reflux and esophageal dysmotility
are often severe and place patients at high risk for aspiration
when they are supine. The patient should be positioned in
bed to limit the likelihood of aspiration.
Even mild hypothermia or vasoconstrictive medications
may cause peripheral, renal, or central vasoconstriction. Se-
vere vasospastic peripheral ischemia may necessitate acute
vasodilator therapy.
OSTEOARTHRITIS
Disease Characteristics and Postoperative Complications
OA is the most common underlying disease warranting arthro-
plasty. Although frequently a multifocal process involving car-
tilage and periarticular bone, OA has no systemic manifesta-
tions affecting the perioperative course. OA is not characterized
by inflammatory joint flares. Patients with acute joint swelling,
particularly with swelling or warmth, should be evaluated by
arthrocentesis for crystal disease or infection. Because the joint
pain is not primarily the result of inflammation in the usual
sense, postoperative joint pain can generally be managed with
pure analgesics. Fever immediately following hip or knee ar-
throplasty (done for any indication) is common and is usually
not related to infection. However, persistent fever for several
days or fever developing a few days postoperatively warrants
detailed evaluation for infection, thrombosis, drug allergy, or
crystalline arthritis.
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PSYCHIATRIC MEDICATIONS
The major classes of psychiatric medications include benzodi-
azepines, tricyclic antidepressants, selective serotonin reup-
take inhibitors (SSRIs), neuroleptic agents, monoamine oxi-
dase (MAO) inhibitors, and lithium. The only agents that are
contraindicated during the perioperative period are the MAO
inhibitors; however, knowledge of the side effect profiles, drug
interactions, and withdrawal syndromes may be helpful in
interpreting clinical problems of patients undergoing surgery.
Perioperative recommendations for different psychiatric medi-
cation classes are summarized in Table 20-1.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed system-
atic reviews of RCTs. B —Case-control or cohort studies, nonrandomized con-
trolled trials, systematic reviews of studies other than RCTs, cross-sectional studies,
retrospective studies. C —Consensus statements, expert guidelines, usual practice,
opinion.
657
Ch20-X2385_657_672.indd 658
TABLE 20-1 Psychiatric Drugs and Perioperative Management
Drug Category Perioperative Concerns Recommendations for Management
Benzodiazepines Abrupt discontinuation can lead to withdrawal Continue perioperatively to avoid withdrawal, using intravenous
symptoms forms if NPO
Mild: insomnia, dysphoria Postoperatively, reduce benzodiazepine doses gradually if concur-
Moderate: agitation, delirium, tremors, abdominal rent narcotics lead to increased side effects
cramps, diaphoresis, seizures
Concurrent narcotics may lead to excessive sedation,
confusion, hypotension, or respiratory depression
Tricyclic Hypotension may be more prevalent with other drugs Consider holding TCA a few days preoperatively and restarting
Antidepressants that also cause hypotension, including some them a few days postoperatively, particularly in patients who
anesthetics (atropine, pancuronium) are at higher risk for falls, hypotension, confusion or arrhyth-
Interactions with sympathomimetics can cause mias or in patients who are taking lower doses of TCAs who
hypertension have less risk of withdrawal symptoms
Interactions with some volatile anesthetics can increase Watch for mild withdrawal symptoms (gastrointestinal symptoms,
potential for arrhythmias dizziness)
Can lead to slowed cardiac conduction No IV form available
Watch for slowed cardiac conduction including P-R and Q-T pro-
longation and bundle branch block, especially with concurrent
atrioventricular node blockers, such as -blockers and calcium
channel blockers
20 • Perioperative Care of the Patient with Psychiatric Illness
Selective Serotonin May interact with warfarin, digoxin, phenytoin Continue SSRI perioperatively; no IV form available
Reuptake Stopping SSRIs suddenly may exacerbate mood disorders In patients on warfarin and SSRI, monitor INR closely
Inhibitors Concurrent use with MAO inhibitors can lead to sero- Monitor for phenytoin toxicity in patients on SSRI
tonin syndrome
12/19/07 3:10:28 PM
MAO Inhibitors Hypertensive crisis with sympathomimetics, caffeine Stop MAO inhibitors at least 2 wk before elective surgery to allow
Interaction with meperidine, dextromethorphan, leading complete elimination
Ch20-X2385_657_672.indd 659
to autonomic instability, agitation, cyanosis (potentially For emergency surgery, or if psychiatrist believes it unsafe to stop
fatal) the MAO inhibitor, anesthesiologist should be notified to avoid
Interaction with SSRIs, leading to autonomic instability, sympathomimetics and to monitor blood pressure closely
rigidity, myoclonus, confusion, coma If MAO inhibitor is continued perioperatively, avoid foods
containing higher amounts of tyramine
Avoid meperidine (Demerol) and dextromethorphan within 2 wk
of using an MAO inhibitor
Avoid SSRIs within 2 wk of using an MAO inhibitor (5 wk with
fluoxetine)
Neuroleptics At high doses, some antipsychotics can prolong the Q-T Continue therapy perioperatively; IV haloperidol available for
interval, leading to risk of torsades de points patients who are NPO
Follow ECG in patients on other agents that can prolong the Q-T
interval and for patients on high doses of antipsychotics
Lithium Narrow safety margin Stop lithium 1–2 days preoperatively and restart when taking
Possible perioperative side effects: nausea, nephrogenic dia- oral medications; no parenteral form available
betes insipidus, delirium, coma, ventricular arrhythmias If continued, follow lithium levels and check baseline ECG
May prolong the effects of neuromuscular blocking agents preoperatively
and anesthetics
May cause T-wave flattening or inversion
ECG, electrocardiogram; INR, international normalized ratio; IV, intravenous; MAO, monoamine oxidase; NPO, nothing by mouth: SSRI, selective
serotonin reuptake inhibitor; TCA, tricyclic antidepressant.
20 • Perioperative Care of the Patient with Psychiatric Illness
659
12/19/07 3:10:28 PM
660 20 • Perioperative Care of the Patient with Psychiatric Illness
Benzodiazepines
Benzodiazepines are used as antianxiety agents and for insom-
nia. They are generally divided into long-acting agents with a
half-life of more than 24 hours (diazepam, chlordiazepoxide,
and flurazepam), intermediate-acting agents with a half-life of
6 to 24 hours (lorazepam, temazepam, and oxazepam), and
short-acting agents with a half-life less than 6 hours (estazolam
and triazolam). These half-lives are determined not only by the
parent compound, but also by the presence and half-life of any
active metabolites. Side effects of benzodiazepines at therapeu-
tic doses may include sedation, dizziness, and confusion.
Perioperatively, the major adverse effect of these agents is the
potential for acute withdrawal if they are discontinued abruptly.
Mild withdrawal symptoms can present as insomnia and dys-
phoria. More severe symptoms include tremors, abdominal
cramps, diaphoresis, agitation, delirium, and seizures. If a pa-
tient taking benzodiazepines requires a surgical procedure, the
drugs should be continued postoperatively to prevent with-
drawal. If the patient is receiving nothing by mouth (NPO) and
is taking a benzodiazepine without a parenteral formulation,
lorazepam, diazepam, and chlordiazepoxide can be used intra-
venously. Postoperatively, benzodiazepine doses may need
to be reduced if concurrently administered narcotics lead to
excessive sedation, confusion, or hypotension.
Tricyclic and Related Antidepressants
The tricyclic antidepressants are used for a variety of prob-
lems, including depression, panic disorder, anxiety, and
neuropathic pain (Table 20-2). These drugs have a 70% re-
sponse rate for depression when therapeutic blood levels are
achieved. Their mechanism of action is by potentiating the
effects of both serotonin and norepinephrine. Unfortunately,
they have many side effects, especially cardiovascular.
Side effects of the tricyclic antidepressants include ortho-
stasis, anticholinergic effects (dry eyes, blurry vision, dry
mouth, urinary hesitancy, constipation), conduction delays, and
12/19/07 3:10:28 PM
662 20 • Perioperative Care of the Patient with Psychiatric Illness
Lithium
Lithium is used to treat mania. It has a narrow margin of
safety and is dangerous when overdosed. Minor side effects
occur even at therapeutic levels (0.8 to 1.5 mEq/L). These
side effects include nausea, anorexia, and nephrogenic diabe-
tes insipidus with polyuria and polydipsia. These last two
symptoms occur in 50% of new patients but in only 5% of
patients taking lithium on a long-term basis. Lithium can also
affect thyroid function. Many drugs can raise lithium levels,
including thiazides, NSAIDs, and metronidazole (Flagyl).
Major side effects may occur at blood levels greater than
2 mEq/L. They consist of progressive delirium, coma, sei-
zures, and ventricular arrhythmias. Unlike many other psy-
chiatric drugs, lithium does not cause sedation at therapeutic
levels. Lithium may also prolong the effects of neuromuscular
blocking and anesthetic agents. Therefore, these agents should
be used with caution in patients receiving lithium. In
addition, lithium may cause changes on the ECG, including
T-wave flattening or inversion, which may provoke confusion
ELECTROCONVULSIVE THERAPY
ECT is one of the most successful methods of treating de-
pression, with up to an 80% response rate. It is also effective
in mania and in some psychoses. In general, ECT is often
used when rapid antidepressant response is necessary or in
refractory psychiatric conditions. The procedure consists of
electrical stimulation lasting approximately 5 seconds, fol-
lowed by a convulsion lasting approximately 30 seconds.
ECT is performed using general anesthesia with cardiac and
blood pressure monitoring. Patients receive mask ventilation
and are given a bite block.
ECT is capable of causing profound changes in hemody-
namics. These include acute hypertension, hypotension, and
arrhythmias, with resultant alterations in cardiac output.
These disturbances result from changes in parasympathetic
and sympathetic tone. Initially, these alterations are mani-
fested by a decrease in blood pressure and heart rate. The
blood pressure may decrease by 10% with the induction of
anesthesia and then increase by up to 80% during the convul-
sion. These hemodynamic changes increase myocardial oxy-
gen consumption and cause ischemia. As a result, hyperten-
sion should be well controlled before ECT. The noncardiac
surgery guideline of the American College of Cardiology/
American Heart Association classifies ECT as a low-risk pro-
cedure. Because ECT is generally an elective procedure, pa-
tients with recent myocardial infarction (ⱕ30 days) should
probably not undergo ECT. The American Psychiatric As-
sociation has suggested that patients with unstable or se-
vere cardiac disease are at increased risk for morbidity
Roose SP, Glassman AH, Dalack GW: Depression, heart disease and tricyclic
antidepressants. J Clin Psychiatry 50(Suppl):12-16, 1989.
Roose SP, Glassman AH, Giardiner EG, et al: Tricyclic antidepressants in
depressed patients with conductive disease. Arch Gen Psychiatry 44:
273-275, 1987.
Wells DG, Davies GG: Hemodynamic changes associated with electrocon-
vulsive therapy. Anesth Analg 66:1193-1195, 1987.
Williams RB Jr, Sherter C: Cardiac complications of tricyclic antidepressant
therapy. Ann Intern Med 74:395-398, 1971.
Yacoub OF, Morrow DM: Malignant hyperthermia and ECT. Am J Psychiatry
143:1027-1029, 1986.
Levels of Evidence:
A —Randomized controlled trials (RCTs), meta-analyses, well-designed systematic
reviews of RCTs. B —Case-control or cohort studies, nonrandomized controlled tri-
als, systematic reviews of studies other than RCTs, cross-sectional studies, retrospec-
tive studies. C —Consensus statements, expert guidelines, usual practice, opinion.
673
Management of Commonly
TABLE 21-2
Prescribed Medications (Continued)
Medication Preoperative Management
Transplantation antirejection medications Continue through surgery
Selective serotonin reuptake inhibitors Administer half dose for 3 days preopera-
tively if NPO period is anticipated post-
operatively
Tricyclic antidepressants Continue through surgery with precautions
Monoamine oxidase inhibitors Consult with anesthesiologist regarding use
of MAO inhibitor–safe anesthesia
Lithium Administer the morning of surgery through
postoperative period
Antipsychotics Administer the morning of surgery through
postoperative period
Multiple IV/IM forms available Long-acting decanoate forms can be administered if a long
period of NPO status is anticipated
␣2-Adrenergic Agonists
Clonidine is the most commonly used agent of this class. The
hypotensive effect of clonidine is mediated primarily by ago-
nism of central nervous system ␣2-receptors, which leads to
increased parasympathetic tone and decreased circulating cat-
echolamines. This global reduction in sympathetic output has
made the drug a useful adjunct in the treatment of opiate with-
drawal. Similarly, in a mechanism likely analogous to that seen
with perioperative -adrenergic blockade, clonidine use is as-
sociated with decreased mortality following vascular surgery
and decreased ischemia and likely decreased mortality follow-
ing cardiac surgery. This appears to be a class effect, because
mivazerol (not available in the United States) has been shown
to improve hemodynamic stability intraoperatively, to reduce
cardiac ischemia during emergence from anesthesia, and to
decrease late postoperative tachycardia and hypertension in
patients at risk for or with coronary artery disease. On the basis
of these findings, the American College of Cardiology sug-
gested that some evidence (level IIB) indicates that ␣2-adrenergic
agonists may be cardioprotective in the perioperative period.
Clonidine should be used for cardioprotective prophylaxis in
patients with a contraindication to -blockers.
Aside from cardiovascular indications, ␣2-agonists are oc-
casionally used de novo perioperatively, because they are
known to have sedative, analgesic, and anxiolytic properties.
Intrathecal clonidine has been used as part of an anesthesia
regimen for postoperative pain control, whereas preoperative
oral clonidine has been associated with decreased postopera-
tive pain. Anesthesia induction with clonidine helps to pre-
vent postoperative nausea and vomiting.
Particular care must be exercised for patients who take
clonidine on a regular basis in the perioperative period.
Cessation of clonidine can be associated with a hyperadren-
ergic withdrawal syndrome characterized by hypertension,
tremor, and agitation. Given the benefits of sympatholysis
in the surgical period and the risks associated with
Antiarrhythmics
Given the proarrhythmic effects of many traditional agents, the
most commonly encountered antiarrhythmic drugs aside from
the -blockers and calcium channel blockers are amiodarone
and sotalol. Amiodarone appears safe in operative patients,
and the drug should be continued until the day before surgery.
The drug has a half-life of 40 to 55 days, with pharmacody-
namic effects lasting up to 50 days after the last dose. In light
of this pharmacokinetic profile, pharmacologic efficacy is
minimally influenced by missed doses. Unless there are ex-
tended periods of NPO status or serious arrhythmia, use of the
intravenous formulation of amiodarone is not indicated. Intra-
venous formulations of flecainide, propafenone, or sotalol are
not available. Patients who take these agents on a long-term
basis should take them with a sip of water on the day of
Nitrates
For the treatment of intraoperative myocardial ischemia, vaso-
spasm, or hypertension, intravenous nitroglycerin is preferable
to transdermal preparations because of more reliable drug
delivery. Unfortunately, nitrates can be associated with intraop-
erative hypotension, especially when these drugs are used in
conjunction with anesthesia in a hypovolemic patient. The
use of prophylactic intravenous nitroglycerin is not associ-
ated with a reduction in ischemia in patients undergoing
noncardiac surgical procedures [ B Dodds et al, 1993].
On the basis of available evidence, the American College of
Cardiology and American Heart Association guidelines en-
dorsed the use of intravenous intraoperative nitroglycerin in
patients with clear signs of myocardial ischemia (level A). In
contrast, even for high-risk patients, the use of intraoperative
nitroglycerin as a prophylactic against ischemia is not well
supported by the evidence (level IIB) and should be reserved
for carefully screened patients. In all cases, nitroglycerin
should be avoided in hypovolemic or hypotense patients.
In long-term users of these agents, a nitrate withdrawal syn-
drome of increased angina and myocardial ischemia has been
suggested, but clinical studies of this possible effect yielded
divergent results. Given inconsistent clinical observations,
when nitrate withdrawal does cause an increase in arterial reacti-
vity, the effect is likely modest. Because of the lack of demonstr-
ated benefit in most patients, the risk of intraoperative hypoten-
sion, and the lack of well-characterized withdrawal syndrome,
oral and transdermal nitrates should be held on the morning of
surgery for patients without active ischemia. These prepara-
tions should be restarted in the postoperative period only when
the patient has demonstrated hemodynamic stability.
Diuretics
Little evidence exists to guide the management of diuretic
therapy in the perioperative period. Decompensated congestive
heart failure is associated with poor surgical outcomes, so in
patients with clinical volume overload, diuretics should be
used until euvolemia is reached. In the more common case of
a stable patient receiving diuretic maintenance therapy, man-
agement is ideally guided by clinical volume status. Hypovole-
mia places patients at risk for intraoperative hypotension and
associated cardiovascular and cerebrovascular complications.
Additionally, hypovolemia and associated hypotension are risk
factors for postoperative renal failure, with diabetic and elderly
patients at particularly high risk. Unfortunately, clinical esti-
mation of volume status and of the risk of postoperative
hypovolemic hypotension in hospitalized and preoperative
patients is often difficult [ C McGee et al, 1999]. For near-
euvolemic patients, diuretics should be discontinued the day
before the surgical procedure. Although diuretic-associated
hypokalemia is well tolerated by patients in the perioperative
period, attention should be paid to this phenomenon in pa-
tients taking digoxin or requiring large doses of 2-agonists.
Anticoagulants
Decisions regarding the management of anticoagulants are
based primarily on the risk of hemorrhage if anticoagulation is
continued in the perioperative period as opposed to the risk and
consequences of thrombosis if anticoagulation is withdrawn
Antiretroviral Medications
Special attention is required for the patient receiving anti-
retroviral medications whose surgical procedure necessi-
tates cessation of oral intake in the perioperative period.
Zidovudine is the only antiretroviral medication that is
available in intravenous formulation. Because even short
periods of monotherapy can generate resistance to antiret-
rovirals, all antiretroviral drugs should be stopped and re-
sumed at the same time. Exceptions to this rule are the
non-nucleoside reverse transcriptase inhibitors nevirapine
and efavirenz, because of their extended half lives (20 to
30 hours and 40 to 55 hours, respectively) and the rapidity
with which human immunodeficiency virus develops resis-
tance to this class of medications. Nevirapine should be
held 2 days and efavirenz 4 days before the cessation of
other antiretrovirals. Patients who receive maintenance
therapy with the subcutaneously administered fusion in-
hibitor enfuvirtide should have this medication held with
other antiretrovirals. Administration of antiretrovirals sensi-
tive to food effects should be resumed when oral intake has
been firmly established. For minor procedures and those
Tricyclic Antidepressants
The clinician should be aware of several risks if patients con-
tinue taking tricyclic antidepressants (TCAs) into the periop-
erative period. These drugs inhibit the reuptake of biogenic
amines in the central and peripheral nervous system. This ac-
tion can predispose patients to cardiac arrhythmias, and the
effect may be increased with the use of pancuronium and
volatile anesthetics such as enflurane. There have also been
case reports of decreased seizure threshold in patients taking
TCAs on a long-term basis who undergo anesthesia with en-
flurane. Agents with sympathomimetic properties may have
exaggerated effects in the presence of TCA, and the dose of
these medications may need to be reduced.
Discontinuation syndromes have been described that
include agitation, irritability, and insomnia. When TCAs are
used to treat depression, these agents should be tapered,
when possible, over a week and held the day before surgery.
For patients taking TCAs for pain, a prudent course is to
allow preoperative withdrawal for a period of three to four
drug half-lives, with control of pain provided by other,
non-TCA agents.
Lithium
Lithium is used in the treatment of bipolar disorder. It is likely
that lithium can potentiate the duration of neuromuscular
blocking agents (e.g., succinylcholine and decamethonium)
that are used during induction of anesthesia and may prolong
the effects of muscle relaxants, but lithium may safely be con-
tinued through the perioperative period with attention paid
to monitoring levels. There is no intravenous preparation of
lithium. Lithium is eliminated entirely by the kidneys, so we
monitor postoperative renal function before restarting this
drug. Additionally, because long-term lithium use can cause
nephrogenic diabetes insipidus resulting in hypernatremia,
the medical consultant should be aware of sodium and free
water balance, especially when patients are not taking oral
hydration.
Antipsychotics
The typical antipsychotics such as haloperidol and chlorpro-
mazine are generally considered safe for use in surgery, and
some of these agents have been used as anesthetic adjuncts for
the treatment of emesis. Aside from the potential for Q-T pro-
longation and some mild anticholinergic effects, the newer
atypical agents such as olanzapine and quetiapine are also con-
sidered safe in the perioperative period. A mild withdrawal
syndrome of insomnia and agitation has been noted. This
would be expected to be more common with the short-acting
agents quetiapine and ziprasidone. Patients unable to take oral
agents who require treatment for psychosis or agitation can be
given parenteral forms of these drugs (e.g., haloperidol). Pa-
tients undergoing procedures with extended anticipated peri-
ods of NPO status can be administered long-acting decanoate
forms (e.g., risperidone or haloperidol).
Herbal Medications
The use of herbal remedies and supplements is common and
has been reported in up to 22% of preoperative patients.
Most patients do not consider these substances “medica-
tions” and do not list them with their medications unless
they are specifically asked about them. Management of pa-
tients taking these products is difficult for a variety of rea-
sons. Preparations often vary in amount of herbal product
present, as well as other ingredients. Neither a mechanism of
purported action nor a dose response has been identified for
most products, and very few have efficacy demonstrated by
well-performed clinical trials. Adverse reactions to some
products have been identified, such as induction of cyto-
chrome P-450 3A4 by St. John’s wort and adverse cardiovas-
cular events from ephedra (ma huang). A proposed manage-
ment approach is outlined in Table 21-3.
Ch21-X2385_673_706.indd 704
TABLE 21-3 Herbal Medicines in the Perioperative Period
Recommended
Herb Purported Indications Potential Drug Interactions Possible Side Effects Discontinuation
Ephedra Increase energy, weight loss, Antidepressants, CNS stimu- Increases in blood pressure, ⱖ24 hr preoperatively
(ma huang) asthma/bronchitis lants, halothane heart rate, arrhythmias
Garlic Hypercholesterolemia, atherosclerotic Aspirin, antiplatelet agents, and Bleeding ⱖ7 days preoperatively
disorders, hypertension anticoagulants
Ginkgo Cognitive disorders, peripheral vascu- Aspirin, antiplatelet agents, anti- Bleeding, decreased seizure ⱖ36 hr preoperatively
lar disease, macular degeneration, coagulants, anticonvulsants, threshold
erectile dysfunction TCAs
Ginseng Protection of the body against stress Corticosteroids, MAO inhibitors, Hypoglycemia, decreased INR ⱖ7 days preoperatively
warfarin
St. John’s wort Depression and dysthymia Antidepressants, piroxicam, tet- Increased photosensitivity, sero- ⱖ5 days preoperatively
racyclines, CNS stimulants, tonin syndrome, induction of
theophylline, cyclosporine, cytochrome P-450 3A4
indinavir, ethinyl estradiol, (reduced INR, cyclosporine
midazolam, lidocaine, calcium levels), possible withdrawal
channel blockers, warfarin syndrome similar to SSRIs
21 • Managing Medication in the Perioperative Period
CNS, central nervous system; INR, international normalized ratio; SSRI, selective serotonin reuptake inhibitor; MAO, monoamine oxidase; TCA,
tricyclic antidepressant.
12/20/07 6:49:16 PM
21 • Managing Medication in the Perioperative Period 705
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Grines CL, Bonow RO, Casey DE Jr, et al: Prevention of premature discon-
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I. Laparoscopic Cholecystectomy
A. Definition: endoscopic removal of the gallbladder
B. Indications: cholelithiasis or cholecystitis, or both, with-
out common duct stenosis
C. Duration of surgery: less than 1 hour
D. Anesthesia: general endotracheal anesthesia
E. Transfusion requirements: rare
F. Mortality: less than 1%
G. Complications
1. Major bleeding: less than 2%
2. Wound infection: less than 1%
3. Biliary injury: less than 1%
4. Bowel injury: less than 1%
5. Need to convert to open procedure: 5% to 10%
H. Specific recommendations
1. Deep venous thrombosis prophylaxis
a. Aggressive early mobilization
b. For patients with additional thromboembolic risk
factors (see Chapter 5, Table 5-1, on risk factors for
deep venous thrombosis and pulmonary embo-
lism), choose one of the following:
i. Unfractionated heparin, 5000 U subcutane-
ously every 12 hours
ii. Low-molecular-weight heparin
(a) Enoxaparin, 40 mg subcutaneously every
24 hours
(d) Dalteparin, 5000 U subcutaneously every
24 hours
iii. Intermittent pneumatic compression sleeves
713
2. Prophylactic antibiotics
a. High risk: ampicillin, 2 g intravenously, and genta-
micin, 1.5 mg/kg, 30 minutes before the proce-
dure, followed by amoxicillin, 1 g orally, intramus-
cularly or intravenously, 8 hours after the procedure;
for penicillin-allergic patients, delete ampicillin
and amoxicillin and add vancomycin, 1 g intrave-
nously, 1 to 2 hours before the procedure
b. Moderate risk: amoxicillin, 2 g orally, or ampicil-
lin, 2 g intravenously, 30 minutes before the proce-
dure; for penicillin-allergic patients, substitute
with vancomycin, 1 g intravenously, 1 to 2 hours
before the procedure
c. Low risk: none suggested
I. Advantages over open procedure
1. Less morbidity
2. Preoperative diagnosis unclear (gallbladder versus ap-
pendix versus gynecologic problem)
V. Laparoscopic Nephrectomy
A. Definition: removal of a kidney by laparoscopy
B. Indication: diseased kidney
C. Duration of surgery: 1 to 2 hours
D. Anesthesia: general anesthesia
E. Transfusion requirements: usually none
F. Surgical mortality: less than 1%
G. Postoperative complications
1. Vascular injury: 7%
2. Other (e.g., small bowel obstruction): 17%
3. Two to three times more complications when com-
pared with open nephrectomy
H. Specific recommendations
1. Deep venous thrombosis prophylaxis
a. Aggressive early mobilization
b. For patients with additional thromboembolic risk
factors (see Chapter 5, Table 5-1, on risk factors for
deep venous thrombosis and pulmonary embo-
lism), choose one of the following:
i. Unfractionated heparin, 5000 U subcutane-
ously every 12 hours
ii. Low-molecular-weight heparin
(a) Enoxaparin, 40 mg subcutaneously every
24 hours
(b) Dalteparin, 5000 U subcutaneously every
24 hours
iii. Intermittent pneumatic compression sleeves
2. Antibiotic prophylaxis: unnecessary
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WB Saunders, 1994.
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review and meta-analysis. JAMA 292:1724-1737, 2004.
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Recommendations by the American Heart Association. JAMA 277:1794-
1801, 1997.
Geerts WH, Pineo GF, Heit JA, et al: Prevention of venous thromboembo-
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University of Maryland 6-year experience. J Urol 171:47-51, 2004.
Matas AJ, Bartlett ST, Leichtman AB, Delmonico FL: Morbidity and mortality
after living kidney donation, 1999-2001: Survey of United States trans-
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Strasberg SM, Soper NJ: An analysis of the problem of biliary injury during
laparoscopic cholecystectomy. J Am Coll Surg 180:101-125, 1995.
I. Vaginal Hysterectomy
A. Definition: removal of the uterus through the vaginal
approach
B. Indications
1. Uterine prolapse
2. Carcinoma in situ of the cervix
3. Obesity with pelvic relaxation
4. Small leiomyomata with some relaxation
C. Duration of surgery: approximately1 hour, longer if lapa-
roscopically assisted
D. Anesthesia: general (usually), spinal, or epidural anes-
thesia
E. Transfusion requirements: infrequent
F. Overall surgical mortality: less than 1%
G. Postoperative complications
1. Ureteral injury (rare for vaginal approach) may occur
during clamping or ligation of the uterine artery, with
resulting flank pain with fever and ileus.
2. Sciatic and peroneal injury (1 in 500) is more com-
mon than in abdominal hysterectomy.
3. Vaginal cuff or adnexal infections are more common
than in abdominal hysterectomy.
4. Postoperative hemorrhage is more common than in
abdominal hysterectomy.
5. Deep venous thrombosis
6. Vesicovaginal fistula
719
719
H. Specific recommendations
1. Antibiotic prophylaxis for wound infection
a. Cefazolin, 1 to 2 g intravenously, cefoxitin, 2 g, or
metronidazole, 1 g as a single dose 30 minutes
before the incision
b. Bacterial vaginosis is a known risk factor for vagi-
nal cuff infection. Metronidazole, 500 mg twice
daily, should be given for 1 week, ideally starting
at least 4 days preoperatively.
2. Deep venous thrombosis prophylaxis
a. Heparin, 5000 U subcutaneously given 2 hours be-
fore surgery and every 8 to 12 hours until the patient
is ambulatory or discharged.
G. Postoperative complications
1. Postoperative ileus
2. Hemorrhage from injury to uterine arteries or veins,
uterine atony, or placenta accreta
3. Injury to bladder or bowel occur in less than 1%
4. Risk of endomyometritis is increased with increased
length of labor and duration of ruptured membranes.
It may present with fever, uterine tenderness, and foul
lochia. Endometritis may progress to pelvic cellulitis
and septic pelvic thrombophlebitis.
5. Wound infections as per previous abdominal surgical
procedures
H. Specific recommendations
1. Antibiotic prophylaxis can decrease the incidence of
endomyometritis, wound infection, and urinary tract
infections. Ampicillin, 2 g intravenously, or cefazolin
1 g intravenously, is administered immediately after
cord clamping. Penicillin-allergic patients may receive
metronidazole, 500 mg intravenously, after the cord is
clamped.
2. Deep venous thrombosis prophylaxis is indicated for
women at high risk.
a. Heparin, 5000 U subcutaneously 12 hours before
surgery and then 5000 U every 8 to 12 hours until
patient is ambulatory or discharged.
b. Pneumatic compression sleeves should be worn
during surgery and then postoperatively until
patient is ambulatory. They may be removed for
out-of-bed activities or bathroom use.
VII. Laparoscopy
A. Definition: insertion of a fiberoptic scope into the abdominal
cavity following needle insertion through abdominal wall
into the peritoneal cavity with carbon dioxide insufflation
B. Indications: surgery for tubal occlusion, biopsy, aspira-
tion of fluid, myomectomy, oophorectomy, ovarian
Selected Readings
ACOG Committee on Practice Bulletins: ACOG Practice Bulletin 74: Antibi-
otic prophylaxis for gynecologic procedures. Obstet Gynecol 108:225-
234, 2006.
Capeless E, Damron DP: Caesarian delivery. Available at http://www
.Uptodate.com
Dajani AS, Taubert KA, Wilson W, et al: Prevention of bacterial endocarditis:
Recommendations by the American Heart Association. Circulation
96:358-366, 1997.
Geerts WH, Pineo GF, Heit JA, et al: Prevention of venous thromboembo-
lism: The Seventh ACCP Conference on Antithrombotic and Thrombo-
lytic Therapy. Chest 126(Suppl):338S-400S, 2004.
Mann WJ Jr: Preoperative evaluation and preparation of women for gynae-
cologic surgery. Available at http://www.Uptodate.com
B. Indications
1. Radical prostatectomies are performed for prostate
cancer.
2. Open simple prostatectomies are performed for urinary
outlet obstruction and are preferred over transurethral
prostate resection if the prostate is larger than 50 to 60 g
or there is a concomitant bladder pathologic condition.
C. Duration of surgery: 2 to 3 hours
D. Anesthesia: general anesthesia is preferred; epidural and
spinal anesthesia are alternatives.
E. Transfusion requirements: often less than 2 U of packed
red blood cells
F. Overall surgical mortality: less than 1%
G. Postoperative complications
1. Simple: Hemorrhage from the prostatic arteries and
venous sinuses may be profuse. Radical: Dorsal ve-
nous plexus bleeding may be profuse.
2. Postobstructive diuresis may result, producing hypo-
volemia and hyponatremia if fluid and electrolytes are
not replaced. This is a rare complication and must be
kept in mind.
3. Deep venous thrombosis occurs in 30% to 50% of
patients with open prostatectomies if no prophylaxis
is used.
4. Epididymitis occurs in 3% to 6% of patients.
5. Urosepsis is common if infected urine is not sterilized
before surgery.
6. Urethrocutaneous fistula, persistent leakage of urine
through the anastomosis, may occur. Prolonged drain-
age almost universally treats this condition.
H. Specific recommendations
1. Antibiotics: No prophylactic antibiotics are required
unless the urine is infected. Infected urine should be
sterilized 24 to 48 hours before surgery. Prophylaxis
for subacute bacterial endocarditis is given to patients
with enterococcal UTIs.
IV. Cystoscopy
A. Definition: insertion of fiberoptic scope into the bladder
through the urethra
B. Indications: evaluation of hematuria; abnormalities of the
urethra, bladder, or prostate; and difficult micturition
C. Duration of surgery: less than 1 hour. Simple diagnostic
cystoscopy may only take 10 minutes.
D. Anesthesia: topical anesthesia if flexible cystoscope is
used; otherwise, general or local anesthesia
E. Transfusion requirements: very rare
F. Overall surgical mortality: very rare, less than 0.01%
G. Postoperative complications
1. Urethral or bladder perforation may occur.
2. Mild hematuria is common.
3. Urinary retention may occur.
4. If urethral dilatation is performed, bacteremia may
occur.
H. Specific recommendations: No prophylactic antibiotics
are necessary, except for prophylaxis against subacute
bacterial endocarditis, in patients with enterococcal
UTIs. Infected urine should be sterilized before the
procedure.
V. Nephrectomy
A. Definition
1. Simple nephrectomy: removal of kidney, usually
through incision or laparoscopy
2. Radical nephrectomy: removal of kidney, Gerota fas-
cia, ipsilateral adrenal gland, and retroperitoneal
lymph nodes, usually by a transabdominal, flank, or
thoracoabdominal approach or by laparoscope for
tumors up to 10 cm in size
B. Indications: neoplasm (radical nephrectomy), severe
trauma, chronic infection, renovascular hypertension, or
renal donation (simple nephrectomy)
C. Duration of surgery: 2 hours for uncomplicated simple
nephrectomy, 3 hours or more for difficult radical ne-
phrectomy or laparoscopic procedures
D. Anesthesia: general anesthesia
E. Transfusion requirements: uncommon for straightfor-
ward cases; 2 to 3 U for radical nephrectomies or
nephrectomies complicated by adhesions or abscesses.
Transfusion for laparoscopic nephrectomy is infre-
quent.
F. Overall surgical mortality: 2% for radical nephrectomy;
1% for simple nephrectomy
G. Postoperative complications
1. Hemorrhage requiring multiple units of packed
red blood cells may occur, especially with radical
nephrectomies.
2. Pneumothorax may occur if the pleural cavity is
entered.
3. Postoperative atelectasis is common, even if the pleu-
ral cavity is not entered. The intraoperative flank posi-
tion decreases vital capacity by 15%.
4. Pancreatic injury may occur intraoperatively with
typical postoperative signs and symptoms of
pancreatitis.
Selected Readings
Geerts WH, Heit JA, Clagett GP, et al: Prevention of venous thromboembo-
lism: The Seventh ACCP Conference on Antithrombotic and Thrombo-
lytic Therapy. Chest 126(3 suppl):338S-400S, 2004.
Taneja SS, et al: Complications of Urologic Surgery: Prevention and Manage-
ment. Philadelphia, WB Saunders, 2001.
Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis:
Guidelines from the American Heart Association: A guideline from the
American Heart Association Rheumatic Fever, Endocarditis, and Kawa-
saki Disease Committee, Council on Cardiovascular Disease in the
Young, and the Council on Clinical Cardiology, Council on Cardiovascu-
lar Surgery and Anesthesia, and the Quality of Care and Outcomes Re-
search Interdisciplinary Working Group. Circulation 116:1736-1754,
2007. Epub 2007 Apr 19.
741
I. Otoplasty/Pinnaplasty
A. Definition: Plastic surgery of the auricle
B. Indications: correction of structural abnormalities of the
auricle
C. Duration of surgery: variable, approximately 1 hour
D. Anesthesia: local anesthesia in adults, general anesthesia
in children
E. Transfusion requirements: none
F. Surgical mortality: less than 1%
G. Postoperative complications
1. Hematoma
2. Perichondritis
H. Deep venous thrombosis prophylaxis
1. Early mobilization
II. Foreign Body Removal from the External Ear
A. Definition: foreign body removal from the external ear
B. Indications: foreign body in ear
C. Duration of surgery: less than 1 hour
D. Anesthesia: local or general anesthesia
E. Transfusion requirements: none
F. Surgical mortality: less than 1%
G. Postoperative complications
1. Local infection
2. Hematoma
H. Deep venous thrombosis prophylaxis
1. Early mobilization
III. Myringotomy
A. Definition: puncture of the tympanic membrane
B. Indications: serous otitis media
C. Duration of surgery: less than 1 hour
D. Anesthesia: general anesthesia
E. Transfusion requirements: none
F. Surgical mortality: less than 1%
G. Postoperative complications
1. Persistent perforation
2. Scarring of tympanic membrane
3. Disruption of ossicular chain
4. Perforation of jugular bulb with bleeding
H. Deep venous thrombosis prophylaxis
1. Early mobilization
V. Stapes Surgery
A. Definition: removal of stapes, replacement with prosthesis
B. Indications: otosclerosis
C. Duration of surgery: 1 to 2 hours
D. Anesthesia: local or general anesthesia
E. Transfusion requirements: none
F. Surgical mortality: less than 1%
G. Postoperative complications
1. Vertigo
2. Nausea
3. Vomiting
4. Acute otitis media
3. Edema
4. Cerebrospinal fluid leak
H. Deep venous thrombosis prophylaxis
1. Intermittent pneumatic compression
IX. Tympanoplasty
A. Definition: repair of injured tympanic membrane
B. Indications: tympanic membrane injury
C. Duration of surgery: 3 to 5 hours
D. Anesthesia: local or general anesthesia
E. Transfusion requirements: none
F. Surgical mortality: less than 1%
G. Postoperative complications: bleeding
H. Deep venous thrombosis prophylaxis
1. Intermittent pneumatic compression
XII. Rhinoplasty
A. Definition: plastic surgery on the nose
B. Indications: cosmetic
C. Duration of surgery: approximately 1 hour
D. Anesthesia: local or general anesthesia
E. Transfusion requirements: none
F. Surgical mortality: less than 1%
G. Postoperative complications: none
H. Deep venous thrombosis prophylaxis
1. Early mobilization
XIII. Caldwell-Luc Sinusotomy
A. Definition: access to the maxillary sinus by creating a
window through the canine fossa
B. Indications
1. Sinusitis refractory to medial or endoscopic surgery
2. Sinus tumors
C. Duration of surgery: 1 to 2 hours
D. Anesthesia: general anesthesia
XIV. Ethmoidectomy
A. Definition: conversion of multichannel ethmoid labyrinth
into a single large cell, thus providing effective drainage
B. Indications: chronic ethmoid sinusitis
C. Duration of surgery: approximately 1 hour
D. Anesthesia: local or general anesthesia
E. Transfusion requirements: none
F. Surgical mortality: less than 1%
G. Postoperative complications
1. Bleeding
2. Cerebrospinal fluid leak
H. Deep venous thrombosis prophylaxis
1. Early mobilization
XVII. Laryngectomy
A. Definition: removal of larynx
B. Indication: malignant laryngeal tumors
C. Duration of surgery: 6 to 7 hours
D. Anesthesia: general anesthesia
E. Transfusion requirements: 0.5 to 1.5 U
F. Surgical mortality: less than 1%
G. Postoperative complications
1. Pneumothorax
2. Pneumomediastinum
3. Hypotension, bradycardia, apnea resulting from ca-
rotid sinus reflex
4. Laryngospasm
5. Bronchospasm
6. Venous air embolism
7. Pharyngeal fistula
8. Hematoma
9. Chylofistula
H. Deep venous thrombosis prophylaxis (one of the follo-
wing)
1. Unfractionated heparin, 5000 U subcutaneously every
8 hours
2. Low-molecular-weight heparin
a. Enoxaparin, 40 mg subcutaneously every 24 hours
b. Dalteparin, 5000 U subcutaneously every 24 hours
3. Intermittent pneumatic compression
XVIII. Tracheostomy
A. Definition: creation of a tracheocutaneous fistula
B. Indications
1. Tracheal stenosis
2. Need for prolonged mechanical ventilation
C. Duration of surgery: approximately 1 hour
D. Anesthesia: local anesthesia
E. Transfusion requirements: none
F. Surgical mortality: none
G. Postoperative complications
1. Early: bleeding, tube displacement, aspiration pneu-
monia, recurrent laryngeal nerve paralysis, subcutane-
ous emphysema, mediastinal emphysema, esophageal
injury
2. Late: ostomy site infection, cannula occlusion, tracheal
stenosis, tracheoesophageal fistula
H. Specific recommendations: none
Selected Readings
Ballenger J, Snow J: Otorhinolaryngology: Head and Neck Surgery, 15th ed.
Baltimore, Williams & Wilkins, 1996.
Cummings CW: Otolaryngology: Head and Neck Surgery, 3rd ed. St Louis,
Mosby–Year Book, 1998.
Dajani AS, Taubert KA Wilson W, et al: Prevention of bacterial endocarditis:
Recommendations of the American Heart Association. JAMA 277:
1794-1801, 1997.
Dickens JR: Comparative study of otologic surgery in outpatient and hos-
pital settings. Laryngoscope 96:774-785, 1986.
Gates GA: Current Therapy in Otolaryngology: Head and Neck, 5th ed.
St. Louis, MO, Mosby, 1994.
Lee K: Essential Otolaryngology: Head and Neck Surgery, 6th ed. Norwalk,
CT, Appleton & Lange, 1995.
Levine SB, Kimmelman CP, Zwillenberg S, Silberstein L: Blood transfusions
in surgery of the larynx and neck. Laryngoscope 96:1095-1098, 1986.
751
E. Specific recommendations
1. Early ambulation is encouraged.
2. Resumption of preoperative medications is encouraged.
III. Trabeculectomy
A. Definition: a partial-thickness scleral flap is created so
that a portion of the sclera and trabecular meshwork can
be removed to create an alternative pathway for the
egress of aqueous humor from the anterior chamber of
the eye. In patients with visually significant cataracts, this
procedure may be combined with cataract extraction.
B. Indications: primary open-angle glaucoma not respon-
sive to medical therapy
C. Duration of surgery: less than 2 hours
D. Anesthesia: local or general anesthesia
E. Specific recommendations
1. Patient may require 1 to 2 days postoperatively in the
hospital.
2. Patients’ carbonic anhydrase inhibitors are typically
stopped postoperatively to encourage the production
and flow of aqueous humor through the surgically
created fistula.
3. Patients often need frequent atropine and phenyleph-
rine drops, which may produce central nervous side
effects.
IV. Cyclocryotherapy
A. Definition: A freezing probe is applied to the bulbar con-
junctiva above the ciliary body to destroy the ciliary body
and thereby to decrease the amount of aqueous humor
produced.
B. Indications: treatment of glaucoma that has not responded
to medical therapy
C. Duration of surgery: less than half an hour
D. Anesthesia: local anesthesia
E. Specific recommendations: none
V. Peripheral Iridectomy
A. Definition: an intraocular procedure to create an opening
in the iris (as compared with peripheral iridotomy [see
later], which is a closed procedure using a laser)
B. Indications
1. Angle-closure glaucoma refractory to medical man-
agement in which the cornea is too clouded to per-
form laser iridotomy
2. Peripheral iridectomy is also often performed as a part
of other intraocular procedures (e.g., cataract extrac-
tion), when there is a concern about a possible ele-
ment of angle closure or pupillary block glaucoma.
C. Duration of surgery: less than half an hour
D. Anesthesia: local or general anesthesia
E. Specific recommendations: none
VI. Laser Trabeculoplasty (Argon Laser
Trabeculoplasty)
A. Definition: production of argon laser burns in the tra-
becular meshwork of the eye to improve aqueous humor
outflow from the anterior chamber
B. Indications: primary open-angle glaucoma refractory to
medical management
C. Duration of surgery: less than 15 minutes
D. Anesthesia: topical anesthesia
E. Specific recommendations: Patients typically need to
have their intraocular pressures checked 1 hour after this
procedure because there can be a significant elevation of
intraocular pressure after laser treatment; the pressure
elevation can be marked enough to necessitate an emer-
gency trabeculectomy.
VII. Temporal Artery Biopsy
A. Definition: removal of a small portion of the temporal
artery for histopathologic examination
B. Indications: suspected cases of temporal arteritis
B. Indications
1. Vitreous hemorrhages that do not clear
2. Often must be performed in cases of neovascularization
or proliferative vitreoretinopathy with retinal tears and
detachments associated with vitreal hemorrhages
C. Duration of surgery: 1 hour
D. Anesthesia: local or general anesthesia
E. Specific recommendations: same as those for scleral
buckle
XI. Enucleation
A. Definition and indications: removal of an eye; performed
for either a blind, painful eye or an eye with an intraocu-
lar malignant tumor
B. Duration of surgery: 1 hour
C. Anesthesia: local or general anesthesia
D. Specific recommendations: Patients typically spend a
postoperative day in the hospital. Note: Vasovagal re-
sponse to ocular pressure may result in bradycardia.
XII. Evisceration
A. Definition and indications: removal of the intraocular con-
tents, leaving the sclera and extraocular muscles intact. It is
performed when inflammation has destroyed the eye irre-
versibly or when severe panophthalmitis has created an
abscess within the eye; its advantage over enucleation (see
earlier) is that the prosthesis will have some mobility; it has
the disadvantage that because the uveal tract is violated,
there is a risk of sympathetic ophthalmia.
XIII. Orbitotomy
A. Definition: an exploratory procedure of the orbit behind
the globe
B. Indications
1. Mass lesions within the orbit
I. Cervical Fusion
A. Definition: immobilization of a joint to create a bony
continuity between two or more adjacent vertebrae (may
be performed by anterior or posterior approach)
B. Indications: intractable pain, instability, or neurologic
deficit (from fracture or dislocation, degenerative disease,
inflammatory lesion, neoplasm, subluxation or impac-
tion, destabilizing procedure) that is not responsive to
nonoperative treatment
C. Duration of surgery: 3 to 4 hours
D. Anesthesia: general anesthesia with nasotracheal or endo-
tracheal intubation
E. Transfusion requirements
1. Usually not required
2. Approximate blood loss commonly 200 to 300 mL
F. Overall surgical mortality: less than 1%
G. Postoperative complications
1. Bleeding
a. The amount depends on the anatomic level, the
number of segments to be fused, and the surgical
approach.
b. Arterial or venous bleeding is most common.
c. Vertebral artery laceration is uncommon and is
usually related to fusions near C1.
d. Hematoma after anterior approach must be evacu-
ated immediately because of the risk of airway
obstruction.
757
2. Wound infection
a. Infection usually occurs after the third postopera-
tive day.
b. Presentation may include wound erythema, indu-
ration, drainage, pain, and elevated white blood
cell count.
c. Incidence is correlated with the type of surgery, the
use of antibiotics, and the length of the procedure.
d. Treatment is determined by culture, early wound
débridement, and pulsed irrigation.
3. Extension of fusion mass (very common)
4. Damage to laryngeal nerve from laceration, edema,
or contusion (may result in temporary or even per-
manent hoarseness)
5. Paresthesias may be associated with passage of wires
into the spinal canal.
6. Damage to or perforation of the esophagus or trachea
7. Graft extrusion with collapse and nonunion of fusion
8. Dural laceration
9. Damage to sympathetic chain (Horner’s syndrome)
10. Pain, bleeding, or infection at the bone graft site
11. Air embolism
a. This can occur intraoperatively during the poste-
rior approach owing to the development of a
gravitational gradient between an open vessel and
the dependent right atrium.
d. Presentation may include sudden hypotension,
alterations in respiratory patterns, electrocardio-
graphic changes, and cardiac arrest.
c. Air embolism can be detected by end-expiratory
carbon dioxide concentration monitoring.
12. Deep venous thrombosis and pulmonary embolism
(see Chapter 5)
H. Specific recommendations
1. Antibiotic prophylaxis
a. Cefazolin, 1 g intravenously within 60 minutes
preoperatively and every 8 hours for 24 hours, or
H. Specific recommendations
1. Antibiotic prophylaxis
a. Cefazolin, 1 g intravenously 60 minutes preopera-
tively and every 8 hours for 24 hours, or cefurox-
ime, 1.5 g intravenously 60 minutes preoperatively
and every 12 hours for 24 hours.
b. -Lactam allergy: vancomycin, 1 g 120 minutes
before surgery and then every 12 hours for
24 hours, or clindamycin, 600 mg intravenously,
60 minutes before surgery and then every 6 hours
for 24 hours
2. Deep venous thrombosis and pulmonary embolism
prophylaxis (see Chapter 5)
d. Periprosthetic fracture
i. Rare after primary total hip arthroplasty (0.1%)
but may be higher in revision arthroplasty
(4.2%)
ii. May be secondary to trauma or to abnormal
stresses placed on the native bone by the pros-
thesis
5. Hip dislocation
a. Most common in first few months after surgery but
can occur several years later
b. Incidence: 0.8% to 2.4%
c. Presents as acute pain in hip with extreme position
as well as inability to stand on hip or return hip to
functional position
6. Heterotopic ossification
a. May occur to some extent in 20% to 50% of pa-
tients undergoing total hip replacement but causes
symptoms in less than 4%
b. Patients at risk include those with previous het-
erotopic ossification, diffuse idiopathic skeletal
hyperostosis, Paget’s disease, or ankylosing spon-
dylitis.
7. Neuropathy
a. Incidence: less than 1%
b. Prognosis for recovery is good.
c. May involve sciatic, femoral, obturator, or gluteal
nerve
d. May be caused by bleeding, surgical trauma, disloca-
tion, stretching of nerve secondary to leg lengthen-
ing, entrapment by wire, or damage from cement
8. Fat embolism
a. This occurs 12 to 72 hours postoperatively.
b. It manifests with sudden tachycardia, respiratory
distress, petechial rash on upper body, fat in retinal
vessels, delirium, and coma
c. Diagnosis is by exclusion of other causes.
Selected Readings
Bratzler D, Houck P: Antimicrobial prophylaxis for surgery: An advisory
statement from the National Surgical Infection Prevention Project. Am J
Surg 189:394-404, 2005.
Greenfield LJ (ed): Complications in Surgery and Trauma. Philadelphia, JB
Lippincott, 1990.
Lawrence VA, Hilsenbeck SG, Noveck H, et al: Medical complications and
outcomes after hip fracture repair. Arch Intern Med 162:2053-2057,
2002.
Quinlet RJ, Winters EG: Total joint replacement of the hip and knee. Med
Clin North Am 76:1235-1251, 1992.
I. Craniotomy
A. Definition: opening of a portion of the skull to obtain ac-
cess for surgical intervention
B. Indications
1. Establishment of histologic diagnosis for optimal ad-
juvant treatment and estimation of prognosis
2. Provision of immediate palliation of increased intra-
cranial pressure
C. Duration of surgery: variable, depending on the reason
for procedure
D. Anesthesia
1. General anesthesia
2. Sedation with local anesthesia (to monitor patient’s
language function)
E. Transfusion requirement: minimal
F. Overall surgical mortality: less than 3%
G. Postoperative complications
1. Postoperative intracranial hemorrhage is most fre-
quently seen in the first 24 to 48 hours postopera-
tively. The cardinal sign is a change in mental status.
2. Cerebral edema
a. Most frequently seen in the first 48 to 72 hours
postoperatively and manifested by a change in
mental status
b. Most frequently seen in central nervous system
neoplastic disease
3. Infection: In clean craniotomies, 2% to 5% will expe-
rience postoperative infections. This rate is decreased
769
769
Selected Readings
Berger RA: Endoscopic tunnel release: A current perspective. Hand Clin
10:625-636, 1994.
Lang EW, Chestnut RM: Intracranial pressure: Monitoring and management.
Neurosurg Clin North Am 5:573-605, 1994.
Rosner M: Complications of craniotomy and trauma. In Greenfield L (ed):
Complications of Craniotomy and Trauma. Philadelphia, JB Lippincott,
1990, pp 677-713.
Young H: Complications of spine surgery and trauma. In Greenfield L (ed):
Complications of Surgery and Trauma. Philadelphia, JB Lippincott,
1990, pp 713-746.
Note: Page numbers followed by the letter b refer to boxes, those followed by the
letter f refer to figures, and those followed by the letter t refer to tables.
A Acetaminophen (Continued)
toxicity cautions, in liver disease, 368
Abdomen
use during pregnancy, 480, 481t
distention of
Acetylcholinesterase inhibitors, myasthenia
anesthesia risks with, 82, 83t, 84
gravis response to, 536
as pulmonary complication factor, 82,
N-Acetylcysteine, for acute renal failure
268, 270
prevention, 629-630
penetrating trauma to
Acid aspiration syndrome, 82-84
antimicrobial prophylaxis for, 41t, 45-46
Acidemia, chronic kidney disease and, 605, 609
during pregnancy, 489-490
management of, 616
Abdominal aorta, resection of, antimicrobial
Acidosis
prophylaxis for, 43t, 48
anion gap, in chronic kidney disease, 616
Abdominal compartment syndrome, 626
diabetic ketoacidosis, 420, 423
Abdominal hysterectomy, 720-721
lactic, as small bowel resection complication,
Abdominal pain, postoperative
337
fever with, 331
metabolic
with cholecystectomy, 332t, 343-344
in ophthalmologic patient, 460
Abdominal surgery
in pregnant patient, 469, 476
gastrointestinal motility and, 298
ACLS (Advanced Cardiac Life Support)
in elderly patient, 599
for arrhythmia management, 217, 219
liver disease and, 364t
for hemodynamic compromise, 517
mortality associated with, 378, 379t
Acoustic neuroma, resection of, 744
preoperative evaluation for, 250, 330
ACTH (adrenocorticotropic hormone), feedback
upper, as pulmonary complication factor,
regulation of, 429-430
258-259
ACTH stimulation test, of HPA function,
management of, 268, 269
432
Abdominal wall
Action potential, cardiac, hypocalcemia impact
herniation of, cirrhotic ascites associated
on, 449
with, 382-383
Activated partial thromboplastin time (aPTT)
nerves traversing, injuries to, 577-578
in hemostasis, 140
pregnancy effect on, 471
in heparin prophylaxis, 110
Ablation techniques, for hepatocellular carci-
preoperative assessment of, 25-26, 25b
noma, 377-378
Active cardiac conditions, in noncardiac surgery,
Abortion, 723
159-160, 160t
antimicrobial prophylaxis for, 42t, 46, 723
evaluation algorithm for, 164, 165f, 166
spontaneous, 148
Activity scales, of functional status
fetal susceptibility to, 472
in healthy patient, 16, 17f
Abscess(es)
preoperative cardiac testing and, 162f, 166
gastrointestinal fistula causing, 342
Acute confusional state. See Delirium.
intra-abdominal, postoperative, 331
Acute renal failure (ARF)
Abstinence, from alcohol use, 496-497, 499
categories of, 607
ACC. See American College of Cardiology (ACC).
in liver disease, operative risk associated
ACCP (American College of Chest Physicians),
with, 354b
on pulmonary embolism prophylaxis, 91,
postoperative, 625-630
94t, 99, 106, 406
diagnosis of, 627-628
ACE inhibitors. See Angiotensin-converting en-
differential diagnosis of, 625-627
zyme (ACE) inhibitors.
incidence and impact of, 625
Acetaminophen
management of, 628-629
postoperative, for chronic kidney disease
prevention of, 629-630
patient, 622
risk factors for, 625
777