Merge From Ofoct
Merge From Ofoct
Merge From Ofoct
• Aging Population.
Diagnosis of respiratory system disease
• Medical history
• Symptoms
• Signs
Cough:
• Acute(bronchitis) or chronic(COPD)?
• Seasonal or associated with wheezing? (Asthma)
• Associated with chest pain(peumonia)
• Associated with fever or sputum?
• Irritation dry cough,persistence.(lung cancer)
• Any associated diseases or risk factors for disease
(e.g., cigarette smoking, risk factors for infection with HIV,
environmental exposures)?
Symptoms
Sputum:
• character, quantity and odour.
• Large amount of yellow phlegm---Bronchiectasis,
lung abscess .
• Iron-rust sputum---Streptococcus Pneumoniae.
• Fetor---combined with anaerobic bacteria infection.
• Thin pink froth sputum---Pulmonary edema patient.
• Coffee like phlegm---lung Amoebiasis 阿米巴--amoeba.
Symptoms
Hemoptysis:
• Originated from the airways: distinguish with
haematemesis[hɛmə'tɛməsɪs] or bleeding from the
nasopharynx[neɪzəʊ'færɪŋks].
→Bronchitis, Bronchiectasis, Cystic fibrosis, Bronchial
carcinoma 肺癌.(smokers)
• Originating from the pulmonary parenchyma:
→ Pneumonia, Lung abscess, Tuberculosis, Infection with
Aspergillus, Goodpasture’s syndrome,
• Originating from the vasculature:
→ Thromboembolic diseases, Arteriovenous malformations 畸形.
Symptoms
Chest pain:
• Related with breath and cough usually be
pleurisy.(sharp pain)
• Continuous and do not relieve may be lung
cancer.
• Company with high fever and chill may be
pneumonia.
• Rib fracture,herpes zoster—localised chest
wall tenderness.
Symptoms
Dyspnea:
Acute (over a period of hours to days):
1.Acute attack of Asthma
2.Acute pulmonary edema (coronary heart disease)
3.Bacterial pneumonia
4.Pneumothorax
5.Pulmonary embolus
Symptoms
Dyspnea:
Subacute (over days to weeks):
1. Asthma
2. Chronic bronchitis
3. Pleural effusion
4. Congestive heart failure
Symptoms
Dyspnea:
Chronic (over months to years):
• 1. COPD
• 2. Chronic interstitial lung disease
• 3. Chronic cardiac disease
Signs
• Pay attention to acropachia ,cyanosis
杵状指 [,saɪə'nəʊsɪs],
• Obstruction:chronic bronchitis,emphasema,asthma
FEV1(forced expiratory volume in one second
)↓FEV1/FVC↓(forced vital capacity)、RV↑、RV/TLC↑
Physical
examination Chest
radiography
Progress of Diagnosis and Therapy
• Respiratory diseases increased in these years,such
as:Obstructive Sleep Apnea Hypopnea
Syndrome(OSAHS).Interstitial Lung Diseases(ILD).
• Basic subject of diagnosing,like molecular biology
oncogene,anti-oncogene in early diagnosing of lung
cancer.
• Sleep monitor for OSAHS.
• PET-CT for identify the nature of enlarged lymph
nodes in mediastinal(Benign or malignant).
• Ultrasonic bronchoscope(EBUS)
Progress of Diagnosis and Therapy
He yuanbing
The First Affiliated Hospital of Xinjiang Medical University
Department of respiratory medicine1
What is Clinical Diagnostics?
• Fundamental theory(Pathology, anatomy,
immunology, etc.)
Techniques of diagnosing disease(laboratory
science,ultrasonic , etc. )
Mode of clinical thinking
What is Clinical Diagnostics?
• Instruct a concise logical approach to recognize
the genius of the diseases
Diagnosis
Identification Analysis
Diagnosis
☆ Medical terminology:
Analysis:
Basic knowledge of medicine
Overall analysis
Scientific way of clinical thinking
Importance of Diagnostics
Essential
Basic courses
Bridge
Tools
Clinical medicine
Content of Clinical Diagnostics
Symptomatic diagnosis
Physical diagnosis
Clinical practice
Bedside activity
Standardized patient
Developmental History of
clinical diagnostics
Hippocrates
• c.130-c.200
• His work in
anatomy/physiology is notable
• Identified artery and vein
• Added greatly to knowledge of the
brain, spinal cord and pulse
Contribution of ancient doctors---Western
Auenbrugger
Laennec RTH
•A French physician
•Invented Auscultation and stethoscope
Contribution of ancient doctors---Western
Laennec RTH
1816
Contribution of Western Physician
17th~19th century
Leenwenhock Microscopy (end of 17th century)
Fahrenheit Thermometer (1724)
Ludwig Hematomanometer (1847)
Welcher Hematinometer (1854)
20th century
X-ray film EKG Endoscopy CT PET
Ultrasonic imaging
CT imaging
MRI
PET
Traditional Chinese Medicine
Wood
Fire
Earth
Metal
Water
Contribution of ancient doctors---Chinese
Inspection
Interrogation
Smell
Pulse palpation
Pay attention to:
n Diagnostic techniques
n Biliary Tumors
Anatomy of biliary tract
Intrahepatic bile duct:
Biliary tract
Pancreatic sphincter
1.Untraumal
2.Low cost
3.Flexibicity
4.First choice
Abdominal Ultrasonography
n Bile leakage
n Haemorrhage
n Sepsis
ERCP
(Endoscopic Retrograde Cholangiopancreatography)
n Acute pancreatitis
n Postprocedure cholangitis
n Other complications
Operative and postoperative
direct cholangiography
Contraindications
n Sensitivity to iodine
n Liver and renal disease
n pregnancy
Choledochoscope
n Intraoperative use:
n Explore the CBD stone
n Tumor,stenosis
n Reduce retained stone rate
n Remove stone
n biopsy
Other examination
n Intravenous cholangiogram
n Angiography
n Isotopic studies
How to choose
1.Ultrasound
2.MRCP and CT
n Acute calculous
cholecystitis 95%
n Acute acalculous
cholecystitis 5%
Etiology
1.Cystic duct obstructed by a gallstone impacting in
Hartmann’s pouch
2.Bacteial infection of the stagnant bile
Aerobic enteric-derived organisms
Escherichia coli, klebsiella pneumoniae, streptococcus faecalis
gallstone impaction →mucosal damage
Lecithin → lysolecithin
↑
phospholipases
Pathology
Cystic duct obstruction →gallbladder →Edema
→suppurate → gangrene → pericholecystic abscess
→perforation
intestinal obstruction
Conservative treatment
1.Intravenons fluid and electrolyte
replacement
2.Nasogastric suction
3.Systemic antibiotics
4.Parenteral analgesia
Surgical Treatment
n Open cholecystectomy
n Laparoscopic cholecystectomy
Indication of Choledochotomy
n Hypotension
n Mental obtundation
Reynold’s Syndromes
Physical examination
n Tenderness
n Abdominal guarding
n Swollen gallbladder
n Hepatomegaly
Laboratory Test
n Leukocytosis
n Hyperbilirubinemia
n Alkaline phosphatase ↑
n Aminotransferases ↑
n Leukopenia
n Profound gram-negative sepsis and
immunosuppression
n Serum amylase ↑
Radiological Evaluation
n Ultrasonography
n CT
n MRCP
n PTC
n ERCP
Treatment
General support
n Dyspepsia
n Right upper quadrant abdominal pain in
association with or shortly after a heavy or fatty
meal
n A feeling of gaseous bloating
n Biliary colic
Physical examination
n Usually normal
n Chronic hydrops of gallbladder→mass
n Some times tenderness
Radiological Test
A plain abdominal roentgenogram
Oral cholecystography
Ultrasonography the initial diagnostic study
CT
MRI
Complications
n Acute cholecystitis
n Jaundice
n Cholangitis
n Pancreatitis
n Mtrizzi syndrome
n cancer
Surgical Indication
n Accelerating symptoms
n Poor visualization or non-visulization on
oral cholecystography
n Diabetas
n Porcelain gallbladder
n stone>2-3cm
Laparoscopic Cholecystectomy
n Indications:
Chronic, uncomplicated cholecystitis
Cholelithiasis
GB polyps
?
n Benefits:
Reducing hospitalization and associated costs
Decreasing pain
Improved cosmetic outcome
Reduced post-operative recovery
Other treatment
n Dietary therapy a low-fat diet, avoidance of
heavy meals
n Antispasmodic medication
n Chenodeoxycholic acid and ursodeoxycholic acid
n Extracorporeal shock wave lithotripsy
Carcinoma of Gallbladder
n Incidence
The most common form of biliary tract malignancy
the fifth gastrointestinal cancer
Encountered in 1-2% of cholecystectomy specimens
Predominantly occurs in elderly females
Over 90% of patients are were 50 years of age
The peak age of incidence is 70-75% years
A male to female ratio of 1:3
Etiology
n Cholelithiasis
n Benign adenoma
n Polypoid gallbladder lesions (polyp greater than
1cm)
n Anomalous pancreatiobiliary junction
n Chronic inflammatory bowel disease
Pathology
n Adenocarcinoma 80% carcinoid
tumours
n Undifferentiated carcinoma 6% sarcoma
n Squamous carcinoma 3%
melanoma
n Mixed tumor or acanthoma 1%
lymphoma
UICC
Ⅰ stage:mucosa and muscular
Ⅱ stage:total layer of the gallbladder
Ⅲ stage:invasion into liver <2cm or
regional lyphatic spread
Ⅳ A stage: invasion into liver >2cm
Ⅳ B stage: spread to distal organ and
lymph node
Clinical Features
n The diagnosis of gallbladder cancer is usually
made when the disease is well advanced. There
are no characteristic features at an early and
curative stage
Laboratory investigations
n FNAC
n ultrasound
Treatment
n UICC Ⅰ cholecystectomy
n UICC Ⅱ
Curative excision procednre
n UICC Ⅲ IVA
extended curative excision
n UICC ⅣB
Palliative procedures
Billiary or duodenal bypass
Prognosis
n Piehler and crichlow
Report of 6000 patients :
1 year survivial rate 11.8%
5 year survival rate 4.1%
Palliative procedure
1.Extra bile drainge
T tube
U tube
PTCD
2.Intra-drainge
Biliary-enteric bypass or intubation
Non-operative endoprosthetic insertion
Clinical Diagnostics
He yuanbing
The First Affiliated Hospital of Xinjiang Medical University
Department of respiratory medicine
What is Clinical
Diagnostics?
• Fundamental theory(Pathology, anatomy,
immunology, etc.)
Techniques of diagnosing disease(laboratory
science,ultrasonic , etc. )
Mode of clinical thinking
What is Clinical
Diagnostics?
• Instruct a concise logical approach to recognize
the genius of the diseases
• A fundamental course of clinical medicine
Fundamental elements of
Diagnostics
Diagnosis
Identification Analysis
Diagnosis
Derived from Greek words☆
distinguish or discern
☆ English term
Diagnostic
The distinguishing sign and symptoms with which
it gerenally begins, continues and goes off…as it
were, a history of the disease
\
In 18th century: Nosography
☆Electrocardiogram, CT, blood test, rash and herpes zoster
nature of pain: Sharp pain, dull pain, knife cut pain, burning pain, colic pain
Persistent pain and paroxysmal pain
☆ In modern usage:
Identification of a disease by investigation of its
signs and symptoms
☆ Medical terminology:
Clinical diagnosis Laboratory diagnosis
X-ray diagnosis Electrocardiographic diagnosis
Gene diagnosis
Identification:
Inquiry
Physical examination
Laboratory tests/Special examination
Analysis:
Basic knowledge of medicine
Overall analysis
Scientific way of clinical thinking
Importance of Diagnostics
Essential
Basic courses
Bridge
Tools
Clinical medicine
Content of Clinical Diagnostics
Symptomatic diagnosis
Physical diagnosis
Laboratory tests or clinical ancillary tests
Medical record
Diagnostic processes and the way of
clinical thinking
Symptomatic Diagnosis
History taking--- Interview
Symptoms --- patient‘s complaints
Symptomatic Diagnosis
Epidemic areas, infectious diseases
family history, genetic diseases
Symptomatic Diagnosis
Symptom
Subjective sensation that patient describes
Physiological & Pathological
Morphological
functional
Sign (Fever, tenderness mass and jaundice )
Abnormality observed by the physician
Physical examination
Conducted with thoroughness , alertness to detect even
slight derivations from normal
Inspection
Palpation
Percussion
Auscultation
stethoscope
Laboratory test or ancillary tests
• Serum, Urine, Stool tests
• X-ray film
• EKG
• Endoscopy
• Ultrasonic imaging( Abdomen )
• CT
• MRI
• PET (Positron Emission Tomography)
Medical record
Medical record is a systematized way of
storing the required data, information and
other relevant documents
Specific requirement in terms of format
and content
Special terms in clinical
diagnosis
Impression
Tentative diagnosis
Differential diagnosis
Evidence based medicine
Differential diagnosis
• Exclusion of other diseases
• Selecting a number of possibilities to explain the
clinical and laboratory findings in the case in question
• The way of exclusion is called Differential diagnosis
Evidence based medicine
It is the conscientious, explicit and judicious use
of current best evidence in making decisions
about the care of the individual patient
It means integrating individual clinical expertise
with the best available external clinical evidence
from systematic research
Evidence based medicine
One need to:
• Be conscientious: it requires effort and thought.
• Be explicit: decisions will need to be backed up by good
evidence
• Relate to specific problems: it is not about a
hypothetical "average" case. Integrate individual clinical
experience: it does not denigrate clinical skills in history
taking, examination and diagnosis.
Evidence based medicine
One need to:
• Look for current best evidence: the perfect study
may not yet have been published, written up or even
commenced. We may have to settle for something
less rigorous, but be on the look out for new
research that will supersede older studies.
Important aspects---
interrogation 问诊
• To get the history in detail of a patient’s illness
• The history is taken at initial contact between
physician and patient
• As some crucial points might be overlooked by the
patients, one will ask many searching questions to
make the history more informative and complete, who
must at the same time avoid suggesting answers
• Occasionally to interrogate his family member
Other important aspects
• The diagnostic process is very complex
• The number of facts that can be collected in a
detailed medical history and in thorough physical
examination are almost without limit
• The laboratory tests or specialized technical
procedures that can employed are numerous and
costly
Other important aspects
• Questions for interrogation, maneuver in P.E.,
laboratory test should be thoughtfully selected
with the view to eliminate some of the possible
diagnosis and guide the search expeditiously to a
specific disease
• Method of approaching a diagnosis:
Analysis of symptoms
Recognition of the syndrome
Consideration of disease mechanisms
Important aspects
• Modern & advanced ancillary techniques:
have their limitations.
It can’t reduced the importance of certain parts
of the classic P. E
• It should be avoided to neglect fundamental
methods
Interrogation
Physical examination
Scientific clinical thinking
Approaches
Basic knowledge learning
Clinical practice
Bedside activity
Standardized patient
Developmental History of clinical
diagnostics
• Western Medicine: from ancient to modern
• Traditional Chinese Medicine
Contribution of ancient doctors---Western
Hippocrates
•Born on the island of Cos,
Greece (c. 460-377 BC)
•The Father of medicine
Hippocratic oath
Hippocratic corpus:
a collection of 70 works
Hippocratic oath
Contribution of ancient doctors---Western
Galen
• c.130-c.200
• His work in
anatomy/physiology is notable
• Identified artery and vein
• Added greatly to knowledge of the
brain, spinal cord and pulse
Contribution of ancient doctors---Western
Auenbrugger
•Born at the village of Graz, Austria (1722)
•Son of an innkeeper
•The working experiences helped him to find
Percussion
•Author of <Inventum Novum>(1761)
translated as ‘On Percussion of the chest’ in 1936
Contribution of ancient doctors---Western
Laennec RTH
•A French physician
•Invented Auscultation and stethoscope
Contribution of ancient doctors---Western
Laennec RTH
1816
Contribution of Western Physician
17th~19th century
Leenwenhock Microscopy (end of 17th century)
Fahrenheit Thermometer (1724)
Ludwig Hematomanometer (1847)
Welcher Hematinometer (1854)
20th century
X-ray film EKG Endoscopy CT PET
Ultrasonic imaging
CT imaging
MRI
PET
Traditional Chinese Medicine
Wood
Fire
Earth
Metal
Water
Contribution of ancient doctors---Chinese
Inspection
Interrogation
Smell
Pulse palpation
Pay attention to:
Good medical ethics
Attach importance to clinical practice
Unit theory with practice
Goals
• Inquiry:
Independent systemic inquiry
Comprehensive understanding of patient’s chief
complains, signs, symptoms and their interrelation
• Physical Examination:
Systemic/thorough
• Familiar with routine tests, EKG manipulation and figure
analysis
• Good case writing and propose the primary diagnosis
• Scientific clinical thinking
InquiryInquiry
He yuanbing
The First Affiliated Hospital of Xinjiang Medical University
Department of respiratory medicine
InquiryInquiry
l It is the method that physician obtain the clinic
data of patient, and further propose clinical
judgment by comprehensive analysis
l Inquiry is the major methods of history taking
l It is a fundamental skill that every physician
should know
BasicBasic principlesprinciples
l Good communication skills are the foundation of
excellent medical care
l It improves health outcomes by resolving symptoms and
reducing patients’ psychological distress and anxiety
l The quality of patient care depends greatly on the skills
of interviewing, because the relationship that a patient
with a physician is probably the most extraordinary
relationship between two human beings
BasicBasic principlesprinciples
l To gather all basic information pertinent to the
patient’s illness and the patient’s adaptation to
illness
l An experienced interviewer considers all the
aspects of the patient’s presentation and follows
the leads that appear to deserve the most attention
BasicBasic principlesprinciples
l The clinician must be keenly aware of all clues, subtle or
obvious
l Although body language is important, the spoken word
remains the central diagnostic tool in medicine
l The art of talking and listening continues to be the central
part of the doctor-patient interaction
l Once all the clues from the history have been gathered, the
assimilation of those clues into an ultimate diagnosis is
relatively easy
BasicBasic principlesprinciples
l Communication is the key to a successful
interviews
l It must be able to ask questions of the patient
freely
l These questions must always be easily understood
and keyed to the medical sophistication of the
patient
ContentContent ofof inquiryinquiry
l General data
l Chief complaint
l History of present illness
l Past history
l Review of systems
l Personal history
l Marital history
l Menstrual history
l Family history
GeneralGeneral datadata
Name Gender
Age birth place
Native place Nation
Marital status Mail address
Profession Data of admission
Data of record Source
Reliability
ChiefChief complaintcomplaint
l It is the patient’s brief statement explaining why
he or she sought medical attention
l It is the answer to the question
“What is the problem that brought you to the
hospital?”
l In the written history, it is frequently a quoted
statement of the patient
ChiefChief complaintcomplaint
l It should be one or two sentences including the
time periods from onset to seeing the doctor
l Not the diagnostic term from the doctor
l Fractures、angina pectoris、 asthma
ChiefChief complaintcomplaint
“Chest pain for the past 5 hours”
“Terrible nausea and vomiting for 2 days”
“Headache for the last week, on and off”
HistoryHistory ofof presentpresent illnessillness
l The history of the present illness refers to the recent
changes in health that led the patient to seek medical
attention at this time
l It describes the information relevant to the chief
complaint
l It should answer the questions what, when, how, where,
which, who, and why
HistoryHistory ofof presentpresent illnessillness
l Chronology is the most practical frameworks for
organizing the history
l It enables the interviewer to comprehend the
sequential development of the underlying
pathologic process
HistoryHistory ofof presentpresent illnessillness
l In this section the doctor gathers all the necessary
information, starting with the first symptoms of
the present illness and following its progression to
present day
l It is important to verify that the patient was
entirely well before the earliest symptom to
establish the beginning of the current illness
HistoryHistory ofof presentpresent illnessillness
l The character of symptoms
location identity during intensity
relief or provoke factors
l Time during may be lasted for years, months, days
l It may also be of hours or minutes (in those with
acute onset)
HistoryHistory ofof presentpresent illnessillness
l Causes and inducing factors
investigate the causes that related with onset of the
disease:
trauma intoxication infection
inducing factors: emotion diet environment
l Caution
the causes that recently occurred may be easily
recognized by the patient
hardly recognized by the patients if the causes are
complicated or if the courses lasted for years
HistoryHistory ofof presentpresent illnessillness
l Progression
including the changes in predominant symptoms or
occurrence of new symptoms
cirrhotic patient manifested some neurological signs,
hepatic encephalopathy should be highly suspected;
chest pain lasted unusually and more severely than
previous episodes of angina, myocardial infarction should
be suspected
HistoryHistory ofof presentpresent illnessillness
l Accompanying symptoms
it is useful in differential diagnosis
e.g. patient manifested nausea, vomiting and
fever,
accompanied with jaundice and/or shock, acute
biliary infection or acute pancreatitis should be
considered
HistoryHistory ofof presentpresent illnessillness
l Course of diagnosis and treatment
The diagnosis and treatment the patient had received in
other medical institution may provide informative data
The diagnosis made by others could not replace one’s
diagnosis
l General condition during the course : diet、sleep、
weight stool urine etc
it may also provide some useful information
PastPast medicalmedical historyhistory
l The past medical history consists of the overall assessment of the
patient’s health before the present illness include a statement of
childhood and adult problems
l Parameters including:
general state of health past illness
injuries hospitalizations
surgery allergies
immunizations substance abuse
diet sleep patterns
current medications alternative therapies
PastPast medicalmedical historyhistory
l The patient should be asked about any prior injuries or accidents
The type of injury and the data are important
l All hospitalization must be indicated, including admissions for
medical, surgical, and psychiatric illness
l All surgical procedures should be specified. The type of procedure,
data, hospital
l All allergies should be described. These include environmental,
ingestible, and drug related
l It is important to determine the immunization history of all patients
Drug allergy
ReviewReview ofof systemssystems
l The review of systems summarizes in terms of
body systems all the symptoms that may have
been overlooked in the history of the present
illness or in the medical history
l By reviewing in an orderly manner the list of
possible symptoms, the interviewer can
specifically check each system and uncover
additional symptoms of “unrelated” illness not yet
discussed
ReviewReview ofof systemssystems
l The review of systems is best organized from the head
down to the extremities
l Patients are told that they are going to be asked whether
they have ever had a particular symptom and should
answer “Yes” or “no”
l Joint pain, dry mouth, rash, shivering
ReviewReview ofof systemssystems
l Respiratory system
cough: identity frequency
sputum production: quantity appearance
coughing up blood shortness of breath
l Cardiovascular system
chest pain shortness of breath with exertion
palpitations shortness of breath lying flat
sudden shortness of breath while sleeping
history of heart attack
ReviewReview ofof systemssystems
l GI system
appetite excessive hunger excessive thirst
nausea constipation diarrhea
heartburn vomiting abdominal pain
change in stool color/caliber/consistency
frequency of bowel movements vomiting blood
rectal bleeding black tarry sto
ols
diabetes , bowel cancer
ReviewReview ofof systemssystems
l Urinary system
frequency urgency incontinence difficulty in the
starting the stream
excessive urination pain on urination
burning blood in the urine
bed-wetting waist pain history of retention
urine color urine odor
ReviewReview ofof systemssystems
l Hematological system pallor yellow skin
hemolytic petechia purpura ecchymosis
hematoma
l Endocrinological system and metabolite
weakness profound sweating
abnormal appetite weight change
ReviewReview ofof systemssystems
l Neurologic system
fainting dizziness mood changes
loss of memory speech disorders
general behavioral change disorientation
l Musculoskeletal system
weakness paralysis muscle stiffness
limitation of movement joint pain
joint stiffness arthritis gout deformities
ReviewReview ofof systemssystems
l Review of systems may involved lots of clinical
diseases
l One has to understand the pathophysilogical meaning
of these signs and symptoms
l In each systems, it is practical to ask several symptoms
l The inquire may be intensified if there is positive
symptoms/signs is elicited
PersonalPersonal historyhistory
l Social experiences
birth place
living area and duration particularly those
epidemical areas Liver cirrhosis, schistosomiasis, infectious diseases
education living condition hobby
l Profession and working place/condition
l Habit smoking (amount and duration)
drinking anesthetic drug
UnhealthyUnhealthy sexualsexual historyhistory
l Unhealthy sexual history:
Sexually transmitted disease
MaritalMarital historyhistory
l Marital history:
single or married
age of marriage
health condition of spouse
MenstrualMenstrual historyhistory
l Menstrual history: only for women
age of menarche (first menstrual cycle)
cycles and flow lasting
amount of vaginal bleeding/discharges
menopause and age of menopause
l Format
flow lasting(day)
menarche last menopause
cycle(day)
FamilyFamily historyhistory
l It provides information about the health of the
entire family,living and dead
l Pay attention to possible genetic and
environmental aspects of disease that might have
implications for the patient
SkillSkill andand methodsmethods inin inquireinquire
l Getting started
l The narrative
l The closing
GettingGetting startedstarted
l The diagnostic process begins at the first moment of
meeting
l One should be dressed appropriately, wearing a white
coat with one’s name badge identifying one as a
physician
l One should make patient as comfortable as possible
l One should sit in a chair directly facing the patient in
order to make good eye contact
GettingGetting startedstarted
l The interviewer should sit in a relaxed position
without crossing arms across the chest
l The crossed-arms position is not appropriate, as
this body language projects an attitude of
superiority and may interfere with the progress of
the interview
GettingGetting startedstarted
l Making the patient feel that you are interested and concerned
l Once the introduction has been made, you may begin the
interview by asking a general ,open-ended question
“What medical problem has brought you to the hospital?”
l This type of opening remark allows the patient to speak first
l The interviewer can determine the patient’s chief complaint
or the problem that is regarded as paramount
GettingGetting startedstarted
l If the patient says “Haven’t you read my records?”
l It is correct to say “No, I’ve been asked to interview you
without any prior information”
or “I would like to hear your story in your words”
l Patients can determine very quickly if you are friendly
and personally interested in them
TheThe narrativenarrative
l Novice interviewers are often worried about
remembering the patient’s history
l It is poor form to write extensive notes during the
interview
l Attention should be focused more on what the
person is saying and less on the written word
TheThe narrativenarrative
l After the introductory story, the interviewer should
proceed to questions related to the chief complaint
l These should naturally evolve into questions related to the
other formal parts of the medical history, such as the
present illness,past illnesses, social and family history,
and review of body system
TheThe narrativenarrative
l Patients should largely be allowed to conduct the
narrative in their own way
l The interviewer must select certain aspects that
require further details and guard the patient toward
them
TheThe narrativenarrative
l Overdirection is to be avoided, because this stifles
the interview and prevents important points from
being clarified
l When patients use vague terms such as “often”,
“a little”, “sometimes”, the interviewer must
always for clarification, ask “What does
‘sometimes’ mean?” or “How often is ‘often’?”
TheThe narrativenarrative
l The interviewer should be alert for subtle clues
from the patient to guide the interview further
l There are a variety of technique to encourage and
sustain the narrative
TheThe closingclosing
l By the conclusion of the interview, the
interviewer should have a clear impression of the
reason why the patient sought medical help, the
history of the present illness, the patient’s past
medical history
l If any part of the history needs clarification, this
is the time to obtain it
TheThe closingclosing
l At the conclusion, it is polite to encourage the patient to
discuss any additional problems or to ask any questions
“Is there anything else you would like to tell me that I
have not already asked?”
l Thank the patient and tell him or her that you are ready
to begin the physical examination
BasicBasic interviewinginterviewing techniquestechniques
l Questioning
l Silence
l Facilitation
l Confrontation
l Interpretation
l Reflection
l Support
QuestioningQuestioning
Open ended questions
l They are used to ask the patient for general information
l It is most useful in opening up the interview or for
changing the topic to be discussed
l An open-ended question allows the patient to tell his
story spontaneously and does not presuppose a specific
answer
Open-endedOpen-ended questioningquestioning
What kind of medical problem are you having?
Can you describe your feelings when you get the pain?
Are you having stomach pain? Tell me about it
DirectDirect questioningquestioning
l After a period of open-ended questioning, the interviewer
should direct the attention to specific facts learned during
the open-ended question period
l This type of question gives the patient little room for
explanation
l A direct question can usually be answered in one word or
a brief sentence
DirectDirect questioningquestioning
Where does it hurt?
When do you get the burning
How do you compare this pain with your ulcer pain?
Notice: avoid asking direct questions in a manner that
might bias the response
DirectDirect questioningquestioning
l Symptoms are classically characterized into
several dimensions or elements, including bodily
location, quality, quantity, chronology, setting,
precipitating or palliating factors and associated
manifestations
l These elements may be used as a framework to
clarify the illness
DirectDirect questioningquestioning
l Bodily location
Can you tell me where you feel the pain?
Do you feel it anywhere else?
l Onset (chronology)
When did you first notice it?
How long did it last?
DirectDirect questioningquestioning
l Precipitating factors
What makes it worse?
What seems to bring on the pain?
l Palliating factors
What do you do to get more comfortable?
Does lying quietly in bed help you?
Does eating make it better?
DirectDirect questioningquestioning
l Quality
What does it feel like?
Can you describe the pain?(Blunt pain, acute pain,
knife cut pain, burning pain?)
l Radiation
When you get the pain in your chest, do you feel it in any
other part of your body?
When you experience your abdominal pain, do you have
pain in any other area of your body?
DirectDirect questioningquestioning
l Severity (quantity)
How many times did you vomit?
Can you fall asleep with the pain?
l Setting
Does it ever occur at rest?
Does the pain occur with your menstrual cycle?
DirectDirect questioningquestioning
l Associated manifestation
Do you ever have nausea with the pain?
Have you noticed other changes that happen when
you start to sweat?
O-P-Q-R-S-TO-P-Q-R-S-T
It stands for onset (chronology), precipitating
(palliative), quality, radiation, severity (setting),
and temporal, is useful to help you remember
these important dimensions of a symptom
QuestionQuestion typestypes toto avoidavoid
l Suggestive question
It may provide the answer to the question
“Do you feel the pain in your left arm when you
get it in your chest?” x
A better way to ask the same question would be:
“When you get the pain in your chest, do you
notice it anywhere else?” √
QuestionQuestion typestypes toto avoidavoid
l Why question
It carries tones of accusation
This type of question almost always asks a patient to
account for his/her behavior and tends to put the person
on the defensive
Why did you stop taking the medication?
Why did you wait so long to call me?
Try rephrasing the “Why” questions to “What is the
reason…?”
QuestionQuestion typestypes toto avoidavoid
l Multiple question
The patient can easily become confused and
respond incorrectly, answering no part of the
question adequately
“How many brothers and sisters do you have, and
has any one of them ever had asthma, heart
disease, pneumonia, or tuberculosis?”
QuestionQuestion typestypes toto avoidavoid
l Medical jargon
“You seem to have a homonymous hemianopsia”
l Leading question or biased question
It carries a suggestion of the kind of response the
interviewer is looking for
Always ask questions in the positive, not the negative
“You don’t have diabetes, do you?”
it should be “Do you have diabetes?”
Thank you
Pneumonia
The First Affliated Hospital of XinJiang
Medical University
Respiratory Unite
Bin Jia
Aim and Demand
Learn about the classification of pneumonia.
Discuss diagnosis and management of CAP.
Describe common pathogens, pathology, clinical
manifestation and treatment of Pneumococcal
pneumonia.
Master the clinical feature,diagnostic criteria and
therapy of Pneumococcal pneumonia, Staphylococcal
Pneumonia, Klebsiellar pneumonia, Legionella
pneumonia and Mycoplasma pneumonia.
Definition
Inflammation of the lung parenchyma,include
terminal airway, alveolar space and pulmonary
interstitium.
Caused by varities of pathogens,Such
as:Bacteria,Virus,Fungus,etc.
Come with fever, chills, cough, pleuritic chest pain,
sputum production, hyper- or hypothermia, increased
respiratory rate, dullness to percussion, bronchial
breathing, crackles, wheezes, pleural friction rub.
Opacity on chest radiography.
Epidemiology
Pneumonia is the sixth leading cause of death in the
United States;Among infectious causes of death,it
ranks number one.
An estimated 4 million cases of CAP occur each year
in the United States.Approximately 20% of these
cases require hospitalization,and among these
patients,mortality average is 15%,compared to <1%
of patients who can be managed as outpatients.
High incidence mortality and drug resistance rate.
Etiology
Pathogenic microorganism
Physical and chemical factors
Immunologic injury
Allergy
Drugs
Pneumonia or not?
There are two factors involved in the formation of
pneumonia.
☆ Pathogen:quantity and virulence.
☆ Host defenses:Respiratory defense and systemic
immunity.
Host factors:age,socioeconomic status,smoking,prior
antibiotic use,underlying medical condition.(alcohol
abuse,COPD,DM,chronic liver disease,chronic renal
insufficiency,CHF,use of immunosuppressive drugs)
Route of infection
Air suction.
Blood dissemination.
Spread by the near infection site.
Aspirated the colonized bacteria of upper respiratory
tract and gastrointestinal.
Invasive operation.
Etiological classification:
Bacterial Pneumonia:Streptococcus pneumoniae,
Staphylococcus aureus. Klebsiella pneumoniae, Colibacillus,
Pseudomonas aeruginosa, Anaerobic bacteria. Legionella
pneumonia and Mycoplasma pneumonia.
Virus pneumonia: Adenovirus,Respiratory Syncytial Virus,
Influenza virus.
Fungal pneumonia: Candida albicans, aspergillus.
Other pathogens: Chlamydia[klə'mɪdɪə] , Rickettsia,
衣原体
Lobular Pneumonia
(bronchopneumonia)
Interstitial pneumonia
Lobar Pneumonia
Community-Acquired Pneumonia
Hospital-Acquired Pneumonia
Community-Acquired Pneumonia
Occure in community within 48 hours.S.pneumonia is
the most common CAP in elderly people.
Incidence:5~10/1,000/year; 6th leading cause of
death in U.S; Number one among the infectious
diseases.Mortality vary between 6 to 20%.
Pathogens:Streptococcus pneumoniae, Haemophilus
influenzae, M catarrhalis, Legionella species,
Mycoplasma pneumoniae,etc.
Community-Acquired Pneumonia
Manifestations:sudden onset, shaking chill, Fever ,
nausea, vomiting, malaise[mæ'leɪz], and myalgias[maɪ'ældʒəs] .
pain with breathing on the affected side (pleurisy).
Cough, dyspnea, and sputum production.
Signs:T: 38~ 40.5℃; tachycardia[,tækɪ'kɑːdɪə];
Tachypnea(respirations accelerate to 20 to 45
breaths/min). lobar consolidation; crackles; pleural
effusion.
Community-Acquired Pneumonia
General Lab Examinations:
Blood tests:leukocytosis with a shift to the left
hypoxemia +respiratory alkalosis.
Diagnosis
Fever>380 C
New cough, ± sputum, hemoptysis[hɪ'mɒptɪsɪs]+Pleuritic
chest pain.WBC>10×109 or <4×109
Rales, rhonci, wheezing
New or evolving infiltrate on chest radiograph
High-resolution computed tomography (CT)
Sputum stains and culture
Lower respiratory secrets.
Hospital-Acquired Pneumonia
Certain illness may predispose HAP because
of:impaired defenses,chronic illness,
coma,malnutrition,prolong hospitalization,
intervention and endotracheal intubation,etc
Pathogens:S.aureus,Enterobacteriaceae
['entərəu,bæktəri'eisi,i:] ,Anaerobic bacteria,Aspergillus sp,Viral.
Resolution stage
Pathology
He yuanbing
The First Affiliated Hospital of Xinjiang Medical University
Department of respiratory medicine1
Inquiry
It is the method that physician obtain the clinic
data of patient, and further propose clinical
judgment by comprehensive analysis
Parameters including:
general state of health past illness
injuries hospitalizations
surgery allergies
immunizations substance abuse
diet sleep patterns
current medications alternative therapies
Past medical history
Cardiovascular system
chest pain shortness of breath with exertion
palpitations shortness of breath lying flat
sudden shortness of breath while sleeping
history of heart attack
Review of systems
GI system
appetite excessive hunger excessive thirst
nausea constipation diarrhea
heartburn vomiting abdominal pain
change in stool color/caliber/consistency
frequency of bowel movements vomiting
blood(haematemesis)
rectal bleeding (hematochezia) black tarry stools
diabetes , bowel cancer
Review of systems
Urinary system
frequency urgency incontinence difficulty in the
starting the stream
excessive urination pain on urination
burning blood in the urine (hematuria)
bed-wetting waist pain history of retention
urine color urine odor
Review of systems
Hematological system pallor yellow skin
hemolytic petechia purpura ecchymosis
hematoma
Musculoskeletal system
weakness paralysis muscle stiffness
limitation of movement joint pain
joint stiffness arthritis gout deformities
Review of systems
Review of systems may involved lots of clinical
diseases
The narrative
The closing
Getting started
The diagnostic process begins at the first moment of
meeting
One should be dressed appropriately, wearing a white
coat with one’s name badge identifying one as a
physician
One should make patient as comfortable as possible
One should sit in a chair directly facing the patient in
order to make good eye contact
Getting started
Once the introduction has been made, you may begin the
interview by asking a general ,open-ended question
“What medical problem has brought you to the hospital?”
Thank the patient and tell him or her that you are ready
to begin the physical examination
Basic interviewing techniques
Questioning
Silence
Facilitation
Confrontation
Interpretation
Reflection
Support
Questioning
Open ended questions
Can you describe your feelings when you get the pain?
Bodily location
Can you tell me where you feel the pain?
Do you feel it anywhere else?
Onset (chronology)
When did you first notice it?
How long did it last?
Direct questioning
Precipitating factors
What makes it worse?
What seems to bring on the pain?
Palliating factors
What do you do to get more comfortable?
Does lying quietly in bed help you?
Does eating make it better?
Direct questioning
Quality
What does it feel like?
Can you describe the pain?(Blunt pain, acute pain,
knife cut pain, burning pain?)
Radiation
When you get the pain in your chest, do you feel it in any
other part of your body?
When you experience your abdominal pain, do you have
pain in any other area of your body?
Direct questioning
Severity (quantity)
How many times did you vomit?
Can you fall asleep with the pain?
Setting
Does it ever occur at rest?
Does the pain occur with your menstrual cycle?
Direct questioning
Associated manifestation
Do you ever have nausea with the pain?
Have you noticed other changes that happen when
you start to sweat?
O-P-Q-R-S-T
It stands for onset (chronology), precipitating
(palliative), quality, radiation, severity (setting),
and temporal, is useful to help you remember
these important dimensions of a symptom
Question types to avoid
Suggestive question
It may provide the answer to the question
“Do you feel the pain in your left arm when you
get it in your chest?” x
A better way to ask the same question would be:
“When you get the pain in your chest, do you
notice it anywhere else?” √
Question types to avoid
Why question
It carries tones of accusation
This type of question almost always asks a patient to
account for his/her behavior and tends to put the person
on the defensive
§ To master:
§ The pathological type of lung cancer and the type of clinical
characteristics
§ Lung cancer clinical manifestations
§ staging of lung cancer treatment
§ To familiar :
§ Lung cancer definitions, etiology, pathogenesis.
What is lung cancer?
§ It’s malignant.
epidemiology
§ Lung cancer is the most common cancer in both men and women.
§ It accounts for about 14% of all new cancers in both men and women.
§ Lung cancer mainly occurs in older people. peak incidence occur
between ages 55-65 years . there is a 3:1 male : female ratio.
§ For smokers the risk is much higher.
§ Lung cancer is the leading cause of cancer death among both men and
women.
§ Lung cancer accounts for about 1 in 4 cancer deaths each year.
§
Etiology
§ The etiology of lung cancer is not clear, but there are many
risk factors.
§ Risk factors are anything that can increase or decrease a
person’s chance of getting a disease, such as cancer.
§ There are many known risk factors for lung cancer.
Etiology
changeschanges
Occupational exposure
If the workplace exposure to carcinogenic substance, to all
workmen, it is also a risk factor for lung cancer. especially
in smokers.
Occupational exposure
§ Asbestos
§ ( 石棉)
Occupational exposure
§ Arsenic(砷)
Air pollution
Come from:
• medical exposure:X-ray
• Nature radiation
Lung cancer risk factors
SCLC:(10-15%)
including
Large cell carcinoma
(10%)
NSCLC Squamous cell carcinoma
(30-60%)
Adenocarcinoma(10-
30%)
Epidermiod [squamous]
carcinoma -35% :
§ occurs most frequently in men and old
people
§ It is strongly associated with smoking.
§ usually starts on one breathing tubes,
and cause obstructive pneumonia or
atelectasis.
§ tend to be localized in the chest longer
than other types of lung cancer.
§ does not tend to metastases early.
§ Tend to necrosis, and form cavity.
Adenocarcinnoma-30%:
§ small cell lung cancer also called oatcell because SCLC cells have oat
grain appearance.
§ It arises from endocrine cells [kulchitisky cells] where many hormones are
secreted.
§ spread to lymph nodes and other organs more quickly than NSCLC .
§ usually started in one larger breathing tube,
§ Tend to grow rapidly .
§ commonly has spread by the time diagnosis and is considered a systemic
disease.
§ It is the only one of the bronchial carcinomas that respond to chemotherapy
Clinical stage
Primary tumor classification
Primary tumor classification
Primary tumor classification
Primary tumor classification
(5-15% no symptom)
⑴ Persistent cough:
⑵ hemoptysis :
⑶ wheezing:
⑸ weight loss:
⑹ fever:
Symptoms caused by tumor
4- Pleural pain :
5. fever
cause by the necrosis of tumor tissue or obstructive
pneumonia.
6. Weight loss
emaciation, cachexia.
Symptoms due to tumor expansion
1. Chest pain
2. Hoarseness
§ Cause by the compression of
recurrent laryngeal nerve because
of tumor or large lymph nodes.
§ causing unilateral vocal cord
paresis with hoarseness of voice.
3. dysphagia
Involvement of esophagus
4.Invassion of phrenic nerve ,
causing paralysis of the diaphragm.
Symptoms due to tumor expansion
5. Pleural effusion:
§10% of cases have pleural effusion
§Caused by invasion of pleura or blocking of pulmonary
lymphatic reflux.
Symptoms due to tumor expansion
⑵ to bone:
⑶ to abdomen:
⑴ hypertrophic pulmmonary
Osteoarthropathy
(肥大性肺性骨关病)
⑵ gynaecomastia
(男性乳房育)
large cell lung cancer
⑶ Cushing's syndrome:
§ Common in SCLC.
§ ACTH increase in tumor tissue or blood.
§ central obesity, muscle weakness, skin thinning,
hypertension,hairiness, etc.
ExtraExtra thoracicthoracic manifestationsmanifestations
⑸ neuromyopathic syndromes:
• Common in SCLC.
• Cortical degeneration(皮质变性), cerebellar degeneration(小脑变性)
, peripheral neuropathy, myasthenia gravis(重症肌无力),
myopathy(肌病)
• Occur before the tumor or at the same time or after operation
• No associated with the position of tumor and metastasis.
⑹ hypercalcemia
• Common in squamous cell carcinoma.
• Sleepiness, Anorexia, nausea, vomit, weight loss
ExtraExtra thoracicthoracic manifestationsmanifestations
§ 7. carcinoid syndrome
§ episodic flushing or edema at face or upper extremities
or trunk; acceleration of gastrointestinal peristalsis;
diarrhea; tachycardia; wheeze.
§ Because of releases of 5-hydroxytryptamine, bradykinin,
catecholamine.
Auxiliary examination
1.X-ray
. chest x-ray:
common radiological presentation of bronchial
carcinoma.
1- unilateral hilar-enlargement.
2- peripheral pulmonary opacity.
3- lung, lobe or segmental collapse.
4- pleural effusion .
5- broadening of the mediastinum,
enlarged cardiac shadow, elevation
of hemidiaphram.
6- rib distruction.
肺癌
Auxiliary examination
2. CT scan
Auxiliary examination
2. CT scan
Auxiliary examination
2. CT scan
Auxiliary examination
2. CT scan
lymphagitis carcinomatosa
Investigation:
. Sputum cytology: high yield for
endobronchial tumors such as
squamous cell and small cell
carcinoma.
Auxiliary examination
5. Fiberoptic bronchoscopy:
euthyphoria, needle biopsy,brush biopsy, forceps biopsy,
sucking
Squamous Cell
Normal Trachea Normal Carina
Carcinoma, Trachea
Adenocarcinoma
Adenocarcinoma Extrinsic Pressure
Left Lingular Bronchus Right Truncal Intermedus Trachea
EBUS
Electromagnetic navigation
fine needle aspiration under
CT.
Auxiliary examination
others:
.Head CT scan.
.liver US.
§ Diagnosis procedure:
Treatment
1.Resection by operation: especially for NSCLC.
5. immunotherapy
6.Traditional Chinese medicine therapy etc.
Treatment
NSCLC:
Ⅰ-Ⅲa operation.
• Implications:
- “Biological Effective Dose” rather than “Maximal Tolerated
Dose”
-Patient Selection Possible by assaying some aspect of the
target
EGFR 信号通路
SCLC:
chemotherapy
+
radiotherapy /chemotherapy.
prognosis
§ squamous carcinoma
>
adenocarcinoma
>SCLC
acuity card
Reflex hammer Lubricant gel
Preparation for examination
Wash your hands before examination
washing with soap and water is an effective way
to reduce the transmission of disease
It is preferable to use daylight for illumination.
skin color changes may be masked by artificial
light.
Become facile in each organ system examination.
the complete examination with the least amount
of movement of the patient is an excellent
manipulation.
Preparation for examination
Light palpation
Deep palpation
Light palpation
Indirect percussion
Direct percussion
Indirect percussion
Resonance:
Can be heard when checking a normal
person’s chest.
Tympany:
Can be heard when checking a normal
person’s abdomen and aerogastria.
Percussion sound
Hyperresonance:
Can be heard when checking a normal
child’s chest.
In normal adult, there is no such
percussion sound. It can just be heard
in patients with emphysema.
Percussion sound
Dullness
Can be heard when checking heart or
liver part covered by lung,ascites.
Flatness
Can be heard when checking the
heart or liver part not be covered by
lung, or parenchyma organs.
Auscultation
Auscultation involves listening to
sounds produced by internal organs.
This technique gives information
about an organ’s pathophysiology.
Smell
Breath
Sputum
Vomitus
Feces
Urine
pus
PLEURAL EFFUSIONS
Anatomy of pleural membrane
and pleural space
Oncotic
pressure
← Permeability of pleural
fluid (8)
Exudative effusions
( capillary permeability exudation of fluid, protein, cells )
The cause may be
Lung and pleural cancer
TB pleuritis
pneumonia
pulmonary embolism
viral infection
Two kinds of pleural effusions
Transudates and exudates
Transudate Exudate
Cause non-inflammatory flammatory,tumor
Apperance light yellow yellow, purulent
Specific gravity <1.018 >1.018
Coagulability unable able
Revalta test negative positive
Protein content <30g/L >30g/L
LDH < 200 I U/ L > 200 I U / L
Cell count < 100×10 6/ L > 500×10 6 / L
Differential cell Lymphocyte Different
Haemorrhagic effusion
l. Trauma
2. Tumor
3. Pulmonary infarction
4. TB
5. Spontaneous pneumothorax
Empyema
l. TB
2. Pulmonary infection
3. Trauma
T B ( Tuberculosis ) is the most
common cause of pleural effusion ,
especially in young people, the common
symptom include: fever 、chest pain expicially
during inspiction,chest tightness, night sweat,
fatigue, bad appitide , weight loss
Malignant pleural effusion is frequently
History(primary diseases)
clinical signs
physical examinations
clinical signs
pleural pain,
dyspnea,
tachypnea,
mild outward bulging of the intercostal
spaces,
decreased tactile fremitus,
dullness or flatness,
decreased transmission of breath and vocal
sounds in the area of the effusion,
and pleural friction sound in its
early stage (dry pleurisy)
Diagnostic procedures 12345
Chest X-ray examination
Blunting of the normally sharp costophyrenic
angle, a concave shadow with its highest margin
along the pleural surface, shift of the tracheal and
mediastinum toward the normal side if pleural is
huge
Pleural effusion
Diagnostic procedures 12345
B- Ultrasonic examination
To localize a small pleural effusion and
determine the correct site for performance
of a thoracentesis
Diagnostic procedures 12345
Thoracentesis is importmant to
diagnosis the cause and alleviated the
sign
To aspirate the pleural effusion for laboratory
examination:
Appearance, Specific gravity, Protein content,
Cell counts, LDH lipid content, ADA
bacteria culture,
Cytologic examination, etc.
Diagnostic procedures 12345
Pleural biopsy
To obtain a specimen for histologic
examination and culture usually
under B ultrasonic or CT guidance
Treatment
to establish the
diagnosis, aspirration of pleural fluid may be
necessary to relieve breathlessness. It is
inadvisable to remove more than 1 litre on
the first occasion because “re-expansion”
amountslly follows the aspiration of
pulmonary edama occasionally follow the
aspiration
Tuberculous pleural effusion
杆菌
不典型分支杆菌
Types of mycobacteria causing disease in
humans
• Pleurisy
• Exudate Pleural
effusion
Extra-pulmonary tuberculosis
isoniazid(INH),200-300mg(children10mg/kg),
side effects: hypersensitivity, polyneuropathy,
lack of mental concentration
pyrazinamide(PZA),20-35mg/kg, side
effects: hepatitis,gout,hypersensitivity
status asthmaticus
On the contrary, in patients with lower respiratory tract
is obstructed, because the airflow out of the lung is
impedent, exhalation with exertion may lead to bulging
of the interspaces. This is associated with prolonged
expiration, called expiratory dyspnea, it usually occurs
in asthma and obstructive emphysema.
1.Respiratory rate:
normal adult at rest, the respiratory rate is 10-20 per
minute.
The ratio of respiratory rate to pulse rate is 1:4. The
respiratory rate in newborn is about 44 per minute, and
decreases gradually upon growing up.
1) tachypnea: Indicates the increased respiratory rate that
over 24 per minute, usually seen in fever, pain, anemia,
hyperthyroidism and heart failure. Usually the respiratory
rate increases approximately four additional cycles per
minute for each 1°above the normal temperature.
2) bradypnea: Indicates the decreased respiratory rate
that less than 10 per minute. The respiration becomes
superficial, seen in over dose of anesthetics or sedatives
and elevated intracranial pressure.
3) Change of the breath depths:
Hypopnea could be seen in respiratory palsy, ascites
and fatness, etc. And also could be seen in pneumonia,
pleurisy, pleural effusion and pneumothorax.
Hyperpnea, could be found during strenuous
exercises, for increased body oxygen supply needs more
air exchange through the lung. It can also appear when
one is excited or nervous, because of over ventilation.
Decreased PaCO2 ensues and could induce respiratory
alkalosis.
Deep and slow breath could appear during serious
metabolic acidosis. This is because the HCO3 in the
extracellular fluid is not enough, and PH is lower, for
compensation, CO2 is eliminated by the lung to
maintain the acid-base balance. This kind of deep and
slow breath is also named as Kussmaul breath, seen
in diabetic ketoacidosis and uremic acidosis.
(3) Rhythm of the breath
Normal adult respiration is basically regular and smooth in
testing status. The rhythm of the breath usually changes in
diseases.
1. Tidal breathing Also called as cheyne-stokes respiration.
Respiration waxes and wanes cyclically so that periods of
deep breathing alternate with periods of apnea(no breathing).
The periods of the tidal breath can last from 30s to 2min. The
periods of apnea can persist 5-30s. So only through carefully
and long enough observation, the whole process could be
realized.
30 秒—2 分 5—30 秒
2. Ataxic breathing Also called Biot’s breahting.
Ataxic breathing is characterized by unpredictable
irregularity. Breaths may be shallow or deep, and stop
for short periods . Ataxic breathing is more severe than
the tidal breathing, the prognosis is worse, often
happening before demise. Aging people normally may
show tidal breathing in sleep, this is a sign of
cerebrovascular sclerosis.
3.Inhibitory breath
The inspiration is suspended while a severe pain in the
chest happened, the respiratory movement restrained
suddenly and momently. The expression of the patient is
suffering, breath become shallow and frequent. Causes
include acute pleurisy, tumor, costal fracture and severe
trauma of the thorax.
4. sighing respiration
Breathing punctuated by frequent sighs should alert you
to the possibility of hyperventilation syndrome – a
common cause of dyspnea and dizziness. Occasional
sighs are normal.
2. PALPATION
(1) Thoracic expansion
It is the movement range of the thorax during respiration.
Easy to obtain when examine the antero-inferior part of the
thorax, where the respiratory movement is much obvious.
Place your thumbs along each costal margin, and your hands
along the lateral rib cage. When the patient inhales deeply,
watch the divergence of your thumbs as the thorax expands,
and feel the range and symmetry of respiratory movement.
Causes of unilateral diminution of or delay in chest
expansion include huge pleural effusion, pneumothorax,
pleural thickening and atelectasis etc
(2) Vocal fremitus Also called tactile fremitus. Vocal
fremitus refers to the palpable vibrations transmitted through
the bronchopulmonary system to the chest wall when the
patient speaks. Ask the patient to repeat the words “yi—“. If
fremitus is faint, ask the patient to speak more loudly or in a
lower voice.
Palpate and compare symmetrical areas of the lungs using
either the ball of your hand (the bony part of the palm at the
base of the fingers) or the ulnar surface of your hand.
In either case you are using the vibratory sensitivity of
the bones in your hand to detect fremitus.
Identify, describe, and localize any area of increased or
decreased fremitus. Fremitus is typically more prominent
in the interscapular area than in the lower lung fields, and
is often more prominent on right side than on the left. It
disappears below the diaphragm.
Fremitus is decreased or absent when the voice is soft or
when the transmission of vibrations from the larynx to the
surface of the chest is impeded.
Causes include an obstructed bronchus, chronic
obstructive pulmonary disease, separation of the pleural
surfaces by fluid (pleural effusion), fibrosis ( pleural
thickening), air (pneumothorax) or an infiltrating tumor;
and also a very thick chest wall.
Fremitus is increased when transmission of sound is
increased, as through the consolidated lung of lobar
pneumonia.
(2) pleural friction fremitus
During acute pleurisy, the fibrin deposit between the
two layers of the pleura, the visceral pleura and the
parietal pleura rub with each other, this can be felt by the
examiner’s hand, so it is called pleural friction fremitus.
It can be palpated both in inspiration and expiration. It is
most obvious at the lower part of the thorax for the
movement range here is the greatest.
The other method of evaluating tactile
fremitus is to use the fingertips instead of
the ulnar side of the hand.
shown in figure 12-13
Table 12-5 lists some of the important
pathologic causes for changes in tactile
fremitus .
Percussion
In percussion of the chest, the examiner
places the middle finger of one hand firmly
against the patient’s chest wall parallel to
the ribs in an interspace, with the palm and
other fingers held off the chest.
The tip of the right middle finger of the
other hand strikes a quick, sharp blow to
the terminal phalanx of the left finger on
the chest wall.
The motion of the striking finger should
come from the wrist and not from the
elbow.
The technique of percussion is
diagrammed in Figure 12-14 and shown
in Figure 12-15.
1. Classification of the percussion notes
The sound heard and the tactile sensation
felt are dependent on the air-tissue ratio.
● Percussion over a solid organ, such as the
liver, produces a dull, low-amplitude, short-
duration note without resonance.
● Percussion over a structure containing air
within a tissue, such as the lung, produces a
resonant, higher- amplitude, lower-pitched note.
● Percussion over a hollow air-containing
structure, such as the stomach, produces
a tympanic, high-pitched, hollow-quality
note.
● Percussion over a large muscle mass,
such as the thigh, produces a flat, high-
pitched note.
● in the chest, dullness over the heart
and resonance over the lung
● pneumonia, resonance is replaced by
dullness.
●Hyperresonance: found in emphysema.
Hyperresonance is a low-pitched, hollow-
quality,sustained resonant note bordering
on tympany.
2. Percussion of the pulmonary boundary
(1)Upper pulmonary boundary
that is the width of the apics. The method is: percuss
from the middle trapezius muscle outwards to lateral side
little by little, when the sound turns from resonance to
dullness gradually, the lateral termination of the upper
border is identified.
inferior
Infer.(6th)
(8th)
(10th)
(3) The anterior pulmonary boundary
The heart normally produces an area of dullness to the
left of sternum. The right anterior pulmonary boundary is
at the sternal line,
the left one is at the parasternal line from 4th to 6th
interspace. It is influenced by the size of heart, pericardial
effusion, aortic aneurysm, enlarged lymph nodes of the
pulmonary portal and also by the emphysema.
Percuss the Posterior Chest
Echocardiogram
ECG
Lung biopsy (rarely done)
Measurement of blood oxygen by checking
arterial blood gas (ABG)
Pulmonary (lung) function tests
Right heart catheterization
Ventilation and perfusion scan of the lungs (V/Q
scan)
Tests for autoimmune lung disease
Treatment
The goal of treatment is to control symptoms. It is
important to treat medical problems that cause
pulmonary hypertension, because they can lead to cor
pulmonale.
Many treatment options are available. In general, the
cause of your cor pulmonale will determine which
treatment you receive.
If your provider prescribes medicines, you may take
them by mouth (oral), receive them through a vein
(intravenous or IV), or breathe them in (inhaled). You
will be closely monitored during treatment to watch
for side effects and to see how well the medicine
works for you. Never stop taking your medicines
without first talking to your doctor.
Other treatments may include:
Blood thinners to reduce the risk of blood clots
Medicines to manage heart failure symptoms
•Oxygen therapy at home
•A lung or heart-lung transplant, if medicine does not
work
Important tips to follow:
•Avoid strenuous activities and heavy lifting.
•Avoid traveling to high altitudes.
•Get a yearly flu vaccine, as well as other vaccines,
such as the pneumonia vaccine.
•If you smoke, stop.
•Use oxygen if your doctor prescribes it.
•Women should not get pregnant.
Pulmonary hypertension
Pulmonary hypertension
is high blood pressure in the arteries of the
lungs. It makes the right side of the heart
work harder than normal
Causes
The right side of the heart pumps blood
through the lungs, where it picks up oxygen.
Blood returns to the left side of the heart,
where it is pumped to the rest of the body.
When the small arteries (blood vessels) of
the lungs become narrowed, they cannot
carry as much blood. When this happens,
pressure builds up. This is called pulmonary
hypertension.
The heart needs to work harder to
force the blood through the vessels
against this pressure. Over time, this
causes the right side of the heart to
become larger. This condition is called
right-sided heart failure, or cor
pulmonale.
Pulmonary hypertension may be caused by:
•Autoimmune diseases that damage the
lungs, such as scleroderma and rheumatoid
arthritis
•Birth defects of the heart
•Blood clots in the lung (pulmonary embolism)
•Heart failure
•Heart valve disease
•HIV infection
•Low oxygen levels in the blood for a long
time (chronic)
•Lung disease, such as COPD or pulmonary
fibrosis or any other severe chronic lung
condition
•Medicines (for example, certain diet
drugs)
•Obstructive sleep apnea
In rare cases, the cause of pulmonary
hypertension is unknown. In this case, the
condition is called idiopathic pulmonary
arterial hypertension (IPAH). Idiopathic
means the cause of a disease is not known.
IPAH affects more women than men.
If pulmonary hypertension is caused by a
known medicine or medical condition, it is
called secondary pulmonary hypertension.
Symptoms
Shortness of breath or lightheadedness during activity
is often the first symptom. Fast heart rate
(palpitations) may be present. Over time, symptoms
occur with lighter activity or even while at rest.
Other symptoms include:
•Ankle and leg swelling
•Bluish color of the lips or skin (cyanosis)
•Chest pain or pressure, usually in the front of the
chest
•Dizziness or fainting spells
•Fatigue
•Increased abdomen size
•Weakness
People with pulmonary hypertension often have symptoms
that come and go. They report good days and bad days.
Exams and Tests
Your health care provider will perform a physical exam and
ask about your symptoms. The exam may find:
•Abnormal heart sounds
•Feeling of a pulse over the breastbone
•Heart murmur on the right side of the heart
•Larger-than-normal veins in the neck
•Leg swelling
•Liver and spleen swelling
•Normal breath sounds if pulmonary hypertension is
idiopathic or due to congenital heart disease
•Abnormal breath sounds if pulmonary hypertension is from
other lung disease
In the early stages of the disease, the exam may be normal or
almost normal. The condition may take several months to
diagnose. Asthma and other diseases may cause similar
symptoms and must be ruled out.
Tests that may be ordered include:
•Blood tests
•Cardiac catheterization
•Chest x-ray
•CT scan of the chest
•Echocardiogram
•ECG
•Lung function tests
•Nuclear lung scan
•Pulmonary arteriogram
•6-minute walk test Sleep study Tests to check for
autoimmune problems
•
Treatment
There is no cure for pulmonary hypertension. The goal
of treatment is to control symptoms and prevent
more lung damage. It is important to treat medical
disorders that cause pulmonary hypertension, such as
obstructive sleep apnea, lung conditions, and heart
valve problems.
Many treatment options for pulmonary arterial
hypertension are available. If you are prescribed
medicines, they may be taken by mouth (oral),
received through the vein (intravenous, or IV), or
breathed in (inhaled).
Your provider will decide which medicine is
best for you. You will be closely monitored
during treatment to watch for side effects
and to see how well you are responding to
the medicine. DO NOT stop taking your
medicines without talking to your provider
Other treatments may include:
•Blood thinners to reduce the risk of blood clots,
especially if you have IPAH
•Oxygen therapy at home
•Lung, or in some cases, heart-lung transplant, if
medicines do not work
Other important tips to follow:
•Avoid pregnancy
•Avoid heavy physical activities and lifting
•Avoid traveling to high altitudes
•Get a yearly flu vaccine, as well as other vaccines such
as the pneumonia vaccine
•Stop smoking
Acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) is
a life-threatening lung condition that prevents
enough oxygen from getting to the lungs and
into the blood. Infants can also have respiratory
distress syndrome
Causes
ARDS can be caused by any major direct or
indirect injury to the lung. Common causes
include:
•Breathing vomit into the lungs (aspiration)
•Inhaling chemicals
•Lung transplant
•Pneumonia
•Septic shock (infection throughout the body)
•Trauma
Depending on the amount of oxygen in the blood
and during breathing, the severity of ARDS is
classified as:
•Mild
•Moderate
•Severe
ARDS leads to a buildup of fluid in the air sacs
(alveoli). This fluid prevents enough oxygen from
passing into the bloodstream.
The fluid buildup also makes the lungs heavy and
stiff. This decreases the lungs' ability to expand.
The level of oxygen in the blood can stay
dangerously low, even if the person receives
oxygen from a breathing machine (ventilator)
through a breathing tube (endotracheal tube).
ARDS often occurs along with the failure of other
organ systems, such as the liver or kidneys.
Cigarette smoking and heavy alcohol use may be
risk factors for its development.
Symptoms
Symptoms usually develop within 24 to
48 hours of the injury or illness. Often,
people with ARDS are so sick they cannot
complain of symptoms. Symptoms can
include any of the following:
•Shortness of breath
•Fast heartbeat
•Low blood pressure and organ failure
•Rapid breathing
Exams and Tests
Listening to the chest with a stethoscope
(auscultation) reveals abnormal breath sounds,
such as crackles, which may be signs of fluid in
the lungs. Often, blood pressure is
low. Cyanosis (blue skin, lips, and nails caused by
lack of oxygen to the tissues) is often seen.
Tests used to diagnose ARDS include:
Tests used to diagnose ARDS include:
•Arterial blood gas
•Blood tests, including CBC (complete blood count)
and blood chemistries
•Blood and urine cultures
•Bronchoscopy in some people
•Chest x-ray or CT scan
•Sputum cultures and analysis
•Tests for possible infections
An echocardiogram may be needed to rule
out heart failure, which can look similar to
ARDS on a chest x-ray.
Treatment
ARDS often needs to be treated in an intensive
care unit (ICU).
The goal of treatment is to provide breathing
support and treat the cause of ARDS. This may
involve medicines to treat infections, reduce
inflammation, and remove fluid from the lungs.
A ventilator is used to deliver high doses of
oxygen and positive pressure to the damaged
lungs. People often need to be deeply sedated
with medicines. During treatment, health care
providers make every effort to protect the lungs
from further damage. Treatment is mainly
supportive until the lungs recover.
Sometimes, a treatment called
extracorporeal membrane oxygenation
(ECMO) is done. During ECMO, blood
is filtered through a machine to
provide oxygen and remove carbon
dioxide
Acute Respiratory Distress Syndrome And
Multiple Organ Dysfunction Syndrome
Professor Xu sicheng
contents
keys:
difinition
causes
clinical features
diagnosis and differential diagnosis
treatment
understanding:
pathogenesis and pathology
Variety of systemic or pulmonary insults can lead to injury of
multiple organs including the lungs, Severe injury can result in
acute lung injury (ALI) or acute respiratory distress syndrome (
ARDS ) and multiple organ dysfunction syndrome ( MODS) .
ALL/ARDS is usually the first presentation of MODS and plays
important role in determining the outcome of MODS. Proper
application of mechanical ventilation is important intervention
for ALL/ARDS.
ACUTE LUNG INJURY AND ACUTE RESPIRATORY
DISTRESS SYNDROMEDEFINITION
ARDS denotes acute hypoxemic respiratory failure following a
systemic or pulmonary insult without evidence of heart failure.
ARDS is the most severe form of acute lung injury and is
characterized by bilateral, widespread radiographic pulmonary
infiltrates,normal pulmonary capillary wedge pressure (≤18 mmHg)
and a PaO2/FiO2 ratio ≤200. ARDS may follow variety of severe
systemic or pulmonary insults, which can induce systemic
inflammatory response. Pro-inflammatory cytokines released from
stimulated inflammatory cells appear to be pivotal in lung injury.
Although the mechanism of lung injury varies with the
cause, damage to capillary endothelial cells and alveolar
epithelial cells is common to ARDS regardless of cause.
Damage to these cells causes increased vascular permeability
and decreased production and activity of surfactant; these
abnormalities lead to interstitial and alveolar pulmonary
edema, alveolar collapse, and hypoxemia.
ARDS first was described in 1967 as the abrupt onset of diffuse
lung injury characterized by severe hypoxemia and generalized
pulmonary infiltrates on the chest radiograph in the absence of overt
cardiac failure. In the early 1990s , the term acute lung injury
officially was introduced to include traditional ARDS and less
severe forms of lung injury. The definitions of ALI and ARDS
require bilateral pulmonary infiltrates compatible with pulmonary
edema in the absence of clinical heart failure(usually as determined
by no evidence of elevated left atrial pressures), but the two are
differentiated by the degree of abnormal oxygenation: Patients are
defined as having ALI if the PaO2 divided by the FiO2 ( PaO2/
FiO2) is less than or equal to 300 mmHg; when the PaO2/ FiO2 is
less than or equal to 200 mmHg, the patient meets criteria for
ARDS.
CAUSES AND PATHOGENESIS CAUSES
ARDS may follow a wide variety of clinical events (Table 1-14-
1). Common risk factors for ARDS include sepsis , aspiration of
gastric contents, shock , infection, lung contusion, nonthoracic
trauma, toxic inhalation , near-drowning , and multiple blood
transfusions. About one third of ARDS patients initially have
sepsis syndrome.
Systemic insults
Pulmonary insults
Sepsis
Aspiration of gastric contents
Trauma Miliary
tuberculosis
Pancreatitis Diffuse
pneumonia(e. g, SARS)
Burns Free-
base cocaine smoking
Drugs and drug overdose, such as Opioids, Aspirin, Phenothiazines, Tricyclic Near-
drowning
antidepressants, Amiodarone , Chemotherapeutic agents, etc.
High-
altitude exposure
Lung
reexpansion or reperfusion
PATHOGENESIS
Although the pathogenesis of ARDS is not fully understood yet
, ARDS occurs primarily as the result of inflammatory injury to
the alveoli producing diffuse alveolar damage, which is part of
systemic inflammatory response syndrome (SIRS) in response to
variety of insults . The lungs probably are particularly vulnerable
to inflammatory injury because mediators are released into the
bloodstream, and the lungs receive the entire cardiac output.
Pro-inflammatory cytokines such as tumor necrosis factor ,
interleukin 1, interleukin-6, and interleukin-8 are released in
response to any of a variety of precipitants . Neutrophils are
recruited to the lungs , become activated, and release toxic
mediate such as reactive oxygen species and proteases which
damage the capillary endothelium and alveolar epithelium.
Impaired neutrophil apoptosis in the early stages of ARDS may
amplify this phenomenon, and may result from increased
concentrations of G-CSF and GM-CSF within alveolar fluid.
As a result, the normal barriers to alveolar edema are lost.
Protein escapes from the vascular space, and the osmotic
gradient favoring resorption of fluid is lost. Fluid pours into the
interstitium and overwhelms the capacity of the lymphatics . Air
spaces fill with bloody, proteinaceous edema fluid and debris
from degenerating cells. Functional surfactant is lost , resulting
in alveolar collapse. The main physiologic derangements
responsible for clinical presentation of hypoxemia and
respiratory distress are as following:.
Impaired Gas EXchange
Ventilation-perfusion mismatching and physiologic shunting
are the major causes of hypoxemia.Increased physiologic dead
space may interfere with CO2 elimination. Although
hypercapnia is uncommon, the minute volume required to
maintain a normal PaCO2 rises significantly.
Impaired Compliance
Decreased pulmonary compliance is one of the hallmarks of
ARDS. The low compliance is due to the stiffness of poorly or
nonaerated lung rather than changes in the pressure-volume
characteristics of residual functioning lung units. Because only
the remaining portions of normally functioning lung
meaningfully participate in gas exchange, even small tidal
volumes may exceed the lung’s inspiratory capacity and cause a
dramatic rise in airway pressures .
Other Mechanisms
Other mechanisms may be involved in the development of
respiratory distress in ARDS. These include stimulation of J-
receptor adjacent to pulmonary capillary by pulmonary
hyperemia and edema, pulmonary hypertension and increased
airways resistance.
PATHOLOGY
The pathologic abnormalities in acute lung injury and ARDS
are nonspecific and are described as diffuse alveolar damage by
pathologists. Abnormalities of epithelial cells, particularly type I
alveolar cells, and pulmonary vascular endothelial cells are seen.
The initial process is inflammatory in nature,with neutrophils
usually predominating in the alveolar fluid. Hyaline membranes,
similar to those seen in premature infants with infant respiratory
distress syndrome, develop, presumably related to the presence
of large-molecular-weight proteins that have leaked into the
alveolar space. Alveolar flooding leads to impairment of
surfactant, which is abnormal in quantity and quality.
The result is microatelectasis , which may be associated with
an impairment of immune function. Cytokines and other
inflammatory mediators usually are markedly elevated , although
with different patterns over time in the bronchoalveolar lavage
and the systemic blood. Lung repair also is disturbed; there is
early evidence of profibrotic processes manifest by the
appearance of breakdown products of procollagen in the
bronchoalveolar lavage fluid, followed by subsequent scarring.
Because lung function improves over time in survivors of ARDS.
however, it has been assumed that this scarring is potentially
reversible.
The pathology of ARDS can be arbitrarily divided as
exudative, proliferative and fibrotic stages. These pathologies are
often overlapped..
CLINICAL FEATURES
ARDS is marked by the rapid onset of profound dyspnea and
hypoxemia that usually occurs within five days( mean time from
12-48 hours) from the onset of underline diseases process.
Respiratory distress presenting as labored breathing, tachypnea ,
intercostals retractions are often accompanied with cyanosis,
agitation, anxiety and diaphoresis ,which are refractory to
oxygen therapy. These abnormalities can not be explained by the
underline diseases and the possibility of cardiogenic pulmonary
edema could be excluded. Abnormal signs on physical
examination are not remarkable or fine crackles can be noted.
LABORATORY FINDINGS
CHEST X-RAY
Chest radiography shows diffuse or patchy bilateral infiltrates
that rapidly become confluent. Air
bronchograms occur in about 80% of cases. The abnormality on
chest X-
ray varies from interstitial infiltrate to bilateral generalized opaci
ties(white
lungs). Interstitial lung fibrosis can persist for several months in
patients recovering from ARDS.
ARTERIAL BLOOD GASES
Arterial blood gases usually show severe hypoxemia, acute res
piratory alkalosis, and elevated alveolar-
arterial oxygen gradient. Pa02/F102 is less than
or equal to 300 mmHg in ALI and less than or equal
to 200 mmHg in ARDS( PaO2 is measured in mmHg
and the FiO2 is expressed as a value between 0.21 and 1.00).
BEDSIDE MONITORING
Decreased compliance of lungs and increased Vo/Vt
ratio are common finding in ARDS, which is helpful
in severity assessment. Swan-
Ganz catheter is sometime necessary to measure the pulmonary c
apillary
wedge pressure(PCWP) in patient suspecting cardiac failure.A P
CWP≤18 mmHg will help to exclude the possibility of
cardiac fallure.
DIAGNOSIS
The diagnosis of ARDS should met all the five criteria in follo
wing:
a. Evidence of underline diseases( predisposing
factors) just as mentioned above.
b. Acute onset of tachypnea and respiratory distress.
C. Hypoxemia: Hypoxemia with PaO2,/FiO2, ratio≤200 mmH
g in ARDS and≤300 mmHg in ALI.
d. Bilateral infiltrates on radiography.
e. PCWP< 18 mmHg or without evidence of left
atrial hypertension or congestive heart failure.
DIFFERENTIAL DIAGNOSIS.
Since ARDS is a physiologic and radiographic syndrome rather
than a specific disease, the concept of differentialosis do diagnes
not strictly apply. Carbiogenic or hydrostatic pulmonary edema
must be excluded. Measurement of PCWP may be required in
selected patients with suspected cardiac dysfunctionbut routine
use of the Swan-Ganz catheter in ARDS is discouraged.
TREATMENT
Treatment of ARDS must include identification and specific
treatment of the underlying precipitating and secondary
conditions(e. g, sepsis). Meticulous supportive care must then be
provided to compensate for the severe dysfunction of the
respiratory system associated with ARDS and to prevent
complications.
OXYGEN THERAPY
Ensure adequate oxygenation is important for vital organs.
Oxygen therapy of high inspiratory oxyger concentration with
mask to maintain arterial hemoglobin saturation
of≥90%(PO2≥60mmHg)is ussually the first step of
management in ARDS, although the response to oxygen
therapy is generally poor and majority of the patients need
mechanical ventilation.
MECHANICAL VENTILATION
Treatment of the hypoxemia seen in ARDS usually requires
tracheal intubation and positive-pressure mechanical ventilation
although there have been some reports on the use of
noninvasive positive pressure ventilation in ALI or less severe
ARDS.The indications and criteria for initiating intubation are
not fully established yet.
The main purposes of mechanical ventilation are to improve
oxygenation and maintain adequate ventilation.A variety of
mechanical ventilation strategies are available,but there is no
universal standard for proper selection of ventilation
mode.Current recommendations for mechanical ventilation via
endotracheal intubation emphasize lower tidal volumes based
on a patient's predicted body weight(6-8mL/kg),limitation of
peak inspiratory pressure(30-35 cmH20),proper use of PEEP
and permissive hypercapnia.
PEEP remains a mainstay in the ventilatory strategy for
ARDS,although the method for determining the optimal level of
PEEP has not been convincingly established.PEEP can increase
end expiratory lung volume,maintain open of alveoli,improve
oxygenation and allow a lower FiO2.A“lung
protective"ventilation strategy in which patients underwent
ventilation with levels of PEEP above the lower inflection point
of a respiratory system pressure-volume curve,which was
intended to maintain patency and reduce cyclic opening and
closing of injured alveoli,a process that is thought to be a major
cause of ventilator-induced lung injury.
FLUID MANAGEMENT
Proper fluid management is important in the treatment of
ARDS.The goal of fluid management is to maintain pulmonary
capillary wedge pressure at the lowest level compatible with
adequate cardiac output and hemodynamic
stability.Administering fluids to increase intravascular volume
should be done only with great caution because increases in
pulmonary capillary pressure worsen pulmonary edema in the
presence of increased capillary permeability.
Management of serum total protein and oncotic pressure are
subject to controversy.Some recent studies suggested that
infusion of albumin and diuretics to achieve a proper colloid
pressure and negative fluid balance improve short-term
oxygenation,longer-term hemodynamic stability,and trends
toward reduction in mechanical ventilation days and length of
stay in the ICU,although no benefit in overall mortality was
observed.
GENERAL SUPPORTIE MEASURES
General supportive measures in ARDS include proper
nutritional support,prevention of nosocomial
infection,pulmonary thromboembolism and gastric stress
ulceration as well as careful nursing.
PHARMACOTHERAPIES
A number of pharmaceutical agents have been tried in
management of ARDS,which include systemic
corticosteroids,surfactant replacement therapy,inhaled nitric
oxide,etc.The efficacy and safety of these pharmaceutical
agents demand further investigation.
PROGNOSIS
The mortality rate associated with ARDS is 30%-
40%,depending on the underline diseases and severity.The
major causes of death are the primary illness and secondary
complications such as multiple organ system failure or
sepsis.Most survivors of ARDS are left with some pulmonary
symptoms(cough,dyspnea,sputum production)which tend to
improve over time.
ESTABLISHMENT AND MANAGEMENT OF
ARTIFICIAL AIRWAY
Artificial airway is important in maintaining air-way patency and
ensuring adequate ventilation and oxygenation,which is crucial in
the management of ARDS.
PURPOSES OF ARTIFICIAL AIR-WAY
ESTABLISHMENT
a. Ensure airway patency.b. Manage airway secretion.c. Protect
airway from aspiration.d. Connect ventilator for mechanical
ventilation.
METHODS OF ARTIFICIAL AIR-WAY
ESTABLISHMENT
Artificial airway can be established through oral
intubation,nasal intubation,or tracheotomy,depend on the
clinical situation and expertise of responsible doctor.Some
other airway devices(e.g.,laryngeal mask airway,esophageal
obturator airway,etc.)may be acceptable and useful in acute
emergent situation,although they do not provide the airway
control and protection afforded by an endotracheal tube.
MECHANICAL VENTILATION
Mechanical ventilation supplied through artificial
airway(e.g.,endotracheal intubation or tracheoto-my)is called
invasive mechanical ventilation.Non-invasive ventilation can be
provided by devices that apply intermittent negative
extrathoracic pressure or furnish intermittent positive pressure
through a tight-fitting nasal or face mask without an artificial
airway in place.In the following paragraph,only invasive
mechanical ventilation will be discussed.
INDICATIONS
Indications for invasive mechanical ventilation in-clude cardiac
respiratory arrest and severe respirato-ry failure due to variety of
underline diseases.The following crileria are general guides for
initiating invasive mechanical ventilation,although there are no
universal agreement yet.
a.Acute inerease in PaCO2 to >50 mmHg with a decrease in
pH to<7.30.b.Respiratory rate>35 breaths/min for prolonged
period.c.Tidal volume <5 ml/kg body weight.d.Ratio of
respiratory rate(breaths/min)to tidal volume(L)>105.e.Minute
ventilalion>10 L/min.f.Vital capacity <10 mL/kg body
weighi.g.Maximum inspiratory pressure between O and 20
cmH20.h.Dead space to tidal volume fraction 0.60 or
more.i.Acute hypoxemia(PaO2<60 mmHg or
Sa0,<90%,especially if inspired oxygen fraction is 0.4 or more,or
P(A-a)02>300 mmHg on inspired FiO2 of 1.0).j.Clinical
instability.
CONTRAINDICATION
There is no absolute contraindication for mechanical
ventilation.Obvious pneumothorax and pneumomediastinum
without adequate drainage are relative contraindication.
MODES OF MECHANICAL VENTILATION
As the progress of mechanical ventilation,variety of modes of
mechanical ventilation has been used in clinical practice.Basically
the modes of mechanical ventilation can be classified as controlled
or assisted mechanical ventilation,the former is mainly used in
patients with weak or no respiratory effort and the later is used in
patients with satisfactory level of respiratory effort.The commonly
used modes include volume controlled ventilation(CMV),pressure
controlled ventilation(PCV),synchronized intermittent mandatory
ventilation(SIMV),pressuresupport ventilation(PSV)and
continuous positive airway pressure(CPAP)or positive end-
expiratorypressure(PEEP).
COMPLICATIONS
The complications of mechanical ventilation inchude positive
ventilation induced and artificial airway induced
complications.The commonly encountered complications are
ventilator induced lung injury(VILI),cardiovascular system
compromise,ventilator associated pneumonia and tracheal
injury.
WEANING
Weaning is the process of discontinuing assisted mechanical
ventilation.Mechanical ventilatory support can generally be
discontinued when there is complete or near-complete
resolution of the patient's disease process.This process may be
accomplished by trial of connecting the endotracheal tube to a
piece of tubing(T-piece)with oxygen therapy,synchronized
intermittent mandatory ventilation,or pressure-support
ventilation.
III SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME(SIRS)
SIRS is defined as the systemic inflammatory response to a wide
variety of severe clinical insults,manifested by two or more of
the following conditions:(1) temperature>38 C or <36 C;(2)heart
rate>90 beats/min;(3) respiratory rate>20 breaths/min or
PaCO2<32 mmHg;and (4)WBC count>12,000/mm3
or<4,000/mm3,or>10% immature(band)forms.
SEPSIS
SEPSIS is defined as the systemie inflammatory response to
infection.In association with infection,mainfestations of sepsis
are the same as those previously defined for SIRS.
SEVERE SEPSISSevere sepsis is defined as sepsis associated
with organ dysfunction,hypoperfusion,or hypotension.
SEPTIC SHOCK
Septic shock is a subset of severe sepsis and defined as sepsis-
induced hypotension despite adequate fluid resuscitation along
with the presence of perfusion abnormalities.Patients receiving
inotropic or vasopressor agents may no longer be hypotensive
by the time they manifest hypoperfusion abnormalities or
organ dysfunction,yet they would still be considered to have
septicshock
MULTIPLE ORGAN DYSFUNCTION
SYNDROME(MODS)
MODS is a frequent complication of an exaggerated
proinflammatory state in the setting of sepsis,SIRS,and
ARDS,which is defined as the development of organ system
dysfunction involving two or more organs such that normal
homeostasis cannot be maintained in the setting of a systemic
inflammatory response to a variety of insults.
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24
25
PATHOPHYSIOLOGYPATHOPHYSIOLOGY
26
PathologyPathology
27
hepatic fibrosis and nodular regeneration28
MANIFESTATIONSMANIFESTATIONS
fatigue,fatigue, anorexia,anorexia, weightweight loss,loss, musclemuscle
wasting,wasting, markedmarked ascites,ascites, andand severesevere
hepatichepatic encephalopathy,encephalopathy, withwith mildmild oror
deeplydeeply jaundicejaundice
spiderspider angiomata,angiomata, skinskin telangiectasiastelangiectasias ,,
30
PulmonaryPulmonary andand cardiaccardiac
manifestationsmanifestations
PatientsPatients withwith cirrhosiscirrhosis maymay havehave impairedimpaired
31
qqManifestationManifestation relatedrelated toto
hepatocellularhepatocellular necrosisnecrosis andand chronicchronic
hepatichepatic dysfunctiondysfunction
PPascitesascites ,, jaundicejaundice
PPfatigue,dyspepsiafatigue,dyspepsia ,, palmarpalmar erythemaerythema
PPspiderspider angiomas,angiomas, bleedingbleeding problemsproblems
PPGynecomastiaGynecomastia (men),(men), menstrualmenstrual
irregularitiesirregularities (women)(women)
PPparotidparotid hypertrophyhypertrophy
PPtesticulartesticular atrophyatrophy
32
qqManifestationManifestation ofof portalportal
hypertensionhypertension
PPascitesascites
33
Anatomy of
the portal
venous
system : the
portal vein
is formed by
the union of
the splenic
vein and
superior
mesenteric
veins
34
Endoscopy:Endoscopy:
A:esophageal varices B:gastric varices
35
36
37
38
39
40
CLINICALCLINICAL HistoryHistory
41
42
43
CLINICALCLINICAL HistoryHistory
DeterminingDetermining thethe presencepresence ofof thethe
complicationscomplications ofof
portalportal hypertensionhypertension involvesinvolves thethe
following:following:
–– HematemesisHematemesis oror melenamelena (gastroesophageal(gastroesophageal
–– HematocheziaHematochezia 44
CLINICALCLINICAL PhysicalPhysical
SignsSigns ofof liverliver diseasedisease includeinclude thethe
following:following:
–– AscitesAscites
–– JaundiceJaundice
–– SpiderSpider angiomasangiomas
–– PalmarPalmar erythemaerythema
–– TesticularTesticular atrophyatrophy
–– GynecomastiaGynecomastia
–– MuscleMuscle wastingwasting
–– SplenomegalySplenomegaly
45
Clinical
manifestations
of portal
hypertension
46
Spider angiomas palmar erythema
47
48
Jaundice Spider angiomas
49
gynecomastiagynecomastia
50
dilateddilated abdominalabdominal wallwall andand umbilicalumbilical
veinsveins51
52
53
54
ascitesascites andand umbilicalumbilical herniahernia 55
rupture of an umbilical hernia scrotal edema
56
scrotalscrotal edemaedema
57
58
59
60
61
62
63
64
ComplicationsComplications
67
ComplicationsComplications
BleedingBleeding fromfrom esophagealesophageal
varicesvarices
AsAs aa resultresult ofof thethe increasedincreased flowflow ofof
bloodblood andand
thethe resultingresulting increaseincrease inin pressure,pressure, thethe
veinsveins inin
thethe lowerlower esophagusesophagus andand upperupper stomachstomach
expandexpand andand thenthen areare referredreferred toto asas
esophagealesophageal andand gastricgastric varices;varices; thethe
higherhigher thethe
portalportal pressure,pressure, thethe largerlarger thethe varicesvarices
andand thethe
moremore likelylikely aa patientpatient isis toto bleedbleed fromfrom
thethe
varicesvarices intointo thethe esophagusesophagus oror stomach.stomach.
68
69
ComplicationsComplications BleedingBleeding
BleedingBleeding fromfrom varicesvarices usuallyusually isis
severesevere ,, withoutwithout
immediateimmediate treatment,treatment, cancan bebe fatal.fatal.
SymptomsSymptoms ofof
bleedingbleeding fromfrom varicesvarices includeinclude vomitingvomiting
bloodblood (the(the
vomitusvomitus cancan bebe redred bloodblood mixedmixed withwith
clotsclots oror
"coffee"coffee grounds"grounds" inin appearance,appearance, thethe
latterlatter duedue toto
thethe effecteffect ofof acidacid onon thethe blood),blood),
passingpassing stoolstool
thatthat isis blackblack asas itit passespasses throughthrough thethe
intestineintestine
(melena),(melena), andand orthoortho staticstatic dizzinessdizziness oror
faintingfainting
(caused(caused byby aa dropdrop inin bloodblood pressurepressure
especiallyespecially
whenwhen standingstanding upup fromfrom aa lyinglying position).position).
72
ComplicationsComplications Hepatic encephalopathy
73
ComplicationsComplications Hepatic encephalopathy
WhenWhen thethe toxictoxic substancessubstances accumulateaccumulate
sufficientlysufficiently inin thethe blood,blood, thethe functionfunction
ofof thethe
brainbrain isis impaired,impaired, aa conditioncondition calledcalled
hepatichepatic encephalopathy.encephalopathy.
SleepingSleeping duringduring thethe dayday ratherrather thanthan atat
nightnight ((reversalreversal ofof thethe normalnormal sleepsleep
pattern)pattern)
isis amongamong thethe earliestearliest symptomssymptoms ofof hepatichepatic
encephalopathy.encephalopathy.
SevereSevere hepatichepatic encephalopathyencephalopathy causescauses
comacoma andand death.death.
74
ComplicationsComplications 44 Hepatorenal syndrome
PatientsPatients withwith worseningworsening cirrhosiscirrhosis cancan
developdevelop thethe hepatorenalhepatorenal syndrome.syndrome. ThisThis
syndromesyndrome isis aa seriousserious complicationcomplication inin
whichwhich thethe functionfunction ofof thethe kidneyskidneys isis
reduced.reduced. ItIt isis aa functionalfunctional problemproblem inin
thethe
kidneys,kidneys, thatthat is,is, therethere isis nono physicalphysical
damagedamage toto thethe kidneys.kidneys. Instead,Instead, thethe
reducedreduced functionfunction isis duedue toto changeschanges inin thethe
77
ComplicationsComplications 66 hepatocellular carcinoma
CirrhosisCirrhosis duedue toto anyany causecause increasesincreases thethe
riskrisk ofof
primaryprimary liverliver cancercancer (hepatocellular(hepatocellular
carcinoma).carcinoma).
PrimaryPrimary refersrefers toto thethe factfact thatthat thethe
tumortumor
originatesoriginates inin thethe liver.liver. AA secondarysecondary
liverliver cancercancer isis
oneone thatthat originatesoriginates elsewhereelsewhere inin thethe
bodybody andand
spreadsspreads toto thethe liver.liver.
TheThe mostmost commoncommon symptomssymptoms andand signssigns ofof
primaryprimary liverliver cancercancer areare abdominalabdominal painpain
andand
swelling,swelling, anan enlargedenlarged liver,liver, weightweight
loss,loss, andand
fever.fever. InIn addition,addition, liverliver cancerscancers cancan
produceproduce andand
releaserelease aa numbernumber ofof substances,substances,
includingincluding onesones
thatthat causecause anan increasedincreased inin redred bloodblood
cellcell countcount
((erythrocytosiserythrocytosis),), lowlow bloodblood sugarsugar
((hypoglycemiahypoglycemia),), andand highhigh bloodblood calciumcalcium
(hypercalcemia(hypercalcemia).). 78
79
80
DiagnosisDiagnosis
TheThe singlesingle bestbest testtest forfor diagnosingdiagnosing
cirrhosiscirrhosis isis
biopsybiopsy ofof thethe liverliver.. LiverLiver biopsies,biopsies,
however,however, carrycarry
aa smallsmall riskrisk forfor seriousserious complications,complications,
and,and,
therefore,therefore, biopsybiopsy oftenoften isis reservedreserved forfor
thosethose
patientspatients inin whomwhom thethe diagnosisdiagnosis ofof thethe
typetype ofof
liverliver diseasedisease oror thethe presencepresence ofof
cirrhosiscirrhosis isis notnot
clear.clear.
TheThe possibilitypossibility ofof cirrhosiscirrhosis maymay bebe
suggestedsuggested byby
thethe history,history, physicalphysical examination,examination, oror
routineroutine
testing.testing. IfIf cirrhosiscirrhosis isis present,present, otherother
teststests cancan bebe
usedused toto determinedetermine thethe severityseverity ofof thethe
cirrhosiscirrhosis
andand thethe presencepresence ofof complications.complications.
TestsTests alsoalso maymay bebe usedused toto diagnosediagnose thethe
underlyingunderlying diseasedisease thatthat isis causingcausing thethe
cirrhosis.cirrhosis.
81
DiagnosisDiagnosis
InIn takingtaking aa patient'spatient's history,history, thethe
physicianphysician
maymay uncoveruncover aa historyhistory ofof hepatitishepatitis ,a,a
historyhistory ofof excessiveexcessive andand prolongedprolonged intakeintake
82
DiagnosisDiagnosis
SomeSome patientspatients withwith cirrhosiscirrhosis havehave
enlargedenlarged liverslivers
and/orand/or spleens.spleens. AA doctordoctor cancan oftenoften feelfeel
(palpate)(palpate)
thethe lowerlower edgeedge ofof anan enlargedenlarged liverliver belowbelow
thethe
rightright ribrib cagecage andand feelfeel thethe tiptip ofof thethe
enlargedenlarged
spleenspleen belowbelow thethe leftleft ribrib cage.cage. AA
cirrhoticcirrhotic liverliver
alsoalso feelsfeels firmerfirmer andand moremore irregularirregular thanthan
aa
normalnormal liver.liver.
83
DiagnosisDiagnosis
84
DiagnosisDiagnosis
Esophagea
l and
gastric
varices with
correspond
ing
endoscopic
views.
85
DiagnosisDiagnosis
86
87
88
DiagnosisDiagnosis
AdvancedAdvanced cirrhosiscirrhosis leadsleads toto aa reducedreduced
levellevel ofof albuminalbumin inin thethe bloodblood andand reducedreduced
90
LabLab StudiesStudies
LabLab studiesstudies areare directeddirected towardstowards
investigatinginvestigating
etiologiesetiologies ofof cirrhosis,cirrhosis, whichwhich isis thethe
mostmost commoncommon
causecause ofof portalportal hypertension.hypertension. LabLab studiesstudies
includeinclude
thethe following:following:
– Liver function tests
– Prothrombin time
– Albumin
– Viral hepatitis serologies
– Platelet count
– Antinuclear antibody, anti-mitochondrial antibody
– Iron index
– Ceruloplasmin, 24-hour urinary copper - To be
considered only in individuals aged 3-40 years who
have unexplained hepatic, neurologic, or psychiatric
disease 91
ImagingImaging StudiesStudies
Duplex-DopplerDuplex-Doppler ultrasonographyultrasonography
–– UltrasoundUltrasound (US)(US) isis aa safe,safe, economical,economical,
andand effectiveeffective
methodmethod forfor screeningscreening forfor portalportal
hypertension.hypertension. ItIt alsoalso
cancan demonstratedemonstrate portalportal flowflow andand helpshelps inin
diagnosingdiagnosing
cavernouscavernous transformationtransformation ofof thethe portalportal
vein,vein, portalportal
veinvein thrombosisthrombosis,, oror splenicsplenic veinvein
thrombosis.thrombosis.
–– FeaturesFeatures suggestivesuggestive ofof hepatichepatic cirrhosiscirrhosis
withwith portalportal
hypertensionhypertension includeinclude thethe following:following:
–– NodularNodular liverliver surfacesurface isis suggestive.suggestive.
However,However, thisthis
findingfinding isis notnot specificspecific forfor cirrhosiscirrhosis
andand cancan bebe
observedobserved withwith congenitalcongenital hepatichepatic
fibrosisfibrosis andand
nodularnodular regenerativeregenerative hyperplasia.hyperplasia.
Splenomegaly is a suggestive finding.
Patients may demonstrate the presence of collateral
circulation. 92
ImagingImaging StudieStudie CTCT scanscan
CTCT scanscan isis aa usefuluseful qualitativequalitative studystudy
inin
casescases wherewhere sonographicsonographic evaluationsevaluations areare
inconclusive.inconclusive.
–– CTCT scanscan isis notnot affectedaffected byby patients'patients'
bodybody
habitushabitus oror thethe presencepresence ofof bowelbowel gas.gas.
–– WithWith improvementimprovement ofof spiralspiral CTCT scanscan andand 3-
3-
dimensionaldimensional angiographicangiographic reconstructivereconstructive
techniques,techniques, portalportal vasculaturevasculature maymay bebe
visualizedvisualized moremore accurately.accurately.
–– FindingsFindings suggestivesuggestive ofof portalportal
hypertensionhypertension
includeinclude thethe following:following:
–– CollateralsCollaterals arisingarising fromfrom thethe portalportal
systemsystem areare
suggestivesuggestive ofof portalportal hypertension.hypertension. 93
ImagingImaging StudiesStudies
94
ImagingImaging StudiesStudies
Liver-spleenLiver-spleen scanscan
–– ThisThis isis describeddescribed forfor historicalhistorical
interestinterest only.only.
95
ProceduresProcedures
EndoscopyEndoscopy
–– PerformPerform upperupper endoscopy,endoscopy, asas appropriate,appropriate,
toto
screenscreen forfor varicesvarices inin everyevery patientpatient withwith
suggestivesuggestive findingsfindings ofof portalportal
hypertension.hypertension.
Additionally,Additionally, allall patientspatients withwith cirrhosiscirrhosis
shouldshould
bebe consideredconsidered forfor thethe presencepresence ofof varicesvarices
atat
thethe timetime ofof thethe initialinitial diagnosisdiagnosis ofof
cirrhosis.cirrhosis.
96
GastroesophagealGastroesophageal varicesvarices confirmconfirm thethe
diagnosisdiagnosis ofof portalportal hypertension;hypertension;
however,however,
theirtheir absenceabsence doesdoes notnot rulerule itit out.out. AtAt
times,times,
gastroesophagealgastroesophageal varicesvarices areare incidentalincidental
findingsfindings inin patientspatients undergoingundergoing upperupper
endoscopyendoscopy forfor otherother reasonsreasons (eg,(eg,
dyspepsiadyspepsia refractoryrefractory toto medications,medications,
dysphagia,dysphagia, weightweight loss).loss). TheseThese patientspatients
shouldshould undergoundergo furtherfurther investigationsinvestigations forfor
97
ProceduresProcedures
–– VariousVarious indirectindirect indices(index),indices(index), suchsuch asas
plateletplatelet
count,count, spleenspleen size,size, albumin,albumin, andand Child-PughChild-
Pugh
score,score, havehave beenbeen studiedstudied toto helphelp diagnosediagnose
TricuspidTricuspid RegurgitationRegurgitation
TuberculosisTuberculosis
MyeloproliferativeMyeloproliferative DiseaseDisease
Pericarditis,Pericarditis, ConstrictiveConstrictive
99
TREATMENTTREATMENT
earlyearly
4)4) liverliver transplantation.transplantation.
100
TREATMENTTREATMENT
::
-Consume-Consume aa balancedbalanced dietdiet andand oneone
multivitaminmultivitamin daily.daily. PatientsPatients withwith
impairedimpaired
absorptionabsorption ofof fatfat solublesoluble vitaminsvitamins maymay
needneed additionaladditional vitaminsvitamins DD andand K.K.
-Avoid-Avoid drugsdrugs (including(including alcohol)alcohol) thatthat
causecause
liverliver damage.damage.
101
TREATMENTTREATMENT NutritionNutrition
ManyMany patientspatients gotgot anorexia,anorexia, whichwhich maymay bebe
compoundedcompounded byby thethe directdirect compressioncompression ofof
ascitesascites onon thethe GIGI tract.tract. CareCare shouldshould bebe
takentaken toto
ensureensure thatthat patientspatients receivereceive adequateadequate
caloriescalories
andand proteinprotein inin theirtheir diets.diets. PatientsPatients
frequentlyfrequently
benefitbenefit fromfrom thethe additionaddition ofof commonlycommonly
availableavailable
liquidliquid andand powderedpowdered nutritionalnutritional
supplementssupplements toto
thethe diet.diet.
OnlyOnly rarelyrarely cancan patientspatients notnot toleratetolerate
proteinsproteins inin
thethe formform ofof chicken,chicken, fish,fish, vegetables,vegetables,
andand
nutritionalnutritional supplements.supplements. InstitutionInstitution ofof aa
low-low-
proteinprotein dietdiet inin thethe fearfear thatthat hepatichepatic
encephalopathyencephalopathy mightmight developdevelop placesplaces thethe
patientpatient
atat riskrisk forfor thethe developmentdevelopment ofof profoundprofound
musclemuscle
wasting.wasting. 102
DosesDoses ofof manymany drugsdrugs thatthat normallynormally areare
detoxifieddetoxified byby thethe liverliver havehave toto bebe
reducedreduced
toto avoidavoid aa toxictoxic buildupbuildup inin cirrhosis,cirrhosis,
particularlyparticularly sedativessedatives andand drugsdrugs thatthat areare
103
DrugDrug hepatotoxicityhepatotoxicity inin thethe patientpatient
withwith cirrhosiscirrhosis
TheThe institutioninstitution ofof anyany newnew medicalmedical
therapytherapy
warrantswarrants thethe performanceperformance ofof moremore frequentfrequent
106
TreatingTreating thethe complicationscomplications ofof cirrhosis:cirrhosis:
110
2)2) varicealvariceal bleedingbleeding
EndoscopicEndoscopic
therapytherapy
111
2)2) varicealvariceal bleedingbleeding
EndoscopicEndoscopic
therapytherapy
EndoscopicEndoscopic varicealvariceal ligationligation (EVL)(EVL) isis
achievedachieved byby aa bandingbanding devicedevice attachedattached toto
thethe tiptip ofof thethe endoscope.endoscope. TheThe varixvarix isis
aspiratedaspirated intointo thethe bandingbanding chamber,chamber, andand aa
triptrip wirewire dislodgesdislodges aa rubberrubber bandband carriedcarried
liverliver transplantation.transplantation.
DecompressiveDecompressive shunts:shunts: TheseThese includeinclude
totaltotal
portalportal systemicsystemic shunts,shunts, partialpartial portalportal
systemicsystemic shunts,shunts, andand otherother selectiveselective
shunts.shunts.
DevascularizationDevascularization procedures:procedures: TheseThese
includeinclude splensplen ectomyectomy,, gastroesophagealgastroesophageal
devascularization,devascularization, andand esophagealesophageal
transectiontransection .. 113
2)2) varicealvariceal bleedingbleeding TIPSTIPS
114
TreatingTreating thethe complicationscomplications ofof cirrhosis:cirrhosis:
3)3) SBPSBP
Most patients with spontaneous bacterial peritonitis are
hospitalized and treated with intravenous antibiotics such
as ampicillin, and one of the newer generation
cephalosporin. Patients usually treated with antibiotics
include:
Patients with blood, urine, and/or ascites fluid cultures
that contain bacteria.
Patients without bacteria in their blood, urine, and ascitic
fluid but who have elevated numbers of white blood cells.
Elevated neutrophil numbers in ascitic fluid often means
that there is bacterial infection. Doctors believe that the
lack of bacteria with culturing in some patients with
increased neutrophils is due either to a very small
number of bacteria or ineffective culturing techniques.
115
TreatingTreating thethe complicationscomplications ofof cirrhosis:cirrhosis:
3)3) SBPSBP
PatientsPatients withwith cirrhosiscirrhosis whowho areare
hospitalizedhospitalized forfor
bleedingbleeding varicesvarices havehave aa highhigh riskrisk ofof
developingdeveloping
spontaneousspontaneous bacterialbacterial peritonitisperitonitis andand
shouldshould bebe
startedstarted onon antibioticsantibiotics earlyearly duringduring thethe
hospitalizationhospitalization toto preventprevent spontaneousspontaneous
bacterialbacterial
peritonitisperitonitis
116
SurgicalSurgical CareCare
33、、LiverLiver transplantationtransplantation
CirrhosisCirrhosis isis irreversibleirreversible.. ManyMany
patients'patients'
liverliver functionfunction willwill graduallygradually worsenworsen
despitedespite
treatmenttreatment andand complicationscomplications ofof cirrhosiscirrhosis
willwill increaseincrease andand becomebecome difficultdifficult toto
treat.treat.
Therefore,Therefore, whenwhen cirrhosiscirrhosis isis farfar
advanced,advanced,
liverliver transplantationtransplantation oftenoften isis thethe onlyonly
optionoption
forfor treatment.treatment.
117
MonitoringMonitoring thethe patientpatient withwith cirrhosiscirrhosis
118
MonitoringMonitoring thethe patientpatient withwith cirrhosiscirrhosis
119
MonitoringMonitoring thethe patientpatient withwith cirrhosiscirrhosis
120
MonitoringMonitoring thethe patientpatient withwith cirrhosiscirrhosis
chestchest andand abdominalabdominal CTCT scansscans andand byby
bonebone scanscan
PreventionPrevention andand earlyearly detectiondetection ofof liverliver
cancercancer::mostmost patientspatients withwith cirrhosis,cirrhosis,
particularlyparticularly hepatitishepatitis BB andand C,C, areare
screenedscreened yearlyyearly oror everyevery sixsix monthsmonths withwith
ultrasoundultrasound examinationexamination ofof thethe liverliver andand
measurementsmeasurements ofof cancer-producedcancer-produced
proteinsproteins inin thethe blood,blood, e.g.e.g.
alphafetoproteinalphafetoprotein
(AFP(AFP levellevel ofof greatergreater thanthan 400400 ng/mLng/mL isis
believedbelieved toto havehave thethe samesame diagnosticdiagnostic
powerpower toto
122
reviewreview
11、、WhatWhat areare thethe symptomssymptoms andand signssigns ofof
cirrhosis?cirrhosis?
22、、WhatWhat areare thethe complicationscomplications ofof cirrhosis?
cirrhosis?
33、、WhatWhat areare thethe commoncommon causescauses ofof cirrhosis?
cirrhosis?
(Chronic viral hepatitis ,Alcohol Autoimmune
hepatitis, Primary biliary cirrhosis , drugs ,
Nonalcoholic fatty liver disease (NAFLD) , chronic
heart failure )
44、、CommonCommon clinicalclinical manifestationsmanifestations ofof
portalportal
hypertensionhypertension
55、、HowHow isis cirrhosiscirrhosis diagnoseddiagnosed andand evaluated?
evaluated?
123
THANKTHANK YOUYOU
124
Respiratory Failure
Professor Xu sicheng
contents
keys:
difinition
causes
classification
acute respiratory failure
chronic repiratory failure
understanding:
pathophysiology
Respiratory Failure
Arterial blood gas criteria for respiratory failure are a PO2, under
60 mmHg and/or a PCO2, over 50mmHg under the condition of room
air breathing during rest at sea level of altitude and exclusion of the
arterial blood gas abnormality due to cardiac shunt or low cardiac
output etc.
CAUSES
PATHOGENESIS
CLASSIFICATION BASED ON ARTERIAL BLOOD GAS
Hypoxemic(Type I) Respiratory Failure
• The characteristics of hypoxemic respiratory failure is PaO2<60 mmHg with
reduced or normal PaCO2,. Hypoxemic respiratory failure is usually associated with
Hypoventilation
Diffusion Abnormality
Ventilation/Perfusion(V/Q)Mismatch
Shunt
•
Hypoventilation
PaCO2=(K x VCO2)/Va
MECHANISMS OF HYPOXEMIA AND HYPERCAPNIA
Hypoventilation
Diffusion Abnormality
Ventilation/Perfusion(V/Q)Mismatch
Shunt
•
Diffusion Abnormality
Diffusion abnormalities refer to the abnormality of gas exchange
between the alveoli and pulmonary capillary.
The diffusion capacity is determined by the partial pressure of
gas,diffusion coefficient and the characteristics of alveolar
membrane(area,thickness and permeability).
As the diffusion coefficient of oxygen is only one twentieth of
that of carbon dioxide,disease leading to abnormal diffusion,such as
acute respiratory distress syndrome,results in mainly hypoxemia rather
than hypercapnia.
MECHANISMS OF HYPOXEMIA AND HYPERCAPNIA
Hypoventilation
Diffusion Abnormality
Ventilation/Perfusion(V/Q)Mismatch
Shunt
•
Ventilation/Perfusion(V/Q)Mismatch
During ideal gas exchange,ventilation and blood flow match
each other perfectly with V/Q ratio of 0.8.V/Q mismatch is the most
common cause of hypoxemia.
(1)Low V/Q ratio: The low V/Qratio may occureither from a decrease in ventilation
secondary
toairway or interstitial lung disease(such as in pneumonia or atelectasis)or from
overperfusion in
thepresence of normal ventilation,Low V/Q ratio is also named as functional
shunt,as it results in
inadequately oxygenated blood returning to systemic circulation and hypoxemia.
(2)High V/Q ratio: HighV/Q ratio usually occurs when local blood decreases,which
wastes
ventilation and results in deadspace effect(also named as physiological
deadspace).So,high V/Q
ratio augments ventilatorydemand and work of breathing.
MECHANISMS OF HYPOXEMIA AND HYPERCAPNIA
Hypoventilation
Diffusion Abnormality
Ventilation/Perfusion(V/Q)Mismatch
Shunt
•
Shunt
Shunt is defined as deoxygenated blood(mixed venous blood) by
passes the ventilated alveoli and mixes with oxygenated blood that has
flowed through the ventilated alveoli, consequently leading to a reduction in
arterial blood content.
Shunt can be distinguished from V/Q mismatch by the persistence of
hypoxemia despite 100% oxygen inhalation.
Anatomical shunt exists in normal lungs because of the direct return
of bronchial circulations to pulmonary vein, accounting for 2%-3% of shunt.
Increased shunt as a cause of hypoxemia is observed primarily in
pneumonia, atelectasis and severe pulmonary edema of either cardiac or
noncardiac origin.
SYSTEMIC EFFECTS OF HYPOXEMIA AND HYPERCAPNIA
CAUSES
As mentioned above,acute respiratory failure may occur in a variety of severe
pulmonary and nonpulmonary disorders involving the chain of breathing ac
tivities,leading to acute development of hypoxemia and/or hypercapnia.
CLINICAL FINDINGS
Symptoms and signs of acute respiratory failure are those of the underlying
disease combined
with those of hypoxemia or hypercapnia.
1.DYSPNEA
Dyspnea is the early and most common symptom of acute respiratory
failure.Signs associated
with dyspnea include tachypnea and activation of accessory respiratory
muscles.However,signs
of dyspnea can be complete absent in acute respiratory failure due to suppression
of central
nervous system,such as overuse of sedative medication.
2.CYANOSIS
Cyanosis is the typical presentation of hypoxia.It develops when oxygen
saturation drops
below 90%.However,cyanosis is affected by other factors,such as content of
hemoglobin in
blood,peripheral perfusion,cardiac output,etc.
3.PSYCHIATRIC AND NEURAL SYMPTOMS
These include headache,restlessness,anxiety,asterixis,impaired
consciousness,confusion and
delirium,Coma can occur in severe hypoxemia and hypercapnia.
4.CIRCULATORY PRESENTATION
Tachycardia is common.Peripheral and conjunctival hyperemia is often associated
with
hypercapnia.Severe hypoxemia and acidosis can result in myocardial
injury,hypertension,cardiac
dysrhythmias,bradycardia and cardiac arrest.
5.PRESENTATIONS OF DIGESTIVE AND URINARY SYSTEMS
Severe acute respiratory failure can result in multiple organs dysfunction.The
common
presentation of digestive system includes dyspepsia and elevated hepatic
enzymies.Upper
digestive track bleeding can occur in severe cases.The presentations of urinary
system include
decreased urine discharge,abnormal urine test and elevated BUN.
DIAGNOSIS
The principles of treatment of the patient with acute respiratory failure consist
of:
① Inspired O2 Concentration(FiO2)
Inspired oxygen concentration should be the lowest value that results in an
arterial hemoglobin
receiving O2.The level of O2 can be adjusted by the flow rate to the nasal
prongs.The drawback of
nasal cannula is the limitation in providing higher FiO2.At flows of greater than 6
L/min,only a small
further augmentation in FiO2 can be achieved with maximal FiO2 of approximately
0.50.
B.Masks
Masks for oxygen therapy include nonrebreathing mask,Venturi mask and
nonrebreathing mask with
O2 reservoir.Oxygen therapy with mask can deliver 50% to 100% 02 depend on the type
of the mask.
Venturi Oxygen facemask has the advantages of able to regulate FiO 2.The drawback
of mask is
interfering cough and eating.
(3)AUGMENTATION OF VENTILATION
① Respiratory Stimulants
The overall usefulness of respiratory stimulants in management of
respiratory failure is
limited. The principle of administering respiratory stimulants is under the
condition of adequate
airway patency. Respiratory stimulant might be effective in hypoventilation due to
suppression
of central nervous system, but no effect in hypoxemic respiratory failure due to
abnormal gas
exchange in the lungs, such as pneumonia and pulmonary fibrosis. The commonly used
medications are nikethamide and lobeline, although the effectiveness is limited.
Doxapram is
new generation of respiratory stimulant, which is more effective than the old one.
② Mechanical Ventilation
Noninvasive mechanical ventilation may also be provided via a full face mask,
nasal mask,
nasal pillow or mouthpiece etc. It has become first-line therapy in COPD patients
with
hypercapnic respiratory failure who can protect and maintain the patency of their
airway, handle
their own secretions, and tolerate the mask apparatus.
CAUSES
Most of the causes of respiratory failure(as mentioned above) can lead to
chronic respiratory failure. In general, chronic respiratory failure results
usually
from chronic bronchial and pulmonary diseases, such as COPD, severe
tuberculosis, interstitial pulmonary fibrosis, pneumoconiosis, etc. Other severe
chronic thoraxic and neuromuscular disorders can also result in chronic respiratory
failure.
CLINICAL PRESENTATIONS
In general, the symptoms and signs of chronic respiratory failure are similar
lo
acute respiratory failure. However, there are also some differences in clinical
characteristics in the following aspects.
① DYSPNEA
Dyspnea may exist long before the occurrence of chronic respiratory failure. A
typical
presentation of mild chronic respiratory failure resulting from COPD is strenuous
breathing with
expiratory prolongation. As the severity of chronic respiratory failure progresses,
rapid shallow
breathing develops. Bradypnoea and Cheyne-Stokes respiration are life-threatening
presentation, usually as the result of rapid progress or severe hypercaprua.
②PSYCHIATRIC AND NEURAL SYMPTONS
As hypercapnia progresses from mild to severe, the presentations turn from
excitatory to
inhibitory symptoms. The excitatory symptoms include insomnia, agitation,
restlessness, sleepy
at daytime with insomnia at nighttime, etc. It is contraindicated to use sedative
medication in
this situation as it will lead to inhibition and deterioration of hypercapnia. In
severe hypercapnia,
pulmonary narcosis may occur, presenting as impaired consciousness, confusion,
delirium,
flapping tremor and coma. Abnormal central neural reflex can occur occasionally. A
differential
diagnosis from disorders of central neural system is necessary.
③CIRCULATORY PRESENTATION
Chronic hypercapnia can lead to dilatation of veins, with manifestation of
dilatation of
peripheral veins, hyperemia of skin, diaphoresis, hypertension and increased
cardiac output.
Tachycardia is common. Pulse headache can occur as the result of dilatation of
intracranial veins.
DIAGNOSIS
failure, it is common to have arterial blood gas results of PaO2>60 mmHg and
PaCO2>50 mmHg in patients after oxygen therapy.
TREATMENT
The principles of treatment of chronic respiratory failure are similar to
those of acute respiratory
failure.
Oxygen therapy for chronic respiratory failure is usually administered low
oxygen flow(1 to 3