Critical Care Nursing of The Oncology Patient 1St Edition Lisa Parks Online Ebook Texxtbook Full Chapter PDF
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CRITICAL CARE NURSING
OF THE ONCOLOGY PATIENT
Edited by
Meghan Routt, MSN, ANP/GNP-BC, AOCNP®
Lisa Parks, MS, ANP-BC
Copyright © 2018 by the Oncology Nursing Society. All rights reserved. No part of the material protected
by this copyright may be reproduced or utilized in any form, electronic or mechanical, including
photocopying, recording, or by an information storage and retrieval system, without written permission
from the copyright owner. For information, visit www.ons.org/sites/default/files/Publication%20
Permissions.pdf, or send an email to [email protected].
Publisher’s Note
This book is published by the Oncology Nursing Society (ONS). ONS neither represents nor
guarantees that the practices described herein will, if followed, ensure safe and effective patient care. The
recommendations contained in this book reflect ONS’s judgment regarding the state of general knowledge
and practice in the field as of the date of publication. The recommendations may not be appropriate
for use in all circumstances. Those who use this book should make their own determinations regarding
specific safe and appropriate patient care practices, taking into account the personnel, equipment, and
practices available at the hospital or other facility at which they are located. The editors and publisher
cannot be held responsible for any liability incurred as a consequence from the use or application of
any of the contents of this book. Figures and tables are used as examples only. They are not meant to
be all-inclusive, nor do they represent endorsement of any particular institution by ONS. Mention of
specific products and opinions related to those products do not indicate or imply endorsement by ONS.
Websites mentioned are provided for information only; the hosts are responsible for their own content
and availability. Unless otherwise indicated, dollar amounts reflect U.S. dollars.
ONS publications are originally published in English. Publishers wishing to translate ONS
publications must contact ONS about licensing arrangements. ONS publications cannot be translated
without obtaining written permission from ONS. (Individual tables and figures that are reprinted or
adapted require additional permission from the original source.) Because translations from English may
not always be accurate or precise, ONS disclaims any responsibility for inaccuracies in words or meaning
that may occur as a result of the translation. Readers relying on precise information should check the
original English version.
Editors
Authors
iii
iv CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
Cynthia Chernecky, PhD, RN, AOCN®, Catherine Hydzik, MS, CNS, AOCN®
FAAN Clinical Nurse Specialist
Professor Memorial Sloan Kettering Cancer Center
Augusta University New York, New York
Augusta, Georgia Chapter 5. Gynecologic Cancers
Chapter 18. Vascular Access
Patricia Jakel, RN, MN, AOCN®
Yelena Drexler, MD Advanced Practice Nurse—Solid Tumor
Assistant Professor of Medicine University of Los Angeles Health
Montefiore Medical Center/Albert Einstein Santa Monica Medical Center
College of Medicine Santa Monica, California
Bronx, New York Chapter 22. Ethics Concepts, Complexities,
Chapter 8. Renal Failure and Obstructive and Controversies
Uropathy
Donald D. Kautz, RN, PhD, CRRN, ACNS-
Brenda Freymiller, BSN, MBA, RN, CWON, BC
CWS Associate Professor Emeritus
Wound and Skin Director University of North Carolina Greensboro
Intermountain Healthcare School of Nursing
Salt Lake City, Utah Greensboro, North Carolina
Chapter 16. Wounds and Critical Care Chapter 15. Early Mobility in the Intensive
Care Unit
Anthony T. Gerlach, PharmD, BCPS, FCCP,
FCCM Lisa Koser, DNP, RN, ACNP-BC, CPNP-AC
Specialty Practice Pharmacist, Surgical Acute Care Nurse Practitioner, Trauma,
Critical Care Critical Care and Burn
Department of Pharmacy The James Cancer Hospital
The Ohio State University Wexner Medical The Ohio State University Wexner Medical
Center Center
Clinical Associate Professor Columbus, Ohio
The Ohio State University College of Chapter 11. Respiratory Failure
Pharmacy
Columbus, Ohio Neelja Kumar, MD
Chapter 17. Pharmacology Assistant Professor of Medicine
Montefiore Medical Center/Albert Einstein
Ladan Golestaneh, MD, MS College of Medicine
Associate Professor of Medicine Bronx, New York
Montefiore Medical Center/Albert Einstein Chapter 8. Renal Failure and Obstructive
College of Medicine Uropathy
Bronx, New York
Chapter 8. Renal Failure and Obstructive Denise Macklin, BSN, RN, VA-BC
Uropathy Consultant
Satellite Beach, Florida
Aimee S. Hoskins, BSN, RN Chapter 18. Vascular Access
Research Nurse Specialist III, Delirium and
Cognitive Impairment Study Group Ainsley Malone, MS, RD, LD, CNSC, FAND,
Vanderbilt University Medical Center FASPEN
Nashville, Tennessee Nutrition Support Dietitian
Chapter 13. Delirium Mt. Carmel West Hospital
Columbus, Ohio
Christine Hull, RN, MSN, OCN® Chapter 14. Nutritional Support
Registered Nurse
Inova Loudoun Hospital
Leesburg, Virginia
Chapter 19. Transitions in Care
Contributors v
DaiWai M. Olson, PhD, RN, CCRN, FNCS Laetitia Simeral, RN, MSN, CRNP
Associate Professor Nurse Practitioner
Neurology and Neurotherapeutics, Neuro- Abramson Cancer Center at Pennsylvania
logical Surgery Hospital
University of Texas Southwestern Medical Philadelphia, Pennsylvania
Center Chapter 7. Bone and Soft Tissue Sarcomas
Dallas, Texas
Chapter 1. Brain Cancer and Neurocritical William H. Tettelbach, MD, FACP, FIDSA,
Care FUHM, CWS
Medical Director
Carol Pavlish, PhD, RN, FAAN Intermountain Healthcare
Associate Professor Salt Lake City, Utah
University of California, Los Angeles School Program Director, Hyperbaric Medicine
of Nursing Fellowship
Los Angeles, California Adjunct Assistant Professor, Duke University
Professor Emerita, St. Catherine University School of Medicine
St. Paul, Minnesota Durham, North Carolina
Chapter 22. Ethics Concepts, Complexities, Chapter 16. Wounds and Critical Care
and Controversies
Yolanda Michelle VanRiel, PhD, RN-BC,
Karen M. Perialis, MSN, RN, ANP-BC, OCN® OCN®, CNE, ANEF
Adult Nurse Practitioner Associate Professor of Nursing
Memorial Sloan Kettering Cancer Center MSN Nursing Education Concentration
New York, New York Program Coordinator
Chapter 5. Gynecologic Cancers University of North Carolina Greensboro
School of Nursing
Alex A. Rollo, BS Greensboro, North Carolina
Medical Student Chapter 15. Early Mobility in the Intensive
University of Texas Southwestern Medical Care Unit
Center
Dallas, Texas Anna Vioral, PhD, MEd, RN, OCN®,
Chapter 1. Brain Cancer and Neurocritical BMTCN®
Care Director, Oncology Education and Research
Allegheny Health Network
Catherine Sargent, MS, RN, BC, AOCNS® Pittsburgh, Pennsylvania
Infusion Unit Supervisor Chapter 12. Sepsis
Mercy Fitzgerald Hospital
Darby, Pennsylvania
Chapter 9. Cardiovascular Complications
Brenda K. Shelton, DNP, APRN-CNS, RN,
CCRN, AOCN®
Clinical Nurse Specialist
Sidney Kimmel Comprehensive Cancer
Center at Johns Hopkins Hospital
Affiliate Faculty, Johns Hopkins University
School of Nursing
Baltimore, Maryland
Chapter 3. Hematologic Malignancies;
Chapter 9. Cardiovascular Complications
vi CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
Disclosure
Editors and authors of books and guidelines provided by the Oncology Nursing Society
are expected to disclose to the readers any significant financial interest or other relationships
with the manufacturer(s) of any commercial products.
A vested interest may be considered to exist if a contributor is affiliated with or has a finan-
cial interest in commercial organizations that may have a direct or indirect interest in the sub-
ject matter. A “financial interest” may include, but is not limited to, being a shareholder in
the organization; being an employee of the commercial organization; serving on an organiza-
tion’s speakers bureau; or receiving research funding from the organization. An “affiliation”
may be holding a position on an advisory board or some other role of benefit to the commer-
cial organization. Vested interest statements appear in the front matter for each publication.
Contributors are expected to disclose any unlabeled or investigational use of products
discussed in their content. This information is acknowledged solely for the information of the
readers.
The contributors provided the following disclosure and vested interest information:
Leanne M. Boehm, PhD, RN, ACNS-BC: American Association of Critical-Care Nurses, research
funding; Sigma Theta Tau International Iota Chapter, employment or leadership position
Anthony T. Gerlach, PharmD, BCPS, FCCP, FCCM: Merck Research Laboratories, research fund-
ing; Society of Critical Care Medicine Council, employment or leadership position
Ladan Golestaneh, MD, MS: AbbVie Inc., research funding; Relypsa, Inc., consultant or advi-
sory role
Patricia Jakel, RN, MN, AOCN®: Genentech, Inc., consultant or advisory role
Ainsley Malone, MS, RD, LD, CNSC, FAND, FASPEN: Academy of Nutrition and Dietetics Posi-
tions Committee, American Society for Parenteral and Enteral Nutrition, employment or
leadership position
DaiWai M. Olson, PhD, RN, CCRN, FNCS: Journal of Neuroscience Nursing, Neuroscience Nursing
Research Center, employment or leadership position; NeurOptics, Inc., research funding
Carol Pavlish, PhD, RN, FAAN: American Association of Critical-Care Nurses, research funding
Karen M. Perialis, MSN, RN, ANP-BC, OCN®: Memorial Sloan Kettering Cancer Center, research
funding
William H. Tettelbach, MD, FACP, FIDSA, FUHM, CWS: MiMedx Group, research funding
Anna Vioral, PhD, MEd, RN, OCN®, BMTCN®: American Society of Clinical Oncology, employ-
ment or leadership position, consultant or advisory role; Celgene Corporation, honoraria
Contents
Preface.............................................................................................................................. xiii
vii
viii CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
Cholangiocarcinoma...................................................................................................................... 109
Cholangitis...................................................................................................................................... 109
Pancreatic Cancer........................................................................................................................... 111
Summary........................................................................................................................................ 113
References...................................................................................................................................... 113
Summary........................................................................................................................................ 265
References...................................................................................................................................... 265
Chapter 21. The Older Adult With Cancer in the Intensive Care Unit.................................. 433
Introduction ................................................................................................................................... 433
Physiology ...................................................................................................................................... 433
Polypharmacy ................................................................................................................................ 438
Frailty .............................................................................................................................................. 439
Older Adult Failure to Thrive ......................................................................................................... 440
Summary ........................................................................................................................................ 440
References ...................................................................................................................................... 441
Index................................................................................................................................ 467
Preface
The care of patients with cancer has evolved over the past 10 years. Patients
who are in intensive care units today would not have been alive a decade ago;
patients on medical-surgical floors in the present would have been in intensive care
units in the past; and patients discharged home today would still be in the hospi-
tal in yesteryears. In this ever-changing environment, it is important that nurses
understand the entire continuum of cancer care. The idea that a cancer diagno-
sis is incompatible with aggressive treatment is outdated; therefore, many more
patients with cancer are requiring care in a an intensive care unit after treatment.
Traditionally, oncology nurses and critical care nurses have viewed patients
through their own respective lenses, which are not always compatible and cer-
tainly require different competencies in providing patient care. The most optimal
strategy in caring for critically ill patients with cancer is leveraging the strengths
of both specialties as well as working collaboratively throughout the transition
from the medical-surgical floor to the intensive care unit and back to the medical-
surgical floor. Many cancer centers are developing oncology-specific intensive care
units. Nurses staffing these new units may be oncology nurses with little critical
care training or critical care nurses with little oncology training. It is our hope
that this book will serve as a reference for nurses working in these settings and
empower them to consider themselves as both oncology nurses and critical care
nurses. As more complex cases of patients with cancer transition from the inten-
sive care setting to the progressive care unit or medical-surgical floor, this text will
become a valuable reference for nurses who care for these patients. Understanding
previous nursing treatments and the complications of the critically ill will enable
nurses to better create a nursing care plan. As editors, we hope that our readers
will find this text helpful.
Meghan M. Routt
Lisa S. Parks
xiii
CHAPTER 1
Introduction
Symptom Monitoring
eyelid droop). These signs and symptoms can be early indicators of brain complica-
tions. Identification of any sign of brain dysfunction triggers the need for diagnostic
testing, which can result in early detection of brain metastasis or the worsening of
treatment side effects. Prompt treatment based on test results can prevent the occur-
rence of irrevocable secondary brain damage (Bader, Littlejohns, & Olson, 2016).
Tumor localization within the brain dictates the likely symptoms and monitor-
ing. For example, a tumor located in or near the ventricles might occlude the flow
of cerebrospinal fluid (CSF), requiring methods of measuring intracranial pres-
sure (ICP) or possibly the insertion of an external ventricular drain (EVD) to alle-
viate the increased pressure (see Figure 1-1) (Olson et al., 2015). It is important
to distinguish between primary neoplasms of the central nervous system (CNS)
and brain metastases encountered in late-stage cancer of other organs. The type
of lesion will affect treatment options. The differentiation of brain tumor etiology
and treatment plans involves several different diagnostic methodologies.
Diagnosis
The diagnostic process typically begins with the patient’s primary complaint,
which may be the patient’s description of symptoms or a description of the patient’s
presenting condition (neurologic examination) by a family member or another practi-
tioner (e.g., nurse, referring physician). Initial symptoms may be noticed at home, dur-
ing an office visit, or in the emergency department. If the patient’s chief complaint and
presenting symptoms are consistent with neurologic dysfunction, diagnostic imaging
is typically ordered. The choice procedure for neurologic assessment is magnetic res-
onance imaging (MRI) because of its high anatomic definition of normal neurologic
structures and absence of any radiation. Computed tomography (CT) scans are often
ordered to rule out acute hemorrhage (see Figure 1-2).
The presence of abnormalities can be accurately detected and localized when
using diagnostic imaging. The pathologic significance of these findings (malig-
nant vs. benign) can be characterized using the various imaging techniques avail-
able with an MRI. When a more definitive diagnosis is required (tissue diagnosis
for tumor type), a biopsy of the lesion may be performed using a CT scan or MRI
to guide the biopsy needle directly into the lesion. Imaging and biopsy results are
used to determine the most appropriate treatment, such as surgery, chemother-
apy, radiation, or a combination. Depending on the level and extent of injury, the
focus of nursing care is toward monitoring for secondary brain injury.
Treatment
The goals of monitoring are to provide early detection at each stage of treat-
ment and to act as a marker of success or failure following each intervention.
Because of the variety of treatment options available, it is imperative to under-
stand which monitoring method will provide the most meaningful information
to guide the most appropriate treatment. Because of the complexity and inter-
Chapter 1. Brain Cancer and Neurocritical Care 3
Note. Image courtesy of Alex A. Rollo and DaiWai M. Olson. Used with permission.
Note that the bone appears bright white. Blood (hemorrhage) appears white and non-
uniform. The small white circle (dot) marks the location of the external ventricular
drain.
Note. Image courtesy of Alex A. Rollo and DaiWai M. Olson. Used with permission.
term use or large doses of chemotherapy agents treating late-stage lung cancer can
adversely affect the ability of oxygen to reach the brain. Reduced cerebral oxy-
genation may lead to cerebral ischemia and result in permanent brain damage or
death. Awareness of neurocritical care is essential not only for nurses caring for
patients being treated for brain cancer, but also for nurses involved in the general
treatment of all cancer types.
Primary CNS tumors begin in the CNS tissues (i.e., brain, meninges, and
spinal cord). Primary brain tumors, including neoplasms of the meninges, neu-
ral sheaths, and glial cells, occur at a rate of 21.42 per 100,000 age-adjusted per-
Chapter 1. Brain Cancer and Neurocritical Care 5
sons in the United States (Ostrom, Gittleman, et al., 2014). These tumors can be
benign (nonmalignant) or malignant based on their rate of growth, tendency to
spread, and histologic appearance. The cells that characterize the tumor will define
its treatment. Some of the most common benign primary brain tumors originate
from astrocytes (support cells), oligodendrocytes (myelin sheaths for neurons),
ependymal cells (lining the ventricles), cells of the meninges (cushion the brain),
and the pituitary (secretes hormones) (Ostrom, Gittleman, et al., 2014).
Although laypeople may use the term benign to describe something non-
threatening, a benign brain tumor does not always mean a favorable prognosis. A
tumor’s location within the brain and rate of growth affect prognosis. For exam-
ple, a rapidly growing benign tumor in the pons can easily compromise critical
brain stem vasculature. Similarly, a benign intraventricular tumor can cause an
obstruction of ventricular CSF flow and result in obstructive hydrocephalus.
Nonmalignant Tumors
Pituitary Adenomas
Pathophysiology: Pituitary adenomas account for 22.7% of nonmalignant
tumors (Ostrom, Gittleman, et al., 2014). Despite being benign, pituitary adeno-
mas can have far-reaching effects through their influence on the secretion of adre-
nal hormones, such as adrenocorticotropic hormone (ACTH), growth hormone
(growth factor), prolactin (PRL; milk production/secretion), thyroid-stimulating
hormone, and sex hormones (luteinizing hormone and follicle-stimulating hor-
mone). The specific effects of pituitary adenomas can vary depending on the cell
within the pituitary that begins the monoclonal expansion, because each hor-
mone is synthesized by a specific cell type (Arafah & Nasrallah, 2001).
Symptoms: Symptoms can result from an excess of one of the hormones listed
in Table 1-1 (e.g., unexpected milk secretion in prolactinomas). Although the
overproduction of these hormones may wreak havoc on the body and pituitary
tumors may impinge on surrounding brain structures, they seldom advance to
malignant cancers or spread to other areas of the CNS. A possible explanation for
this is that the trophic effects of these hormones intrinsically restrain cells from
indefinitely proliferating (Melmed, 2011).
Diagnosis and treatment: Prolactinomas are pituitary tumors most easily
diagnosed and monitored with a combination of an MRI and assays for hor-
mones. PRL is the most common hormone oversecreted by pituitary tumors, and
prolactinomas are indicated when a patient presents with PRL that is greater than
250 ng/ml (Glezer & Bronstein, 2015). Elevated PRL also can be seen in preg-
nancy, primary hypothyroidism, and renal failure. An MRI is often used to con-
firm the presence of a mass in the anatomic location of the pituitary gland. Pro-
lactinomas are usually treated with dopamine agonists, which often will cause
shrinkage and a drop in PRL levels (Freda & Wardlaw, 1999).
Somatotroph adenomas are growth hormone–secreting tumors that com-
prise up to 20% of pituitary tumors. They often result in acromegaly and are
6 CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
Primary
Tumor Hormone Prevalence Symptoms
Meningiomas
Pathophysiology: Meningiomas are tumors originating from the arach-
noid cells lining and cushioning the brain. More than 97% of meningiomas are
benign, and they are the most common type of primary brain tumor (36.1%)
(Ostrom, Gittleman, et al., 2014).
Chapter 1. Brain Cancer and Neurocritical Care 7
Diagnosis
When required, biopsies are obtained using an MRI. Treatment monitoring
also uses a conventional MRI. When characterization of a high-grade glioma (III
or IV) is required, metabolic imaging with positron-emission tomography (PET)
and 2-[18F]fluoro-2-deoxy-D-glucose (FDG) is used (Pedersen & Romner, 2013).
Treatment
The treatment for low-grade gliomas (grade II) is typically a combination of
surgery and adjuvant radiation. Recently, temozolomide (TMZ) chemotherapy
has been used for salvage therapy; however, interest has grown in larger cohort
studies of low-grade gliomas treated with a combination of procarbazine, lomus-
tine, and vincristine (Pedersen & Romner, 2013).
Grade II gliomas almost invariably transform to more malignant tumors, such
as anaplastic gliomas (grade III) or glioblastoma multiforme (GBM; grade IV)
(Stupp, Brada, van den Bent, Tonn, & Pentheroudakis, 2014). Although GBM
accounts for more than 45% of malignant primary brain tumors, it is responsi-
ble for only 15.4% of all primary brain tumors (Ostrom, Gittleman, et al., 2014).
Patients with GBM present nearly 50% of the time with a primary complaint of a
headache, usually with unilateral localization and progressive severity, and 20%–
40% present with a seizure, often with a focal onset (Omuro & DeAngelis, 2013).
Obtaining a brain MRI is essential to help with staging because GBM metastases
outside the CNS are rare. First-line treatment is almost always surgical resection,
8 CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
Nursing Implications
Because of the fast rate of growth in GBM as well as the increased risk of
thromboembolic events, patients should be assessed regularly for performance sta-
tus and neurologic function. An increased risk of stroke and deep vein thrombosis
is attributed to a tumor-induced hypercoagulable state, neurologic deficits, immo-
bilization, and steroid use. ICP monitoring should be considered with a change
in neurologic status. Cerebral and tumor-associated edema may be alleviated with
steroids such as dexamethasone. Steroid treatment is usually followed with rapid
tapering and discontinuation after surgical resection to avoid toxicity. Radiation
often follows surgery, and 4–12 weeks after completion of radiation treatment, an
MRI is used to evaluate the tumor’s initial response (Stupp et al., 2014). A pseu-
doprogression may be observed in 60% of patients, as radiation therapy may result
in increased contrast enhancement (Stupp et al., 2014).
Most brain tumors originate in other tissues and metastasize to the brain
(secondary or metastatic brain tumor), making early recognition of the primary
tumor that much more vital. Metastatic brain tumors are estimated to occur at a
rate of 7–14 per 100,000 age-adjusted persons (Fox, Cheung, Patel, Suki, & Rao,
2011); however, true incidence is difficult to measure because many brain metas-
tases are identified during autopsy (Fox et al., 2011). Up to 40% of all systemic
cancers originating outside of the brain eventually will metastasize to it, and the
incidence of metastatic brain cancer is as high as 10 times that of primary brain
cancer (Patchell, 2003).
Lung cancer (primarily small cell and adenocarcinoma) is the most common
source of brain metastases. Brain metastasis secondary to lung cancer is thought
to be related to the advanced progression of the disease before presentation of
symptoms. In fact, a diagnosis of lung cancer often follows with the presentation
of neurologic symptoms of brain metastases. Equally important, 91% of patients
with lung cancer with a working diagnosis of localized disease have been found
to have brain metastases within one year of their initial diagnosis for lung cancer
(Schouten, Rutten, Huveneers, & Twijnstra, 2002).
Nurses caring for patients with cancer should note that other primary can-
cers have significantly high rates of metastasis to the brain. Breast cancer is the
Chapter 1. Brain Cancer and Neurocritical Care 9
second most common cause of secondary brain tumors, followed by skin cancer
(melanoma), and then cancer of the gastrointestinal tract (colorectal) (Langley &
Fidler, 2013). Many attribute the rising incidence of secondary brain tumors to
the improved efficacy of cancer treatment options, which has resulted in increased
survival time of patients with cancer but also has allowed more time for cancer
cells to enter the bloodstream and metastasize to the brain.
The process of metastasizing to the brain requires cancer cells to overcome sev-
eral barriers, beginning with normal cells being converted to cancer cells in the
host organ. After the cancer cells attach to the extracellular matrix, the malig-
nant cells rapidly degrade the matrix by producing proteolytic enzymes and pro-
inflammatory cytokines. The degradation process allows the cancer cells to enter
the bloodstream (Ridley et al., 2003). The entry can occur either by penetrating
the thin-walled endothelium of small vessels or by circulating in the lymphatic
system until entry to the blood vessels is achieved.
After entering the bloodstream, the cancer cells must overcome the predisposi-
tion of cells toward apoptosis (normal cell death) and avoid host immunity (death
from natural killer cells). Cancer cells also can seed the venous capillary bed of the
lungs before reaching the arterial circulation through the left heart. This process
is the basis for the strong correlation between lung cancer and brain metastasis,
as the lung capillary bed is the last site for metastatic localization before the met-
astatic cells enter the left heart and are then transported via the arterial system to
the brain (Gavrilovic & Posner, 2005).
water soluble. This makes it difficult for the chemotherapy agent to pass through
the tight junctions of the BBB, therefore providing a sanctuary for tumorigene-
sis and growth. Most current treatments will not be able to reach the tumor until
it has developed its own leaky vasculature (i.e., a breakdown in the BBB). This
breakdown is typically through the process of angiogenesis, or the natural forma-
tion of new blood vessels.
One experimental technique to provide reversible BBB disruption is the addi-
tion of concentrated solutions into the carotid artery. This method works by
osmotically drawing water out of the endothelial cells of brain vessels, resulting in
cell shrinkage and cracks in the tight junctions, allowing chemotherapy agents to
leak into the CNS. The vessels eventually resume their normal BBB function after
the hypertonic bolus enters venous drainage (Kroll & Neuwelt, 1998).
action relieves it. A thorough personal and family history should also be gathered
to better understand the potential etiology of the symptoms; however, these find-
ings can only suggest the cause and should never rule out other pathologic pro-
cesses (Gates, 2010).
A neurologic examination should fully investigate the primary complaint
and explore the patient’s mental status, cranial nerves, sensory and motor sys-
tems, reflexes, cerebellum, meninges, and system survey (Bader et al., 2016). Any
irregular findings on neurologic examination can point to a brain tumor or at
least neural involvement. An observant caregiver checking the cognitive status or
reflexes of a patient with cancer could identify and aid in the early treatment of
brain metastasis.
Diffusion-weighted imag- DWI is an MRI technique used to weight the signal by the
ing (DWI) amount of diffusion of water molecules in selected voxels.
Fluid-attenuated inver- FLAIR is an MRI technique that nulls the effect of fluid
sion recovery (FLAIR) on the image.
Functional MRI (fMRI) fMRI observations are made to assess how different
parts of the brain respond to stimuli.
Positron-Emission Tomography
PET detects photons when a positron is emitted from a radioactive agent
interacting with an electron. The most commonly used positron-emitting iso-
tope is fluorine-18, and the most commonly used imaging agent is FDG, a glu-
cose analog that mimics glucose uptake in metabolically active tissue. It can
reveal regional differences between the metabolic activity in normal tissue and
fast-growing tumors (Hauser & Josephson, 2010). PET imaging has the advan-
tage of pinpointing small, metabolically active tumors that an MRI might over-
look; however, its usage is limited by the already high metabolism of glucose
in healthy brain tissue. Although PET may not be used in the initial diagnosis
of most brain tumors, it can aid in differentiating recurrent tumor from radia-
tion necrosis. High uptake in a previously low-grade tumor that had low uptake
establishes the diagnosis of anaplastic transformation. Currently, high inter-
est exists in the future of novel PET tracers, such as [18F]fluoro-methionine and
[18F]fluorodopa to target tumors that FDG may miss, 3'-deoxy-3'-[18F]fluorothy-
midine to evaluate tumor cell proliferation, and [18F]fluoromisonidazole for the
imaging of tumor hypoxia (Chen, 2007).
Combined PET/MRI machines are being developed to perform integrated
metabolic/anatomic imaging with a single machine; however, MRI alone is the
superior option for almost any brain tumor indication when available. Although
PET/MRI is a hopeful possibility in development, its availability has been largely
limited by cost (Buchbender et al., 2012).
Electroencephalogram
The presence of seizure can be accurately ruled out by electroencephalography
(EEG). Patients with both primary and secondary brain tumors may have seizure
as their presentation. Seizure is considered a medical emergency and should be
treated immediately. Status epilepticus is defined as a seizure that lasts longer than
five minutes (Brophy et al., 2012). On stabilization, patients who present with sei-
zures and are found to have brain tumors via MRI analysis may undergo a video
14 CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
process of swelling will eventually lead to cell death. This is a primary example of
cytotoxic cerebral edema.
The brain stores neither oxygen nor glucose, making it entirely dependent
on the oxygen and glucose concentrations in the blood reaching the brain and
the extent of delivery throughout the vasculature of the brain. Brain tumors can
obstruct this delivery. Both cancer and cancer therapy can drastically affect oxy-
gen being carried in the blood (oxygen bound to hemoglobin) and, ultimately, the
blood supply to the brain (cerebral perfusion); continuous monitoring of these
and other factors is vital to the well-being of patients with cancer.
To this end, critically ill and hospitalized patients with cancer should always
have some form of continuous measure of blood oxygen content. Systemic oxy-
gen is best measured by oxygen saturation (SaO2), an expression of the percent-
age of all hemoglobin binding sites in the blood bound to oxygen. Normal SaO2
is greater than 90%.
Pulse Oximetry
Pulse oximetry is a highly reliable and the least invasive method of estimating
SaO2. The abbreviation SpO2 may be used to denote the source of measurement
(e.g., pulsatile flow in the finger) of SaO2. Pulse oximetry is a direct measure of
SaO2 and works by passing light at different wavelengths (usually red and infra-
red) through an ear or finger and measuring the difference in absorption sensed
on the other side, which corresponds to the concentration of saturated to unsatu-
rated hemoglobin (Aoyagi, 2003).
Near-Infrared Spectroscopy
Near-infrared spectroscopy (NIRS) is an enticing alternative to the invasive
methods of measuring brain tissue oxygen level. NIRS is noninvasive and works
similarly to the rather reliable pulse oximeter. By using the near-infrared spectrum
(700–1100 nm), photons from multiple sources can travel several centimeters or
more into the brain tissue. These photons can penetrate the skull and refract or
scatter to surface signal sensors (Scheeren, Schober, & Schwarte, 2012). Like
SaO2, hemoglobin molecules saturated with oxygen will absorb specific portions
of the spectrum. Algorithms have been developed to produce a digital display that
reflects the oxygen content available in the region of the brain corresponding to
the NIRS sensor. Four commercially available models exist, including FORE-
SIGHT® by CAS Medical Systems, Inc., EQUANOX™ by Nonin Medical, Inc.,
INVOS™ by Medtronic, and NIRO® by Hamamatsu Photonics K.K. (Oddo &
Chapter 1. Brain Cancer and Neurocritical Care 17
Bösel, 2014). Although great potential exists for future improvements on this and
similar noninvasive measurements, medical consensus is that NIRS has limita-
tions in adult use and minimal clinical use (Le Roux et al., 2014).
Continuous Electroencephalography
The wide availability of EEG monitoring has extended the use of EEG beyond
a single-time, limited observation. Continuous EEG monitoring is increasingly
being used in the NCCU for several days at a time to evaluate for seizure and
determine the success or failure of treatment regimens. High-speed computing
and microprocessors have helped further the field of electrical signal monitoring.
Consciousness, neurofunction, and hypnosis monitoring have been developed to
acquire and transform raw EEG signals. The bispectral index and SedLine® mon-
itoring systems both rely on computerized algorithms (fast Fourier transform)
to analyze components of the EEG signal and produce a highly reliable numeric
interpretation of an individual’s level of consciousness, ranging from 0 (no brain
activity) to 100 (maximal activity). This technology has been validated intraoper-
atively and in critical care as an adjunct to subjective sedation assessment (Olson,
Zomorodi, Britz, et al., 2013).
Chapter 1. Brain Cancer and Neurocritical Care 19
Nursing Care
The type and intensity of therapy provided for patients with cancer and brain
injury vary widely. The role of the nurse as clinician, educator, and patient advo-
cate cannot be overstated. An accurate and comprehensive neurologic examina-
tion is fundamental in providing the medical team, patients, and families with
information to determine prognosis and treatment options. Because nurses often
have unique relationships with patients and their families, the contributions of
nursing toward education and patient advocacy are essential elements of care.
Surgery
Surgery can be curative or palliative and is indicated for removal of mass (e.g.,
hematoma, neoplasm), repair (e.g., aneurysm clipping), or alleviation of pressure
(e.g., decompressive hemicraniectomy). The most common postsurgical complica-
tions are cerebral edema and hemorrhage. After undergoing surgical resection of
a brain tumor, patients should be observed closely for 12–24 hours in an intensive
care unit to detect and rapidly treat postoperative complications (Ziai, Veralas,
Zeger, Mirski, & Ulatowski, 2003). Beyond cerebral edema, other common post-
operative complications include pulmonary issues, dysphagia/vocal cord paresis,
seizures, cerebral edema, and cardiac arrhythmias (Ziai et al., 2003).
Radiation
Although acute brain injury days to weeks after irradiation is rare in modern
radiation therapy, early delayed brain injury occurs one to six months after treat-
ment and involves transient demyelination and somnolence (Greene-Schloesser et
al., 2012). These can result in serious complications but are usually self-limiting
and reversible.
Late delayed brain injury occurs after six months and is described by irreversible
and progressive vascular abnormalities, demyelination, and white matter necrosis,
which can lead to dementia and death (Greene-Schloesser et al., 2012). Two schools
of thought delineate on how this occurs. One proposes that radiation damages the
vasculature of the brain, leading to ischemic damage to the white matter, while the
other attributes the death of oligodendrocytes (myelin loss) and astrocytes (physical
support) to the collapse of brain infrastructure and vasculature.
Regardless, radiation-induced cognitive impairment, including dementia,
occurs in 50%–90% of patients with brain tumors who survive more than six
months after irradiation (Greene-Schloesser et al., 2012). Symptoms include loss
of verbal and spatial memory, attention, and problem-solving ability. Occasionally,
patients who receive more than 3 Gy progress to dementia with progressive mem-
ory loss, ataxia, and urinary incontinence (Greene-Schloesser et al., 2012).
20 CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
Chemotherapy
Neurotoxic side effects are very common and are often dose limiting in the
treatment of cancer. Vinca alkaloids, cisplatin, and taxanes are most commonly
peripherally neurotoxic, while methotrexate, cytarabine, and ifosfamide are
known for central neurotoxicity (Verstappen, Heimans, Hoekman, & Postma,
2003). Cognitive or neurologic deficits after chemotherapy, such as “chemobrain,”
have been identified as a real phenomenon (Frank, Vance, Triebel, & Meneses,
2015). The exact pathophysiology, identification, and treatment of chemobrain
have yet to be identified (Wang et al., 2015).
Summary
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CHAPTER 2
Lung Cancer
Cindy Byrd, DNP, RN, ACNP-BC
Introduction
Lung cancer is the leading cause of cancer death for both men and women in
the United States, accounting for an estimated 26% (155,870) of all cancer-related
deaths in 2017 (Siegel, Miller, & Jemal, 2017). Currently, more than 400,000
Americans are living with a lung cancer diagnosis, approximately 13% of all
newly diagnosed cancers (American Lung Association [ALA], 2016c; Siegel et al.,
2017). Lung cancer is the most commonly diagnosed cancer worldwide, account-
ing for approximately 1.8 million new diagnoses and 1.6 million deaths each year
(ALA, 2016c).
The far-reaching effects of lung cancer make it a significant health issue. The
National Institutes of Health estimates that lung cancer annually costs the U.S.
healthcare system $13.4 billion (ALA, 2016c). This number does not include
work-related loss of productivity from patients with lung cancer.
Two major types of lung cancer exist: small cell lung cancer (SCLC) and non-
small cell lung cancer (NSCLC) (ALA, 2016b). NSCLC accounts for about 80%
of all newly diagnosed lung cancers (Burdett, Stewart, & Rydzewska, 2007).
NSCLC can be differentiated into three major types: adenocarcinoma, squamous
cell carcinoma, and large cell carcinoma (ALA, 2016b). Adenocarcinoma begins in
the cells that line the alveoli where mucus is produced (NCI, 2016). Squamous cell
carcinoma originates in tissues formed in the surface of the skin, the passages of the
respiratory and digestive tract, and the lining of hollow organs such as the bladder,
23
24 CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
kidneys, and uterus (NCI, 2016). Large cell carcinoma is named after its origin (in
large type cells) and appearance (large cell) under a microscope (National Cancer
Institute [NCI], 2016). Less common forms of NSCLC include pleomorphic, car-
cinoid tumor, salivary gland carcinoma, and unclassified carcinoma. Although dif-
ferent subgroups exist, these types are grouped as NSCLCs because of similar treat-
ment protocols.
SCLC, previously known as oat cell carcinoma, is distinct from other lung
cancers because of its clinical and biologic characteristics (NCI, 2016). It is a
malignancy that originates from cells in the lung tissue, is very aggressive, and
can rapidly metastasize. This cancer is strongly correlated with smoking, expo-
sure to second-hand smoke, a family history of lung cancer, radiation therapy to
the breast or chest, asbestos exposure, and radon exposure at home or in the work-
place. Prompt identification and staging is required. Often, this type of carcinoma
will metastasize early in the disease, with common sites in the mediastinal lymph
nodes, liver, bones, adrenal glands, and brain (NCI, 2016). Frequent paraneoplas-
tic syndromes also are prevalent with this type of malignancy, such as syndrome
of inappropriate antidiuretic hormone secretion and syndrome of ectopic adreno-
corticotropic hormone.
Routine screening is based on risk factors for the development of lung cancer.
Patients who qualify for routine screening include those aged 55–80 years, those
with a 30 pack-year smoking history, current smokers, or smokers who have quit
within the past 15 years (ALA, 2016d). Providers must perform a thorough phys-
ical examination and an evaluation of the patient’s social history. Table 2-1 out-
lines testing options used in the diagnosis and staging of lung cancer.
Once the presence of lung cancer is confirmed, the next step is to determine
the most appropriate treatment modalities through a comprehensive staging pro-
cess. This process includes understanding important universal abbreviations.
Staging occurs by considering the primary tumor location (T), the regional lymph
nodes involved (N), and the distance of metastasis (M). This nomenclature may
be reviewed in its entirety on the American Joint Committee on Cancer website
(https://cancerstaging.org/pages/default.aspx). Treatment options include surgery,
radiation, chemotherapy, or a combination of these therapies.
Radiation Therapy
Radiation therapy is the process of receiving high-energy radiation to decrease
tumor size, destroy cancer cells, and alleviate symptoms. This therapy can be used
as an adjunct to surgical resection and is often used in conjunction with addi-
tional treatment modalities, including surgery and chemotherapy.
Chapter 2. Lung Cancer 25
Procedure Description
Fine needle aspiration Removal of tissue or fluid using a thin needle under
computed tomography scan, ultrasound, or other imag-
ing to identify abnormal tissue
Note. Based on information from American Lung Association, 2016a; National Cancer Institute,
2016.
Three radiation sources exist: gamma rays, x-rays, and charged particles. These
may be administered to a patient in two ways. The first method is the external
delivery of radiation outside the body, termed external beam therapy. Internal radi-
ation therapy, or brachytherapy, is the second method and the process of inserting
or implanting radioactive material into the body.
Radiation therapy for cure is indicated in patients with stage I, II, or III
NSCLC with good performance status and whose disease may be covered in radi-
ation therapy without the risk of damaging healthy tissue (National Collaborat-
ing Centre for Cancer [NCC-C], 2015). Medically inoperable patients with stage
I or II NSCLC should be offered continuous, hyperfractionated, and accelerated
radiation therapy as treatment (NCC-C, 2015).
Nursing implications for patients receiving radiation therapy include careful
attention to external skin sites, as these areas may become irritated from radiation
exposure. Patients should avoid lotions and creams prior to radiation and should
bring severe skin burns to the attention of the radiation team.
it is only curative in a minority of patients (Kurup & Hanna, 2004). Because of the
small proportion of patients with SCLC (20% of all lung cancers) and the aggres-
sive nature of the disease process, chemotherapy options are limited to platinum-
based agents and etoposide.
Platinum-based chemotherapy agents (e.g., cisplatin, carboplatin, oxaliplatin)
are the mainstay of cancer therapy, accounting for almost half of all chemotherapy
agent use (Johnstone, Park, & Lippard, 2014). Side effects include nephrotoxic-
ity (acute renal failure), ototoxicity (tinnitus), neurotoxicity, hematologic suppres-
sion, gastrointestinal distress, hepatic dysfunction, and anaphylaxis (Bristol-
Myers Squibb Co., 2011).
In patients with NSCLC in which platinum-based therapy has been unsuc-
cessful or the tumor is unresectable, locally advanced, or untreated, docetaxel
is used. Docetaxel’s mechanism of action is as an antimitotic agent, meaning it
inhibits mitosis, or cell division, to also inhibit cancer growth (Sanofi-Aventis
U.S. LLC, 2014). Docetaxel is associated with many serious side effects, includ-
ing cardiovascular issues such as body fluid retention and vasodilation (Sanofi-
Aventis U.S. LLC, 2014). Dermatologic effects include alopecia, disorders of the
skin, nail changes, pruritus, rash, and more severe effects such as Stevens-John-
son syndrome and toxic epidermal necrolysis. Gastrointestinal side effects include
diarrhea, inflammatory disease of mucous membranes, nausea, stomatitis, vomit-
ing, and more severe side effects such as colitis. Significant hematologic alterations
include anemia, leukopenia, and neutropenia. These side effects place patients at
significant risk of opportunistic infections, which should always be carefully con-
sidered. Docetaxel also can cause significant organ dysfunction, including renal
failure, hepatic dysfunction, and anaphylactic reaction.
Gemcitabine is used for patients with inoperable, locally advanced (stage
IIIA or IIIB), or metastatic stage IV NSCLC. Gemcitabine’s mechanism of
action is that of a nucleoside metabolic inhibitor that exhibits antitumor activ-
ity by blocking cells from undergoing DNA synthesis (Eli Lilly & Co., 2014).
This medication has a similar side effect profile as docetaxel but also has side
effects of pulmonary toxicity, including pulmonary edema, pulmonary fibrosis,
interstitial pneumonitis, acute respiratory distress syndrome (ARDS), and fatal
respiratory failure.
Paclitaxel is an antimicrotubule agent, meaning it attacks the cells during var-
ious phases of division as an antimitotic, blocks the progression of mitosis, and
prolongs the mitotic checkpoint triggers of apoptosis or reversion of the cell cycle
without cell division (Bristol-Myers Squibb Co., 2011). When surgery and/or
radiation therapy are not suitable for patients with NSCLC, paclitaxel is used as
treatment in combination with cisplatin. It shares a similar side effect profile to
other chemotherapy agents, with the most serious being anaphylaxis.
Vinorelbine is a vinca alkaloid with antitumor activity and is indicated as a
first-line single agent in combination with cisplatin for treatment of patients with
stage III and IV NSCLC. It shares a similar side effect profile with other chemo-
therapy agents.
Chapter 2. Lung Cancer 27
Targeted Therapy
Targeted therapy includes either monoclonal antibodies or small-molecule
drugs that block the action of certain enzymes and proteins (NCI, 2016). This
treatment is indicated for certain cancer types and is used in conjunction with
other treatments. A tumor biopsy is needed to determine if targeted therapy is
appropriate.
Monoclonal antibodies are drugs that work on the outer surface of cancer cells.
They can be used alone or concurrently with other drugs to target defects in can-
cer cells or make the cells more receptive to the body’s immune system. Monoclo-
nal antibodies also can be used as carriers for other drugs or as substrates directly
to the cancer (NCI, 2016). For example, ramucirumab can be used in conjunc-
tion with docetaxel in stage IV NSCLC with continued tumor growth in addition
to a platinum-based therapy (NCI, 2016). Bevacizumab can also be used for the
treatment of nonsquamous cell NSCLC and can be given with traditional chemo-
therapy agents. Small-molecule drugs can enter the cells and inhibit them from
normal function, leading to cell death. Examples include erlotinib, afatinib, crizo-
tinib, ceritinib, and cetuximab.
Immunotherapy
Immunotherapy treats lung cancer by stimulating the body’s immune
response. Nivolumab and pembrolizumab are the two immunotherapy treat-
ments currently approved for lung cancer. Nivolumab is used to treat squa-
mous cell NSCLC that has spread during or after treatment with a platinum-
based therapy. It is both a monoclonal antibody and a checkpoint inhibitor that
addresses the PD-1 (programmed cell death protein 1) pathway (NCI, 2016).
PD-1 binds to PD-L1 (a protein on some normal and cancer cells), allowing an
immune response. Nivolumab binds to PD-1 and allows these pathways to be
active. Pembrolizumab is used in patients with advanced NSCLC of PD-L1–
positive tumor cells.
Surgery
Surgical options are based on tumor size, location, and disease progression (Van
Schil et al., 2013). The three typical goals of surgery are cure, tumor debulking, or
the symptom palliation. If the procedure’s aim is curative, the surgeon’s goal is to
remove the entire tumor. A debulking procedure removes some of the tumor and
may be used if an associated risk of injuring surrounding organs exists (Van Schil
et al., 2013). A palliative surgical approach alleviates symptoms associated with the
tumor, such as pain or obstruction; this is not a curative measure.
Lung cancer resections can be grouped into three major categories: standard
resections, lung parenchymal–sparing procedures, and surgeries that involve
the removal of surrounding organs (Van Schil et al., 2013). Standard resections
include lobectomy (removal of a lobe of the lung), bilobectomy (removal of two
28 CRITICAL CARE NURSING OF THE ONCOLOGY PATIENT
lobes on the right side of the lung), and pneumonectomy (removal of the entire
lung) (Burdett et al., 2007). Pneumonectomy was considered the treatment of
choice through the 1940s; however, if the lesion can be fully resected, lobectomy
currently has a similar survival rate with better patient outcomes (Burdett et al.,
2007).
Lung parenchyma is the portion of the lung responsible for gas exchange and
includes the alveoli, alveolar ducts, and bronchioles. Lung parenchyma–sparing
procedures can be distal or proximal (Van Schil et al., 2013). Distal procedures
include segmentectomies and wedge resections. A wedge resection procedure
removes a wedge-shaped portion of lung that comprises cancerous cells and some
healthy tissue. A segmentectomy is similar but takes out a larger portion of lung
tissue without removing the entire lung.
Proximal procedures include bronchoplastic and tracheoplastic operations.
The sleeve resection is the most common bronchoplastic procedure performed
and is indicated for upper lobe orifice lung cancer. This procedure removes a can-
cerous lobe of lung and a portion of the bronchus.
A final resection procedure involves lung parenchyma with an adjacent tumor-
invaded organ. Common procedures include resection of the chest wall, dia-
phragm, pericardium, left atrium, superior vena cava, or the apex of the chest (Van
Schil et al., 2013). Knowledge of the structures involved during these extended
resections is paramount for postoperative management and detection of poten-
tial complications.
Medically fit patients with NSCLC should be offered lobectomy for cure. This
may be performed as an open thoracic surgery as a first-line choice (NCC-C,
2015); however, debate exists whether this or video-assisted thoracic surgery
(VATS) is the optimal technique. Surgical decision should be based on the pro-
gression of the patient’s condition, the stage of lung cancer, the cell type, and the
surgeon’s preference.
Patients with borderline fitness and smaller tumors (e.g., T1a/b, N0, M0)
should be considered for lung parenchymal–sparing operations if a complete
resection cannot be completed. Pneumonectomies, bilobectomies, and bronchial
angioplasties should only be performed if needed to obtain clear margins. Patients
undergoing surgery with T3 NSCLC with chest wall involvement should receive
a complete resection of the tumor with an accompanied extrapleural or en bloc
resection (NCC-C, 2015).
Postoperative Care
bidities (Iyer & Yadav, 2013). Complications of both open and VATS procedures
include hemorrhage, empyema, air leak, pneumonia, and surgical emphysema.
Postoperative care, such as learning pain management techniques, is aimed at
reducing the risk for complications.
Ventilator Settings
Different ventilator settings use pressure or volume as a basis for breath deliv-
ery. As ventilators evolve and become more complex, the line between settings
becomes increasingly blurred. It is important to understand traditional ventilator
modes and all associated terms, including the following:
••Frequency or respiratory rate—the number of breaths per minute
••Tidal volume—the amount of volume (ml) delivered with each breath
••PEEP—prevents progressive atelectasis by preventing repetitive opening and
closing of alveoli and improves compliance and ventilation–perfusion mismatch
••Fraction of inspired oxygen (FiO2)—percentage of delivered oxygen
Volume Modes
Assist-control ventilation (ACV), also known as continuous mandatory
ventilation, is a set volume delivered with each breath. The patient determines
the absolute respiratory rate, but a minimum rate is also set (Burnes, 2008).
One disadvantage to ACV is that patients breathing rapidly may develop
hyperinflation and respiratory alkalosis because of a prolonged inspiratory-
to-expiratory time ratio (Burnes, 2008). An advantage is that sedation or par-
alytics can be increased in extreme cases to totally control a patient’s respira-
tory function.
Synchronized intermittent mandatory ventilation (SIMV) guarantees a
certain number of breaths, which are synchronized to coincide with the patient’s
spontaneous respirations. The patient is partially breathing independently, reduc-
ing the risk of respiratory alkalosis and hyperinflation (Burnes, 2008). Disadvan-
tages include increased independent breathing and potentially decreased cardiac
output. With few exceptions, provider preference determines ACV or SIMV use.
When a patient’s respiratory status must be totally controlled, ACV is preferred.
If a patient is breathing rapidly on ACV, SIMV is preferred.
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Language: French
LE CANTIQUE
DE L’AILE
CINQUIÈME MILLE
PARIS
Librairie CHARPENTIER et FASQUELLE
EUGÈNE FASQUELLE, ÉDITEUR
11, RUE DE GRENELLE, 11
1922
Tous droits réservés.
Copyright 1922, by Eugène Fasquelle.
Chaque volume 6 75
Un soir à Hernani, poésie 1 75
Discours de réception à l’Académie Française 1 75
Homère.
27 septembre 1910.