Nichole Miller - Clinical Rotation Manual For The Acute Care Nurse Practitioner Student-Springer Publishing Company (2021)
Nichole Miller - Clinical Rotation Manual For The Acute Care Nurse Practitioner Student-Springer Publishing Company (2021)
Miller
for the Acute Care Nurse Practitioner Student
Clinical
“Provide[s] the foundation needed for new graduates as well as seasoned acute care nurse
practitioners to practice at the highest level. This author has taken great care to write this book
in an easy-to-read-and-follow format to meet the needs of acutely ill patients while providing
high-quality, cost-effective care.”
—Mary Ellen Roberts, DNP, APN-C, NP-C, FNAP, FAANP, FAAN
Director, DNP and Acute Care Nurse Practitioner Programs
Seton Hall University, Nutley, NJ
Rotation
From the Foreword
Written specifically for the AGNP-AC student or the incoming Acute Care Nurse
Practitioner, this handy guide provides a quick but thorough reference on the basics
of the many complex challenges encountered in the clinical rotation portion of the
AGNP-AC curriculum. It covers key skills such as patient assessment, billing, labs, im-
Manual
aging, and major diagnoses, among many others in a bulleted format for on-the-go
comprehension. Chapters are deliberately designed to aid in surmounting practice
knowledge gaps by synthesizing resources often found in disparate references, making
them easily accessible and pertinent to the AGNP student.
Nurse Practitioner
appropriate, role-specific guidance
• Serves as a guide for instructors for effective precepting of AGNP-AC students
• Instructs on principles of accurate diagnosis and management of the major acute
conditions by body system
Student
• Cuts through the complexities of billing
• Provides abundant “Clinical Tips and Tricks” boxes in each chapter
ISBN 978‑0‑8261‑8922‑6
Nichole Miller
11 W. 42nd Street
New York, NY 10036-8002
www.springerpub.com
With a contribution by Tish Myers, MSN, APRN, FNP-BC, Burn and Reconstructive Centers
of America, Augusta, Georgia
CLINICAL ROTATION
MANUAL FOR THE
ACUTE CARE NURSE
PRACTITIONER STUDENT
Nichole Miller, AGACNP-BC, MSN
Copyright © 2022 Springer Publishing Company, LLC
All rights reserved.
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Springer Publishing Company, LLC
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Acquisitions Editor: Rachel X. Landes
Compositor: Amnet Systems
ISBN: 978-0-8261-8922-6
ebook ISBN: 978-0-8261-8923-3
DOI: 10.1891/9780826189233
21 22 23 24 / 5 4 3 2 1
The author and the publisher of this work have made every effort to use sources believed to
be reliable to provide information that is accurate and compatible with the standards generally
accepted at the time of publication. Because medical science is continually advancing, our knowl-
edge base continues to expand. Therefore, as new information becomes available, changes in pro-
cedures become necessary. We recommend that the reader always consult current research and
specific institutional policies before performing any clinical procedure or delivering any medi-
cation. The author and publisher shall not be liable for any special, consequential, or exemplary
damages resulting, in whole or in part, from the readers’ use of, or reliance on, the information
contained in this book. The publisher has no responsibility for the persistence or accuracy of
URLs for external or third-party internet websites referred to in this publication and does not
guarantee that any content on such websites is, or will remain, accurate or appropriate.
Library of Congress Cataloging-in-Publication Data
Names: Miller, Nichole, author, editor.
Title: Clinical rotation manual for the acute care nurse practitioner student / Nichole Miller.
Description: New York, NY : Springer Publishing Company, LLC, [2022] |
Includes bibliographical references and index.
Identifiers: LCCN 2021018684 (print) | LCCN 2021018685 (ebook) | ISBN
9780826189226 (paperback) | ISBN 9780826189233 (ebook)
Subjects: MESH: Critical Care Nursing—methods | Nurse Practitioners | Outline
Classification: LCC RC86.7 (print) | LCC RC86.7 (ebook) | NLM WY 18.2 | DDC 616.02/8—dc23
LC record available at https://lccn.loc.gov/2021018684
LC ebook record available at https://lccn.loc.gov/2021018685
Publisher’s Note: New and used products purchased from third-party sellers are not guaranteed
for quality, authenticity, or access to any included digital components.
Printed in the United States of America.
This book is dedicated to my family.
First to my husband, who has supported me every step of
the way in following my dreams.
To my daughters, who have watched me type while at practice,
dance, and even on vacation.
Thank you for always understanding.
To my parents, thank you for always telling me that anything is possible.
It has kept me going even when I have wanted to give up.
To all the mentors that have helped me grow along the way,
thank you for helping me become the nurse and provider that I am today.
CONTENTS
Foreword Mary Ellen Roberts, DNP, APN-C, NP-C, FNAP, FAANP, FAAN ix
Preface xi
Abbreviations xiii
vii
viii CONTENTS
Index179
FOREWORD
This timely book was inspired because of the need for a clinical book that
addresses the needs of acute care nurse practitioners. This new book, Clinical
Rotation Manual for the Acute Care Nurse Practitioner, builds on the work of
acute care nurse practitioners over the past 20 years. Chapters cover complex
care problems in the acute care setting with the most current evidence-based
information. Using an interprofessional approach, this book focuses on clini-
cal decision-making and collaboration.
This manual is divided into chapters by system, beginning with the car-
diovascular system and concluding with infectious diseases. Each chapter
section is divided into common disease states. The easy-to-read-and-follow
book includes clinical tips and tricks, normal lab values, causes, assessment
findings, treatment and management methods, and critical-level treatment.
Dr. Miller has included billing, assessments, and documentation in the
final section. Templates for documentation and billing are included. Docu-
mentation includes a template for history and physicals, tips, and tricks in
documentation.
Critically important clinical information on practice is provided. The in-
formation provided in this book will provide the foundation needed for new
graduates as well as seasoned acute care nurse practitioners information to
practice at the highest level of nurse practitioner practice. Dr. Miller has taken
great care to write this book in an easy-to-read-and-follow format to meet the
needs of acutely ill patients while providing high-quality cost-effective care.
This book will act as a resource for the acute care nurse practitioner at a vari-
ety of stages, from student to novice to expert.
ix
PREFACE
Welcome to the Clinical Rotation Manual for the Acute Care Nurse Practitioner
Student. This book is designed to prepare the acute care nurse practitioner
student for those complicated and complex clinical situations you may not
have yet explored fully in the didactic part of your program. When I was
an acute care nurse practitioner student myself, I recognized that there were
no resources specifically designed for the acute care nurse practitioner. As I
began my practice and began to precept, I noticed that no new resources had
been developed. And after several years of precepting nurse practitioner stu-
dents, I received a lot of feedback that certain disease processes had not yet
been covered in their course work, often leading to frustration and difficulty
working through complex differential diagnoses during clinical rotations.
This book has been developed as a bridge to fill those gaps in knowledge
and help build confidence in the clinical setting. While no resource will re-
place those hours of course work, this book will help guide you through some
complex clinical situations. This book is organized first by body systems then
by disease processes. Each disease process is then broken down into causes,
assessment findings, diagnostic testing, and treatment and management sec-
tions. This hopefully will allow you to correlate assessment findings, order
appropriate diagnostic testing, and identify appropriate management and
treatments.
Another key feature of this book is the Clinical Tips and Tricks boxes. These
are clinical tips that may help as quick tips or bits of information on certain
disease processes. These are important facts and knowledge bits that are used
frequently in practice. Areas that are commonly found in practice are often
found on tests as well, so it is helpful to know this material.
While this book is meant to be a clinical manual, it can also be a great
companion to classroom learning. It takes each complex concept and breaks
it down into its very basic parts. As you grow in your knowledge and your
practice as a nurse practitioner, you build on your knowledge. This book can
be a great building block for those who may benefit from that learning style.
I hope you find this book useful and enjoy its contents.
Nichole Miller
xi
ABBREVIATIONS
ACTH adrenocorticotropic hormone
ADH antidiuretic hormone
ALT alanine transaminase
ANA antinuclear antibody
ARDS adult respiratory distress syndrome
AST aspartate transaminase
BNP brain natriuretic peptide
BP blood pressure
CABG coronary artery bypass graft
CAUTI catheter-associated urinary tract infection
CC chief complaint
CI cardiac index
CLABSI central line blood stream infection
CMV cytomegalovirus
CO cardiac output
CRE carbapenem-resistant enterobacteriaceae
CRP C-reactive protein
CVP central venous pressure
DKA diabtetic ketoacidosis
DRESS drug reaction with eosinophilia and systemic symptoms
EBL estimated blood loss
EBV Epstein–Barr virus
EF ejection fraction
ERCP endoscopic retrograde cholangio-pancreatography
ESR eosinophil sedimentary rate
FENa fraction of excreted sodium
FFP fresh frozen plasma
FWD free water deficit
HEENT head, eyes, ears, nose, and throat
HHS hyperglycemic hyperosmolar state
HPI history of present illness
HSV herpes simplex virus
ICD intracardiac defibrillators
LDH lactate dehydrogenase
MAC monitored anesthesia care
MAP mean arterial pressure
MI myocardial infarction
xiii
xiv ABBREVIATIONS
(continued)
3
4 I CARDIOVASCULAR DISEASE AND DISORDERS
Type IV
■ Infarction due to previous percutaneous intervention (PCI)
Type V
■ Infarction due to coronary artery bypass graft (CABG) intervention
Assessment Findings
■ Chest pain
● Substernal
● Epigastric
● Often described as crushing
● May radiate to the neck or jaw
1 ACUTE CORONARY SYNDROME AND MYOCARDIAL INFARCTION 5
■ Back pain
■ Arm pain
■ Abdominal pain
■ Nausea
■ Tachycardia
■ Bradycardia
■ Arrhythmias
● Ventricular tachycardia
● Ventricular fibrillation
■ Diaphoresis
■ Sudden cardiac death
■ Reports of decreased activity tolerance
Diagnostics
EKG
● ST elevations
■ >2-mm elevation in leads V2 and V3
■ >1-mm elevation in leads I, II, III, aVR, aVL, aVF, and V3 to V6
■ Must be in contiguous leads to be significant
● New left bundle branch block
■ Previously treated like a STEMI
■ Should raise suspicion of acute event
● ST depression
■ In contiguous leads, may indicate ischemia
■ In leads V1 to V4, may indicate posterior wall injury
● Serial EKG
■ May be indicated every 15 to 30 minutes in patients who remain
symptomatic in first hour after presentation
6 I CARDIOVASCULAR DISEASE AND DISORDERS
Laboratory
● Troponin
■ Negative on arrival does not rule out ischemia
■ Repeat should be done within 3 to 6 hours
■ Considered negative if no elevations 6 hours after presentation
● Complete blood count (CBC)
● Coagulation panel
Echocardiogram
● Evaluate for ejection fraction and mechanical
Stress Test
● Nuclear medicine
■ Antiplatelet Therapy
● Indicated in patients with STEMI or with acute coronary syndrome
(ACS) and moderate to high risk for NSTEMI
■ These patients should receive dual-platelet therapy with aspirin and
another antiplatelet therapy.
● Aspirin
■ Aspirin should be given by emergency medical services (EMSs)
prior to arrival.
1 ACUTE CORONARY SYNDROME AND MYOCARDIAL INFARCTION 7
■ STATIN Therapy
● Moderate- to high-dose statin should be initiated in patients with MI
and suspected MI
● Dose recommended prior to PCI
● Dosing should be continued on discharge
■ Nitroglycerin
● Sublingual
● Intravenous
● Contraindicated for hypotension
8 I CARDIOVASCULAR DISEASE AND DISORDERS
■ Beta-Blocker
● Should be given in first 24 hours and continued post discharge
● Decreases heart rate and blood pressure
● Decreases myocardial oxygen consumption
● Decreases risk of reinfarction
● Contraindication
■ Acute heart failure
■ Second- or third-degree heart block
■ Angiotensin-Converting Enzyme (ACE) Inhibitor
● Mortality benefit in acute MI with ejection fraction (EF) <40%
● Consider angiotensin II receptor blocker in patients unable to tolerate
ACE inhibitor
● Patients with a history or diabetes and chronic kidney disease should
be started on an ACE Inhibitor prophylactically to decrease the risk of
renal failure and cardiac events.
■ Aldosterone Antagonist
● Spironolactone 25 to 25 mg daily
● May be beneficial in patients with acute myocardial infarction (AMI)
and EF less than 40%
■ Left Heart Catheterization and/or PCI
● Indications
■ New ST elevation in 2 or more leads
■ Refractory angina
■ Cardiogenic shock
■ Ventricular tachycardia
■ Ventricular fibrillation
● Activation of cardiac catheterization lab on presentation of STEMI
● Goal is intervention within 90 minutes of presentation
■ CABG
● Indicated when PCI not possible
● Usually indicated when there is multivessel disease and stents cannot
be placed.
● Often seen when patients have had previous stents that have failed.
Bibliography
Anderson, J. L., & Morrow, D. A. (2017). Acute myocardial infarction. New England
Journal of Medicine, 376(21), 2053. https://doi.org/10.1056/NEJMra1606915
Bangalore, S., Makani, H., & Radford, M. (2014). Clinical outcomes with B-blockers
for myocardial infarction: A meta-analysis of randomized trials. American Journal
of Medicine, 64(24), 939–953. https://doi.org/10.1016/j.amjmed.2014.05.032
Dewilde, W. J., Oirbans, T., Verheugt, F. W. A., Kelder, J. C., De Smet, B. J. G. L.,
Herrman, J.-P., Adriaenssens, T., Vrolix, M., Heestermans, A. A. C. M., Vis, M. M.,
Tijsen, J. G.P., van ‘t Hof, A. W., & ten Berg, J. M.; WOEST study investigators
et al. (2013). Use of clopidogrel with or without aspirin in patients taking oral
1 ACUTE CORONARY SYNDROME AND MYOCARDIAL INFARCTION 9
HYPERTENSIVE URGENCY
Cause
● Refractory hypertension
● Medication noncompliance
Risk Factors
● Obesity
● Tobacco use
● Excessive alcohol consumption
● Estrogen supplementation
● Pregnancy
● Endocrine disorders
■ Pheochromocytoma
Assessment Findings
■ Systolic blood pressure (SBP) >170 or diastolic blood pressure (DBP) >110
■ May be asymptomatic with only finding being elevated BP
■ Headache but overall asymptomatic
11
12 I CARDIOVASCULAR DISEASE AND DISORDERS
Diagnostics
Laboratory
● Troponin
■ Evaluate for cardiac damage
● Serum chemistry
■ Evaluate renal function
HYPERTENSIVE EMERGENCY
Cause
■ Refractory hypertension
■ Medication noncompliance
■ Aortic dissection
■ Stroke
■ Pulmonary edema
■ Malignant hypertension
■ Preeclampsia or eclampsia
■ Intracranial hemorrhage
■ Myocardial infarction
■ Pheochromocytoma
■ Drug intoxication
● Cocaine
● Amphetamines
2 HYPERTENSION URGENCY AND EMERGENCY 13
AORTIC DISSECTION
■ Severe sudden pain
● Back pain
● Chest pain
■ Hypertension
● Seen with descending aorta dissection
■ Hypotension
● Seen with ascending aorta dissection
■ Weakened pulses
● Carotid
● Brachial
● Femoral
■ Syncope
■ Diastolic decrescendo murmur
■ Wide pulse pressure
■ Widen mediastinum on chest x-ray
Assessment Findings
Cardiovascular
● SBP >180 or DBP >110 to 120
■ No set standard
● Tachycardia
● Bradycardia
● Jugular vein distention (JVD)
● Chest pain
Neurological
● Blurred vision or vision loss
● Agitation
● Stupor
● Delirium
● Headache
● Lethargy
● Seizures
● Nausea and vomiting
■ Can be a sign of increased intracranial pressure
14 I CARDIOVASCULAR DISEASE AND DISORDERS
Fundoscopic Exam
● Should be performed on any patient in whom hypertensive crisis is
suspected
● Optic disk edema
● Flame hemorrhages
● Cotton wool spots
Back Pain
● Specific to aortic dissection
Pulmonary
● Dyspnea
Diagnostics
Laboratory
● Serum chemistry panel
■ Elevated BUN
■ Elevated creatinine
● Serum lactate
■ Elevation indicates hypoperfusion
● Troponin
● Urinalysis
● Urine or serum drug screen
■ When substance abuse is the suspected cause
Radiography
● Chest radiography
● Head CT
■ When concerns for intracranial process such as the following:
● Acute cerebrovascular accident (CVA)
● Intracranial hemorrhage
● Recent head trauma
● Chest CT
■ Suspected aortic dissection
2 HYPERTENSION URGENCY AND EMERGENCY 15
EKG
● Consider in all significantly hypertensive patients for concerns of
ischemia or acute myocardial infarction
● Hydralazine
■ 5 to 20 mg IV push
■ Not used in aortic dissection
● Esmolol
■ Loading dose of 500 to 1,000 mcg
■ 25 to 50 mcg/kg/min with maximum of 300 mcg/kg/min
■ May cause significant bradycardia
● Enalapril
■ 1.25 mg over 5 minutes q6h
■ Cardiac catheterization
● Consider if ischemia is suspected
■ Other underlying conditions
● Identify underlying conditions that may exist
● Treatment for underlying condition as indicated by the system
Bibliography
Jamerson, K., Weber, M. A., Bakris, G. L., Dahlöf, B., Pitt, B., Shi, V., Hester, A.,
Gupte, J., Gatlin, M., & Velazquez, E. J.; ACCOMPLISH Trial Investigators (2008).
Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk
patients. New England Journal of Medicine, 359(23), 2417. https://doi.org/10.1056/
NEJMoa0806182
Karabacak, M., Yiquit, M., Turdogan, K. A., & Sert, M. (2015). The relationship
between vascular inflammation and target organ damage in hypertensive crises.
American Journal of Emergency Medicine, 33(4), 497–500. https:/doi.org/10.1016/
j.ajem.2014.11.014.
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Preston R. A., Arciniegas, R., DeGraff, S., Materson, B. J., Bernstein, J., & Afshartous, D.
(2019). Outcomes of minority patients with very severe hypertension
(>220/>120 mmHg). Journal of Hypertension, 37(2), 415. https://doi.org/10.1097/
HJH.0000000000001906
Varon, K. (2000). The diagnosis and management of hypertensive crises. Chest, 118(1),
214–227. https://doi.org/10.1378/chest.118.1.214
Varon, K. (2008). Treatment of acute severe hypertension: Current and newer agents.
Drugs, 68(3), 283–297. https://doi.org/10.2165/00003495-200868030-00003
Whelton, P. K., Carey, R. M., Aronow, W. S., Casey, D. E., Jr., Collins, K. J.,
Himmelfarb, C. D., DePalma, S. M., Gidding, S., Jamerson, K. A., Jones, D. W.,
MacLaughlin, E. J., Muntner, P., Ovbiagele, B., Smith, S. C., Jr., Spencer, C. C.,
Stafford, R. S., Taler, S. J., Thomas, R. J., Williams, K. A., Sr., … Wright, J. T., Jr.
(2018). 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/
PCNA guideline for the prevention, detection, evaluation, and management of
high blood pressure in adults: A report of the American College of Cardiology/
American Heart Association Task Force on Clinical Practice Guidelines.
Hypertension, 71(6), e13. https://doi.org/10.1161/HYP.0000000000000065
Wong, T. Y., & Mitchell, P. (2007). The eye in hypertension. Lancet, 369, 425. https://
doi.org/10.1016/S0140-6736(07)60198-6
3
MANAGEMENT OF
ACUTE HEART FAILURE
HEART FAILURE WITH REDUCED EJECTION FRACTION
Causes
Left Ventricular Systolic Dysfunction
■ Coronary artery disease
■ Idiopathic dilated cardiomyopathy
■ Muscular dystrophy
■ Alcohol abuse
■ Cocaine abuse
■ Myocarditis
■ Peripartum
■ Untreated valvular heart disease
■ Tachyarrhythmias
■ Hypertension
■ Lupus
■ Rheumatoid arthritis
Assessment Findings
General
■ Cool extremities
■ Altered mentation
Cardiovascular
■ Tachycardia
■ Jugular venous distention
■ Hepatojugular reflux
■ Narrow pulse pressure
17
18 I CARDIOVASCULAR DISEASE AND DISORDERS
■ Hypotension
■ S3 and/or S4
■ Tricuspid murmur
Pulmonary
■ Shortness of breath
■ Cheyne–Stokes respirations
■ Rales
Diagnostics
Laboratory
■ Serum chemistries
■ Complete blood count (CBC)
■ Troponin
■ Brain natriuretic peptide (BNP)
● May be useful in patients in whom cause of dyspnea is not known
Radiology
■ Chest x-ray
EKG
Echocardiogram
■ Especially important in a patient with an unknown ejection fraction (EF)
or first presentation of decompensated heart failure
Respiratory Support
■ Assess ventilation and work of breathing
■ Supplemental oxygen for hypoxia
3 MANAGEMENT OF ACUTE HEART FAILURE 19
■ Bipap
● Help with increased work of breathing
● Improve ventilation
■ Intubation/mechanical ventilation
● For respiratory failure
Medications
■ Bolus dose loop diuretics
● Requires close monitoring of input/output (I/O)
● Consider Foley catheter for accurate assessment of volume status
● Especially important in incontinent patients or critically ill patient’s
● patients on a diuretic infusion should have catheter in place for hourly I&O
● Furosemide
■ Initial dose 40 to 60 mg or double home dose
■ Maximum daily dose 160 to 320 mg
● Bumetanide
■ Initial dose 1 to 2 mg
■ Maximum dose 5 to 10 mg
■ Continuous infusion loop diuretics
● Requires close monitoring of electrolytes
● Monitor closely for symptoms of hypokalemia
● Requires foley catheter placement
● Furosemide
■ 20 to 80 mg loading dose
■ 5 to 20 mg/hr
● Bumetanide
■ 1 mg IV load
■ 0.5 to 2 mg/hr
■ Morphine
● Assists with air hunger
■ Nitrates
● Nitroglycerin
■ 5 to 25 mcg/min
■ max 300 mcg/min
■ Coronary vasodilators
■ Decreases systemic pressure
■ Decreases pulmonary pressure
● Nitroprusside
■ 0.5 to 8 mcg/kg/min
■ max 10 mcg/kg min
■ Extremely potent and can cause extreme hypotension
■ Use with caution and titrate carefully
■ Should be used with arterial line monitoring only
■ Nitroprusside is only used for max 72 hours as it can metabolize
into cyanide
■ Decreases preload and afterload
20 I CARDIOVASCULAR DISEASE AND DISORDERS
■ Inotropes
● Used in patients with known depressed ejection fraction or cardiogenic
shock.
● Used to improve cardiac output and cardiac index.
● Recommend advanced hemodynamic monitoring to assist with titration.
■ Dobutamine
● 2.5 to 20 mcg/kg/min
● max dose 40 mcg/kg/min
■ Milrinone
● Initial bolus 50 mcg/kg over 10 min
● 0.375 to 0.75 mcg/kg/min
Follow-Up
■ Intracardiac defibrillators (ICDs)
● Recommended in patients with EF <30% due to increased risk of
sudden cardiac death
● Some patients may have Life Vest placed initially if ICD cannot be
implanted or are expected to have improvement in EF
Causes
■ Infiltrative heart disease
■ Constrictive pericarditis
■ Hypertension
■ Anemia
■ Thyrotoxicosis
■ Arteriovenous (AV) communication
■ Obesity
■ Right-side heart failure from pulmonary disease
Assessment Findings
General
■ Cool extremities
■ Altered mentation
Cardiovascular
■ Tachycardia
■ Jugular venous distention
■ Hepatojugular reflux
■ Narrow pulse pressure
■ Hypotension
■ S3 and/or S4
■ Tricuspid murmur
3 MANAGEMENT OF ACUTE HEART FAILURE 21
Pulmonary
■ Shortness of breath
■ Cheyne–Stokes respirations
■ Rales
Diagnostics
Laboratory
■ Serum chemistries
■ CBC
■ Troponin
■ BNP
● May be useful in patients in whom cause of dyspnea is not known
Radiology
■ Chest x-ray
EKG
Echocardiogram
Respiratory Support
■ Assess ventilation and work of breathing
■ Supplemental oxygen for hypoxia
■ Bipap
●Help with increased work of breathing
●Improve ventilation
■ Intubation/mechanical ventilation
● For respiratory failure
22 I CARDIOVASCULAR DISEASE AND DISORDERS
MEDICATIONS
Diuretic Infusions
■ Foley catheter highly recommended for accurate I/O
■ Frequent monitoring of electrolytes (every 4–6 hours)
■ Replacement of potassium and other electrolytes
■ Set 24-hr goal for net urine output
Bibliography
Maddox, T. M., Stanislawski, M. A., Grunwald, G. K., Bradley, S. M., Ho, P. M., Tsai, T.
T., Patel, M. R., Sandhu, A., Valle, J., Magid, D. J., Leon, B., Bhatt, D. L., Fihn, S. D., &
Rumsfeld, J. S. (2014). Nonobstructive coronary artery disease and risk of myocardial
infarction. JAMA, 312(17), 1744–1763. https://doi.org/10.1001/jama.2014.14681
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
3 MANAGEMENT OF ACUTE HEART FAILURE 23
Ponikowski, P. (2016). 2016 ESC guidelines for the diagnosis and treatment of acute
and chronic heart failure: The Task Force for the diagnosis and treatment of acute
and chronic heart failure of the European Society of Cardiology (ESC) developed
with the special contribution of the Heart Failure Association (HFA) of the ESC.
European Heart Journal, 37(27), 2129. https://doi.org/10.1093/eurheartj/ehw128
Preston R. A., Arciniegas, R., DeGraff, S., Materson, B. J., Bernstein, J., & Afshartous,
D. (2019). Outcomes of minority patients with very severe hypertension
(>220/>120 mmHg). Journal of Hypertension, 37(2), 415. https://doi.org/10.1097/
HJH.0000000000001906
Whelton, P. K., Carey, R. M., Carey, R. M., Aronow, W. S., Casey, D. E., Jr., Collins, K. J.,
Himmelfarb, C. D., DePalma, S. M., Gidding, S., Jamerson, K. A., Jones, D. W.,
MacLaughlin, E. J., Muntner, P., Ovbiagele, B., Smith, S. C., Jr., Spencer, C. C.,
Stafford, R. S., Taler, S. J., Thomas, R. J., Williams, K. A., Sr., … Wright, J. T., Jr. (2018).
2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA
guideline for the prevention, detection, evaluation, and management of high blood
pressure in adults: A report of the American College of Cardiology/American Heart
Association Task Force on Clinical Practice Guidelines. Hypertension, 71(6), e13. https://
doi.org/10.1161/HYP.0000000000000065
Yancy, C. W., Januzzi, J. L., Jr., Allen, L. A., Butler, J., Davis, L. L., Fonarow, G. C.,
Ibrahim, N. E., Jessup, M., Lindenfeld, J., Maddox, T. M., Masoudi, F. A.,
Motiwala, S. R., Patterson, J. H., Walsh, M. N., & Wasserman, A. (2017). ACC
expert consensus decision pathway for optimization of heart failure treatment:
Answers to 10 pivotal issues about heart failure with reduced ejection fraction:
A report of the American College of Cardiology Task Force on expert consensus
decision pathways. Journal of the American College of Cardiology, 71(2), 201. https://
doi.org/10.1016/j.jacc.2017.11.025
SECTION II
PULMONARY DISORDERS
AND MANAGEMENT
4
RESPIRATORY FAILURE
Causes
Neurological
■ Change in level of consciousness
● Opiate overdose
■ Neuromuscular disease
● Guillain–Barré syndrome
● Myasthenia gravis
■ Spinal cord injury
Chest
■ Trauma to chest wall
■ Obesity
■ Kyphosis
■ Pneumothorax
■ Hemothorax
■ Abdominal distention
■ Pleural effusion
Lung parenchyma
■ Edema
■ Atelectasis
■ Infiltrate
Airway
■ Upper airway
Tumor
●
Edema
●
■ Allergic reaction
■ Angioedema
● Foreign body
● Abscess
● Trauma
■ Lower airway
● Foreign body
● Mucus plug
● Tumor
● Bronchospasm
27
28 II PULMONARY DISORDERS AND MANAGEMENT
Vascular
■ Pulmonary embolism
■ Right ventricular failure
Assessment Findings
General
■ Altered mental status
■ Decreased level of consciousness
■ Anxiety
■ Diaphoresis
■ Cyanosis
Respiratory
■ Increased work of breathing
■ Tachypnea
■ Hypoxia
■ Ancillary muscle use
■ Abnormal lung sounds
● Dependent of pathology
■ Mucus production
■ Cough
Cardiovascular
■ Tachycardia
■ Bradycardia
● Sign of severe hypoxia
■ Hypotension/shock
4 RESPIRATORY FAILURE 29
Diagnostics
Laboratory
■ Arterial blood gas
■ Complete blood count (CBC)
■ Chemistries
■ Lactic
Radiology
(continued)
30 II PULMONARY DISORDERS AND MANAGEMENT
F—Fields
■ Infiltrates
● Identify the location of infiltrates by use of known radiological phenomena, for example,
loss of heart borders or of the contour of the diaphragm.
● Remember that right middle lobe abuts the heart, but the right lower lobe does not.
● The lingula abuts the left side of the heart.
■ Identify the pattern of infiltration
● Interstitial pattern (reticular) versus alveolar (patchy or nodular) pattern
● Lobar collapse
● Look for air bronchograms, tram tracking, nodules, Kerley B lines
● Pay attention to the apices
■ Look for granulomas, tumor, and pneumothorax
G—Gastric Air Bubble
■ Check correct position
■ Beware of hiatus hernia
■ Look for free air
■ Look for bowel loops between diaphragm and liver
H—Hilum
■ Check the position and size bilaterally
■ Enlarged lymph nodes
■ Calcified nodules
■ Mass lesions
■ Pulmonary arteries; if greater than 1.5 cm, think about possible causes of enlargement
■ Chest x-ray
Anterior–posterior (AP)
●
Posterior–anterior (PA) and lateral
●
■ EKG
■ Bronchoscopy
● Diagnostics
■ Evaluation of disease
■ Evaluate structures and mucosa
■ Take biopsies
● Therapeutic
■ Removal of secretions
■ Removal of foreign bodies
■ Removal of mucous plugging
4 RESPIRATORY FAILURE 31
INTUBATION CRITERIA
Degree of distress
■ Evaluate degree of distress
■ Respiratory rate >30
■ Work of breathing
■ Ancillary muscle use
■ Apnea
■ Age and ability to sustain level of distress
Gas exchange
■ Evaluation of arterial blood gas
■ Hypoxemia
■ Ventilation
■ Acidosis with pH <7.25
Progression of underlying process
■ How long will it take to correct the underlying condition?
■ Can patient maintain airway until the condition is corrected?
■ Level of consciousness
■ Hemodynamic instability
Noninvasive Ventilation
■ Continuous positive airway pressure
■ Bilevel positive airway pressure (BiPAP)
■ May be beneficial in patients who do not require more than 48 hours of
support and can protect their airway
Mechanical Ventilation
■ Goals
● Improve ventilation
■ Minute ventilation (MV) = tidal volume × respiratory rate
■ Manipulate respiratory rate
● Increasing respiratory rate will decrease CO2
● Increasing respiratory rate will increase MV
32 II PULMONARY DISORDERS AND MANAGEMENT
BIBLIOGRAPHY
Adler, D., Pépin, J.-L., Dupuis-Lozeron, E., Espa-Cervena, K., Merlet-Violet, R.,
Muller, H., Janssens, J.-P., & Brochard, L. (2017). Comorbidities and subgroups of
patients surviving severe acute hypercapnic respiratory failure in the intensive
care unit. American Journal of Respiratory and Critical Care Medicine, 196(2), 200.
https://doi.org/10.1164/rccm.201608-1666OC
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Ram, F. S., Picot, J., Lightowler, J., & Wedzicha J. A. (2004). Non-invasive positive
pressure ventilation for treatment of respiratory failure due to exacerbations
of chronic obstructive pulmonary disease. The Cochrane Database of Systematic
Reviews, (1), CD004104. https://doi.org/10.1002/14651858.CD004104.pub2
Tobin, M. J., Jubran, A., & Laghi, F. (2001). Patient-ventilator interaction. American
Journal of Respiratory Critical Care Medicine, 163(5), 1059. https://doi.org/10.1164/
ajrccm.163.5.2005125
Wilson, J. G., & Matthay, M. A. (2014). Mechanical Ventilation in acute hypoxemic
respiratory failure: A review of new strategies for the practicing hospitalist.
Journal of Hospital Medicine, 9(7), 469–475. https://doi.org/10.1002/jhm.2192
5
ADULT RESPIRATORY DISTRESS
SYNDROME
Causes
■ Sepsis
■ Pneumonia
● Aspiration pneumonia
■ Blunt force trauma
■ Fat embolism
■ Transfusion-related acute lung injury (TRALI)
● Adult respiratory distress syndrome (ARDS) that develops after
transfusion of blood products
■ Massive blood transfusion
● Required in trauma or massive hemorrhage
33
34 II PULMONARY DISORDERS AND MANAGEMENT
Assessment Findings
General
■ Fever
■ Hemodynamic instability
■ Symptoms of underlying condition such as sepsis or trauma
■ Cyanosis
Respiratory
■ Dyspnea
■ Cough
■ Sudden increase in oxygen requirement
■ Hypoxia
■ Sputum production
■ Elevated peak airway pressures
■ Paradoxical breathing
■ Abnormal lung sounds
● Wheezing
● Rhonchi
● Stridor
Cardiovascular
■ Tachycardia
■ Hypotension
■ Shock symptoms
Neurological
■ Confusion
■ Altered mental status
■ Decreased level of consciousness
■ Restlessness
Diagnostics
Lab
■ Complete blood count (CBC)
■ Serum chemistry
■ D-dimer
■ Brain natriuretic peptide (BNP)
■ Arterial blood gas
Radiology
■ Chest x-ray
● Findings
■ Bilateral diffuse opacities
■ Ground glass opacities
■ “White out” chest x-ray
■ Chest CT
● May be helpful to determine the extent of ARDS
Microbiology
■ Sputum culture
■ Bronchoscopy cultures
Echocardiogram
■ Helpful in determining cardiogenic pulmonary edema versus ARDS
Bibliography
Brodie, D., & Bacchetta, M. (2011). Extracorporeal membrane oxygenation for ARDS
in adults. New England Journal of Medicine, 365(20), 1905–1914. https://doi.org/
10.1056/NEJMct1103720
Cheng, I. W., Eisner, M. D., Thompson, B. T., Ware, L. B., & Matthay, M. A. (2005).
Acute effects of tidal volume strategy on hemodynamics, fluid balance, and
sedation in acute lung injury. Critical Care Medicine, 33(1), 63. https://doi.org/
10.1097/01.ccm.0000149836.76063.71
Chimello, D., & Brioni, M. (2016). Severe hypoxemia: Which strategy to choose.
Critical Care, 20(1), 132. https://ccforum.biomedcentral.com/track/pdf/10.1186/
s13054-016-1304-7.pdf
Fan, E., Brodie, D., & Slutsky, A. S. (2018). Acute respiratory distress syndrome:
Advances in diagnosis and treatment. JAMA, 319(7), 698–710. https://doi.org/
10.1001/jama.2017.21907
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
5 ADULT RESPIRATORY DISTRESS SYNDROME 37
Tobin, M. J., Jubran, A., & Laghi, F. (2001). Patient-ventilator interaction. American
Journal of Respiratory Critical Care Medicine, 163(5), 1059. https://doi.org/10.1164/
ajrccm.163.5.2005125
Wilson, J. G., & Matthay, M. A. (2014). Mechanical ventilation in acute hypoxemic
respiratory failure: A review of new strategies for the practicing hospitalist.
Journal of Hospital Medicine, 9(7), 469–475. https://doi.org/10.1002/jhm.2192
Yonsuck, K. (2014). Update in acute respiratory distress syndrome. Journal of Intensive
Care, 2(2), 1–6. https://doi.org/10.1186/2052-0492-2-2
Zambon, M., & Vincent, J. L. (2008). Mortality rates for patients with acute lung
injury/ARDS have decreased over time. Chest, 133(5), 1120. https://doi.org/
10.1378/chest.07-2134
SECTION III
MANAGEMENT OF
NEUROLOGICAL CONDITIONS
6
TRANSISCHEMIC ATTACKS
AND CEREBROVASCULAR
ACCIDENTS
TRANSISCHEMIC ATTACKS
Causes
Embolic
■ Particles of debris that originate elsewhere in the body block blood flow
to a region of the brain
Thrombosis
■ Manual obstruction of an artery due to disease of the artery wall or
fibromuscular dysplasia
Lacunar or Small Vessel
■ Disease of the small vessels of the brain that may decrease microperfusion
to the brain
Low Flow
■ Due to low blood flow of stenosed vessels in the brain
Systemic Hypoperfusion
■ Due to low blood flow to the brain; may be seen in systemic hemorrhage
or heart failure
41
42 III MANAGEMENT OF NEUROLOGICAL CONDITIONS
Assessment Findings
■ Sudden onset of symptoms
■ Hemiparesis
■ Dysarthria
■ Dysphasia
■ Diplopia
■ Circumoral numbness
■ Imbalance
■ Monocular blindness
Diagnostics
Radiology
■ CT head
● Imaging can be normal or show chronic changes
■ MRI brain
May show areas of ischemia better than CT
●
May still be negative
●
■ Magnetic resonance angiography (MRA) head
● May show occlusion or vascular
Ultrasound
■ Carotid artery dopplers
● Evaluate for plaque or occlusion
Echocardiograph
■ Bubble study
● Evaluate for septal defect
CEREBROVASCULAR ACCIDENTS
Causes
Vascular Disorders
■ Atherosclerosis
Disease in the brain and neck
●
Most common cause in older adults
●
■ Carotid or vertebral artery dissection
6 TRANSISCHEMIC ATTACKS AND CEREBROVASCULAR ACCIDENTS 43
■ Fibromuscular dysplasia
● Common cause in younger adults
■ Giant cell arteritis
■ Systemic lupus erythematosus
■ Cocaine use
Can cause cerebral vasospasm
●
Rupture arteriovenous (AV) malformations
●
■ Moyamoya syndrome
■ Dissection of carotid or vertebral arteries
Embolism
■ Atrial fibrillation
■ Atrial flutter
■ Mitral or aortic valve disease
■ Carotid artery arteriosclerosis
■ Sickle cell disease
■ Prosthetic heart valves
■ Rheumatic heart disease
■ Bacterial endocarditis
● Commonly seen in intravenous (IV) drug users
■ Atrial septal defect
■ Atrial myxoma
Hypercoagulable States
■ Antiphospholipid antibody syndrome
■ Oral contraceptives
■ Polycythemia
■ Sickle cell disease
■ Leukemia
■ Activated protein C resistance
■ Protein C, S, or antithrombin III deficiency
■ Disseminated intravascular coagulopathy
Systemic Hypoperfusion
■ Heart failure with ejection fraction <30%
(continued)
44 III MANAGEMENT OF NEUROLOGICAL CONDITIONS
Assessment Findings
General
■ Sudden onset of symptoms
■ Hemiparesis
■ Dysarthria
■ Dysphasia
■ Diplopia
■ Circumoral numbness
■ Imbalance
■ Monocular blindness
■ Carotid bruits
Subarachnoid Hemorrhage
■ Sudden intense headache
■ May radiate to posterior neck; worsened by neck movement
Intracranial Hemorrhage
■ Hypertension
■ Headache
■ Eye deviation
● Conjugately
● Downward
6 TRANSISCHEMIC ATTACKS AND CEREBROVASCULAR ACCIDENTS 45
■ Pinpoint pupils
■ Coma
■ Vertigo
Diagnostics
Radiology
■ CT head
● Lacunar infarct
■ Degenerative changes from small arteries deep in the brain
● Assessment for intracranial bleeding prior to the administration
of tissue plasminogen activator (tPA)
● Will differentiate between ischemic and hemorrhagic stroke
■ MRI brain
● More sensitive than CT
● May show ischemia
■ MRA head
● Evaluation of intracranial vessels and extracranial vessels
Ultrasound
■ Carotid artery dopplers
■ Evaluate for carotid artery occlusion
Echocardiograph
■ Bubble study
● Evaluate for atrio-septal defect
Laboratory
■ Chemistry
● Hypoglycemia can mimic stroke symptoms
● Electrolyte abnormalities
■ Coagulation panel
● Evaluate for coagulopathy
● Baseline prior to initiating anticoagulation therapy
■ Lipid panel
■ Eosinophil sedimentary rate (ESR)
● Elevated in vasculitis, endocarditis, giant cell arteritis
Microbiology
■ Blood cultures
● Evaluate for endocarditis
EKG
■ Identify atrial fibrillation or atrial flutter.
46 III MANAGEMENT OF NEUROLOGICAL CONDITIONS
Diabetes
■ Adequate glucose management in patients with diabetes
Fibrinolytic Therapy
■ Alteplase
● See Clinical Tips and Tricks (Tissue Plasminogen Activator Guidelines)
● Evaluate bleeding risk
Mechanical Thrombectomy
■ Done for large artery occlusions
■ Can be done up to 24 hours from the last known neurological baseline
■ Can be performed even if the patient has received thrombolytics
6 TRANSISCHEMIC ATTACKS AND CEREBROVASCULAR ACCIDENTS 47
Subarachnoid Hemorrhage
■ Continuous cardiac monitoring
■ Reversal of anticoagulation medications
■ Monitoring for cerebral edema and increase in intracranial pressure (ICP)
■ Neurosurgery consult is generally indicated
■ If aneurysm is the underlying cause, surgical intervention may be indicated
■ Blood pressure management and control
● Being aware to not lower blood pressure too quickly or too low
Intracranial Hemorrhage
■ Reversal of anticoagulation medications
● Infusion of fresh frozen plasma (FFP)
● Vitamin K
● Protamine sulfate
■ For patients receiving heparin infusions prior to bleeding
■ Stop all anticoagulants and antiplatelet medications
■ Blood pressure management and control
■ ICP monitoring and management
● Head of bed at 30 degrees
● Sedation to keep calm
■ Medications
● Mannitol
■ Osmotic therapy
■ Initial dose 0.5 to 1 g/kg
■ Repeat dosing 0.25 to 0.5 g/kg every 4 to 12 hours
■ Dosing should not exceed 250 mg q4h
■ Check serum osmolality
● Goal 300 mOsmol/kg
● Hypertonic saline (3%)
■ Osmotic therapy
■ Serum sodium goal 145 to 155 mEq/L
● Barbiturate coma
■ Pentobarbital is the most used medication
● Initial bolus 10 to 15 mg/kg
● 1 to 4 mg/kg/hr maintenance
● Propofol
■ May help to decrease ICP
● Hyperventilation
Seizure Management
■ Higher risk of seizure in the following:
Intracerebral hemorrhage
●
Subcortical hematoma
●
Cortical location
●
Increased risk with the increase in the severity of the stroke
●
■ Medication for prophylaxis based on degree of risk and benefit for patient
■ Consider medication in higher-risk patients
48 III MANAGEMENT OF NEUROLOGICAL CONDITIONS
Bibliography
Albers, G. W., Caplan, L. R., Easton, J. D., Fayad, P. B., Mohr, J. P., Saver, J. L., &
Sherman, D. G.; TIA Working Group (2002). Transient ischemic attach: Proposal
for a new definition. New England Journal of Medicine, 347(21), 1713–1716. https://
doi.org/10.1056/NEJMsb020987
Chan, L., Hu, C.-J., Fan, Y.-C., Li, F.-Y., Hu, H.-H., Hong, C.-T., & Bai, C.-H. (2018).
Incidence of post stroke seizures: A meta-analysis. Journal of Clinical Neuroscience,
47(2), 347–351. https://doi.org/10.1016/j.jocn.2017.10.088
Del Zoppo, G. J., Saver, J. L., Jauch, E. C., & Adams, H. P., Jr.; American Heart
Association Stroke Council (2009). Expansion of the time window for treatment
of acute ischemic stroke with intravenous tissue plasminogen activator: A science
advisory from the American Heart Association/American Stroke Association.
Stroke, 40(8), 2945–2948. https://doi.org/10.1161/STROKEAHA.109.192535
6 TRANSISCHEMIC ATTACKS AND CEREBROVASCULAR ACCIDENTS 49
51
52 III MANAGEMENT OF NEUROLOGICAL CONDITIONS
Assessment Findings
During seizure
■ Neurological
● Aura
■ Sense prior to seizure
■ Can be visual disturbance or smell
Tonic–clonic movements
●
Nystagmus
●
Uncontrolled movements
●
Altered mental status
●
Memory loss
●
Blank stare
●
Posturing
●
■ Decortication
■ Decerebrating
■ Cardiovascular
● Tachycardia
● Hypertension
■ Respiratory
● Ictal cry
■ A moan or noise that escapes the pharynx due to contracture of the
muscles
● Cyanosis
● Apnea
● Bleeding from mouth or tongue
■ Genitourinary
● Incontinence of bowel or bladder
Memory loss
●
Confusion
●
Weakness
●
Sleeping
●
■ Cardiovascular
● Tachycardia
● Hypotension
■ Respiratory
● Bleeding from mouth or tongue
● Excessive salivation
■ Musculoskeletal
● Muscle flaccidity
● Muscle pain
TYPES OF SEIZURES
Typical absence seizures: Sudden brief loss of consciousness. Body control remains intact.
Atypical absence seizures: Sudden loss of consciousness but lasts longer than typical absence
seizures.
Generalized tonic–clonic seizures: Starts abruptly without warning and causes tonic muscle
contractions.
Atonic seizures: Sudden loss of tone that lasts only seconds.
Myoclonic seizures: Sudden brief muscle contraction that can range from one area of the body
to the whole body.
Epileptic seizures: Sustained spasms of flexion and extension.
Diagnostics
Laboratory
■ CBC
● Elevated white blood cell (elevated WBC count)
■ Chemistry
● Hypokalemia
● Hypocalcemia
● Hypoglycemia
■ Endocrine studies
■ Elevated lactic
■ Elevated LDH
■ Elevated creatinine kinase
■ Elevated prolactin level
● Accurate only if obtained within 30 minutes of seizure activity
54 III MANAGEMENT OF NEUROLOGICAL CONDITIONS
■ Urinalysis
■ Blood alcohol level
■ Urine drug screen
■ Valproic acid level
● Check for therapeutic level
● Therapeutic level 50 to 100 mcg/mL
■ Phenytoin level
● Check for therapeutic level
● Therapeutic level 10 to 20 mcg/mL
Lumbar puncture
■ If infection suspected
■ Culture
EEG
■ Normal EEG does not rule out seizure activity
■ Focal abnormalities—partial seizures
■ Generalized abnormalities—primary generalized seizures
Radiology
■ Head CT
● To evaluate acute intracranial pathology
■ MRI
STATUS EPILEPTICUS
■ Definition
● Continuous or repetitive seizures in which patient does not regain
wakefulness between events
● Emergent situation
● Can cause significant neurological injury
■ Management
● D50 bolus
● Thiamine 100 mg IM
● Diazepam
■ IV ideal dosing
■ 0.2 mg/kg
■ 20 mg maximum in one dose
● Lorazepam
■ IV ideal dosing
■ 0.1 mg/kg
■ 10 mg maximum in one dose
● Risk for airway compromise with high dose of benzodiazepines
56 III MANAGEMENT OF NEUROLOGICAL CONDITIONS
Bibliography
Beghi, E., Carpio, A., Forsgren, L., Hesdorffer, D. C., Malmgren, K., Sander, J. W.,
Tomson, T., & Hauser W. A. (2010). Recommendation for a definition of acute
symptomatic seizure. Epilepsia, 51(4), 671–675. https://doi.org/10.1111/j.1528
-1167.2009.02285.x
Bottaro, F. J., Martinez, O. A., Pardal, M. M., Bruetman, J. E., & Reisin, R. C. (2007).
Nonconvulsive status epilepticus in the elderly: A case-control study. Epilepsia,
48(5), 966. https://doi.org/10.1111/j.1528-1167.2007.01033.x
Droney, J., & Hall, E. (2008). Status epilepticus in a hospice inpatient setting. Journal
of Pain and Symptom Management, 36(1), 97–105. https://doi.org/10.1016/
j.jpainsymman.2007.08.009
Huff, J. S., Morris, D. L., Kothari, R. U., & Gibbs, M. A. (2001). Emergency
department management of patients with seizures: A multicenter study. Academic
Emergency Medicine, 8(6), 622–628. https://doi.org/10.1111/j.1553-2712.2001.
tb00175.x
Matz, O., Heckelmann, J., Zechbauer, S., Litmathe, J., Brokmann, J. C., Willmes, K.,
Schulz, J. B., & Dafotakis, M. (2018). Early postictal serum lactate concentrations
are superior to serum creatine kinase concentrations in distinguishing generalized
tonic-clonic seizures from syncopes. Internal Emergency Medicine, 13(5), 749.
https://doi.org/10.1007/s11739-017-1745-2
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Pellock, J. M. (1998). Management of acute seizure episodes. Epilepsia, 39 (1), S28–S35.
Walker, M. C. (2003). Status epilepticus on the intensive care unit. Journal of
Neurology, 250(4), 401. https://doi.org/10.1007/s00415-003-1042-z
SECTION IV
MANAGEMENT OF RENAL AND
ELECTROLYTE DISORDERS
8
ACUTE KIDNEY INJURY
AND RENAL FAILURE
RENAL FAILURE
■ Renal dysfunction is common in acutely ill patients.
■ Up to 80% of all ICU patients will have some level of renal dysfunction during their stay.
■ Prevention of dysfunction is ideal, but early recognition and treatment of kidney injury can be
key to preserving or restoring function.
■ Age can also be a complicating factor, with many older patients having some underlying degree
of renal dysfunction.
■ Advanced age can complicate or exacerbate renal injury in acutely ill patients.
Prerenal
Causes
■ Hypovolemia
● Volume depletion
■ Hemorrhage
■ Dehydration
■ Diabetes insipidus
● Decreased circulating volume
■Hepatorenal syndrome
■Cirrhosis
■Congestive heart failure
■Nephrotic syndrome
■ Hypotension
● Sepsis
● Shock states
■ Renal artery stenosis
■ Vasculitis
■ Drugs affecting perfusion
● Cyclosporine
● Tacrolimus
59
60 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
AZOTEMIA UREMIA
● Significantly increases in BUN with or ● Cluster of symptoms associated with
without increase in creatinine renal failure
● Not associated with specific symptoms ● Pruritis
● May not be related to kidney injury ● Encephalopathy/alterations in mental
status
● Nausea and/or vomiting
BUN, blood urea nitrogen
Assessment Findings
■ Decreased urine output
■ Tachycardia
■ Shock symptoms
■ Altered mental status
■ Nausea
■ Vomiting
RISK STAGE I
INJURY STAGE II
URINE OUTPUT <0.3 mL/kg/hr for more >300% of baseline or >4 mg/dL
than 12 hours with an acute increase of >0.5
mg/dL or on RRT
Diagnostics
■ Laboratory
● Basic metabolic panel
■ BUN-to-creatinine ratio 20:1
■ Hyperkalemia
● Complete blood count (CBC)
■ Leukocytosis
■ Urinalysis
Hyaline casts in urinalysis
●
Decreased urine sodium
●
Increased urine-specific gravity
●
■ Fraction of excreted sodium (FENa)
● FENa <1%
INTRARENAL
INTRARENAL (INTRINSIC)
■ Intrinsic injuries can be classified by ischemic and nephrotoxic injuries.
■ These are conditions that lead to damage to the functionality of the kidney by damaging part of
the structure.
■ Decreased urine output and increase in serum BUN and creatinine after event or exposure.
■ Many different causes with different diagnostics.
Causes
■ Most common intrarenal condition
■ Hypoperfusion causes damage and destruction to the renal tubules
■ Caused by prolonged prerenal conditions
Assessment Findings
■ Current or recent shock state
■ Symptom of volume depletion
■ Decreased urine output
■ Tachycardia
■ Hypotension
Diagnostics
■ BUN/creatinine ratio of 10:1
■ Urine osmolality approximately 300 mOsm/kgH2O
■ Urine sodium > 40 mEq/L
■ FENa >2%
■ Muddy brown casts on urinalysis
CONTRAST-INDUCED NEPHROPATHY
Causes
■ Renal vasoconstriction and direct cytotoxicity of contrast material
● Patients should be well hydrated with isotonic fluids prior to
studies requiring dye injections to decrease risk for contrast-induced
nephropathy
● Benefits of testing should also be considered
Assessment Findings
■ Sudden decrease in urine output
■ Recent contrast administration
■ Edema
■ Malaise
Diagnostics
■ FeNa <1%
■ Serum creatinine increases quickly over 24 to 48 hours after contrast
media
GLOMERULONEPHRITIS
Causes
■ Medications
■ Immunologic conditions
■ Infection
■ Vasculitis
Assessment Findings
■ Hematuria
■ Proteinuria
■ Hypertension
64 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
■ Edema
■ Bleeding
Diagnostics
■ Laboratory findings
Hyponatremia
●
Elevated partial thromboplastin time (PTT)
●
Elevated international normalized ratio (INR)
●
Low fibrinogen
●
■ Urinalysis
● Blood
● Red blood cells
● Protein
● Dysmorphic erythrocytes
● Erythrocyte casts
■ Biopsy
INTERSTITIAL NEPHRITIS
Causes
■ Drug induced
Most common cause
●
Sulfonamides
●
Aminoglycosides
●
Vancomycin
●
Mannitol
●
■ Infection
■ Immunological
Assessment Findings
■ Decreased urine output
■ Fever
■ Rash
■ Arthralgias
8 ACUTE KIDNEY INJURY AND RENAL FAILURE 65
Diagnostics
■ Classic triad (10%–30% of patients)
● Fever
● Rash
● Eosinophilia
● Mild proteinuria
■ BUN-to-creatine ratio variable among patients
■ Urine osmolality variable
POSTRENAL
POST RENAL
■ Urinary obstruction that causes a rise in the renal tubular pressure and eventually decreases
the tubular function.
■ If obstruction is not removed or urine diverted, permanent damage to the kidney may result.
■ If obstruction is bilateral, it can be the cause of permanent renal failure.
■ Progressive disease where vascular supply is disrupted and leads to loss of renal function over
a period.
■ it goes untreated, permanent renal failure may result.
If
■ Risk increases with advanced age.
■ Suprapubic catheter may be indicated in emergent situations where obstruction cannot be
bypassed by other methods.
Causes
Renal Calculi
■ Types of calculi
● Hypercalciuric calcium
● Hyperoxaluric calcium
● Hyperuricosuria calcium
● Struvite
● Uric acid
● Cystine
● Hypocitraturia
66 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
Assessment Findings
■ Renal colic
■ Nausea
■ Vomiting
■ Costovertebral angle tenderness
■ Dysuria
■ Abdominal or flank pain
■ Bladder distention
NEPHROLITHIASIS
■ Nephrolithiasis is a condition when stones are in the pelvis, kidney, or ureters.
■ These stones are made up of calcium phosphate uric acid, calcium oxalate, struvite, or cystine.
■ Some people are more prone to developing stones and may develop many stones over their lifetime.
■ There is a higher incidence of stones in men.
Causes
■ Arteriosclerosis of renal arteries
■ Fibromuscular dysplasia
Risk Factors
■ Advanced age
■ Being female
■ Underlying hypertension
■ Tobacco use
■ Diabetes
Assessment Findings
■ Sudden onset of hypertension
■ Age >50 years
■ Resistant hypertension
■ Pulmonary edema without history
Diagnostics
■ Renal functions
■ Serum chemistries
■ Urinalysis
■ Renal ultrasound
68 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
First-line diagnostic
●
May show asymmetric kidneys
●
■ CT angiography
■ Invasive angiography
■ MRA
Bibliography
Chacko, J. (2008). Renal replacement therapy in the intensive care unit. Indian Journal
of Critical Care Medicine, 12(4), 174–180. https://doi.org/10.4103/0972-5229.45078
Farrar, A. (2018). Acute kidney injury. Nursing Clinics of North America, 53(4), 499–510.
https://doi.org/10.1016/j.cnur.2018.07.001
Hricik, D. E., Chung-Park, M., & Sedor, J. R. (1998). Glomerulonephritis. New
England Journal of Medicine, 339(13), 888–899. https://doi.org/10.1056/
NEJM199809243391306
Huber, W., Schneider, J., Lahmer, T., Küchle, C., Jungwirth, B., Schmid, R. M., &
Schmid, S. (2018). Validation of RIFLE, AKIN, and modified AKIN definition of
acute kidney injury in a general ICU. Medicine, 97(38), 1–8. https://doi.org/
10.1097/MD.0000000000012465
Isaac, S. (2012). Contrast- induced nephropathy: Nursing implications. Critical Care
Nurse, 32(3), 41–48. https://doi.org/10.4037/ccn2012516
Koyner, J. L. (2012). Assessment and diagnosis of renal dysfunction in the ICU. Chest,
141(6), 1584–1594. https://doi.org/10.1378/chest.11-1513
Lao, D., Parasher, P. S., Cho, K. C., & Yeghiazarians, Y. (2011). Atherosclerotic renal
artery stenosis- Diagnosis and treatment. Mayo Clinic Proceedings, 86(7), 694–657.
https://doi.org/10.4065/mcp.2011.0181
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Ronco, C., Bellomo, R., & Kellum, J. A. (2019). Acute kidney injury. Lancet, 394,
1949–1964. https://doi.org/10.1016/S0140-6736(19)32563-2
Ronco, C., & Ricci, Z. (2008). Renal replacement therapies: Physiological review.
Intensive Care Medicine, 34, 2139–2146. https://doi.org/10.1007/s00134-008-1258-6
Safian, R. D., & Textor, S. C. (2001). Renal artery stenosis. New England Journal of
Medicine, 344(6), 431–442. https://doi.org/10.1056/NEJM200102083440607
Vinen, C. S., & Oliveira, D. G. (2002). Acute glomerulonephritis. Postgraduate Medical
Journal, 79, 206–213. https://doi.org/10.1136/pmj.79.930.206
9
ELECTROLYTE DERANGEMENTS
POTASSIUM
Normal Level
■ 3.5 to 5.2 mEq/L
HYPERKALEMIA
POTASSIUM
■ Potassium is a vital electrolyte that plays a large part in muscle function.
■ Approximately 90% of potassium is intracellular.
■ The kidneys are the primary method of excretion.
Causes
■ Transcellular shift
● Rhabdomyolysis
● Metabolic acidosis
● Hemolysis
● Tumor lysis syndrome
● Hyperglycemia
● Succinylcholine administration
● Digoxin toxicity
■ Impaired excretion of potassium
● Acute kidney injury
● Chronic renal failure
● Ingestion of potassium foods
● Potassium supplements
● Transfusion on blood products
● Potassium sparing diuretics
● Sickle cell disease
● Medications
69
70 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
HYPERKALEMIA
■ Peaked T waves are only seen in a small percentage of patients.
■ Chronic hemodialysis patients will often tolerate a high potassium level for a longer period.
■ Patient may not have any symptoms.
■ Hyperkalemia may be present post cardiac arrest due to hypoperfusion.
Assessment Findings
■ Muscle weakness
■ Flaccid paralysis
■ Cardiac abnormalities
■ Symptoms of underlying conditions
Diagnostics
■ Laboratory
● Chemistry
■ Serum K level >5.2 mEq/L
Serum renin
●
Serum aldosterone
●
■ EKG
● Peaked T waves
● Prolonged PR intervals
● Wide QRS
● V-fib
Critical-Level Treatment
■ Regular insulin
● Dose: 10 units IV
9 ELECTROLYTE DERANGEMENTS 71
● Onset: 15 minutes
● D50 given to prevent hypoglycemia if patient is euglycemic
■ Calcium
● Dose: Calcium gluconate 10% 1G IV
● Onset: Immediate
■ Albuterol nebulizer
● Dose: 10 to 20 mg nebulizer over 15 minutes
● Onset: 10 to 30 minutes
■ Sodium bicarb
● Effective only if there is underlying metabolic acidosis
■ Emergent dialysis treatment in severe cases
HYPOKALEMIA
Causes
■ Decreased intake
■ Transcellular shift
● Insulin excess
● Beta 2 adrenergic agonist (albuterol)
● Thyrotoxicosis
■ Renal loss
● Diuretic use
■ Thiazides
■ Loop
■ Acetazolamide
■ Mannitol
■ Gastrointestinal (GI) loss
● Diarrhea
● Vomiting
● Nasogastric (NG) suction
■ Renal tubular acidosis
■ Increased aldosterone
■ Renin secreting tumor
■ Hypomagnesemia
HYPOKALEMIA
■ Most common cause is use of loop diuretics
■ Can also be associated with excess water
■ In the ICU setting, hyponatremia has been shown to be associated with mortality and a high
risk of death
72 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
Assessment Findings
■ Muscle weakness
■ Muscle cramps
■ Diaphragm paralysis
■ Palpitations
■ Flattened T waves on EKG
■ Arrhythmias
Diagnostics
■ Serum K <3.5 mEq/L
■ Lab chemistries
■ EKG with flattened T waves
■ Low serum Mg level
■ Aldosterone
■ Renin
■ Arterial blood gas (ABG)
● pH
● Serum bicarbonate
Critical-Level Treatment
■ Combination of IV and PO (by mouth, if able to tolerate) recommended
■ Continuous cardiac monitoring
■ Watch for arrhythmias
SODIUM
Normal Level
135 to 145 mEq/L
9 ELECTROLYTE DERANGEMENTS 73
HYPERNATREMIA
Causes
Hypovolemia/Euvolemia
■ Decreased water intake
● Older adults
● Nothing by mouth (NPO) due to illness
● Unable to access free water
● Impaired thirst
■ Insensible water loss
● Acute burns
● Large wounds
● Open abdomen
● Febrile states
● Excessive sweating
● Blistering skin diseases
■ Bullous pemphigoid
■ Toxic epidermal necrolysis
■ Osmotic diuresis
● Water loss
● Mannitol therapy
■ GI loss
● Excessive diarrhea or emesis
■ Surgical drains
■ Central diabetes insipidus
■ Nephrogenic diabetes insipidus
Hypervolemia
■ Hypertonic sodium load
Sodium bicarb infusions
●
IV sodium chloride infusion
●
Salt tablets
●
■ Hyperaldosteronism/Cushing’s syndrome
Assessment Findings
■ Neurologic
● Stupor
● Coma
● Lethargy
● Confusion
● Irritability
■ GI
● Nausea
● Vomiting
74 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
■ Hypotension
■ Tachycardia
■ Thirst
■ Polyuria
■ Symptoms of underlying disease process
Diagnostics
■ Serum sodium level greater than 150 mEq/L
■ Serum osmolality
■ Urine osmolality
■ Antidiuretic hormone (ADH) level
HYPONATREMIA
Causes
■ Thiazide diuretics
■ Pseudohyponatremia
● Sodium corrected for hyperglycemia
■ Hypervolemia or excess free water
■ Syndrome of inappropriate diuretic hormone (SIADH)
■ Cerebral sodium salt wasting
Assessment Findings
■ Weakness
■ Lethargy
9 ELECTROLYTE DERANGEMENTS 75
Diagnostics
■ Laboratory
Serum chemistry
●
Serum electrolytes
●
■ Serum sodium level of <135 mEq/L
● Serum osmolality
● Cortisol
● Adrenocorticotropic hormone (ACTH)
■ Urinalysis
● Urinalysis
● Urine electrolytes
● Urine osmolality
CALCIUM
Normal Level
■ Calcium 8.6 to 10.2 mg/dL
■ Ionized calcium 4.6 to 5.3 mg/dL
76 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
CALCIUM
■ Most of the body’s calcium stored in bone
■ Plays a role in muscle and motor function
■ Serum calcium can be inaccurate in patients with low albumin
HYPERCALCEMIA
Causes
■ Hyperparathyroidism
● Most common cause
■ Malignancy
● Especially in lung, renal, or breast cancer
■ Vitamin D toxicity
■ Granulomatous disease
● Sarcoidosis
■ Vitamin A intoxication
■ Hyperthyroidism
■ Immobilization or casting
■ Thiazide diuretic
Assessment Findings
■ Neurologic
● Lethargy
● Coma
● Personality changes
■ GI
Nausea
●
Vomiting
●
Constipation
●
■ Renal
● Renal calculi
● Nocturia
■ Musculoskeletal
● Muscle weakness
● Bone pain
● Depressed deep tendon reflexes
9 ELECTROLYTE DERANGEMENTS 77
■ Hypertension
■ Confusion
■ Weakness
Diagnostics
■ Laboratory
Serum calcium > 10.2 mg/dL
●
Ionized calcium > 5.3 mg/dL
●
Parathyroid hormone (PTH) level
●
Thyroid functions
●
Vitamin D levels
●
■ EKG
● QTc interval
HYPOCALCEMIA
Causes
■ Hypoparathyroidism
● Seen in patients with thyroidectomy
■ Vitamin D deficiency
● Poor PO intake
● Severe liver disease
● P450 enzyme inducers
■ Phenytoin
■ Phenobarbital
■ Isoniazid
■ Rifampin
■ Hypomagnesemia
■ Uremia
■ Hyperphosphatemia
● Rhabdomyolysis
● Tumor lysis syndrome
78 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
■ Pancreatitis
■ Alkalemia
■ Alcoholism
■ Citrate infusion
■ Ethylene glycol toxicity
Assessment Findings
■ Confusion
■ Seizure
■ Bradycardia
■ Prolong QT interval prolongation
■ Bradycardia
■ Complete heart block
■ Circumoral or distal paresthesia
■ Tetany
■ Ataxia
■ Chvostek’s sign
■ Trousseau’s sign
■ Muscle weakness
■ Dry skin and nails
● Seen more in chronic patients
SYMPTOMS OF HYPOCALCEMIA
Trousseau sign: Carpal spasm induced by inflating a blood pressure cuff to upper arm above
systolic blood pressure for 3 minutes.
Cvostek sign: Perioral muscle twitching when tapping the ipsilateral facial nerve.
Diagnostics
Laboratory
■ Serum calcium level < 8.6 mg/dL
● Serum calcium should be corrected for hypoalbuminemia
■ Ionized calcium level < 4.6 mg/dL
■ Albumin
■ Magnesium
■ Parathyroid hormone (PTH) level
■ Thyroid functions
■ Vitamin D levels
EKG
■ Prolonged QTc interval
9 ELECTROLYTE DERANGEMENTS 79
PHOSPHORUS
Normal Level
2.5 to 4.5 mg/dL
PHOSPHORUS
■ Phosphorus is an electrolyte that is important for effective cellular metabolism.
■ Most phosphate is intracellular and only a small amount (about 1%) is extracellular.
■ Phosphate is regulated by the kidneys, and reabsorption is dependent on vitamin D, insulin, and
hormones.
■ Parathyroid hormone plays the biggest role in regulation of phosphorus, but calcitonin, thyroid,
and growth hormone also have some effect.
■ Altered phosphorus levels in ICU are associated with high mortality and morbidity.
HYPERPHOSPHATEMIA
Causes
■ Low renal clearance
■ Increased tubular phosphorus reabsorption
■ Intake from phosphate-based laxatives
■ Tumor lysis syndrome
■ Acromegaly
■ Vitamin D toxicity
HYPOPHOSPHATEMIA
■ Hypophosphatemia is common in the ICU but is most often asymptomatic.
■ However, suboptimal levels can increase duration of mechanical ventilation and increase risk
of ventricular tachycardia.
80 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
Assessment Findings
■ Grainy feeling to skin
■ Pruritis
■ Conduction defects
■ Acute conjunctivitis
Diagnostics
■ Serum phosphorus level > 4.5 mg/dL
■ Renal panel or chemistry profile
● Evaluating for renal insufficiency
Hypophosphatemia
Causes
■ Sepsis
■ Alcohol withdrawal
■ Malnutrition
■ Refeeding syndrome
■ Ketoacidosis
■ Alkalosis
■ Hungry bone syndrome
■ Trauma
■ Surgery
Assessment Findings
■ Generally asymptomatic
■ Irritability
■ Weakness
■ Paresthesia
Diagnostics
■ Serum phosphorus level < 2.5 mg/dL
MAGNESIUM
Normal Level
1.7 to 2.2 mg/dL
HYPERMAGNESMIA
Causes
■ Renal impairment
■ Magnesium intake with renal insufficiency
Magnesium-based laxatives or bowel prep
●
Antacids
●
■ Large intake of magnesium
● Treatment of eclampsia
● Treatment of asthma
Assessment Findings
■ Generalized weakness
■ Lethargy
■ Absent or diminished deep tendon reflexes
■ Hypotension
■ Nausea and vomiting
Diagnostics
Laboratory
■ Serum magnesium level greater than 2.2 mEq/dL
● Not usually symptomatic until level is greater than 4.0 mEq/dL
■ Renal functions
EKG
■ Widening of QRS
■ Prolonged PR interval
■ Possible complete heart block
HYPOMAGNESEMIA
Causes
■ Renal loss
● Diuretics
● Chronic alcohol use
● Nephrotoxic drugs
■ Aminoglycosides (vancomycin)
■ Amphotericin B
■ Cisplatin
■ GI loss
● Diarrhea
● Inflammatory bowel disease
■ Poor intake
■ Diabetic ketoacidosis (DKA)
■ Alcohol withdrawal
Assessment Findings
■ Muscle weakness
■ Tremors
■ Seizures
■ Trousseau’s sign
■ Chvostek’s sign
■ Tremors
Diagnostics
Laboratory
● Serum magnesium level of less than 1.6 mEq/L
● Serum or ionized calcium level
● Potassium
Urinalysis
● Urine magnesium level
EKG
● Prolonged QTc interval
● Ventricular tachycardia
● Ventricular fibrillation
■ Mild
● Oral supplementation
■ Magnesium chloride
■ Magnesium oxide
Bibliography
Adrogue, H. J., & Madias, N. E. (2000). Hypernatremia. The New England Journal of
Medicine, 342(20), 1493–1499. https://doi.org/10.1056/NEJM200005183422006
Demssie, Y. N., Patel, L., Kumar, M., & Syed, A. A. (2014). Hypomagnesaemia:
Clinical relevance and management. British Journal of Hospital Medicine, 75(1),
39–43. https://doi.org/10.12968/hmed.2014.75.1.39
Evans, S. K., & Greenberg, A. (2005). Hyperkalemia: A review. Journal of Intensive Care
Medicine, 20(5), 272–290. https://doi.org/10.1177/0885066605278969
Halperin, M. L., Goldstein, M. B., & Kamel, S. K. (2010). Fluid, electrolyte, & acid-base
balance pathophysiology (4th ed.). Elsevier.
Kamel, K. S., & Wei, C. (2003). Controversial issues in the treatment of hyperkalemia.
Nephology Dialysis Transplant, 18, 2215–2218. https://doi.org/10.1093/ndt/gfg323
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Noel, J. A., Bota, S. E., Petrcich, W., Garg, A. X., Carrero, J. J., Harel, Z., Tangri, N.,
Clark, E. G., Komenda, P., & Sood, M. M. (2019). Risk of hospitalization for serious
adverse gastrointestinal events associated with sodium polystyrene sulfonate us
in patients of advanced age. JAMA Internal Medicine, 179(8), 1025–1033. https://
doi.org/10.1001/jamainternmed.2019.0631
Rose, B. D., & Post, T. (2005). Clinical physiology of acid-based and electrolyte disorders
(5th ed.). McGraw-Hill.
Wang, A. S., Dhillon, N. K., Linaval, N. T., Rottler, N., Yang, A. R., Margulies, D. R.,
Ley, E. J., & Barmparas, G. (2019). The impact of IV electrolyte replacement on the
fluid balance of critically ill surgical patients. The American Surgeon, 85, 1171–1174.
10
MANAGEMENT OF
ACID–BASE BALANCE
ACID–BASE BALANCE AND INTERPRETATION OF
ARTERIAL BLOOD GAS
METABOLIC ACIDOSIS
Causes
■ Elevated Anion Gap
● Ketoacidosis
■ Diabetic
■ Alcoholic
● Lactic acidosis
■ Sepsis
■ Hypotension
■ Localized area of hypoperfusion
● Renal failure
● Rhabdomyolysis
● Poisoning
■ Ethylene glycol
■ Methanol
■ Aspirin
■ Non-anion Gap
● Diarrhea
● Renal tubular acidosis
● Chronic renal failure
85
86 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
● Adrenal insufficiency
● Acetazolamide therapy
Assessment Findings
■ Specific to underlying cause and degree of acidosis
■ C
● Ill appearing
● Weakness
● Lethargy
Respiratory
■ Tachypnea
■ Increased work of breathing
■ Hypoxia
Cardiac
■ Tachycardia
■ Bradycardia
■ New arrhythmia
Diagnostics
Laboratory
■ Arterial blood gas
■ Serum chemistries
■ Lactic
■ Alcohol level
● In suspected alcohol abuse
■ Salicylate level
● If suspected overdose
● Isotonic fluids
■ Sepsis
■ Diabetic ketoacidosis
■ Alcoholic acidosis
■ Poisoning
METABOLIC ALKALOSIS
Causes
■ Low urine chloride (<20)
● Vomiting
● Nasogastric suctioning
● Diuretic use
● Severe congestive heart failure (CHF)
■ Normal or high urine chloride (>30)
● Primary or secondary hyperaldosteronism
● Cushing syndrome
● Licorice ingestion
● Diuretic use
● Excess alkali
■ Baking soda ingestion
■ Massive transfusion (citrate)
■ Total peripheral nutrition (acetate)
■ Excess calcium carbonate ingestion
Assessment Findings
■ May be asymptomatic
● Symptoms generally seen with pH > 7.55
88 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
■ Delirium
■ Neuromuscular irritability
■ Hypoventilation
■ Hypoxia
Diagnostics
Laboratory
● Arterial blood gas
● Serum chemistries
● Lactic
● Urine chloride
RESPIRATORY ACIDOSIS
RESPIRATORY ACIDOSIS
■ As PaCO2 increases, pH decreases
■ PaCO2 rises from hypoventilation
■ Commonly seen in acute and critically ill patients
Causes
■ Acute respiratory acidosis
● Asthma
● Chronic obstructive pulmonary disease (COPD) exacerbation
● Oversedation
● Narcotic overdose
■ Intentional
■ Unintentional
● Pneumonia
● Central nervous system depression
■ Guillain-Barré
■ Myasthenia gravis
● Pneumothorax
10 MANAGEMENT OF ACID–BASE BALANCE 89
■ Chronic
● COPD
● Chronic lung disease
● Chronic central nervous system disorders
● Pregnancy
● High altitude
● Obesity
Assessment Findings
Respiratory
■ Anxiety
■ Agitated
■ Apnea
Neurologic
■ Lethargic
■ Obtunded
■ Unresponsive
■ Myoclonic jerking
■ Tremor
■ Papilledema
Diagnostics
Laboratory
■ Arterial blood gas
■ Serum chemistries
■ Lactic
(continued)
90 IV MANAGEMENT OF RENAL AND ELECTROLYTE DISORDERS
RESPIRATORY ALKALOSIS
RESPIRATORY ALKALOSIS
■ As PaCO2 decreases, pH increases
■ PaCO2 decreases from hyperventilation
■ Less common than respiratory acidosis
Causes
■ Anxiety
■ Pain
■ Sepsis
■ Central nervous system disorders
Assessment Findings
■ Tachypnea
■ Shortness of breath
■ Anxiety
■ Altered/abnormal breathing pattern
● Seen with neurological injury
Diagnostics
Laboratory
■ Arterial blood gas
■ Serum chemistries
■ Lactic
Neurological workup
■ For suspected neurological injury
BIBLIOGRAPHY
Farrar, A. (2018). Acute kidney injury. Nursing Clinics of North America, 53(4), 499–510.
https://doi.org/10.1016/j.cnur.2018.07.001
Halperin, M. L., Goldstein, M. B., & Kamel, S. K. (2010) Fluid, electrolyte, & acid-base
balance pathophysiology (4th ed.). Elsevier.
Koyner, J. L. (2012). Assessment and diagnosis of renal dysfunction in the ICU. Chest,
141(6), 1584–1594. https://doi.org/10.1378/chest.11-1513
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Rose B. D., & Post, T. (2005). Clinical physiology of acid-based and electrolyte disorders
(5th ed.). McGraw-Hill.
Wang, A. S., Dhillon, N. K., Linaval, N. T., Rottler, N., Yang, A. R., Margulies, D. R.,
Ley, E. J., & Barmparas, G. (2019). The impact of IV electrolyte replacement on the
fluid balance of critically ill surgical patients. The American Surgeon, 85, 1171–1174.
SECTION V
MANAGEMENT
GASTROINTESTINAL DISORDERS
11
GASTROINTESTINAL BLEEDING
Helicobacter pylori
■ Bacteria that infects the lining of the stomach
■ Most common cause of peptic ulcer disease
■ Testing methods include noninvasive methods
● Urea breath test
● Stool antigen
● Serum testing
■ Testing can also be performed by biopsy during endoscopy
■ Treated with combination antibiotic therapy and proton pump inhibitor
■ Esophageal varices
■ Gastritis
■ Mallory-Weiss tear
Assessment Findings
HEMORHAGIC SHOCK
■ Tachycardia
■ Hypotension
■ Pallor
■ Decreased urine output
■ Obvious bleeding
95
96 V MANAGEMENT GASTROINTESTINAL DISORDERS
Diagnostics
Endoscopy
■ Standard of care
■ If patient is hemodynamically unstable due to bleeding, endoscopy
should be performed within 12 hours of suspected bleed, but ideally as
soon as clinically possible.
■ C
● Complete blood count (CBC)
■ Low hemoglobin and hematocrit
● Chemistry panel
■ Elevated BUN
■ BUN-to-creatinine ratio > 20:1
● Type and screen
■ Important to have ready if transfusion is needed
■ Blood in gastrointestinal (GI) lavage
Causes
■ Loss of stomach epithelium that penetrates to the muscularis
mucosae
Defined as a mucosal break greater than 5 mm
●
■ H. pylori
● Most common cause
■ Imbalance between acid and stomach mucosa
11 GASTROINTESTINAL BLEEDING 97
■ Medications
● Nonsteroidal anti-inflammatory drugs (NSAIDs)
● Aspirin
■ Alcohol
Assessment Findings
■ Epigastric pain
● Described as gnawing or aching
● Occurs 1 to 3 hours after eating
● Relieved by eating or antacids
■ Pain on palpation slightly left of midline
■ Coffee ground emesis
Diagnostics
■ Same as general GI upper bleed
Esophageal Varices
Causes
■ Portal vein hypertension seen in liver disease
Assessment Findings
■ Signs of liver failure
● Ascites
● Jaundice
Diagnostics
■ Same as general GI upper bleed
MALLORY-WEISS TEAR
Causes
■ Lacerations of the mucosa at the junction of the esophagus and the
proximal stomach
● Chronic vomiting
● Heavy alcohol use, especially with vomiting
● Bulimia
● Hiatal hernia
● Blunt abdominal injury
● Seizures
● Coughing
● Advanced age
Assessment Findings
■ Pain that radiates to the back
■ Non-bloody emesis
Diagnostics
■ Same as general GI upper bleed
Assessment Findings
■ Abdominal pain
■ Hematochezia
■ Nausea
■ Vomiting
■ Anorexia
■ Hypovolemic shock symptoms due to blood loss
● Hypotension
● Pallor
● Tachycardia
● Altered level of consciousness
100 V MANAGEMENT GASTROINTESTINAL DISORDERS
Diverticulosis
■ Reports of the urge to defecate
■ Bloating
■ Abdominal cramping
Neoplasm
■ Palpable abdominal mass
Diagnostics
Colonoscopy
● Standard initial method of assessment
● Occult or nonemergent bleeding may need additional workup
Laboratory
■ CBC
● Low hemoglobin and hematocrit
■ Type and screen
Bibliography
Cook, D., & Guyatt, G. (2018). Prophylaxis against upper gastrointestinal bleeding
in hospitalized patients. New England Journal of Medicine, 378(26), 2506–2516.
https://doi.org/10.1056/NEJMra1605507
Gerson, L. B., Fidler, J. L., Cave, D. R., & Leighton, J. A. (2015). ACG clinical
guideline: Diagnosis and management of small bowel bleeding. American Journal
of Gastroenterology, 110, 1265–1287. https://doi.org/10.1038/ajg.2015.246
Laine, L., & Jensen, D. (2012). Management of patients with ulcer bleeding. American
Journal of Gastroenterology, 107, 345–360. https://doi.org/10.1038/ajg.2011.480
Meehan, C. D., & McKenna, C. G. (2018). Stopping acute upper- GI bleeds: Risk
stratification and quick intervention can save lives. American Nurse Today, 13(3), 6–8.
Mitra, V., Marrow, B., & Nayar, M. (2012). Management of acute upper
gastrointestinal bleeding. Gastrointestinal Nursing, 10, 34–39. https://doi.org/
10.12968/gasn.2012.10.7.34
Oakland, K., Chadwick, G., East, J. E., Guy, R., Humphries, A., Jairath, V.,
McPherson, S., Metzner, M., Morris, A. J., Murphy, M. F., Tham, T., Uberoi, R.,
Veitch, A. M., Wheeler, J., Regan, C., & Hoare, J. (2019). Diagnosis and
management of acute lower gastrointestinal bleeding guidelines from the
British Society of Gastroenterology. Gut, 68, 776–789. https://doi.org/10.1136/
gutjnl-2018-317807
Strate, L. L., & Gralnek, I. M. (2016). ACG clinical guideline: Management of patients
with acute lower gastrointestinal bleeding. American Journal of Gastroenterology,
111, 459–474. https://doi.org/10.1038/ajg.2016.41
12
ACUTE LIVER DYSFUNCTION
LIVER FAILURE
Causes
■ Viral hepatitis
● Hepatitis C most common viral cause
■ Cirrhosis
■ Alcohol abuse
■ Cytomegalovirus
■ Drug toxicity
■ Toxins
■ Metabolic disorders
■ Autoimmune disease
Assessment Findings
General
■ Weakness
■ Fatigue
■ Weight loss
■ Hypoglycemia
Gastrointestinal
■ Anorexia
■ Change in bowel habits
■ Nausea and vomiting
■ Abdominal discomfort
■ Diarrhea
■ Gastrointestinal (GI) bleed
■ Malnutrition
Skin
■ Jaundice
■ Angiomas
■ Pruritis
Cardiovascular
■ Edema
■ Hypotension
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104 V MANAGEMENT GASTROINTESTINAL DISORDERS
Hematologic
■ Anemia
■ Coagulopathy
■ Thrombocytopenia
●Not usually less than 50,000
●Caused by splenic pooling and increased destruction
■ Increase in von Willebrand's factor
■ Increase D-dimer
■ Decreased protein C levels
Neurologic
■ Confusion
■ Altered mental status
■ Cerebral edema
Pulmonary
■ Dyspnea
■ Hypoxemia
Renal
■ Azotemia
■ Oliguria
■ Hyponatremia
■ Hepatorenal syndrome
JAUNDICE LOCATIONS
■ Sclera
■ Skin
■ Urine
■ Mucus membranes
■ Nail beds
■ Tears
Diagnostics
■ Laboratory findings
Elevated bilirubin
●
Low albumin
●
Coagulopathy
●
Elevated ammonia
●
Elevated transaminases
●
Aspartate transaminase (AST)
●
Alanine transaminase (ALT)
●
Alkaline phosphatase
●
■ Abdominal/pelvis CT scan
12 ACUTE LIVER DYSFUCTION 105
■ Liver ultrasound
■ Liver biopsy
● Definitive for cirrhosis
HEPATORENAL SYNDROME
Causes
■ Liver failure
■ Abnormal vasodilation that leads to central hypovolemia
Symptoms
■ Decreased urine output
● Can be non-oliguric
■ Hypotension
■ Ascites
■ Uremia
Diagnostics
■ Renal panel
● Slow rise in serum creatinine
● Hyperkalemia
● Acidosis
■ Vasoconstrictors
●Norepinephrine
●Vasopressin
●Dopamine
■ Octreotide
■ Midodrine
Bibliography
Acevedo, J. G., & Cramp, M. E. (2017). Hepatorenal syndrome: Update on diagnosis
and therapy. World Journal of Hepatology, 9(6), 293–299. https://doi.org/10.4254/
wjh.v9.i6.293
Erly, B., Carey, W. D., Kapoor, B., McKinney, J. M., Tam, M., & Wang, W. (2015).
Hepatorenal syndrome: A review of pathophysiology and current treatment
options. Seminars in Interventional Radiology, 32, 445–454. https://doi.org/
10.1055/s-0035-1564794
European Association for the Study of the Live. (2010). EASL clinical practice
guidelines on the management of ascites, spontaneous bacterial peritonitis, and
hepatorenal syndrome in cirrhosis. Journal of Hepatology, 53, 397–417.
Francoz, C., Durand, F., Kahn, J. A., Genyk, Y. S., & Nadim, M. K. (2019). Hepatorenal
syndrome. Clinical Journal of the American Society of Nephrology, 14, 774–781.
https://doi.org/10.2215/CJN.12451018
Herrera, J. L., & Rodriguez, R. (2006). Medical care of the patient with compensated
cirrhosis. Gastroenterology & Hepatology, 2(2), 124–133.
Kamath, P. S., & Kim, R. (2007). The model for end-stage liver disease (MELD).
American Association for the Study of Liver Diseases, 45(3), 797–805. https://doi.org/
10.1002/hep.21563
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Peck-Radiosavljevic, M., Angeli, P., Cordoba, J., Farges, O., & Valla, D. (2015).
Managing complications in cirrhotic patients. United European Gastroenterology
Journal, 3(1), 80–94. https://doi.org/10.1177/2050640614560452
13
ACUTE DYSFUNCTION OF THE
PANCREAS AND BILIARY SYSTEM
ACUTE PANCREATITIS
PANCREATITIS CLASSIFICATION
Causes
■ Stone in biliary tract
■ Alcohol abuse
■ Medications
● Azathioprine (Imuran)
● Sulfonamides
● Furosemide
● Valproic acid
■ Post endoscopic retrograde cholangiopancreatography (ERCP)
■ Uncontrolled hyperlipidemia
■ Abdominal trauma
■ Ischemia
Assessment Findings
■ Symptoms occurred suddenly
■ Sudden onset of epigastric or right upper quadrant pain
Pain is usually described as constant and severe
●
May radiate to back
●
Is worse with movement
●
■ Nausea
109
110 V MANAGEMENT GASTROINTESTINAL DISORDERS
■ Vomiting
■ Diaphoresis
■ Dyspnea
■ Epigastric tenderness
■ Fever
■ Tachycardia
■ Hypotension
■ Jaundice
■ Cullen’s sign
■ Grey Turner sign
SIGNS OF PANCREATITIS
■ Cullen’s sign
● Ecchymosis of the periumbilical region
● Can be a sign of pancreatic necrosis
■ Grey Turner’s Sign
● Ecchymosis to the flank
● Can be a sign of retroperitoneal bleeding
APACHE II SCORE
Developed for use in the ICU to evaluate the severity of pancreatitis
■ Age
■ Glasgow Coma Scale
■ Mean arterial pressure
■ FiO2
■ PaO2
■ pH
■ Serum sodium
■ Serum potassium
■ Hct
■ White blood cell (WBC)
■ Chronic disease
Diagnostics
Laboratory
■ Elevated serum amylase
● Usually 3× the upper limit of normal
● Elevation within 6 to 12 hours
13 ACUTE DYSFUNCTION OF THE PANCREAS AND BILIARY SYSTEM 111
ACUTE CHOLECYSTITIS
Causes
■ Gall stones
● Stones lodge in cystic duct
● Inflammation due to blockage
■ Acalculous cholecystitis
● Seen in critically ill patients
● Increases mortality
■ Ischemia
■ Infection
■ Tumor
■ Stricture of the bile duct
112 V MANAGEMENT GASTROINTESTINAL DISORDERS
MURPHY SIGN
Murphy sign
Examiner places hand over the right subcostal area (right upper quadrant) and has patient take a
deep breath. If patient has pain on inspiration, the sign is positive.
Pain occurs when gallbladder comes in contact with provider’s hand.
Sonographic Murphy sign
Pain on inspiration while ultrasound probe is visualizing the gallbladder.
Assessment Findings
■ Biliary colic
● Sudden severe pain to the right upper quadrant
● May radiate to shoulder or back
■ Nausea
■ Vomiting
■ Anorexia
■ Fever
■ Murphy’s sign
■ Jaundice
■ May have several episodes before patient seeks care
RANSON’S CRITERIA
Hour zero (each worth 1 point)
■ Age >55 years
■ WBC >16,000 mcL
■ Glucose >200 mg/dL
■ Lactate dehydrogenase (LDH) >350 IU/L
■ Aspartate transaminase (AST) >250 IU/L
48 hours (each worth 1 point)
■ Hct drop of 10% or more
■ BUN increase by 5 mg/dL
■ Serum calcium <8 mg/dL
■ PaO2 <60 mmHg
■ Base deficit >4 mEq/L
■ Fluid sequestration >6,000 mL
Results
0 to 2 points: Mortality 0% to 3%
3 to 5 points: Mortality 11% to 15%
6 to 11 points: Mortality >40%
13 ACUTE DYSFUNCTION OF THE PANCREAS AND BILIARY SYSTEM 113
Diagnostics
■ Right upper quadrant ultrasound
● Best study for diagnosing gallstones
■ Leukocytosis
■ Elevated serum bilirubin
■ Elevated alanine transaminase (ALT)
■ Elevated AST
■ Elevated LDH
■ Elevated alkaline phosphatase
■ Elevated amylase
■ HIDA scan
Bibliography
Banks, P. A. (1997). Practice guidelines in acute pancreatitis. The American Journal of
Gastroenterology, 92(3), 377–396. https://doi.org/10.1111/j.1572-0241.2006.00856.x
Banks, P. A., & Freeman, M. L. (2006). Practice guidelines in acute pancreatitis. The
American Journal of Gastroenterology, 101(10), 2379–2400. https://doi.org/10.1111/
j.1572-0241.2006.00856.x
Ganpathi, I. S., Diddapur, R. K., Euguene, H., & Karim, M. (2007). Acute acalculous
cholecystitis: Challenging the myths. HPB, 9, 131–134. https://doi.org/10.1080/
13651820701315307
Indar, A. A., & Beckinham, I. J. (2002). Acute cholecystitis. British Medical Journal, 325,
639–643. https://doi.org/10.1136/bmj.325.7365.639
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Pandol, S. J., Saluja, A. K., Imrie, C. W., & Banks, P. A. (2007). Acute pancreatitis:
Bench to bedside. Gastroenterology, 132(3), 1127–1151. https://doi.org/10.1053/
j.gastro.2007.01.055
Swaroop, V. S., Chari, S. T., & Clain, J. E. (2004). Severe acute pancreatitis. JAMA,
291(23), 2865–2868. https://doi.org/10.1001/jama.291.23.2865
Trowbridge, R. L., Rutkowski, N. K., & Shojania, K. G. (2003). Does this patient have
acute cholecystitis. JAMA, 289(1), 80–86. https://doi.org/10.1001/jama.289.1.80
Whitcomb, D. C. (2006). Acute pancreatitis. New England Journal of Medicine, 354(20),
2142–2150. https://doi.org/10.1056/NEJMcp054958
14
MANAGEMENT OF
ACUTE INFLAMMATORY
GASTROINTESTINAL DISORDERS
DIVERTICULITIS
Types
■ Uncomplicated
■ Complicated
● Considered complicated if one or more is present
■ Abscess formation
■ Peritonitis
■ Obstruction
■ Fistula
■ Sepsis
■ No improvement with medical management
Causes
■ Inflammation or perforation of diverticulum
■ Abscess formation within a diverticulum
■ Diverticulum occurs for a variety of reasons
● Low fiber diet
115
116 V MANAGEMENT GASTROINTESTINAL DISORDERS
■ Some research shows that this may not have as much impact as
previously thought.
● Decreased bowel motility
● Weakness in the colon wall
● Deranged microbiome
● Diet high in red meat
● Smoking
● Obesity
● Physical inactivity
● Nuts, corn, seeds are no longer considered risk factors
Assessment Findings
■ Abdominal pain
● Pain is acute or subacute
● Left quadrant in most patients
● Suprapubic pain
● Tenderness on palpation
● Guarding
● Pain worse with movement
■ Fever
■ Nausea without vomiting
■ Reports change in bowel habits
■ Constipation alternating with diarrhea
■ Hypoactive bowel sounds on auscultation
■ Urinary symptoms from inflamed colon near bladder
● Dysuria
● Urgency
● Frequency
■ Abdominal distention may indicate bowel obstruction
■ May have symptoms of sepsis or septic shock
Diagnostics
Laboratory
■ Complete blood count (CBC)
● Leukocytosis
■ C-reactive protein
● Elevated
Imaging
■ CT scan with oral and IV contrast if appropriate
● Showing abscess form
■ Abdominal ultrasound
■ Abdominal x-ray (KUB)
● Not diagnostic for diverticulitis
● Will be useful in diagnosis of pneumoperitoneum in perforation
● Diagnostic for bowel obstruction
14 MANAGEMENT OF ACUTE INFLAMMATORY GASTROINTESTINAL DISORDERS 117
DIVERTICULUM PERFORATION
Microperforation: Small amounts of gas or air bubbles seen on CT. No obvious free air or free
contrast media.
Perforation: Noted free air on CT with possible fluid or contrast spillage. Will lead to peritonitis.
■ Surgical consult
● Indications
• Abscess
• Peritonitis
• Patient not improving with medical management
APPENDICITIS
Causes
■ Acute inflammation of the vermiform appendix
■ Luminal obstruction with a fecalith
● Can lead to perforation and gangrene
■ Inflammation
■ Tumors
■ Strictures
■ Alterations in the colonic microbiome
Assessment Findings
■ Abdominal pain
● Initially central abdomen
● Migrates right lower quadrant pain
■ Guarding
■ Tenderness on palpation
● Rovsing’s sign
● Psoas sign
● Obturator sign
● Flexion of thigh lessens pain
● Movement usually worsens pain
SIGNS OF APPENDICITIS
■ Rovsing’s sign
● Right lower quadrant pain when pressure applied to left lower quadrant
■ Psoas sign
● Pain with extension of right thigh
■ Obturator sign
● Pain with internal rotation of flexed right thigh
■ Anorexia
■ Nausea without vomiting
■ Urge to defecate
■ Low-grade fever
14 MANAGEMENT OF ACUTE INFLAMMATORY GASTROINTESTINAL DISORDERS 119
Diagnostics
Laboratory
■ CBC
● Leukocytosis
● Usually 10,000 to 20,000/mcL
■ Urinalysis
● Elevated specific gravity
● Hematuria
● Pyuria
Ultrasound
■ Accurate when appendix can be visualized
■ Generally used as first approach when perforation not suspected
CT scan
■ Used to identify perforation or possible abscess
PERITONITIS
Causes
■ Primary
● Spontaneous bacterial peritonitis in patients with cirrhosis
● Escherichia coli most common cause
■ Secondary
● Peritoneal dialysis
120 V MANAGEMENT GASTROINTESTINAL DISORDERS
● Abdominal trauma
● Penetrating abdominal wounds
● Colon perforation
● Postoperative
PERITONEAL DIALYSIS
■ Usually caused by skin bacteria
● Staphylococcus epidermidis
● Staphylococcus aureus
■ Translocation
● From gastrointestinal (GI) source
Assessment Findings
■ Abdominal pain
● Worse with motion
● Rebound tenderness
● Rigidity
■ Abdominal distention
● Possible ascites
■ Decreased bowel sounds
■ High fever
■ Nausea
■ Vomiting
■ Constipation
■ Tachypnea
■ Dyspnea
Diagnostics
Laboratory
■ CBC
●Leukocytosis
●Elevated hematocrit
■ Renal panel
● Elevated BUN
■ Elevated amylase
Peritoneal aspirate
■ Elevated WBC
■ Elevated LDH
■ Protein level elevated
■ Glucose less than 50 mg/dL
■ Bacteria on gram stain
14 MANAGEMENT OF ACUTE INFLAMMATORY GASTROINTESTINAL DISORDERS 121
Blood cultures
■ Positive in approximately 25% of patients
Imaging
■ Chest x-ray
● Elevated diaphragm
■ CT scan
● Intra-abdominal mass
Bibliography
Flum, D. R. (2015). Acute appendicitis: Appendectomy or the “antibiotic first”
strategy. New England Journal of Medicine, 372(20), 1937–1943. https://doi.org/
10.1056/NEJMcp1215006
MacIntosh, T. (2018). Emergency management of spontaneous bacterial peritonitis: A
clinical review. Cureus, 10(3), e2253. https://doi.org/10.7759/cureus.2253
Morris, A. M., Regenbogen, S. E., Hardiman, K. M., & Hendren, S. (2014). Sigmoid
diverticulitis: A systematic review. JAMA, 311(3), 287–297. https://doi.org/
10.1001/jama.2013.282025
122 V MANAGEMENT GASTROINTESTINAL DISORDERS
Siletz, A., Grotts, J., Lewis, C., Tillou, A., Cheaito, A., & Cryer, H. (2018). Monitoring
complications of medically managed acute appendicitis. The American Surgeon, 84,
1684–1690.
Soares-Weiser, K., Paul, M., Brezis, M., & Leibovici, L. (2002). Antibiotic treatment for
spontaneous bacterial peritonitis. BMJ, 324, 100–102. https://doi.org/10.1136/
bmj.324.7329.100
Such, J, & Runyon, B. A. (1998). Spontaneous bacterial peritonitis. Clinical Infectious
Disease, 27, 669–676. https://doi.org/10.1086/514940
Swanson, S. M., & Strate, L. L. (2018). In the clinic: Acute colonic diverticulitis.
Annals of Internal Medicine, 168(9), ITC65–ITC80. https://doi.org/10.7326/
AITC201805010
SECTION VI
MANAGEMENT OF ENDOCRINE
DISORDERS
15
ACUTE MANAGEMENT OF
DIABETIC EMERGENCIES
DIABETIC KETOACIDOSIS
Causes
■ New-onset type I diabetes
■ Infection
■ Noncompliance
● Lack of insulin
● Poor regulation of food intake
■ Pancreatitis
■ Surgical intervention
■ Trauma
■ Medications that alter the metabolization of carbohydrates
● Glucocorticoids
■ Cocaine use
Assessment Findings
General
■ Flushed dry skin
■ Weight loss
■ Weakness
■ Fruity breath
■ Hypothermia
■ Dry mucous membranes
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126 VI MANAGEMENT OF ENDOCRINE DISORDERS
Cardiovascular
■ Tachycardia
■ Hypotension
■ Orthostatic hypotension
Neuro
■ Headache
■ Encephalopathy
■ Coma
Gastrointestinal
■ Nausea
■ Vomiting
■ Abdominal pain
Pulmonary
■ Tachypnea
■ Kussmaul respiration
Renal
■ Polyuria
■ Polydipsia
COMPLICATIONS OF DIABETES
■ Diabetic retinopathy
■ Cardiovascular disease
■ Cataracts
■ Glaucoma
■ Neuropathy
■ Increased risk for infections
● Vaginal and oral yeast infections
■ Foot wounds
Diagnostics
Laboratory
■ Chemistries
● Serum glucose greater than 250 mg/dL
■ Usually between 350 and 500 mg/dL
■ Not usually >800 mg/dL
● Hyperkalemia
■ Due fluid loss
● Anion gap
● Increased BUN
● Hyponatremia
● Normal serum osmolality
15 ACUTE MANAGEMENT OF DIABETIC EMERGENCIES 127
■ Serum ketones
■ Hemoglobin A1c
■ Complete blood count (CBC)
● Leukocytosis
● Elevated hematocrit
■ Arterial blood gas
● Arterial pH less than 7.3
■ Urinalysis
● Ketones in serum and urine
● Glucose in urine
EKG
■ Surgical intervention
■ Trauma
■ Medications that alter the metabolization of carbohydrates
● Glucocorticoids
Assessment Findings
General
■ Flushed dry skin
■ Weight loss
■ Weakness
■ Hypothermia
■ Dry mucus membranes
Cardiovascular
■ Tachycardia
■ Hypotension
■ Orthostatic hypotension
Neuro
■ Headache
■ Encephalopathy
■ Coma
Gastrointestinal
■ Nausea
■ Vomiting
■ Abdominal pain
Pulmonary
■ Tachypnea
Renal
■ Polyuria
■ Polydipsia
Diagnostics
Laboratory
■ Chemistries
● Serum glucose greater than 500 mg/dL
■ Usually >1,000 mg/dL
● Hyperkalemia
■ Due fluid loss
No anion gap
●
Increased BUN
●
Increased creatinine
●
Hyponatremia
●
Elevated serum osmolality
●
■ Hemoglobin A1c
15 ACUTE MANAGEMENT OF DIABETIC EMERGENCIES 129
■ CBC
● Leukocytosis
● Elevated hematocrit
■ Arterial blood gas
● Arterial pH less than 7.3
■ Urinalysis
● In serum and urine
● Glucose in urine
■ Not always good indicator in type 2 diabetes; many oral
medications increase glucose excretion in urine
EKG
● Bolus initially
■ Should be given IV
■ Continuous insulin infusion
● IV insulin should be continued until anion gap is resolved
HYPERGLYCEMIA
■ Fluid resuscitation is priority in both DKA and hyperglycemic hyperosmolar state (HHS) and
should be initial method of treatment.
■ Insulin infusion is usually required for gradual glycemic control.
■ As serum glucose is lowered, serum potassium level decreases. Frequent potassium monitoring
and replacement are often required in both DKA and HHS.
Bibliography
Filers, E., Bianco, A. C., Langouche, L., & Boelen, A. (2015). Endocrine and metabolic
considerations in critically ill patients. Lancet Diabetes Endocrinology, 3(10),
816–825. https://doi.org/10.1016/S2213-8587(15)00225-9
Finfer, S., Chittock, D., Li, Y., Foster, D., Dhingra, V., Bellomo, R., Cook, D.,
Dodek, P., Hebert, P., Henderson, W., Heyland, D., Higgins, A., McArthur,
C., Mitchell, I., Myburgh, J., Robinson, B., & Ronco, J. (2009). Intensive versus
conventional glucose control in critically ill patients. New England Journal of
Medicine, 360(13), 1283–1297. https://doi.org/10.1007/s00134-015-3757-6
Finney, S. J., Zekveld, C., Elia, A., & Evans, T. W. (2003). Glucose control and
mortality in critically ill patients. JAMA, 290(15), 2041–2047. https://doi.org/
10.1001/jama.290.15.2041a
French, E. K., Donihi, A., & Korytkowski, M. T. (2019). Diabetic ketoacidosis and
hyperosmolar hyperglycemic syndrome: Review of acute decompensated diabetes
in adult patients. BMJ, 365, 1–15. https://doi.org/10.1136/bmj.l1114
Gillespie, G. L., & Campbell, M. (2002). Diabetic ketoacidosis. AJN, 102, 13–16.
Johnston, J. A., & Van Horn, E. R. (2011). The effects of correction insulin and basal
insulin on inpatient glycemic control. Medsurg Nursing, 20(4), 187–193.
Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic
crises in adult patients with diabetes. Diabetes Care, 32(7), 1335. https://doi.org/
10.2337/dc09-9032
Kraut, J. A., & Madias, N. E. (2012). Treatment of acute metabolic acidosis: A
pathophysiologic approach. Nature Reviews: Nephrology, 8(10), 589–601. https://
doi.org/10.1038/nrneph.2012.186
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Van Den Berghe, G., Wouters, P., Weekers, F., Verwaest, C., Bruyninckx, F., Schetz, M.,
Vlasselaers, D., Ferdinande, P., Lauwers, P., & Bouillon, R. (2001). Intensive insulin
therapy in critically ill patients. New Journal of Medicine, 345(19), 1359–1367.
https://doi.org/10.1056/NEJMoa011300
16
THYROID EMERGENCIES
MYXEDEMA COMA
Causes
Underlying preexisting hypothyroidism and one of the following:
■ Infection
■ Sepsis
■ Myocardial infarction
■ Congestive heart failure
■ Cold exposure
■ Postoperative
■ Sedation
■ Illicit drug use
● Opiates
● Marijuana
Amiodarone
■ With or without preexisting hypothyroidism
MYXEDEMA COMA
■ Medical emergency
■ High mortality
■ Patient requires ICU admission
■ Occurs more often in winter months
■ Not usually seen as the initial presentation of undiagnosed hypothyroidism
■ Causes global decrease in organ function
■ Can be secondary to noncompliance with medication use
Assessment Findings
Neurological
■ Decreased level of conscious
■ Altered mental status
■ Confusion
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132 VI MANAGEMENT OF ENDOCRINE DISORDERS
Hemodynamics
■ Hypotension
■ Hypothermia
■ Bradycardia
■ Low respiratory rate
■ Decreased cardiac output
General
■ Non-pitting edema
● Face
● Tongue
● Lips
● Hands
● Nose
Gastrointestinal
■ Abdominal distention
■ Hypoactive or absent bowel sounds
■ Constipation
Musculoskeletal
■ Muscle weakness
■ Woltman’s sign
● Delayed relaxation of deep tendon reflexes
Diagnostics
Laboratory
■ Chemistry
● Hypocalcemia
● Hyponatremia
● Hypoglycemia
■ Thyroid functions
● High thyroid stimulating hormone (TSH)
■ In primary hypothyroidism
● Low or normal TSH
■ In central hypothyroidism
● Low T3
● Low T4
■ Complete blood count (CBC)
● Anemia
● Thrombocytopenia
■ Cortisol
● May be low if concurrent adrenal insufficiency
■ Coagulation
● Elevated partial thromboplastin time (PTT)
● Elevated international normalized ratio (INR)
● Decreased fibrinogen
16 THYROID EMERGENCIES 133
Radiography
■ Chest x-ray
● Pleural effusion
■ Kidney, ureter, and bladder (KUB)
● Ileus
● Constipation
ECHO
■ Pericardial effusion
Hemodynamic Support
■ Vasopressors may be required for blood pressure support until
underlying condition can be corrected
■ Dopamine
● May treat both bradycardia and hypotension
■ Norepinephrine
■ Epinephrine
Respiratory
■ Consider intubation for the following:
● Hypoventilation
● Airway protection for altered consciousness
■ Follow arterial blood gas (ABG) for ventilatory status
■ Follow chest x-ray 24 to 48 hours
■ Pleural effusions will generally resolve without intervention when
myxedema resolves
134 VI MANAGEMENT OF ENDOCRINE DISORDERS
Hypothermia
■ Aggressive warming measures not indicated due to risk of vasodilation
and increased hypotension
■ Warm room
■ Apply room temperature blankets
Hypoglycemia
■ Frequent blood glucose monitoring
■ May require dextrose boluses and infusion
Adrenal Insufficiency
■ Hydrocortisone bolus dosing 100 mg IV q8h
■ Dexamethasone 8 mg IV daily
Pericardial Effusion
■ Will usually resolve without intervention when myxedema resolved
THYROID STORM
THYROID STORM
■ Medical emergency
■ Requires ICU admission
■ Rare disorders
■ Caused by inadequately controlled hyperthyroidism
■ High risk of death
Causes
■ Trauma
■ Stress
■ Infection
■ Thyroid surgery
■ Pregnancy
Assessment Findings
General
■ Fever
● Fever can be extreme, as high at 105
■ Flushing
■ Diaphoresis
■ Exophthalmos
■ Eyelid lag
■ Infrequent blinking
16 THYROID EMERGENCIES 135
Neurological
■ Psychosis
■ Stupor
■ Delirium
Hemodynamics
■ Tachycardia
■ Atrial fibrillation
■ Palpitation
Gastrointestinal
■ Diarrhea
■ Increase appetite
■ Weight loss
Musculoskeletal
■ Hyperreflexia
Diagnostics
Laboratory
■ TSH
■ T3 and T4
■ Erythrocyte sedimentation rate (ESR)
■ Antinuclear antibody (ANA)
■ Chemistry
● Hypercalcemia
■ CBC
● Anemia
Bibliography
Ashton, N. (2005). Pituitary, adrenal and thyroid dysfunction. Anesthesia Intensive
Care Medicine, 6(12), 346–349. https://doi.org/10.1383/anes.2005.6.10.346
Fliers, E., Bianco, A. C., Langouche, L., & Boelen, A. (2015). Thyroid function in
critically ill patients. Lancet Diabetes Endocrinol, 3, 816. https://doi.org/10.1016/
S2213-8587(15)00225-9
Holcome, S. S. (2005). Detecting thyroid disease. Nursing, 35(10), 4–9.
Jonklaas, J., Bianco, A. C., Bauer, A. J., Burman, K. D., Cappola, A. R., Celi, F. S.,
Cooper, D. S., Kim, B. W., Peeters, R. P., Rosenthal, M. S., & Sawka, A. M. (2014).
Guidelines for the treatment of hypothyroidism: Prepared by the American
thyroid association task force on thyroid hormone replacement. Thyroid, 24(12),
1670. https://doi.org/10.1089/thy.2014.0028
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
Willis, G., Alhisabs, S., & Glouser, J. (2017). The great mimicker: Thyroid
emergencies. Investigative Medial Alert, 20(9), 5–18.
SECTION VII
MANAGEMENT OF INFECTIOUS
DISEASES
17
SEPSIS AND SEPTIC SHOCK
CLINICAL TIPS AND TRICKS
Causes
Infection
■ Bacteria
■ Fungus
■ Yeast
■ Viruses
Patients at Increased Risk for Sepsis
■ Diabetes
■ HIV/AIDS
■ Chronic obstructive pulmonary disease (COPD)
■ Cancer
■ Chemotherapy
■ Immunosuppressive drugs
■ Solid organ transplant
■ Extremes of age
Common Source of Infection
■ Pneumonia
■ Most common source of infection
■ Intraabdominal Infection
■ Infections of the urinary tract
■ Wounds
■ Invasive lines
■ Meningitis
139
140 VII MANAGEMENT OF INFECTIOUS DISEASES
Assessment Findings
General
■ Fever
■ Ill appearance
■ Cold clammy skin
■ Hot dry skin
■ Reports symptoms consistent with active infection
Cardiovascular
■ Tachycardia
■ Hypotension
●Systolic blood pressure (SBP) <90
●Mean arterial pressure (MAP) <70
■ Elevated cardiac index (CI)
■ Low central venous pressure (CVP)
Pulmonary
■ Shortness of breath
■ Tachypnea
■ Respiratory failure
■ Cough
● Especially when pneumonia is the source
Renal
■ Decreased urine output
■ Acute oliguria
● Urine output less than 0.5 mL/kg/hr
Genitourinary
■ Dysuria
■ Frequency
■ Cloudy urine
■ Foul-smelling urine
Gastrointestinal
■ Hypoactive or absent bowel sounds
■ Nausea
■ Vomiting
Neuro
■ Altered mental status
■ Obtunded
■ Confusion
● May be early symptom in older adults
Integumentary
■ Cellulitis
■ Open wounds
■ Pressure wounds
■ Rash
■ Punctures
17 SEPSIS AND SEPTIC SHOCK 141
Endocrine
■ Reports of hyperglycemia
Diagnostics
Laboratory Findings
■ CBC
● WBCs >12 or <4
● Bandemia >10%
● Decrease platelets
■ Chemistry
● Elevated glucose without history of diabetes
● Elevated BUN and creatinine
■ Creatinine increased >0.5 than baseline
■ Lactate >2 mmol/L
142 VII MANAGEMENT OF INFECTIOUS DISEASES
■ Coagulation
● Elevated PT
● Elevated PTT
● Decreased fibrinogen
■ Elevated procalcitonin level
● Data support use in de-escalation of antibiotics and not as confirmation
of sepsis
■ Elevated CRP (C-reactive protein)
■ Urinalysis
● If source consistent with infection
■ Color: Dark
■ Clarity: Hazy
■ Bacteria/yeast: 1 to 4+
■ Nitrites: Positive
■ WBC: Present
■ Leukocyte esterase: Present
■ Arterial blood gas (ABG)
● P/F ratio <300
● Metabolic acidosis
■ Mixed venous blood gas
● SpO2 >70%
Radiology
■ Chest x-ray
● Pneumonia
● Adult respiratory distress syndrome (ARDS)
■ Broad-spectrum antibiotics
● Ideally in the first 1 hour of identification of sepsis
● Make sure suspected sources are covered by therapy being initiated
■ Commonly vancomycin and
■ Piperacillin/tazobactam OR cefepime OR a carbapenem
■ Supplemental oxygen
● Sepsis often causes increased oxygen demand
● Titrate for optimal SpO2 or PaO2
● Intubation for respiratory distress
■ Pulmonary
● Risk for respiratory failure
● Follow ABG for hypoxemia
● High risk of requiring intubation
● Low tidal volume strategies recommended due to increased risk of
ARDS
■ Renal
● Acute kidney injury is seen in more than 50% of patients with sepsis
and is linked to an increase in mortality
● Follow serial chemistries for renal function
● Follow urine output
● Patient may require renal replacement therapy due to renal injury
■ Gastrointestinal (GI)
● Ileus
● Nasogastric or orogastric tube to low intermittent wall suction
● If GI tract nonfunctioning, consider IV route for medications
● Liver dysfunction
■ Hematology
● Coagulopathy
■ Fresh frozen plasma
■ Vitamin K
■ Cryoprecipitate
● Anemia
■ Transfuse packed red blood cells
■ Usually to keep hgb >7
17 SEPSIS AND SEPTIC SHOCK 145
■ Neuro
●Encephalopathy
●Follow acidosis and liver dysfunction for possible causes of acute
encephalopathy
■ Adrenal
● Adrenal insufficiency in septic shock
● Hydrocortisone replacement
■ Generally, IV dosed q8 to 12h
■ Seen as a late complication of sepsis and the critically ill
Bibliography
Angus, D. C., & van der Poll, T. (2013). Severe sepsis and septic shock. Critical Care
Medicine, 369(9), 840–851. https://doi.org/10.1056/NEJMra1208623
Dellinger, R. P., Levy, M. M., Rhodes, A., Annane, D., Gerlach, H., Opal, S. M.,
Sevransky, J. E., Sprung, C. L., Douglas, I. S., Jaeschke, R., Osborn, T. M.,
Nunnally, M. E., Townsend, S. R., Reinhart, K., Kleinpell, R. M., Angus, D. C.,
Deutschman, C. S., Machado, F. R., Rubenfeld, G. D., … Moreno, R.; Surviving
Sepsis Campaign Guidelines Committee including the Pediatric Subgroup (2013).
Surviving sepsis campaign: International guidelines for management of severe
sepsis and septic shock: 2013. Intensive Care Medicine, 41, 580–637. https://doi.org/
10.1097/CCM.0b013e31827e83af
Gaileski, D. F., Mikkelsen, M. E., Band, R. A., Pines, J. M., Massone, R., Furia, F. F.,
Shofer, F. S., & Goyal, M. (2010). Impact of time to antibiotics on survival in
patients with severe sepsis or septic shock in whom early goal-directed therapy
was initiated in the emergency department. Critical Care Medicine, 38(4), 1045–
1053. https://doi.org/10.1097/CCM.0b013e3181cc4824
Gupta, S., Sakhuja, A., Kumar, G., McGrath, E., Nanchal, R. S., & Kashani, K. B.
(2016). Culture-negative severe sepsis. Chest, 150(6), 1251–1259. https://doi.org/
10.1016/j.chest.2016.08.1460
Hohn, A., Balfer, N., Heising, B., Hertel, S., Wiemer, J. C., Hochreiter, M., &
Schröder, S. (2018). Adherence to a procalcitonin-guided antibiotic treatment
protocol in patients with severe sepsis and septic shock. Annals of Intensive Care,
68(8), 1–10. https://doi.org/10.1186/s13613-018-0415-5
Howell, M. D., & Davis, A. M. (2017). Management of sepsis and septic shock. JAMA,
317(8), 847–848. https://doi.org/10.1001/jama.2017.0131
Kaukonen, K., Bailey, M., Suzuki, S., Pilcher, D., & Bellomo, R. (2014). Mortality
related to severe sepsis and septic shock among critically ill patients in
Australia and New Zealand, 2000–2012. JAMA, 311(13), 1308–1316. https://
doi.org/10.1001/jama.2014.2637
Kaukonen, K., Bailey, M., Suzuki, S., Pilcher, D., Cooper, J. D., & Bellomo, R. (2015).
Systemic inflammatory response syndrome criteria in defining severe sepsis.
New England Journal of Medicine, 372(17), 1629–1638. https://doi.org/10.1056/
NEJMoa1415236
Marik, P. E., Khangoora, V., Rivera, R., Hooper, M. H., & Catravas, J. (2016).
Hydrocortisone, vitamin C, and thiamine for the treatment of severe sepsis and
septic shock. Chest, 151(6), 1229–1236. https://doi.org/10.1016/j.chest.2016.11.036
Puskarich, M. A., Marchick, M. R., Kline, J. A., Steuerwald, M. T., & Jones, A. E.
(2009). One year mortality of patients treated with an emergency department
146 VII MANAGEMENT OF INFECTIOUS DISEASES
based early goal directed therapy protocol for severe sepsis and septic shock: A
before and after study. Critical Care, 13(5), R167. https://doi.org/10.1186/cc8138
Raith, E. P., Udy, A. A., Bailey, M., McGloughlin, S., MacIsaac, C., Bellomo, R., &
Pilcher, D. V.; Australian and New Zealand Intensive Care Society (ANZICS)
Centre for Outcomes and Resource Evaluation (CORE). (2017). Prognostic
accuracy of the SOFA score, SIRS criteria, and qSOFA score for in-hospital
mortality amount adults with suspected infection admitted to the intensive care
unit. JAMA, 317(3), 290–300. https://doi.org/10.1001/jama.2016.20328
Seymour, C. W., Liu, V. X., Iwashyna, T. J., Brunkhorst, F. M., Rea, T. D., Scherag, A.,
Rubenfeld, G., Kahn, J. M., Shankar-Hari, M., Singer, M., Deutschman, C. S.,
Escobar, G. J., & Angus, D. C. (2016). Assessment of clinical criteria for sepsis: For
the third international consensus definitions for sepsis and septic shock (Sepsis-3).
JAMA, 315(8), 762–774. https://doi.org/10.1001/jama.2016.0288
18
FEVER OF UNKNOWN ORIGIN AND
NOSOCOMIAL INFECTIONS
Causes
■ Infection
● Bacterial
■ Intraabdominal abscess
■ Appendicitis
■ Cholecystitis
■ Diverticulitis
■ Endocarditis
■ Pelvic inflammatory disease
■ Liver abscess
■ Osteomyelitis
■ Sinusitis
● Specific bacteria
■ Lyme disease
■ Chlamydia
■ Mycoplasma
■ Syphilis
■ Tick-borne illnesses
■ Tuberculosis
● Fungal
■ Aspergillosis
■ Candidiasis
■ Cryptococcosis
■ Histoplasmosis
● Viral
■ Coxsackievirus
■ Cytomegalovirus (CMV)
■ Epstein–Barr virus (EBV)
■ Hepatitis (A, B, C, D, E)
■ Herpes simplex (HSV)
■ HIV
● Parasitic
■ Giardia
147
148 VII MANAGEMENT OF INFECTIOUS DISEASES
■ Neoplasm
● Malignant lymphoma (most common)
● Leukemia
■ Vasculitis syndromes
■ Granulomatous disorders
■ Autoimmune disorders
● Rheumatoid arthritis
● Lupus
■ Drug-induced fever
● Drug reaction with eosinophilia and systemic symptoms (DRESS)
DRESS
■ Rare but potentially fatal drug reaction
■ Delayed onset of reaction
■ Delay can be between 2 and 10 weeks from last dose of offending agent
■ Clinical manifestations include cutaneous rash, atypical lymphocytes, and lymphadenopathy
Assessment Findings
■ Fever (101 F)
■ Illness lasting greater than 2 to 3 weeks
■ Tachycardia
■ Ill appearing
■ Hypotension
■ Complaints specific to etiology
18 FEVER OF UNKNOWN ORIGIN AND NOSOCOMIAL INFECTIONS 149
FACTIOUS FEVER
■ Fever falsely elevated by the patient
■ Suspected when no suspected source or no other hemodynamic changes
■ Seen more in females with healthcare knowledge
■ May be symptom of Munchausen syndrome
Diagnostics
Laboratory
■ CBC
● Ideally with manual differential
■ Chemistries
■ Lactic
■ Lactate dehydrogenase
■ Interferon gold
● If tuberculosis is suspected
■ Inflammatory markers
● C-reactive protein (CRP)
● Eosinophil (ESR or sedimentation rate)
● Antinuclear antibodies (ANA)
● Rheumatoid factor
■ Hepatitis panel (A, B, C)
● Indicated when there are abnormal liver functions, or
● Suspected exposure
■ HIV
● Indications
● Risk factors present
● Low cd4/cd8 count
● Other opportunist infections
150 VII MANAGEMENT OF INFECTIOUS DISEASES
Blood cultures
■ Ideally obtained from two different locations
■ If possible, obtain when fever present
■ Obtain set prior to initiation of antibiotics
Wound cultures
■ If wounds present
Urinalysis and urine culture
Radiology
■ Chest x-ray
■ Right upper quadrant ultrasound
● Evaluate liver and gallbladder
● If liver functions abnormal
■ CT abdomen and pelvis
● If abdominal abscess or intrabdominal process
suspected
ECHOCARDIOGRAM
■ Suspected or concerns of endocarditis
Lumbar puncture
■ Indicated when symptoms of central nervous system (CNS) infection, or
■ If no other source is found
Punch biopsy
■ May be indicated if a rash is present
Bone marrow biopsy
■ Suspected malignancy
● Infectious disease
● Other specialties as indicated
NOSOCOMIAL INFECTIONS
Causes
■ Gram-positive bacteria
● Staphylococcus
■ Including methicillin-resistant Staphylococcus aureus (MRSA)
Streptococcus
●
Enterococcus
●
■ Gram-negative bacteria
● Klebsiella
● Enterobacter
● Pseudomonas
■ Fungal
● Candida
Assessment Findings
■ Fever
■ Chills
■ Tachycardia
■ Redness drainage at insertion site
■ Extending cellulitis
■ Hypoglycemia
● Seen in systemic fungal infections
■ Ill appearing
■ Shock
■ Sepsis
Diagnostics
Laboratory
■ CBC
● Leukocytosis
■ Trend from start of fever or suspected worsening of illness
● Thrombocytopenia
■ Chemistry
● Rising creatinine
■ Lactic
● Elevated as sepsis marker
152 VII MANAGEMENT OF INFECTIOUS DISEASES
Blood cultures
■ One from suspected line
■ One from peripheral stick
■ Ideally prior to initiation of antibiotics
Causes
■ Gram-negative bacteria
Escherichia coli
●
Klebsiella
●
Pseudomonas
●
Proteus
●
■ Gram-positive bacteria
● Staphylococcus epidermis
● Staphylococcus aureus
■ Including MRSA
● Enterococcus faecalis
■ Yeast
● Less common
Risk Factors
■ Advanced age
■ Females
■ Diabetes
Assessment Findings
■ Pyuria
■ Suprapubic discomfort
■ Dysuria
■ Sudden fever
■ Flank pain
■ Signs of sepsis without source
18 FEVER OF UNKNOWN ORIGIN AND NOSOCOMIAL INFECTIONS 153
Diagnostics
Laboratory
■ CBC
● Leukocytosis
■ Trend from start of fever or suspected worsening of illness
■ Urinalysis and culture
● Culture generally not treated unless >100,000 colonies or other
indications that urinary tract is the source of infection
■ Chills
■ Rigors
■ Malaise
■ The elderly may be more difficult to assess
● May have increased confusion
● Increased risk for falls
● However, symptoms may indicate other pathology
● Signs of upper tract infection
■ Flank pain
■ Nausea and vomiting
■ Costovertebral tenderness
● Treatment
■ Evaluate risk of resistance
■ No risk of resistance
● Ceftriaxone 1 g daily or piperacillin–tazobactam 3.375 g q6h
■ Risk of resistance
● Gram-negative resistance
• Carbapenem
• Meropenem 1 g q8h
• Doripenem 500 mg q8h
● Gram-positive resistance
• Vancomycin
• Dosing based on weight and renal function
• Daptomycin 4 to 6 mg/kg IV
• Linezolid 600 mg IV q12h
Other Assessments
■ Assess need for catheter
■ Discontinue foley if appropriate
■ Change foley if unable to be discontinued
■ Evaluate risk factors for resistant infection
18 FEVER OF UNKNOWN ORIGIN AND NOSOCOMIAL INFECTIONS 155
Ventilator-Associated Pneumonia
Causes
■ Pneumonia that occurs more than 48 hours after the initiation of
mechanical ventilation
■ Gram-positive bacteria
● S. aureus
■ Gram-negative bacteria
● Pseudomonas aeruginosa
● Other gram-negative bacilli
Assessment Findings
■ Fever
■ Tachypnea
■ Increased secretions
■ Purulent secretions
■ Increased inspiratory pressures on ventilator
■ Decreased tidal volumes
■ Hypoxia
■ Increased oxygen demand
■ Bronchospasm
Diagnostics
Laboratory
■ CBC
● Increased leukocytosis
Radiology
■ Chest x-ray
● New or worsening infiltrate
156 VII MANAGEMENT OF INFECTIOUS DISEASES
Bronchoscopy
■ Bronchoalveolar lavage
● Allows for sampling of lower airways for culture
RESISTANT BACTERIA
TABLE
BACTERIA COMMON SITES RISK FACTORS TREATMENT
OF INFECTION
Bibliography
Cunha, B.A., Lortholary, O., & Cunha, C. B. (2019). Fever of unknown origin: A
clinical approach. American Journal of Medicine, 128(10), e1–e15. https://doi.org/
10.1016/j.amjmed.2015.06.001
Davis, C. (2019). Catheter-associated urinary tract infection: Signs, diagnosis,
prevention. British Journal of Nursing, 28(2), 96–100. https://doi.org/10.12968/
bjon.2019.28.2.96
Horowitz, H. (2013). Fever of unknown origin or fever of too many origins?
New England Journal of Medicine, 368(3), 197–199. https://doi.org/10.1056/
NEJMp1212725
Ibn Saied W., Mourvillier, B., Cohen, Y., Ruckly, S., Reignier, J., Marcotte, G., Siami, S.,
Bouadma, L., Darmon, M., de Montmollin, E., Argaud, L., Kallel, H., Garrouste-
Orgeas, M., Soufir, L., Schwebel, C., Souweine, B., Glodgran-Toledano, D.,
Papazian, L., & Timsit, J.-F.; OUTCOMEREA Study Group. (2019). A comparison
of the mortality risk associated with ventilator-acquired bacterial pneumonia and
non-ventilator ICU-acquired bacterial pneumonia. Critical Care Medicine, 47(3),
345. https://doi.org/10.1097/CCM.0000000000003553
Leuck, A. M., Wright, D., Ellingson, L., Kraemer, L., Kuskowski, M. A., & Johnson, J. R.
(2012). Complications of Foley catheters: Is infection the greatest risk? Journal of Urology,
187(5), 1662–1666. https://doi.org/10.1016/j.juro.2011.12.113
Lo, E., Nicolle, L. E., Coffin, S. E., Gould, C., Maragakis, L. L., Meddings, J., Pegues,
D. A., Pettis, A. M., Saint, S., & Yokoe, D. S. (2014). Strategies to prevent catheter-
associated urinary tract infections in acute care hospitals: 2014 update. Infect
Control Hospital Epidemiology, 35(5), 464–479. https://doi.org/10.1086/675718
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in
adults children (8th ed.). Mosby.
158 VII MANAGEMENT OF INFECTIOUS DISEASES
National Healthcare Safety Network. (2021, January). Urinary tract infection (Catheter-
Associated Urinary Tract Infection [CAUTI] and Non-Catheter-Associated Urinary
TractInfection [UTI]) events. http://www.cdc.gov/nhsn/PDFs/pscManual/
7pscCAUTIcurrent.pdf
Nicolle, L. E. (2001). A practical guide to antimicrobial management of complicated
urinary tract infection. Drugs Aging, 18(4), 243. https://doi.org/10.2165/00002512-
200118040-00002
Parisi, M., Gerovasili, V., Dimopoulos, S., Kampisiouli, E., Goga, C., Perivolioti, E.,
Argyropoulou, A., Routsi, C., Tsiodras, S., & Nanas, S. (2016). Use of ventilator
bundle and staff education to decrease ventilator associated pneumonia in
intensive care patients. Critical Care Nurse, 36(5), e1–e7. https://doi.org/10.4037/
ccn2016520
SECTION VIII
BILLING, ASSESSMENTS, AND
DOCUMENTATION
Nichole Miller and Tish Myers
19
NOTE TEMPLATES
OLD CARTS
■ ONSET
■ LOCATION
■ DURATION
■ CHARACTER
■ AGGRAVATING FACTORS
■ RELIEVING FACTORS
■ TIMING
■ SEVERITY
Medical History
■ Any significant medical history
Surgical History
■ Any surgical history
Allergies
■ Drug
■ Food
■ Latex
■ Include reaction to each medication/food if allergies are present
161
162 VIII BILLING, ASSESSMENTS, & DOCUMENTATION
Home Medications
■ Medication
■ Dose
■ Schedule
Social History
■ Tobacco
■ Alcohol
■ Drug use
■ Vaccine status
■ Occupation
Family History
■ Mother
■ Father
■ Siblings
■ Grandparents
Review of Systems
General
■ Fever
■ Chills
■ Weight loss
■ Fatigue
Skin
■ Rashes
■ Lesions
■ Changes in hair
Head/Neck
■ Headache
■ Dizziness
■ Trauma
Eyes
■ Vision changes
■ Eye pain
■ Photophobia
Ears
■ Pain
■ Drainage
■ Vertigo
19 NOTE TEMPLATES 163
Nose
■ Epistaxis
■ Discharge
■ Sneezing
Mouth/Throat
■ Pain
■ Exudate
■ Oral ulcers
Cardiovascular
■ Chest pain
■ Palpitations
■ Edema
INTERVIEW TECHNIQUES
■ Open-ended questions will elicit more information than closed-ended questions.
■ Avoid “why” questions. This can make patients defensive.
■ Use active-listening skills.
■ Avoid leading questions.
Pulmonary
■ Dyspnea on exertion
■ Cough
■ Sputum
■ Orthopnea
Breasts
■ Drainage
■ Pain
Gastrointestinal
■ Nausea vomiting
■ Hematemesis
■ Abdominal pain
■ Diarrhea
■ Constipation
■ Melena
■ Change in bowel habits
Genitourinary
■ Dysuria
■ Frequency
■ Hematuria
■ Penile/vaginal discharge
164 VIII BILLING, ASSESSMENTS, & DOCUMENTATION
Endocrine
■ Temperature intolerance
■ Polyuria
■ Polydipsia
■ Polyphagia
Musculoskeletal
■ Arthralgias
■ Myalgias
■ Erythema/tenderness
Neurology
■ Syncope
■ Vertigo
■ Weakness
■ Numbness
Psychiatric
■ Anxiety
■ Mania
■ Depression
■ Suicide ideology
REVIEW OF SYSTEMS
■ Information is subjective
■ Is what the patient states
■ May differ at times from physical assessment
Vital Signs
■ Temperature
■ Blood pressure
■ Heart rate
■ Respiratory rate
■ SpO2
■ Central venous pressure (CVP)
■ Cardiac index (CI)
■ Cardiac output (CO)
■ Systemic vascular resistance (SVR)
Physical Exam
General
■ Age
■ Sex
■ What does the patient look like?
Head, Eyes, Ears, Nose, and Throat
■ Atraumatic normocephalic
■ Mucus membrane assessment
Cardiovascular
■ Rate rhythm
■ Heart sounds
■ Jugular vascular distention
Pulmonary
■ Rate
■ Rhythm
■ Mechanical ventilation
Mode
●
Ventilator settings
●
■ Lung auscultation
■ Chest tubes
Gastrointestinal
■ Abdomen
■ Abdomen sign findings
● Murphy
● Cullen
Genitourinary
■ Urine color
■ Urine output
■ Foley
■ Vaginal/penile drainage
■ Pelvic exam findings
Neurology
■ Mental status
■ Cranial nerves
■ May not be able to assess fully in sedated/intubated patients
Musculoskeletal
■ Extremity movement
■ Edema
■ Compartment pressure
Psychiatry
■ Mental state
166 VIII BILLING, ASSESSMENTS, & DOCUMENTATION
Diagnosis
■ Your diagnoses or differential
Plan
■ What are you going to do for each patient?
CONSULT NOTE
■ If working with a specialty service, you may be completing a consultation note instead of an
H&P.
■ Consult notes are similar to H&P and contain all the same parts.
■ Physical exam may be more specific to the specialty (e.g., cardiology may have a focused
assessment of the cardiovascular system).
■ Plan will also be more specific to the specialty and may not address all aspects of the patient’s
care.
Technique/Procedure
● Describe in detail the procedure performed.
● This section is often completed by the surgeon if the procedure is
completed with a surgeon.
Specimens Removed
● Tissue sent to microbiology or pathology
● Body parts removed and disposition
Implants
● Name of or type of any implants such as orthopedic or plastics devices
● Include serial number of implanted products and lot number
Complications
Fluids
● Type of fluids given and amount infused
● Can include blood or blood products
Estimated Blood Loss
● Noted in milliliters
Findings
● Any important data about the procedure
● Often include measurements
● Tourniquet times
● Pump times
● Abnormal findings
● Exploration findings
DISCHARGE SUMMARY
Name and Title of Person Dictating the Summary
● NPs and PAs state name of MD they are dictating on behalf of
Patient Identifiers
● Name
● Date of birth
● Medical record number
Date of Admission
● Specify date
Date of Discharge
● Specify date
19 NOTE TEMPLATES 169
Admitting Diagnosis
● Initial reason for admission to the hospital
Name of Attending Physician
Name of Primary Care Physician
● State “PCP unknown” if this is the case
Name of Referring Physician
● This is important information to include in the admission H&P and can
be located there if available; otherwise, state “unknown.”
Names of Any Consulting Physicians
● Include here any other physicians who assisted in the patient’s care
while hospitalized other than the admitting physician (also referred to
as the “attending physician”)
Date and Description of Operative or Other Procedures
● Include name of healthcare providers who completed the procedures if
available
Brief History
● Summarize why the patient was admitted to the hospital and include
the following:
● Age and gender
■ Where patient was admitted from
■ ED
■ Direct admit
● Outside facility
■ Reason for admission to include symptoms and any diagnoses if known
Hospital Course
● Summarize pertinent laboratory and other diagnostic data
● White blood cell (WBC) elevated
● Low hemoglobin
● Platelet counts (high or low)
● Abnormal chemistry results
● Results of CAT scans, MRIs, x-rays, and so forth
● Biopsy, urinalysis, or tissue culture results
● What was the result or action performed in relation to these findings
● Antibiotics
■ Unexpected or untoward occurrences and the outcome
Discharge Diagnosis or Diagnoses
● May be multiple depending on patient and length of stay
Patient Condition on Discharge
● Stable
● Improved
● Fair
● Guarded
● Critical
Discharge Medications
● Include name of drug, dosage, frequency, and duration of any new
medications prescribed
170 VIII BILLING, ASSESSMENTS, & DOCUMENTATION
Subjective
■ Chief complaint
Use patient’s own words to describe how they feel
●
What do they report?
●
■ Nursing reports
■ Note any reported concerns, events, or changes in condition
Objective
■ Vital signs
■ I&O
■ Weight or changes in weight
■ Physical assessment data
● General appearance
● HEENT
● Neck
● Respiratory
19 NOTE TEMPLATES 171
● Cardiovascular
● Abdomen
● Genitourinary
● Musculoskeletal
● Neurological
● Psych
● Wounds/incisions
■ Pertinent laboratory data
■ Other diagnostic findings
■ Treatment and prophylaxis
■ Include pertinent changes to medications, antibiotics, lines or other
invasive devices, ventilator, oxygen, tube feeds, intravenous fluids,
and so forth
Diagnosis
■ Any applicable diagnoses
■ List and update all diagnosis
BILLING
■ Billing captures the services provided and allows reimbursement from insurance.
■ These will vary by specialty, location, and supervision type.
■ Location of patient does not mean they qualify for billing at that level.
■ Some places validate positions by hours billed.
■ Billing can be used to justify raises or bonuses.
■ Medical history
■ Family medical history
■ Social history
■ Review of all body systems
■ Physical exam
Medical Decision-Making
■ Moderate
■ Two of the following three must be met or exceeded:
● Multiple number of diagnoses or management options
● Moderate amount and/or complexity of data to be reviewed
● Moderate risk of significant complications, morbidity, and/or mortality
99231—Problem Focused
■ Approximately 15 minutes at bedside
■ Medical decision-making is low/straightforward
99233—Detailed
■ Approximately 35 minutes
■ Medical decision-making high or complex
OBSERVATION CODES
■ Observation codes are used when a patient is not expected to spend
greater than two nights in the hospital.
■ Severity of patient condition can range from low to high in the same
manner as a full inpatient admission.
CONSULTING SERVICES
■ Consults will be billed under a consult code 99251 to 99253.
■ Initial consults should contain the same information as an H&P based on the acuity and
complexity of the patient.
■ Plan should reflect specialty.
20 BILLING FOR SERVICES 177
99291 30 to 74 minutes
99292 Each additional 30 minutes (added to initial code)
■ Both codes can be used together.
Documentation Required Every Hospital Day
■ Chief complaint
■ HPI
■ Review of all body systems
■ Physical exam
■ Diagnosis to support need for ICU level of care
■ Plan for each diagnosis
BILLABLE PROCEDURES
Many procedures are reimbursable.
■ Central line placement
● Peripherally inserted central catheter line
● Central venous catheter
● Dialysis catheter
■ Arterial line placement
■ Incision and drainage
■ Laceration repair
■ Chest tube placement
■ Thoracentesis
■ Paracentesis
INDEX
abdominal compartment syndrome, 111 Allen test, 86
abdominal x-ray, 111, 116, 133 allergies, 161
ABG. See arterial blood gas alpha blockers, for cocaine-induced
acalculous cholecystitis, 113 hypertensive emergency, 15
ACE inhibitors, 8, 68 alteplase, for cerebral vascular
acetaminophen, 117, 135, 143, 150 accident, 46
acid-base balance, 85 amikacin, for carbapenem resistant
formulas, 87 enterobacteriaceae, 157
metabolic acidosis, 85–87 aminoglycosides
metabolic alkalosis, 87–88 for carbapenem resistant enterobacte-
respiratory acidosis, 88–90 riaceae, 157
respiratory alkalosis, 90 for diverticulitis, 117
acute cholecystitis, 111–113 amiodarone, 131
acute coronary syndrome, 3–8 anatomic shunt, 28
acute heart failure, 17–22 anemia, 144
acute kidney injury, 59–66 angiotensin II (Giapreza), for sepsis, 144
azotemia vs. uremia, 60 anion gap, 87
fraction of excreted sodium, 61 anterior cerebral artery occlusion, 44
intrarenal (intrinsic), 62–65 antibiotics, 36, 66
postrenal, 65–66 for appendicitis, 119
prerenal, 59–61 beta lactam, for diverticulitis, 117
RIFLE and AKIN classification, 60–61 broad spectrum, 143
RIFLE criteria, 60–61 for CLABSI, 152
and sepsis, 144 for sepsis, 143
acute pancreatitis, 109–111 for spontaneous bacterial
APACHE II score, 110 peritonitis, 121
classification, 109 for diverticulitis, 117
signs of, 110 for esophageal varices, 98
acute tubular necrosis, 62 for peritonitis, 121
adrenal insufficiency, 134, 145 for ventilator associated pneumonia,
adult respiratory distress syndrome 156
(ARDS), 33–36, 144 anticoagulants, reversal of, 47
P/F ratio, 34 antiemetics, for Mallory-Weiss tear, 98
severity, 35 antiepileptics, 54–55
stages of, 33 antihistamines, for pruritis, 105
albumin infusions, 105, 106 antiplatelet therapy, for myocardial
albuterol, 36 infarction, 6–7
nebulizer, for hyperkalemia, 71 aortic dissection, 13
for ventilator associated pneumonia, 156 APACHE II score, 110
alcohol withdrawal, and seizures, 55 appendectomy, 119
aldosterone antagonists, for myocardial appendicitis, 118–119
infarction, 8 ARBS, 68
179
180 INDEX