Critical Care Medicine

American Thoracic Society BOARD REVIEW ATS REVIEW FOR THE CRITICAL CARE BOARDS First Edition Senior Editorial Team Susan Pasnick, MD | Jason Poston,...
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American Thoracic Society


ATS REVIEW FOR THE CRITICAL CARE BOARDS First Edition Senior Editorial Team Susan Pasnick, MD | Jason Poston, MD | Tisha Wang, MD

Copyright © 2018 by American Thoracic Society All rights reserved. This book or any portion thereof may not be reproduced or used in any manner whatsoever without the express written permission of the publisher except for the use of brief quotations in a book review. Printed in the United States of America First Printing, 2018 ISBN 978-0-9776442-1-6 American Thoracic Society 25 Broadway, 18th Floor New York, NY 10004

Foreword and Dedication The creation of this book was a truly collaborative project between trainees and both junior and senior faculty from a number of academic institutions brought together by the ATS. Through the efforts of all these dedicated individuals and multiple levels of reviews, it is our hope that we have provided you with a useful resource for both board review and the most current up-to-date clinical care within critical care. This project would not have been possible without the volunteer work and efforts of all the pulmonary/critical care fellows, the faculty reviewers (largely taken from the ATS Education Committee), and the dedicated editorial staff of superstar clinician educators who worked tirelessly to complete this in the midst of our busy day jobs and lives. We owe a significant thank you to the wonderful ATS staff who helped us from start to finish – Odalys Jimenez, Eileen Larsson, Lauren Lynch, and especially Jennifer Siegel-Gasiewski who kept us on track and provided an immense amount of both administrative and moral support. We also owe a great deal of appreciation to our family, friends, and loved ones who tolerated the countless hours of editing on weekends, nights, and during vacations. Our careers and impact in education and medicine would simply not be possible without your support. And lastly, this book is dedicated to all of our trainees, past and present, who constantly inspire us to continue learning and teaching at every stage of our careers. There is no doubt that we are better people, physicians, and educators because of you. Good luck with the boards and the patients and thanks for reading… Tisha Wang MD on behalf of the editorial team


Senior Editors Susan Pasnick, MD Director of Critical Care Process Improvement CHRISTUS St. Vincent Regional Medical Center, Santa Fe, NM Jason T. Poston, MD Assistant Professor of Medicine University of Chicago Medicine Tisha Wang, MD Associate Professor of Clinical Medicine Fellowship Program Director and Clinical Division Chief UCLA Pulmonary and Critical Care Medicine

Associate Editors W. Graham Carlos, MD, MSCR Associate Professor of Clinical Medicine Division of Pulmonary, Critical Care, Sleep and Occupational Medicine Indiana University School of Medicine Shazia M. Jamil, MD, FCCP, FAASM Clinical Associate Professor of Medicine University of California, San Diego School of Medicine Division of Pulmonary, Critical Care and Sleep Medicine Department of Medicine, Scripps Clinic Medical Copyeditor: Kerry M. Ledbetter


chapter 1 Renal, Endocrine, and Metabolic Disorders

chapter 6 Surgery, Trauma, and Transplantation

Zafia Anklesaria, MD; Nancy Hsu, MD; Ishan Mehta, MD; Kathryn H. Melamed, MD

Ayodeji Adegunsoye, MD, MS; Anthony F. Arredondo, MD

chapter 2 Infectious Disease Christine M. Bojanowski, MD; Bryan Joshua Garber, DMD; Anas Khalil,MD; Tessy Paul, MD; Alexander Zider, MD

chapter 3 Pharmacology and Toxicology Gabriel Wardi, MD, MPH

chapter 4 Pulmonary Disease Ryan Boente, MD; Nancy Hsu, MD; Christopher Kniese, MD; Patrick G. Lyons, MD; Claudia Daniela Onofrei, MD, MSc; Nathan Schoettler, MD., PhD

chapter 5 Gastrointestinal Disorders Emily Cochard, MD; Laura Hinkle, MD


chapter 7 Cardiovascular Laura K. Frye, MD; William F. Parker, MD; Krysta S. Wolfe, MD; David Wu, MD, PhD

chapter 8 Neurologic Disorders Karen C. Dugan, M.D; Heng T. Duong, MD; Juan C. Rojas, MD

chapter 9 Hematologic/Oncologic Disorders Başak Çoruh, MD; James Town, MD

chapter 10 Research/Administration/ Ethics Juan C. Rojas, MD

Contributing Authors Ayodeji Adegunsoye. MD, MS Clinical Instructor, Division of Pulmonary, Critical Care and Sleep Medicine The University of Chicago Zafia Anklesaria MD Fellow, Division of Pulmonary and Critical Care University of California, Los Angeles Anthony F. Arredondo, MD Associate Medical Director Pulmonary and Critical Care Medicine Martin Luther King Jr. Community Hospital Associate Staff Physician UCLA Pulmonary and Critical Care Medicine

Bryan J. Garber, MD Fellow, Division of Pulmonary and Critical Care University of California, Los Angeles Laura Hinkle, MD Assistant Professor of Clinical Medicine Division of Pulmonary, Critical Care, Sleep, & Occupational Medicine Indiana University School of Medicine Anas Khalil,MD Assistant Professor of Pulmonary and Critical Care Medicine Taibah University, Saudi Arabia

Ryan Boente, MD Fellow, Division of Pulmonary and Critical Care Medicine Indiana University School of Medicine

Christopher Kniese, MD Fellow, Division of Pulmonary and Critical Care Medicine Indiana University School of Medicine

Christine M. Bojanowski, MD Fellow, Division of Pulmonary, Critical Care and Sleep Medicine University of California, San Diego

Patrick G. Lyons, MD Fellow, Division of Pulmonary and Critical Care Medicine Washington University in St. Louis

Emily Cochard, MD Fellow, Division of Pulmonary and Critical Care Medicine Indiana University School of Medicine

Ishan Mehta, MD Fellow, Division of Pulmonary and Critical Care University of California, Los Angeles

Başak Çoruh, MD Assistant Professor Division of Pulmonary, Critical Care and Sleep Medicine University of Washington

Kathryn H. Melamed, MD Fellow, Division of Pulmonary and Critical Care University of California, Los Angeles

Karen C. Dugan, MD Fellow, Division of Pulmonary, Critical Care and Sleep Medicine The University of Chicago


Laura K. Frye, MD Assistant Professor of Medicine The University of Chicago

Nancy Hsu, MD Fellow, Division of Pulmonary and Critical Care University of California, Los Angeles

Claudia Daniela Onofrei, MD, MSc Fellow, Division of Pulmonary and Critical Care Medicine Indiana University School of Medicine

David Wu, MD, PhD Fellow, Division of Pulmonary, Critical Care and Sleep Medicine The University of Chicago

William F. Parker, MD Fellow, Division of Pulmonary, Critical Care and Sleep Medicine The University of Chicago

Alexander Zider, MD Pulmonary Associates Burlingame, CA

Tessy Paul, MD Assistant Professor, Division of Pulmonary and Critical Care University of Virginia Juan C. Rojas, MD Fellow, Division of Pulmonary, Critical Care and Sleep Medicine The University of Chicago Nathan Schoettler, MD, PhD Fellow, Division of Pulmonary, Critical Care and Sleep Medicine The University of Chicago James Town, MD Clinical Instructor Division of Pulmonary, Critical Care and Sleep Medicine University of Washington Gabriel Wardi, MD, MPH Fellow, Department of Emergency Medicine and Division of Pulmonary, Critical Care, and Sleep Medicine University of California, San Diego Krysta S. Wolfe, MD Fellow, Division of Pulmonary, Critical Care and Sleep Medicine The University of Chicago


Faculty Reviewers Shozab Ahmed, M.B.B.S, F.C.C.P Assistant Professor Associate Program Director Internal Medicine Residency Program Associate Program Director Critical Care Fellowship Program Department of Internal Medicine Division of Pulmonary, Critical Care and Sleep Medicine University of New Mexico Colleen L. Channick, MD Assistant Professor of Medicine, Harvard Medical School Division of Pulmonary and Critical Care Medicine Massachusetts General Hospital Daniel Crouch, MD Assistant Professor of Medicine Division of Pulmonary and Critical Care Medicine University of California, San Diego Margaret M. Hayes, MD Assistant Professor of Medicine, Harvard Medical School Associate Program Director, Beth Israel Internal Medicine Residency Division of Pulmonary, Critical Care, and Sleep Medicine Beth Israel Deaconess Medical Center Abigail Lara, MD Associate Professor of Medicine Division of Pulmonary Sciences and Critical Care Medicine University of Colorado School of Medicine


Ryan C. Maves, MD, FCCP, FIDSA Commander, Medical Corps, U.S Navy Program Director, Infectious Diseases Fellowship Faculty Physician, Critical Care Medicine Service Naval Medical Center, San Diego, California Associate Professor of Medicine Uniformed Services University, Bethesda, Maryland Jakob I. McSparron, MD Assistant Professor of Medicine Division of Pulmonary and Critical Care Medicine University of Michigan Gaetane Michaud, MS, MD, FRCPC Associate Professor of Medicine, Pulmonary, Critical Care and Cardiothoracic Surgery Chief, Interventional Pulmonology NYU School of Medicine Samaan Rafeq, MD Senior Associate Director, Interventional Pulmonology Section Director, Interventional Pulmonary Fellowship NYU School of Medicine Jeremy B. Richards, MD, MA Assistant Professor of Medicine Beth Israel Deaconess Medical Center and Harvard Medical School

Carey C. Thomson, MD, MPH Associate Chair, Department of Medicine Chief, Pulmonary and Critical Care Division Mount Auburn Hospital Associate Professor, Harvard Medical School Carolyn H. Welsh, MD Professor of Medicine Division of Pulmonary Sciences and Critical Care Medicine Staff physician and Sleep Program Director at The Eastern Colorado VA Health Care System University of Colorado Denver Bishoy Zakhary, MD Assistant Professor of Medicine Department of Pulmonary and Critical Care Medicine Oregon Health and Sciences University Anna L. Zisman, MD Assistant Professor of Medicine Department of Medicine and Section of Nephrology The University of Chicago



renal, endocrine, and metabolic disorders Kathryn Melamed, MD; Ishan Mehta, MD; Nancy Hsu, MD; Zafia Anklesaria, MD

►►ELECTROLYTE DISORDERS Maintaining electrolyte balance and homeostasis is integral to organ function. Electrolyte disorders are common indications for ICU admission and can be primary or secondary.

►SODIUM ► AND WATER BALANCE Sodium and water regulation are tightly linked yet involve separate mechanisms. Changes in water balance can lead to hyponatremia or hypernatremia, and similarly changes in Na homeostasis can lead to hypovolemia or hypervolemia. In general: • • • •

Hypovolemia → loss of water and Na Edema → Na and water retention Hyponatremia → excess water that is not excreted Hypernatremia → water loss that is not replaced

Sodium Regulation • Cell membrane: Na/K-adenosine triphosphatase (ATPase), actively transports Na out of cell • Kidney: 99% of filtered Na is reabsorbed (60% in proximal tubules, 30% in loop of Henle, 10% in distal segments) • Several transporters aid in Na reabsorption into bloodstream (Figure 1-1) ◦◦ Na/H antiporter: proximal tubule ▪▪ Primary mechanism for Na absorption ▪▪ The H secreted into proximal tubule lumen then binds bicarbonate


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(HCO3), forming carbon dioxide (CO2) for passive reabsorption back into cell → H returns via Na/H antiporter, and HCO3 is absorbed

flash card Q. What are the results of treatment with aldosterone antagonists such as spironolactone?

A. Hyperkalemia, metabolic acidosis, and occasionally hyponatremia. These drugs prevent insertion of Na channels and decrease stimulation of H/K antiporter in the collecting duct.

Figure 1-1. Nephron with Na and K channels, symporters, and antiporters. Drugs, hormones, and conditions that stimulate (green arrow) or inhibit (red arrow) reabsorption are indicated. (Courtesy of Dr. Kathryn Melamed.)

Water Regulation • Both the hypothalamus-posterior pituitary-antidiuretic hormone (ADH) system and function/structure of nephron are necessary for maintaining normal plasma tonicity (280-290 mOsm/kg) • Proximal tubule + thin descending limb of loop of Henle = water passively absorbed • Ascending limb of loop of Henle + distal tubules = impermeable to water • The glomerular filtration rate (GFR) is regulated by: ◦◦ Effective circulating blood volume – the portion of total body volume in arterial circulation (decreased effective circulating blood volume = decreased GFR) ◦◦ Volume expansion → decreased reabsorption of isosmotic fluid (Na and water) in proximal tubule ◦◦ Volume contraction → increased reabsorption of isosmotic fluid in proximal tubule


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◦◦ Sympathetic innervation: causes vasoconstriction of afferent arteriole • Renin-angiotensin-aldosterone system (RAAS) (Figure 1-2) ◦◦ Decreased effective circulating blood volume activates RAAS ◦◦ Angiotensin II causes preferential constriction of efferent arteriole to increase GFR while aldosterone promotes Na reabsorption; therefore both increase Na and water reabsorption • ADH ◦◦ ADH is released by: ▪▪ Hyperosmolality (>295 mOsm/kg) stimulates osmoreceptors in hypothalamus → posterior pituitary secretes ADH ▪▪ Thirst, hypotension, hypovolemia stimulate baroreceptors in carotid sinuses, aortic arch, cardiac atria → ADH release ◦◦ ADH is suppressed by: ▪▪ Isotonic or hypotonic plasma ◦◦ ADH stimulates V2 receptors on collecting duct cells → increased aquaporin expression → water absorption in collecting duct

ACE = angiotensin-converting enzyme; ADH = antidiuretic hormone.

Figure 1-2. Renin-angiotensin-aldosterone system (RAAS).

(CC-BY-SA-3.0 (], via Wikimedia Commons.)

Hyponatremia Low plasma Na, defined as 20 mEq/La

>200 mOsm/kg

Cerebral salt wasting


Cerebral injury → BNP → renal Na wasting + inhibition of renin

>40 mEq/L

>300 mOsm/kg



Inappropriately elevated ADH causes excess water retention

>20 mEq/L

>100 mOsm/kg

Psychogenic polydipsia


Ingestion of large volume of water overwhelms kidney’s ability to dilute urine and excrete water

200 mOsm/kg



Profound salt loss during exercise followed by large intake of free waterb

100 mOsm/kg



Administration of excess hypotonic fluid (eg, D5W)c

100 mOsm/kg

Heart failure


200 mOsm/kg



200 mOsm/kg

Nephrotic syndrome


Low effective circulating volume →ADH secretion + RAAS activation → water retention out of proportion to Na retention

200 mOsm/kg

ACE=angiotensin-converting enzyme; ADH=antidiuretic hormone; ATN=acute tubular necrosis; BNP=brain natriuretic peptide; CRH=corticotropin-releasing hormone; D5W=5% dextrose in water; GFR=glomerular filtration rate; Osm=osmolality; RAAS= renin-angiotensin-aldosterone system; SIADH=syndrome of inappropriate antidiuretic hormone. a Eventually, even with diuretics, the urine Na will become very low as proximal tubule Na reabsorption will predominate. b This is largely because of extreme hypovolemia that then is corrected with free water intake alone. c Occurs in setting of low-solute intake or chronic kidney disease (ineffective ability to excrete free water), as under normal circumstances, liters of free water can be excreted.


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Antidiuretic hormone is elevated when not physiologically appropriate.

• Etiology ◦◦ Pulmonary: pneumonia, asthma/chronic obstructive pulmonary disease, pulmonary edema ◦◦ Neurologic: trauma, stroke, hemorrhage, meningitis ◦◦ Paraneoplastic: small cell lung carcinoma ◦◦ Medications: psychogenic medications (particularly selective serotonin reuptake inhibitors, chemotherapy) ◦◦ Pain ◦◦ Nausea, stomach cramping NOTE: Elevated ADH levels may be physiologic and still cause hyponatremia (eg, in hypovolemia).

PSYCHOGENIC POLYDIPSIA—ingestion of large amounts of water such that the

kidney is unable to dilute the urine any further

• Requires ingestion of 12+ L of water per day • Extremely low solute-to-water ratio dilutes concentrating power of medulla • Similar pathophysiology exists in a low-solute diet (eg, “tea and toast” diet or “beer potomania”) CLINICAL MANIFESTATIONS—due to osmotic water shifts and cerebral edema

• Asymptomatic: most often, hyponatremia causes no symptoms, particularly if onset is subacute or chronic • Symptoms related to underlying cause (eg, congestive heart failure, dehydration, hypothyroidism) • Altered mental status, headache, seizures • Death DIAGNOSIS

• Serum Na 145 mEq/L • Always occurs with hypertonic plasma (>295 mOsm/kg) • Due to loss of hypotonic fluids + decreased access to water • Rarely, it can result from iatrogenic infusion of hypertonic Na solutions Table 1-2. Hypernatremia Causes, Physiology, and Urine Studies




Urine Osm

Urine Na

Central diabetes insipidus

Loss of ADH production  inability to concentrate urine and absorb free water

100 mEq/L

Mineralocorticoid excess

Leads to Na channel insertion into collecting duct principal cells  Na reabsorption

>600 mOsm/kg

600 mOsm/kg

145 mEq/L • Serum osmolality >295 mOsm/L • Urine Na and osmolality (Table 1-2) • Water deprivation test: evaluates etiology of polyuria ◦◦ Deprive patient of free water until one of three occurs: A. Serum osmolality >295 mOsm/kg or Na >145 mEq/L B. Urine osmolality remains stable >3 h C. Urine osmolality >600 mOsm/kg ◦◦ If A or B: Then administer desmopressin and check urine osmolality every 30 min for 2 h


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▪▪ If urine osmolality increases by >50% = central DI ▪▪ If urine osmolality remains stable = nephrogenic DI ▪▪ NOTE: DI often partial such that urine osmolality only increases ≤50% ◦◦ If C = primary polydipsia ◦◦ Partial DI ▪▪ Central: Urine osmolality may only increase by 15-50% but should increase to >300 mOsm/kg ▪▪ Nephrogenic: Urine osmolality may only increase ≤45% but should remain 5.0 mEq/L ETIOLOGY—important to distinguish between: • True elevated total body K levels—due to decreased GFR; or normal GFR with decreased renal K secretion ◦◦ Renal failure ◦◦ Renal tubular acidosis (RTA) ◦◦ Adrenal insufficiency ◦◦ Medications ◦◦ Blood transfusions • Elevated serum K with normal or low total body K due to transcellular shifts of K out of cells ◦◦ Acidosis ◦◦ Insulin deficiency ◦◦ Hyperglycemia/hyperosmolality ◦◦ Medications (eg, β-blockers, succinylcholine) ◦◦ Cell lysis (eg, rhabdomyolysis, tumor lysis, trauma)


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◦◦ GI bleed • Pseudohyperkalemia RTA TYPE 4 (HYPOALDOSTERONISM)

Hypoaldosteronism → hyperkalemia + metabolic acidosis • Hypoaldosteronism → decreased Na channels → loss of negative electrochemical gradient → loss of K secretion • Nongap metabolic acidosis ◦◦ Direct effect of hypoaldosteronism on proton secretion by α-intercalated cells ◦◦ Decreased ammonia production by proximal tubule in setting of hyperkalemia and increased intracellular pH via K/H exchange ◦◦ Decreased ammonium production as a result of combination of above • Etiology ◦◦ Decreased aldosterone production ▪▪ Primary adrenal insufficiency (see below) ▪▪ Hyporeninemic hypoaldosteronism ▪▪ Diabetic nephropathy ▪▪ HIV infection ▪▪ Medications: nonsteroidal anti-inflammatory drugs (NSAIDs), calcineurin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), heparin ▪▪ Pseudohypoaldosteronism type 2 (Gordon syndrome): hypertension, hyperkalemia, metabolic acidosis, normal renal function ◦◦ Aldosterone resistance ▪▪ Medications: K-sparing diuretics, trimethoprim, pentamidine ▪▪ Pseudohypoaldosteronism type 1: rare inherited resistance to aldosterone • Diagnosis ◦◦ Remove any offending medication ◦◦ Measure plasma renin activity, serum aldosterone under appropriate setting (either 3 h of being upright or loop diuretic challenge), serum cortisol • Treat underlying cause ADRENAL INSUFFICIENCY (AI)—Please review section below on Adrenal Disorders

for details.

DRUG-INDUCED—medications can lead to extracellular shift of K into serum or

decreased renal secretion of K into the urine • Extracellular shift of K ◦◦ β-blockers ◦◦ Succinylcholine ◦◦ Digoxin (dose-dependent toxicity) ◦◦ Calcineurin inhibitors (eg, tacrolimus, cyclosporine)


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• Decreased renal secretion of K ◦◦ ACE inhibitors/ARBs (eg, lisinopril) ◦◦ Aldosterone antagonists (eg, spironolactone) ◦◦ Other K-sparing diuretics (eg, amiloride) • Iatrogenic overdose of K supplementation PSEUDOHYPERKALEMIA—artificially elevated serum K level due to blood draw

technique or K shifts after blood collection

• Hemolysis during or after venipuncture • Prolonged use of tourniquet, causing acidosis and local extracellular K shift • Leukocytosis or thrombocytosis CLINICAL MANIFESTATIONS • Symptoms: muscle weakness, nausea, palpitations • Signs: decreased deep tendon reflexes, irregular heart rate • EKG changes: occur in stepwise fashion as K rises (Figure 1-5) ◦◦ Peaked T waves ◦◦ Shortened QT interval ◦◦ Prolonged PR and QRS intervals ◦◦ Sine wave pattern ◦◦ Ventricular fibrillation and cardiac arrest

Figure 1-5. EKG changes in hyperkalemia. (A) Peaked T waves, (B) prolonged QRS, (C) sine wave.

(EKGs courtesy of: [A and B] Guthrie K. Hyperkalemia. Life in the Fast Lane website. Published January 12, 2010 Accessed 2017; [C] Cornelius BG, Cornelius A, Desai B. Identification of sine wave in early suspicion for hyperkalemia. West J Emerg Med. 2010;11(1):94.)


key fact A widened QRS >240 msec is due to hyperkalemia: Do not confuse it with ventricular tachycardia (QRS 5.0 mEq/L • Basic metabolic panel and blood gas to investigate other causes of hyperkalemia (eg, renal failure, acidosis) • Serum cortisol level (when clinically appropriate) TREATMENT • Indications ◦◦ EKG changes (Figure 1-5) ◦◦ Muscle weakness ◦◦ K >6.0 to 6.5 mEq/L ◦◦ K >5.5 mEq/L + renal disease + ongoing tissue breakdown (eg, rhabdomyolysis, tumor lysis) or K uptake (eg, GI bleed) • Stabilize cardiac membrane (temporizing) ◦◦ Ca gluconate or Ca citrate IV push ◦◦ Caution in those with hyperphosphatemia: Ca will precipitate and deposit in tissues ◦◦ Ca works within minutes, but effects last only 30-60 min ▪▪ It can be re-administered as needed ▪▪ Additional therapy must be given with Ca to have lasting benefit • Shift K intracellularly (temporizing) ◦◦ Insulin + glucose ▪▪ Regular insulin 10 U IV with 1 amp D50 to prevent hypoglycemia ▪▪ Insulin activates Na/K-ATPase → K shift into cells ◦◦ NaHCO3 ▪▪ 1 amp IV push to rapidly increase pH ▪▪ Increased pH → H shift out of cells + K shift into cells ◦◦ β-agonists (eg, albuterol) ▪▪ Rarely used in clinical practice • Remove K from body (more definitive) ◦◦ Na polystyrene sulfonate: binds K in GI tract for excretion in the stool ▪▪ Caution with constipation or recent abdominal surgery, as they can cause bowel perforation ◦◦ Loop diuretics (eg, furosemide to cause renal loss) ◦◦ Hemodialysis: quickest way to lower plasma K

flash card Q. What are rapidly acting treatments for hyperkalemia, and what are the indications for their use?

A. Acute treatment includes IV Ca, insulin, and NaHCO3. Beta-agonists are rarely used in practice. Indications for acute reversal of hyperkalemia are arrhythmia, muscle weakness, K >6.5 mEq/L or K >5.5 mEq/L + renal disease and ongoing source of K.

Hypokalemia Low-plasma K, defined as 4.8 mg/dL and significantly symptomatic when >7.2 mg/dL ETIOLOGY • Renal failure • Cell lysis: burns, rhabdomyolysis • Iatrogenic: Mg infusion in obstetrics; excessive ingestion of Mg-containing laxative or antacids CLINICAL MANIFESTATIONS • Symptoms ◦◦ Mg 4.8-7.2 mg/dL: nausea, weakness, flushing ◦◦ Mg 7.2-12 mg/dL: facial paresthesias, somnolence, hypotension, bradycardia ◦◦ Mg >12 mg/dL: flaccid quadriplegia, apnea, complete heart block, cardiac arrest


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• Signs ◦◦ Mg 4.8-7.2 mg/dL: decreased deep tendon reflexes ◦◦ Mg >7.2 mg/dL: absent deep tendon reflexes, complete heart block • EKG changes: similar to hyperkalemia (Figure 1-5) DIAGNOSIS • Serum Mg >2.5 mg/dL TREATMENT • Ca gluconate IV for EKG changes • IVF + furosemide • Dialysis if severe or in renal failure

Hypomagnesemia Low plasma Mg, defined as Mg normal and elevation is less than decrease in HCO3 (ΔAG < ΔHCO3), follow pathway for AGMA and NAGMA (Figures 1-9 and 1-10) 6. If AG > normal and elevation is > decrease in HCO3 (ΔAG > ΔHCO3), follow pathway for AGMA and consider cause of metabolic alkalosis (Figure 1-10 and see below on Metabolic Alkalosis)

key fact Remember Winter’s Formula for metabolic acidosis: PaCO2 = [1.5 × (serum HCO3)] + 8 (± 2)

NON-ANION GAP METABOLIC ACIDOSIS (NAGMA) (AG 6.5, with polyuria, or if urine Na is 10 is considered high (Table 1-8). Ethanol is the most common cause of OG elevation; however, it is accounted for in the formula below. OG = measured osmoles – calculated osmoles Calculated osmoles = 2*Na + glucose/18 + BUN/2.8 + ETOH/3.7 Table 1-8. Causes of Osmolal Gap Elevation (OG >10) Ingestions



Altered mentation and blurred vision

Ethylene glycol

Altered mentation, cardiopulmonary manifestations, and AKI

Propylene glycol

Similar to ethylene glycol but less toxic

Isopropyl alcohol

Altered mentation, fruity breath, normal anion gap

AKI = acute kidney injury; OG = osmolal gap.

Figure 1-10. Workup of anion gap metabolic acidosis (AGMA). (Courtsey of Dr. Ishan Mehta)


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LOW ANION GAP METABOLIC ACIDOSIS (AGMA) —Common etiologies include:

• Multiple myeloma (or other monoclonal gammopathies) • Lithium toxicity A negative AG can develop in patients with pseudohyperchloremia in bromide and iodide toxicity. TREATMENT—Treatment of underlying disorder should correct acute etiologies of

metabolic acidosis (eg, DKA or lactic acidosis).

In chronic metabolic acidosis, particularly if NAGMA and if underlying disorder cannot be reversed, alkali therapy may be useful. One common scenario is the use of NaHCO3 in chronic kidney disease and metabolic acidosis to target serum HCO3 between 23 and 29 mEq/L (per 2013 Kidney Disease: Improving Global Outcomes [KDIGO] guidelines). For the critically ill with pH 300 mg/dL


>400 mg/dL

Respiratory depression and possible death

Blood alcohol level can be used to determine the amount of alcohol intake; however, metabolism is based on genetic background. Ethanol is the most common cause of OG elevation and is accounted for in the equation: OG = measured osmoles – calculated osmoles Calculated osmoles = (2 × Na ) + glucose/18 + BUN/2.8 + EtOH/3.7 TREATMENT • Mild ethanol intoxication does not require specific treatment other than supportive care • Patients with volume depletion/hypotension should receive IVF • Patients with ethanol poisoning/severe intoxication with diminished respiratory drive and loss of consciousness may require endotracheal intubation and mechanical ventilation • Any patient with severe alcohol intoxication should receive IV thiamine


key fact Wernicke encephalopathy is an acute neurologic complication of chronic alcohol intoxication due to poor nutrition and malabsorption, while Korsakoff syndrome is a late neurologic complication with marked anterograde and retrograde amnesia. Both are associated with thiamine (Vitamin B1) deficiency.

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• Glucose by itself can exacerbate Wernicke encephalopathy so thiamine should be administered before glucose administration • Due to likelihood of concomitant nutritional deficiencies, patients with alcohol intoxication should also receive folic acid supplementation Patients with alcohol withdrawal should be monitored and routinely assessed to ensure withdrawal symptoms are not progressing. Table 1-12 highlights the common progression of alcohol withdrawal with associated findings. Delirium tremens, a severe complication of alcohol withdrawal, presents as global confusion, tachycardia, hyperthermia, and diaphoresis in the setting of alcohol withdrawal or abstinence. Table 1-12. Alcohol Withdrawal Syndromes and Timing Since Last Drink Time Since Last Drink (h)



Minor withdrawal






Delirium tremens

The following medications can be used: • Thiamine (oral or IV) should be administered in all patients with alcohol withdrawal • Benzodiazepines stimulate GABA receptors, resulting in relative sedation and should be given as symptom-triggered therapy, using an objective scoring system for withdrawal such as the Clinical Institute Withdrawal Assessment for Alcohol Scale • Long-acting benzodiazepines with active metabolites such as diazepam and chlordiazepoxide are preferred; however, patients with severe liver disease should receive short-acting benzodiazepines to prevent oversedation • Adjunctive blockers can be initiated in patients with coronary artery disease to off-load the cardiovascular system • Clonidine can help with autonomic withdrawal symptoms • For severe alcohol withdrawal symptoms, including delirium tremens and seizures, high-dose benzodiazepines (often requiring drip) or a propofol drip can be used once an airway is secured. Phenobarbital is also used in rare refractory cases • Dexmedetomidine has been successfully used as an adjunct for severe withdrawal in small studies; however, it can lower the seizure threshold


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Methanol Methanol commonly is found in antifreeze/deicing products and windshield wiper fluid. It is also used in the manufacturing of numerous chemicals and frequently used as a lab solvent. PATHOPHYSIOLOGY—As seen in Figure 1-14, methanol is metabolized to

formaldehyde and to formic acid: an end metabolite with toxic effects to the eye and CNS.

Figure 1-14. Methanol metabolism to formic acid.


• Damage to optic nerve with resultant visual change and blindness • Headache, dizziness, and confusion • Respiratory failure if significant amount is ingested LAB FINDINGS

• Severe metabolic acidosis; increased AG and OG • Co-ingestion often present, particularly with suicide attempts, and levels of other toxins, especially acetaminophen and salicylates, should be measured TREATMENT—Goal of therapy is to increase elimination and reduce production of

toxic metabolites of methanol.

• Fomepizole competitively inhibits alcohol dehydrogenase and reduces enzyme availability to convert methanol to toxic metabolites: formaldehyde and formic acid (Figure 1-15) • IV ethanol: use only if fomepizole is unavailable • Hemodialysis rapidly clears toxic metabolites (particularly if evidence of end organ damage, AGMA, high OG) • NaHCO3 neutralizes acid species (particularly formic acid) and prevents endorgan damage • Thiamine and folic acid supplementation are important, as deficiencies due to alcoholism can lead to neurologic and cardiac complications


key fact Home distilled spirits (eg, moonshine) can be contaminated with methanol. Consumption can lead to ethanol intoxication as well as blindness or death from methanol poisoning.

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Figure 1-15. Ethanol and fomepizole inhibition of alcohol dehydrogenase.

Ethylene Glycol Ethylene glycol is also commonly used in many commercial products, including antifreeze and metal cleaners. PATHOPHYSIOLOGY—As seen in Figure 1-16, ethylene glycol is metabolized to

glycolic acid and oxalic acid: both are toxic metabolites, resulting in cardiac, neurologic, and renal toxicity.

Figure 1-16. Ethylene glycol metabolism to glycolic and oxalic acids.

CLINICAL MANIFESTATIONS • Renal toxicity: Hematuria and renal failure are cardinal symptoms • Cardiac toxicity: CHF and circulatory collapse have been reported in addition to arrhythmias from severe acidosis and electrolyte abnormalities • Disorientation, ataxia, stupor, coma, and death can occur and are dependent on dose as well as time from ingestion LAB FINDINGS • Severe metabolic acidosis, increased AG and OG • Urine exam for Ca oxalate crystals, urine fluorescence, and UV light can serve as diagnostic tools. Ca oxalate crystals, however, are a nonspecific finding and fluorescin, the cause of fluorescence under UV light, is absent in many commercially available ethylene glycol solutions

key fact Methanol is associated with vission loss, and ethylene glycol is associated with renal failure.

TREATMENT—Similar to methanol, treatment of ethylene glycol ingestion

involves competitively inhibiting alcohol dehydrogenase to prevent production of glycolaldehyde. Please see treatment detailed above.


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Isopropyl Alcohol Isopropyl alcohol is commonly found in hand sanitizers, rubbing alcohol, and disinfecting pads. PATHOPHYSIOLOGY—As seen in Figure 1-17, isopropyl alcohol is metabolized to


Figure 1-17. Isopropyl alcohol metabolism to acetone.

CLINICAL MANIFESTATIONS—Isopropyl alcohol ingestion is not as lethal as

methanol or ethylene glycol poisoning and rarely results in death. • • • •

Often presents with fruity odor to breath due to the metabolite acetone Usually presents with CNS depression to various degrees Hemorrhagic gastritis has been reported All patients presenting with isopropyl alcohol ingestion should be evaluated for co-ingestion of other lethal agents

LAB FINDINGS • High OG with normal AG and absence of acidosis despite presence of ketosis due to acetone • For significant ingestions, creatinine is often falsely elevated and can be a diagnostic clue in the setting of normal blood urea nitrogen (BUN) and pH TREATMENT • Because of the less severe effects of isopropyl alcohol, supportive care with airway management and IVF resuscitation are mainstays of therapy • Must rule out other toxic alcohol ingestions so as to not miss the potentially fatal effects of concomitant methanol and ethylene glycol toxicity

Propylene Glycol Propylene glycol is used in various food products and in several IV medications (eg, lorazepam and diazepam). CLINICAL MANIFESTATIONS • No toxic effects on humans are reported in low to moderate doses over a short time frame


key fact Methanol and ethylene glycol ingestions present with a high AGMA, but pure isopropyl alcohol ingestion presents with a normal AG and absence of metabolic acidosis, easily remembered as “ketosis without acidosis.” All three of these ingestions have a high OG.

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• Prolonged exposure → hemolysis, acidosis, and multi-organ failure • Patients in ICU on prolonged IV benzodiazepines can present with a worsening AGMA because of the presence of propylene glycol. They also have an associated OG correlating with the severity of exposure TREATMENT • Early recognition, discontinuation of offending agent, and supportive care • Hemodialysis if toxicity is severe

Salicylates Aspirin is the most commonly used salicylate and converts to salicylic acid. Oil of wintergreen (methyl salicylate), a topical analgesic, and salicylic acid, a topical wart remover, are other types of salicylates available over the counter. Data suggest ingestion of 10-30 g can result in acute toxicity. PATHOPHYSIOLOGY—Aspirin toxicity occurs due to increased acid-base

disturbance, uncoupled oxidative phosphorylation, and disordered glucose metabolism. CLINICAL MANIFESTATIONS • Nonspecific symptoms: fever, nausea, vomiting, tinnitus, altered mentation to coma • Chronic salicylate use also associated with toxicity and presents with nonspecific symptoms, resulting in delay of diagnosis • Noncardiogenic pulmonary edema frequently seen in chronic salicylate ingestion

flash card Q. A patient with respiratory failure requiring prolonged intubation and sedation with IV lorazepam for 2 wk develops a new AGMA. There is no evidence of uremia, ketosis, or lactic acidosis, and the rest of the workup is unremarkable. What other lab investigation should be performed?

A. Serum propylene glycol level.

LAB FINDINGS • Hypoglycemia, high lactate with AGMA, hyperventilation (due to effect on medullary respiratory center) → primary respiratory alkalosis • High salicylate level TREATMENT • Aggressive resuscitation and correction/prevention of potentially fatal effects, including hypoglycemia, metabolic acidosis, and electrolyte abnormalities • Activated charcoal should be considered in cooperative patients with an acute ingestion • Evidence of respiratory failure should trigger immediate intubation and mechanical ventilation • NaHCO3 used to alkalinize serum and urine to prevent harmful effects of acidosis and to promote excretion of salicylate: essential to correct hypokalemia in these patients or alkalinization will not be effective


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• Acetazolamide, which also results in alkalinization of urine and increases urinary excretion of salicylate, should be avoided, as it can potentially worsen neurologic effects by allowing salicylate molecules to easily cross the bloodbrain barrier • For critically ill patients with severe metabolic acidosis, hemodialysis should be initiated • Early toxicology consultation, if available, should be considered

►►ACUTE RENAL FAILURE DEFINITION Acute renal failure or acute kidney injury (AKI) represents a sudden decline in the kidneys’ ability to regulate volume, electrolytes, and nitrogenous waste.

In 2012, the KDIGO guidelines merged the RIFLE (Risk, Injury, Failure, Loss and End-stage renal disease and AKIN (Acute Kidney Injury Network) criteria (Table 1-13) to standardize the definition of AKI. Table 1-13. KDIGO Diagnosis and Staging of Acute Kidney Injury Stage


Urine Output


Rise of 0.3 mg/dL within 48 h or 50-99% rise in Cr from baseline within 7 d

6 h


100-199% rise in Cr from baseline within 7 d

12 h


◦◦ ≥200% rise in Cr from baseline within 7 d

65%, and its development is associated with worse outcomes and increased risk for future chronic kidney disease (CKD). PRERENAL DISEASE Renal blood flow autoregulation maintains the GFR over a wide range of systemic blood pressures. Hypotension leads to afferent arteriolar vasodilation, causing activation of the renin-angiotensin system. Angiotensin II causes preferential efferent arteriolar vasoconstriction, which maintains renal blood flow (Figure 1-18).


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ACEi = angiotensin-converting enzyme inhibitor; ATII = angiotensin II; NSAID = nonsteroidal anti-inflammatory drug.

Figure 1-18. Glomerular changes during renal blood flow regulation. (Courtesy of Dr. Nancy Hsu)

Prerenal azotemia occurs due to reduced renal perfusion despite compensatory mechanisms and occurs in the following settings: Table 1-14. Etiologies of Prerenal Acute Kidney Injury Diagnosis


Clinical Features



Total body volume depletion (eg, acute blood loss, diarrhea)

Clinical history of blood or fluid loss

Resuscitation with blood or IVF as appropriate

Hepatorenal syndrome

◦◦ Dilation of splanchnic arterial vascular bed ◦◦ Excessive RAS activation → renal vasoconstriction or vasospasm

◦◦ Advanced cirrhosis or acute liver failure ◦◦ Lack of GFR normalization with volume expansion and diuretic cessation

◦◦ Systemic vasoconstrictors increase resistance in splanchnic circulation and redistribute blood flow to the kidneys ◦◦ Terlipressin (not available in U.S.), norepinephrine or octreotide + midodrine

Cardiorenal syndrome

◦◦ Decreased cardiac output ◦◦ Renal venous congestion

◦◦ Volume overload ◦◦ Hypotension may be present

◦◦ Diuresis ◦◦ Ultrafiltration ◦◦ Inotropes


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Etiologies of Prerenal Acute Kidney Injury Abdominal compartment syndrome

◦◦ Compression of IVC reduces cardiac preload and output ◦◦ Renal venous congestion

◦◦ Recent abdominal surgery or trauma, large-volume resuscitation, severe pancreatitis ◦◦ Elevated IAP >20 mm Hg on intravesical manometry via a urinary catheter

◦◦ Diuresis or ultrafiltration ◦◦ Bowel decompression ◦◦ Decompressive laparotomy ◦◦ HoB >30° and minimizing sedation/ paralytics may worsen IAP


Interference with normal renal blood flow autoregulation

Use of ACEi, ARB, and NSAIDs

Cessation of causative medication

ACEi = angiotensin converting enzyme inhibitor; ARB = angiotensin II receptor blocker; GFR = glomerular filtration rate; HoB = head of bed; IAP = intra-abdominal pressure; IVC = inferior vena cava; NSAID = nonsteroidal anti-inflammatory drug; RAS = renin angiotensin system.

• Actual decrease in intravascular volume (eg, blood loss, severe diarrhea) • Effective decrease in intravascular volume (eg, hepatorenal syndrome, cardiorenal syndrome, abdominal compartment syndrome, and medications)

►INTRINSIC ► RENAL DISEASE Epidemiology Intrinsic AKI occurs due to damage of the glomerulus, vasculature, tubule, or interstitium. Acute tubular necrosis (ATN) is by far the most common cause of AKI in the ICU, with an incidence ranging from 40% to 88% in various cohorts.

Diagnosis Table 1-15. Urinary Diagnostic Indices in Acute Kidney Injury Prerenal

Intrinsic Renal


Urine Na (mEq/L)

40 (ATN, AIN)



2% (ATN, AIN)




48 h in patients with normal GFR and >72 h in patients with diabetes or preexisting CKD ◦◦ Non-iodinated contrast is preferred over iodinated. If iodinated contrast media is used, iso-osmolar or low-osmolar are less nephrotoxic than ionic high-osmolar agents

• N-acetylcysteine (NAC): Administration of oral NAC (either 1200 mg once or 600 mg q12h before and after contrast administration) with isotonic saline has been shown to be beneficial in some (but not all) studies • Other approaches: Attempts to improve renal vasodilation with dopamine or increase clearance of contrast agent with prophylactic hemodialysis or diuretics have not shown benefit DIAGNOSIS— rise in serum creatinine within 24-72 h of contrast administration,

which usually peaks within 5 d, with/without oliguria


key fact Though CI-AKI is overall rare, the risk is most substantial in patients with preexisting CKD, DM, advanced age, and intraarterial contrast injection.

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OUTCOMES • In most cases, CI-AKI is mild, and full recovery of renal function is expected • In patients with preexisting CKD, CI-AKI can be irreversible and severe • Overall, CI-AKI is associated with excess cardiovascular events, prolonged hospitalization, and increased risk for death, even in patients who do not require dialysis

Pigment-Induced Acute Kidney Injury

flash card Q. What intervention has been shown to be most effective for prevention of contrastinduced nephropathy?

A. Intravenous fluid hydration for 12 h pre- and postprocedure.

The release of hemoglobin and myoglobin in the setting of hemolytic anemias and rhabdomyolysis, respectively, can cause AKI. PATHOPHYSIOLOGY—Myoglobin and hemoglobin are heme pigment-containing

proteins that cause direct toxicity to and obstruction in the proximal tubules and collecting ducts.

mnemonic You may get rhabdomyolysis if you CAN HOIST excessive weight: Crush injuries Activity (eg, exercise)

RISK FACTORS • Rhabdomyolysis results from destruction of muscle tissue via trauma, exertion, immobilization, or medications (eg, statins) • Hemolytic anemia has been associated with malaria, glucose-6-phosphate dehydrogenase (G6PD) deficiency, cardiopulmonary bypass circuits, and autoimmune antibody-mediated states. Transfusion-related causes (eg, ABOincompatibility) are now rare CLINICAL FEATURES—Patients may be asymptomatic or present with symptoms

of the underlying etiology of hemolytic anemia or rhabdomyolysis. Urine can be discolored (ranging from pink to cola-colored). DIAGNOSIS Table 1-17.

Table 1-17. Laboratory Findings in Pigment-Induced Acute Kidney Injury Rhabdomyolysis

Necrosis of muscles Heat stroke Overdose of drugs (eg, cocaine, phencyclidine) Immobilization Seizures Trauma

key fact Creatine kinase has a half-life of 48 h and remains elevated for 1-3 d. Thereafter, the levels will fall unless the patient has end-stage renal disease, ongoing muscle ischemia or necrosis, or compartment syndrome.

Hemolytic Anemia

Urinalysis is positive for blood, but no red blood cells are seen on microscopy. ↑CK, up to 5-10× ULN



↑Reticulocyte index

↓Ca (↑during recovery phase)



Peripheral smear: schistocytes, spherocytes

Rarely DIC (↓platelet and fibrinogen; ↑INR)

Positive Coomb test

CK = creatine kinase; DIC = disseminated intravascular coagulation; INR = international normalized ratio; K = potassium; LDH = lactate dehydrogenase; ULN = upper limit of normal.

key fact In rhabdomyolysis, damaged myocytes release thromboplastin and tissue plasminogen, which can promote disseminated intravascular coagulation.


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MANAGEMENT—In rhabdomyolysis, sequestration of fluid in necrotic muscle

can lead to shock and impaired renal blood flow. Prevention of AKI rests on aggressive IVF resuscitation for patients with rising CK levels or total CK >5000 U/L. Correction of electrolytes and treating the precipitating cause make up the remaining components of management. • Volume resuscitation ◦◦ Early resuscitation with isotonic saline to maintain urine output of 200-300 mL/h ◦◦ Maintaining urine pH >6.5 with NaHCO3 may decrease renal toxicity of heme/myoglobin but has not been shown to be superior to isotonic saline in the prevention of AKI. Potential risks include Ca phosphate precipitation within the renal tubules and worsening of hypocalcemia (leading to arrhythmias, tetany, or seizures) ◦◦ Optimal fluid type and rate in hemolytic anemia is unclear • Diuretics ◦◦ Loop diuretics do not prevent AKI, may worsen hypocalcemia, and cause other electrolyte derangements. Their use is justified in setting of volume overload ◦◦ Mannitol is an osmotic agent that scavenges free radicals and minimizes myoglobin cast formation, but evidence regarding its use is conflicting • Electrolyte derangements (eg, hypocalcemia, hyperkalemia, hyperphosphatemia) are common and should be closely monitored. In the absence of tetany or treatment for hyperkalemia, hypocalcemia should not be corrected, as it will promote hypercalcemia during the renal recovery phase • Dialysis may be required to treat severe hyperkalemia; however, its role in removing myoglobin, hemoglobin, or uric acid to prevent AKI has not been demonstrated • Allopurinol is usually given if uric acid levels are >8 mg/dL

Acute Interstitial Nephritis (AIN) Acute interstitial nephritis (AIN) is most often a hypersensitivity reaction to certain medications but can be due to an infectious or autoimmune process. CLINICAL MANIFESTATIONS—Classic triad of fever, rash, and eosinophilia/

eosinophiluria is seen in 20 mL/kg/h; typical prescriptions target 25-35 mL/kg/h

flash card Q. What is the dialysis adequacy of a 70-kg man who is receiving IHD at a dialyzer clearance of 300 mL/min during a session that lasts 3 h ?

A. Kt/V = 300 mL/min × 180 min/(70 × 0.6 × 1000 mL/L) = 1.3.


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►►TUMOR-RELATED SYNDROMES ►PHEOCHROMOCYTOMA ► Pathophysiology Pheochromocytomas are catecholamine-secreting endocrine tumors that originate from the chromaffin cells of the adrenal medulla.

Epidemiology • Up to 30% of pheochromocytomas are associated with a genetic mutation (RET, NF-1, VHL, SDH) • Presentation is generally in fourth to fifth decade, although those due to hereditary syndromes tend to present at an earlier age • Pheochromocytomas are considered rare (despite a relatively high prevalence of 1:2000 in autopsy series) and account for 0.2% of hypertension cases

Clinical Features (Table 1-22) • Catecholamines act via α, β, and dopaminergic receptors to cause vasoconstriction and increased cardiac inotropy and chronotropy • The “classic triad” refers to the paroxysmal diaphoresis, headaches, and tachycardia

Rule of 10s for pheochromocytoma:

Table 1-22. Signs and Symptoms of Pheochromocytoma Common


Hypertension (sustained or episodic)

Aortic aneurysms




Cerebrovascular accidents


CHF from dilated or hypertrophic cardiomyopathy


Myocardial infarctions

CHF = congestive heart failure.

Diagnosis Serum catecholamines have a very short half-life, so measurement of normetanephrine and metanephrine metabolites are performed instead. • 24-h urine fractionated metanephrines and catecholamines • Serum fractionated metanephrines drawn from a supine patient



10% malignant 10% bilateral 10% extra-adrenal

key fact Hypertension, either sustained or episodic, is the most common presenting symptom of pheochromocytoma. Uncommon presentations such as CHF and strokes result from catecholamine excess, untreated hypertension, and consequent end-organ damage.

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After biochemical confirmation of catecholamine excess, CT or MRI of abdomen/ pelvis (Figure 1-20) or 123I-metaiodobenzylguanidine (123I-MIBG) scans are performed to localize the tumor.

flash card Q. What triad of symptoms can be seen during a catecholamine surge in pheochromocytoma?

A. The classic presenting triad is paroxysmal diaphoresis, headaches, and tachycardia.

Figure 1-20. MRI abdomen showing left adrenal pheochromocytoma (white arrow).

(Reproduced from Roghi A, Pedrotti P, Milazzo A, Bonacina E, Bucciarelli-Ducci C, et al. Adrenergic myocarditis in pheochromocytoma. J Cardiovasc Magn Reson. 2011;13(1):1-3.)

Management Adrenalectomy is the treatment of choice for pheochromocytomas. Appropriate perioperative and intraoperative management can minimize hypertensive crises and arrhythmias (Table 1-23). PREOPERATIVE—Goals of therapy are to prevent unpredictable increases in BP

during surgery and to reverse catecholamine-induced volume contraction.

INTRAOPERATIVE/CRITICAL CARE—Increases in BP can occur with moving patients

to operating room table, anesthesia induction, intubation, overall sedation, and manipulation of tumor.

• Heart rhythm and intra-arterial BP should be monitored • General anesthesia is preferred. Most agents can be used except for halothane (associated with arrhythmias) and ketamine (increases catecholamine release) POSTOPERATIVE—Resection of pheochromocytoma removes excess

catecholamines from the circulation.

• Rebound secretion of insulin leads to hypoglycemia, so serum blood sugar should be monitored for >24 h after surgery • Preoperative antihypertensives or adrenal insufficiency (especially in setting of bilateral adrenalectomy) can cause postoperative hypotension


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Table 1-23. Management of Hemodynamics in Pheochromocytoma Blood Pressure

Heart Rate

Volume Status


◦◦ α-adrenergic receptor blockers: doxazosin, phenoxybenzamine ◦◦ CCBs: nifedipine, amlodipine

◦◦ Β-blockade if very tachycardic despite adequate α-blockade: atenolol, propranolol

◦◦ High-Na diet 1 wk prior ◦◦ Saline infusion in evening prior to surgery

Intraoperative or critical care

◦◦ Nitroprusside or nicardipine infusions ◦◦ Phentolamine boluses

◦◦ Lidocaine ◦◦ Esmolol

◦◦ IVF boluses as needed


◦◦ Optimize volume status ◦◦ Stress dose steroids if suspicion for adrenal insufficiency ◦◦ Vasopressors if no response to above


◦◦ Continuous IVF or boluses as needed

IVF = intravenous fluid. CCB = calcium channel blocker

►►CARCINOID SYNDROME Introduction Carcinoid tumors are rare, slow-growing neuroendocrine tumors most commonly found in GI tract (74%; majority in small bowel) or bronchopulmonary system (25%). Carcinoid syndrome typically manifests as a constellation of hypotension, diarrhea, bronchospasm, and flushing, but hypertension and tachycardia can also be seen with secretion of bioactive peptides by the carcinoid tumor.

Pathophysiology Serotonin and other peptides are released into the bloodstream but destroyed after one passage through the liver. It is not until these patients develop liver metastasis that they develop carcinoid syndrome, as these substances bypass portal circulation /hepatic metabolism and directly enter systemic circulation in large amounts. • Serotonin (5-hydroxytryptamine [5-HT]) and kallikrein are the main peptides involved in carcinoid syndrome; other peptides include 5-hydroxytryptophan (5-HTP), 5-hydroxyindoleacetic acid (5-HIAA), histamine, tachykinins, bradykinin, and prostaglandins. Bradykinins are potent vasodilators and increase capillary permeability, causing hypotension/shock and tissue edema


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• In carcinoid tumor cells, tryptophan metabolism is diverted from synthesis of niacin and protein to the synthesis of supraphysiological levels of serotonin

Figure 1-21. Metabolism of tryptophan.

Clinical Features

Figure 1-22. Clinical features of carcinoid syndrome. (Modified courtesy of Wikicommons)


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key fact

Table 1-24. Evaluation of Carcinoid Syndrome Studies Biochemical markers

◦◦ Elevated 24-h urinary HIAA excretion ◦◦ Elevated serum chromogranin A or serotonin

Imaging to localize disease and determine extent of tumor burden

◦◦ Abdominal CT or MRI ◦◦ Nuclear medicine scans (octreotide scan, PET scan) ◦◦ Endoscopy or bronchoscopy ◦◦ Echocardiography


◦◦ Positive staining for ≥1 neuroendocrine markers (eg, chromogranin A, synaptophysin) ◦◦ Ki-67 to determine malignant potential

Carcinoid syndrome typically manifests with flushing, diarrhea, and abdominal pain. Up to 50% develop right-sided valvular disease.

HIAA = hydroxyindoleacetic acid.

Management • • • •

Somatostatin analogue (octreotide or lanreotide) for all symptomatic patients Antidiarrheal agents, such as loperamide Surgical debulking of tumor burden Repair of valvular (tricuspid insufficiency and pulmonic stenosis) disease, which can occur in 50% of carcinoid syndrome

CARCINOID CRISIS is a life-threatening condition that occurs after liberation of

large amounts of peptides from a carcinoid tumor, resulting in sudden changes in BP, tachycardia, hyperthermia, bronchospasm, delirium, and prolonged flushing. • Etiologies: anesthesia induction, tumor manipulation during surgery, and tumor necrosis from arterial embolization or radiofrequency ablation • Prevention: adequate prophylactic measures can decrease crisis response to the stress of surgery ◦◦ Octreotide prophylaxis (subcutaneous for 2 wk with IV infusion started before anesthesia) ◦◦ Use of non–histamine-releasing opiates such as fentanyl (avoid morphine, as it causes both serotonin and histamine release) • Treatment: ◦◦ IV octreotide ◦◦ IVF ◦◦ Hyperglycemia management (serotonin stimulates glycolysis/ glycogenolysis) ◦◦ Electrolyte monitoring and replacement (may develop hypokalemic hyperchloremic metabolic acidosis from severe diarrhea) ◦◦ Refractory hypotension: vasopressin or phenylephrine preferred (β agonists may increase release of vasoactive substances → hypotension) ◦◦ Hypertension: treated with α and β-adrenergic receptor blockers


key fact Hypercortisolism due to an ACTH-secreting tumor (eg, pituitary adenoma, small cell lung cancer) will be associated with adrenal hyperplasia on imaging.

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►►ADRENAL DISORDERS ►ADRENAL ► INSUFFICIENCY (AI) Definition • Inadequate glucocorticoid +/− mineralocorticoid production by adrenal glands • Primary adrenal insufficiency (AI) is due to adrenal dysfunction, whereas secondary (central) AI is due to hypothalamus and/or pituitary dysfunction (Figure 1-23)

Figure 1-23. Regulation of cortisol secretion. (Modified based on Ross AP, Ben-Zacharia A, Harris C, Smrtka J. Multiple sclerosis, relapses, and the mechanism of action of adrenocorticotropic hormone. Front Neurol. 2013;4:21.)

Table 1-25. Comparison of Primary vs Secondary Adrenal Insufficiency Primary


Affected organ

Adrenal gland

Hypothalamus +/− pituitary

ACTH secretion

Cortisol secretion

Mineralocorticoid (ie, aldosterone) secretion


key fact Adrenal crisis occurs in both primary and secondary AI and is precipitated by infection (especially GI illness), surgery, trauma, or abrupt cessation of glucocorticoids.

ACTH = adrenocorticotropic hormone.


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• Adrenal crisis: absolute AI, leading to a range of life-threatening symptoms • Relative AI in critical illness: a form of secondary AI (generally in setting of sepsis) that occurs due to higher systemic cortisol requirements or tissue corticosteroid resistance, but the level of serum cortisol may be normal

Clinical Manifestations Signs/symptoms of AI are nonspecific, and acute AI may mimic other conditions. Table 1-26. Clinical Features of Primary and Secondary Adrenal Insufficiency Features



Fatigue, malaise



Abdominal pain, nausea







+ (Due to hypovolemia)

+ (Due to SIADH)



-- (+ in setting of critical illness)

Skin hyperpigmentation






mnemonic Primary adrenal insufficiency can cause increase skin Pigmentation.

SIADH = syndrome of inappropriate antidiuretic hormone secretion.

Etiologies Table 1-27. Causes of Adrenal Insufficiency Primary




◦◦ Adrenal infiltration by TB ◦◦ Fungal infections (Cryptococcus, histoplasmosis, coccidiodomycosis)

◦◦ Actinomycosis ◦◦ Pituitary infiltration by TB

Medications (eg, etomidate, ketoconazole)

Medications (eg, withdrawal of exogenous steroids)



◦◦ Bilateral metastatic disease ◦◦ Amyloidosis ◦◦ Hemochromatosis

◦◦ Sarcoidosis ◦◦ Histiocytosis


Vascular (eg, Sheehan syndrome or postpartum hypopituitarism)

◦◦ Adrenal hemorrhage (WFS in meningococcal sepsis) ◦◦ Adrenal vein thrombosis from APLS Autoimmune (eg, Addison's disease)

Mass lesions ◦◦ Pituitary tumors, craniopharyngioma ◦◦ Complications of radiotherapy or surgery

APLS = antiphospholipid antibody syndrome; TB = tuberculosis; WFS = Waterhouse-Friderichsen syndrome.


flash card Q. A patient with AIDS presents with fever, hemoptysis, abdominal pain, and hypertension. A CT of the abdomen shows bilateral adrenal gland calcification. What is the most likely diagnosis?

A. Primary adrenal insufficiency due to disseminated Mycobacterium tuberculosis.

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Diagnosis Routine labs suggestive of AI: hyperkalemia, hyponatremia Confirmatory labs: ACTH LEVEL—Serum morning ACTH should be measured with baseline cortisol to

distinguish between primary or secondary AI (Table 1-26).

• Primary adrenal insufficiency = elevated (>52 pg/mL, often >4000 pg/mL) • Secondary adrenal insufficiency from pituitary abnormality = normal or low normal (20-52 pg/mL) SERUM CORTISOL—Circadian cortisol levels generally peak at 8 a.m., and

measurements at other times have little diagnostic use. Morning serum cortisol levels • • • •

Cortisol 15 µg/dL generally excludes AI in the nonstressed individual Cortisol >18 µg/dL generally excludes AI in the critically ill Measurement of random serum cortisol levels is not recommended in critically ill patients


of AI is based on the peak cortisol level after administration of synthetic ACTH (cosyntropin or tetracosactrin) 250 µg.

• Measure serum cortisol in the morning, which serves as baseline level. Practically speaking, in ICU, this is often a random cortisol level • Administer cosyntropin (synthetic ACTH) 250 μg IV or intramuscularly • Measure serum cortisol level at 30 min and 60 min ◦◦ In noncritically ill, peak cortisol level >18 µg/dL excludes diagnosis of AI ◦◦ Diagnosis of relative AI in critically ill patients is not clearly defined, but a serum cortisol 400 mg/dL • Initially normokalemia or hyperkalemia, but insulin therapy may subsequently cause profound hypokalemia (intracellular shift) • Hypophosphatemia may develop with insulin therapy (intracellular shift) • Leukocytosis • Hyperlipidemia due to lipolysis • Acute kidney injury due to volume depletion

key fact Despite presenting with normal K and phosphate (PO4) levels, patients with DKA have a K and PO4 deficit. The true state of the K and PO4 balance is revealed after treatment with insulin and volume expansion.

►HYPEROSMOLAR ► HYPERGLYCEMIC NONKETOTIC STATE • More insidious than DKA and usually presents with days of polyuria, polydipsia, severe dehydration, and, most notably, altered mental status • More common in older patients and people with type 2 diabetes who usually have enough circulating insulin to prevent lipolysis and thus ketoacidosis • Characterized by significant hyperglycemia in absence of ketosis with hyperosmolality and mental status changes • Has same precipitating factors as DKA

Common Lab Findings • Severe hyperglycemia • Elevated plasma osmolality, typically >320 mOsm/kg ◦◦ Calculated osmolality = 2(NaK) + glucose/18 + BUN/2.8 • Electrolyte abnormalities similar to DKA in regards to Na, K, and phosphate (PO4), although K and PO4 deficits less severe • Hyperlipidemia • Absence of ketoacidosis Table 1-29 compares HHS and DKA. There may be significant overlap in approximately one-third of patients.


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Table 1-29.

key fact

Distinction Between DKA and HHS

In HHS, neurological abnormalities are common, and patients present with severe hyperglycemia and elevated plasma osmolality. Ketoacidosis is not present.



Plasma glucose >250 mg/dL

Plasma glucose >600 mg/dL

Arterial pH 7-7.30

Arterial pH >7.30

Urine ketones positive

Urine ketones small

Serum ketones elevated

Serum ketones not elevated

Plasma osmolality varies

Plasma osmolality >320 mOsm/kg

Anion gap elevated

Anion gap variable

Mental status changes vary from alert to severely altered

Mental status changes severe


Severe dehydration

Severe K and PO4 deficit

Less severe K and PO4 deficit

DKA = diabetic ketoacidosis; HHS = hyperosmolar hyperglycemic state.

►MANAGEMENT ► OF DKA AND HHS Cornerstones of treatment for both DKA and HHS are similar and include: • • • •

Correction of fluid deficit Management of electrolyte abnormalities Insulin therapy Identification of precipitating causes

In most ICUs, a protocol is used to manage DKA and HHS (Figure 1-24). FLUIDS Severe Hypovolemia

HCO3 Mild Hypovolemia

pH< 6.9

No HC03

IL/hr 0.9% NaCl

High Na⁺

pH> 6.9


Normal Na⁺

250-500mL/hr* 0.45% NaCL

Low Na⁺

250-500mL/hr* 0.9% NaCL

100mmol HC03 in 400ml H20 +20Meq KCL over 2hrs

Repeat pH and K+ q2h until pH>7

0.1U/Kg IV bolus, then 0.1U/Kg IV infusion OR 0.14U/Kg IV infusion

K⁺ K⁺5.2mEq/L

Hold insulin until K⁺>3.3mEq/L

Do not add K⁺ To fluid

K⁺ 3.3-5.2mEq/L Glucose should decrease by 10% in 1st hr. If not give 0.14U/Kg bolus IV insulin

Add 20-30mEq K⁺ to each L of fluid until K > 4mEq/L

When serum glucose 10 stools/d, bleeding, abdominal pain, distension, and toxic symptoms [eg, fever]) should receive what initial therapy?

A. IVF, electrolyte repletion, transfusions prn, IV glucocorticoids, and empiric IV antibiotics. If poor response, infliximab or cyclosporine should be tried. Colectomy may be required if all medical therapies fail.

SYMPTOMS—Bloody diarrhea, abdominal pain, urgency, tenesmus, and


EXTRAINTESTINAL MANIFESTATIONS—Present in ~25% of patients during

their lifetime and include arthritis, uveitis, erythema nodosum, pyoderma gangrenosum, arterial or venous thromboembolism, and primary sclerosing cholangitis.

flash card Q. A patient with UC presents with acute abdominal pain, distension, fever, tachycardia, and hypotension. On X-ray, the colon measures 8 cm in diameter. After initiating IVF and antibiotics, what is the next step in management?

A. Surgical consultation.

Figure 5-11. Endoscopic images of UC.

(Reproduced. de Lange T, Larsen S, Aabakken L. Inter-observer agreement in the assessment of endoscopic findings in ulcerative colitis. BMC Gastroenterol. 2004;18(4):9.)


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ACUTE COMPLICATIONS • Severe bleeding: massive bleeding may necessitate urgent colectomy • Toxic megacolon: occurs with fulminant colitis and extension of inflammation to muscle layers • Perforation: either due to toxic megacolon or colitis flare

Crohn's Disease Crohn's disease is a chronic inflammatory disease characterized by transmural inflammation of the GI tract. It may involve mucosa from the mouth to perianal area, with the most common areas involved being the terminal ileum and colon. Unlike UC, Crohn's disease usually spares the rectum and is characterized by "skip lesions" rather than contiguous inflammation. • 30% of patients have only terminal ileitis • 50% have ileocolitis • 20% have only colitis (Figure 5-12)

flash card Q. A patient with Crohn's disease presents with acute abdominal pain, fevers, leukocytosis, and a palpable mass. What is the most likely diagnosis?

A. Intra-abdominal abscess: could be caused by a walledoff microperforation or fistula formation.

Figure 5-12. The three most common sites of intestinal involvement in Crohn's disease. (Reproduced courtesy of Wikipedia)

SYMPTOMS—diarrhea, abdominal pain, fatigue, weight loss, and fever. EXTRAINTESTINAL MANIFESTATIONS include arthritis, uveitis, erythema nodosum,

pyoderma gangrenosum, primary sclerosing cholangitis, secondary amyloidosis, venous and arterial thromboembolism, nephrolithiasis, and osteoporosis.

ACUTE COMPLICATIONS • Fistula formation: risk of developing fistula is ~50% after 20 yr and may lead to infection and sepsis • Phlegmon/abscess: sinus tracts can form walled-off abscesses, which can present with sepsis and/or peritonitis (especially if perforation occurs)


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►►LIVER ►ACUTE ► LIVER FAILURE Patients presenting with acute liver failure typically have no prior history of cirrhosis but demonstrate clinical signs of encephalopathy and impaired synthetic function (INR ≥1.5) due to a hepatic insult. This can be further subcategorized as: • Hyperacute: 21 d and 3500 IU/L

Underlying liver disease, concomitant alcohol abuse

See Chapter 2 "Pharmacology and Toxicology" for detailed discussion

Third trimester of pregnancy

Maternal mortality improves after delivery, but fetal mortality risk remains elevated

Bilirubin low INR elevated Drug level dependent on time of ingestion Acute fatty liver of pregnancy

AST, ALT 2000 IU/L

Autoimmune hepatitis

AST, ALT >1000 IU/L Minimal bilirubin, ALP elevation Hyperglobulinemia Anti-smooth muscle Ab ≥1:320 May also see anti-SLA/ LP Ab


Typically occurs 4-8 d after mushroom ingestion More common in women and often seen in setting of other autoimmune disease

Most often diagnosed in third or fourth decade of life

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Causes of Acute Liver Failure Budd-Chiari (hepatic vein thrombosis)

Highly variable depending on degree of liver injury May see elevated AST, ALT, bilirubin, INR

Hemophagocytic lymphohistiocytosis

AST, ALT >3× ULN Elevated triglycerides Elevated INR

Underlying thrombotic Underlying disorder diatheses, paroxysmal commonly present nocturnal hemoglobinuria, UC, celiac disease Primary immunodeficiency syndromes

Genetic or acquired; viral infection (eg, EBV is common inciting factor)

Anemia Ferritin >500 ng/mL, levels commonly in the thousands See Table 5-8

Herpes simplex

Markedly elevated transaminases Leukopenia Low bilirubin

Idiosyncratic drug reactions/DILI

Neonates, immunocompromised state (eg, steroids, HIV, pregnancy), and malignancy

May see cholestatic or hepatocellular pattern.

May see elevated bilirubin

Often do not see skin lesions

May also be caused by cocaine and methamphetamines Particularly seen with breast cancer, small cell lung cancer, lymphoma, melanoma, or myeloma

Severe acute alcoholic hepatitis

AST rarely >300 IU/L

Veno-occlusive disease

Findings similar to ischemic hepatopathy

Stem cell transplant recipients

Wilson disease

Coombs-negative hemolytic anemia

Autosomal recessive disorder due to defect in ATP7B gene

AST/ALT ratio usually >2

AST, ALT 2 ALP may be markedly low

Indeterminate: 14%

key fact

LDH elevated Elevated INR

toxicity: 46%

Dose-independent, usually within 6 mo of initiation

AST, ALT 25-250× the ULN AST, ALT >15× ULN

A. Acetaminophen

Hepatitis A: 3%

Bilirubin elevated

Malignant infiltration

common causes of acute liver failure in the United States?

Hepatitis B: 7%

If hepatocellular, can see AST and ALT >25× the ULN Ischemic hepatopathy (shock liver)

Q. What are the most

Idiosyncratic drug reactions: 12%


Hepatitis A, B, C, D, E

flash card

Chronic alcohol users, with recent increase in amount ingested

Acute liver failure has also been associated with cytomegalovirus, EpsteinBarr virus, and varicella zoster virus.

May not be considered acute liver failure due to frequent occurrence of underlying liver disease

Often see rapidly progressive renal failure +/− signs of CNS involvement Kayser-Fleischer rings may be seen in later stages

Ab = antibody; ALP = alkaline phosphatase; ALT = alanine aminotransferase; AST = aspartate aminotransferase; ATP7B = adenosine triphosphate copper transport β; CNS = central nervous system; DILI = drug induced liver injury; HIV = human immunodeficiency virus; INR = international normalized ratio; LDH = lactate dehydrogenase; SLA/LP = soluble liver antigen/liver pancreas; UC = ulcerative colitis; ULN = upper limit of normal.


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Table 5-8.

key fact

Viral Hepatitis Type


Risk Factors


Hep A IgM

Travel to areas with poor sanitation

Progression to Acute Liver Failure Rare

Incarceration Illicit drug use MSM HBV

Hep B surface Ag

Residing in high risk area

Hep B surface Ab

HIV or HCV infection

Hep B core Ag

IV drug use

Hep B core Ab (IgM)

Multiple sexual partners

Uncommon in absence of superinfection with HDV, but likely underdiagnosed

MSM Hemodialysis Prisoners HCV

Hep C Ab

IV drug use Blood transfusion (prior to 1990)

Rare unless co-infected with HBV

Hemodialysis HDV

Markers of acute or chronic Hep B + Hep D Ab Hep D Ag (frequently not detected)


Hep E IgM

IV drug use

50% survive transplant-free. Of those requiring transplant, the 1-y survival rate is ~80%. Spontaneous recovery from acute liver failure is most dependent on the following factors: • Age: >10 and 6.5), creatinine >3.4 mg/dL, and Grade 3 or 4 encephalopathy ◦◦ All other causes require any three of the following: ▪▪ Age 40 ▪▪ Jaundice preceding onset of encephalopathy by >7 d ▪▪ Prothrombin time >50 sec ▪▪ Serum bilirubin >18 mg/dL ▪▪ Etiology with low rate of transplant-free survival (eg, idiosyncratic drug reactions, non-A/non-B viral hepatitis, Wilson disease)

flash card Q. You have admitted a 23-year-old man to the ICU for acute liver failure after acetaminophen ingestion. What single finding would prompt referral to a transplant center for further evaluation?

A. Per the King’s College Criteria, an arterial pH 15 mm Hg. This leads to formation of portosystemic collateral vessels (Figure 5-13) and increased splanchnic blood flow, which both worsens portal hypertension and causes systemic hypotension. In Western countries, cirrhosis is the most common cause. Schistosomiasis and portal vein thrombosis are the predominant etiologies in other regions.

Figure 5-13. Portosystemic collateral vessels in portal hypertension.

(Reproduced. GP Sangster, Previgliano CH, Nader M, Chwoschtschinsky E, Heldmann MG. MDCT imaging findings of liver cirrhosis: spectrum of hepatic and extrahepatic abdominal complications. HPB Surg. 2013;2013: 129396.)

►PORTAL ► HYPERTENSIVE GASTROPATHY The etiology of portal hypertensive gastropathy is unclear but may be caused by increased splanchnic flow. Severity of gastropathy correlates with severity of portal hypertension. Most often, portal hypertensive gastropathy causes chronic GI bleeding but may also cause severe, acute bleeds. DIAGNOSIS on endoscopy by characteristic appearance of gastric mucosa, which is

commonly described as mosaic or snakeskin-like (Figure 5-14).

TREATMENT—Treatment aimed at measures to reduce portal hypertension such as

propranolol or carvedilol. Transjugular intrahepatic portosystemic shunt (TIPS) or liver transplant reserved for refractory bleeding.


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Figure 5-14. Mosaic pattern seen in portal hypertensive gastropathy. (Reproduced courtesy of Wikicommons.)

Variceal Hemorrhage Esophageal or gastric variceal hemorrhage represents the second most common cause of upper GI bleed and has an index bleed mortality of ~20%. Variceal hemorrhage should be considered in all patients with known or suspected portal hypertension who present with GI bleed. The majority of patients should be admitted to ICU, as only ~50% of variceal bleeds will be controlled without pharmacologic or endoscopic intervention. MANAGEMENT—Initial treatment of variceal hemorrhage is similar to any other

cause of GI bleed, with the following specific considerations:

• Airway: consider intubation in setting of ongoing hemorrhage and vomiting with risk for aspiration. GI bleeding can also lead to worsening of encephalopathy in advanced cirrhosis, which may further compromise the airway. Prophylactic intubation, however, is not indicated and may increase the rate of aspiration pneumonia • Volume resuscitation: aggressive resuscitation to achieve stabilization is important but should be performed with caution. Volume overload may lead to distended varices and cause rebleeding/worsening hemorrhage • Correction of coagulopathy ◦◦ Keep platelets >50,000/uL ◦◦ Vitamin K ◦◦ Consider FFP or administration of clotting factors as needed • Pharmacologic therapy: Table 5-10 outlines pharmacologic therapy that should be administered empirically to all patients with known or suspected portal hypertension presenting with GI bleed • Balloon tamponade: temporizing measure if unable to control bleeding until definitive treatment is possible (Figure 5-15)


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Table 5-10. Pharmacologic Treatment of Variceal Hemorrhage Octreotide

Reduces mortality, may lead to hemostasis in >50% of patients

Bolus: 50 μg IVP


Reduces rebleeding risk, lowers rate of infection, and reduces mortality

Ceftriaxone 1 g IV daily

May reduce risk of post-banding ulcers and associated rebleeding

Bolus: 80 mg IVP


Infusion: 50 μg/h for 5 d or Fluoroquinolone

Infusion: 8 mg/h No convincing evidence that IV PPI drip is superior to intermittent IV dosing or oral PPI

IVP = intravenous push; PPI = proton pump inhibitor.

Figure 5-15. Balloon tamponade of bleeding varices. (Reproduced courtesy of Wikicommons.)

• Endoscopy ◦◦ Esophageal varices: band ligation is first line treatment with reduced risk of rebleeding and mortality compared with sclerotherapy. Achieves hemostasis in >80% of patients (Figure 5-16) ◦◦ Gastric varices: difficult to treat, with high risk for treatment failure and/or rebleeding. Cyanoacrylate injection appears to provide superior results to banding, but more studies are needed


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key fact Cirrhotics with GI bleeding are at increased risk for various infections. Prophylactic antibiotics reduce this risk and the risk of rebleeding.

flash card Q. You are preparing to perform balloon tamponade in a patient with refractory variceal bleed. What are the complications of this procedure?

A. Complications related

Figure 5-16. Bleeding esophageal varix (A) and same varix after banding (B).

(Reproduced with permission, Khan NM, Shapiro AB. The White Nipple Sign: Please Do Not Disturb. Case Reports in Gastroenterology 2011;5:386–390.)

• Treatment of refractory bleeding ◦◦ TIPS (Figure 5-17) ◦◦ Surgical shunt ◦◦ Embolization ◦◦ Transplant: if patient is a transplant candidate, consult with transplant team before TIPS or surgical shunt, as this can make the transplant surgery more difficult Hepatic vein

Inferior vena cava Varices

Guided wire with needle



Portal vein

to balloon tamponade are reported in >10% of patients and include esophageal rupture, esophageal mucosal ischemia and ulceration, and pulmonary aspiration.

flash card Q. Endoscopy was unsuccessful in achieving hemostasis in your patient with severe bleeding esophageal varices. Balloon tamponade has been performed as a temporizing measure. What therapy would you consider next?

A. TIPS is indicated for management of complications of portal hypertension refractory to medical management. In refractory variceal bleeding, TIPS resulted in hemostasis in >90% of cases, with the most common significant complication being hepatic encephalopathy.

Stent in place Guidewire

Figure 5-17. TIPS placement and changes in flow (Courtesy of Dr. Laura Hinkle)


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PROGNOSIS—Below are the risk factors for early vs late rebleeding. In addition

to endoscopic treatment of varices, further reduction in recurrence risk can be achieved with a nonselective β-blocker (propranolol, carvedilol). Caution should be taken, however, as β-blockers may lead to increased mortality in patients with decompensated cirrhosis manifested by refractory ascites and spontaneous bacterial peritonitis. Risk Factors for Rebleeding Early Rebleed: 6 wk

• Active bleeding or stigmata of recent bleed on endoscopy • Advanced age • Advanced liver disease +/− other apparent complications: encephalopathy, ascites • Bleeding from large varices or gastric varices • Renal failure • Sepsis • Severity of initial bleed • Thrombocytopenia

• Advanced age • Advanced liver disease +/− other apparent complications: encephalopathy, ascites • Hepatoma • Ongoing alcohol abuse • Stigmata of recent bleed on initial endoscopy

key fact Risk factors for development of post-TIPS encephalopathy include pre-TIPS encephalopathy, MELD >15 or Child-Pugh score >10, and older age. Often encephalopathy will respond to usual medical therapies, but some patients may require shunt revision or reversal.

key fact Contraindications to elective TIPS include heart failure, significant tricuspid regurgitation or pulmonary hypertension, and systemic infection. Caution should also be taken in patients with high MELD scores, as the MELD was originally developed to predict 90-d mortality in patients undergoing TIPS.

Spontaneous Bacterial Peritonitis (SBP) Spontaneous bacterial peritonitis (SBP) almost always occurs in the setting of ascites secondary to cirrhosis, and the diagnosis should be considered in any patient with cirrhosis who presents with hepatic encephalopathy, systemic signs of infection, or abdominal pain. DIAGNOSIS—Any patient with suspected SBP should undergo diagnostic

paracentesis, with fluid sent for gram stain, culture, and cell count. Consider also sending albumin, total protein, glucose, lactate dehydrogenase, and amylase, depending on the clinical picture. TREATMENT—Most cases are due to gut flora, with most common organisms being

Escherichia coli, Streptococcus species, and Klebsiella pneumoniae.

• Broad-spectrum antibiotic such as cefotaxime or another third-generation cephalosporin or fluoroquinolone • Albumin 1.5g/kg on day 1 and 1.0 g/kg on day 3 has been shown to reduce inhospital mortality and the incidence of new or worsening renal dysfunction • Discontinue β-blockers until infection has resolved. Continued use has been shown to increase mortality • Repeat paracentesis is not routinely indicated but should be considered if there is an atypical presentation or lack of response to treatment


key fact If culture reveals polymicrobial infection, glucose 1 g/dL, or elevated LDH, consider diagnosis of secondary bacterial peritonitis.

flash card Q. What are the criteria for diagnosis of SBP?

A. Positive culture and ascitic polymorphonuclear (PMN) count ≥250 cells/mm3. Sensitivity of ascitic fluid cultures is low, so treat as SBP based on PMN count alone.

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Hepatorenal Syndrome (HRS) Hepatorenal syndrome (HRS) most often occurs in patients with cirrhosis but can be seen in acute or chronic liver failure of any cause. It is thought to be triggered by a decline in renal perfusion caused by the combination of: • Splanchnic vasodilation • Increased cardiac output due to decreased systemic vascular resistance • Systemic hypotension DIAGNOSIS of exclusion occurring in ~13-17% of patients with acute kidney

injury who also have underlying liver disease. Diagnostic studies

• Urine ◦◦ Sodium 55 yr Obesity (BMI >30 kg/m2) Altered mental status Comorbid disease

Presence of SIRS

At least two of the following: Heart rate >90 bpm RR >20 /min or PaCO2 38°C or 12,000 cells/mm3 or 10%


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Risk Factors for Development of Severe Acute Pancreatitis on Initial Assessment Laboratory evaluation

BUN > 20 mg/dL or rising BUN Hct >44% or rising Hct Elevated creatinine

Radiologic evaluation

Pleural effusions Pulmonary infiltrates Extrapancreatic fluid collections

BMI = body mass index; BUN = blood urea nitrogen; Hct = hematocrit; PaCO2 = partial pressure of carbon dioxide; SIRS = systemic inflammatory response syndrome; WBC = white blood cell.

Epidemiology Acute pancreatitis is the most common GI disease resulting in hospitalization in the U.S., and incidence is rising in Europe and Scandinavia. Gallstones are the most common cause worldwide, followed by alcohol.


key fact Severe acute pancreatitis is associated with a mortality rate of 17-30%.

key fact

Table 5-12. Causes of Acute Pancreatitis Etiology (% of cases)

Risk Factors

Alcohol (30%)

Longstanding alcohol abuse

Gallstones (35-40%)

Female sex Smaller stone size

Patients with HIV are at risk for development of acute pancreatitis due to medications, opportunistic infections, and lymphoma.


Post-ERCP (3-5% of patients undergoing ERCP)

ERCP procedure within the previous 24 h

Biliary sludge (20-40% of patients with no other identifiable cause)

Total parenteral nutrition, biliary obstruction, prolonged fasting state

Causes of pancreatitis: GET SMASHED

Hypertriglyceridemia (1-4%)

Serum triglycerides >1000 mg/dL

Drug-induced (0.1-2%)

Many common drugs associated with acute pancreatitis including diuretics, ACE inhibitors, oral contraceptives, HAART, steroids

Gallstones Ethanol Trauma

Infectious (unknown)

Multiple etiologies, including bacterial, fungal, viral, and parasitic infections

Autoimmune (rare)

Presence of other autoimmune disorders

Hypercalcemia (rare)

Elevated serum calcium of any etiology

Toxin exposure (rare)

Brown recluse spiders, scorpions, Gila monster lizard

Trauma (rare)

History of blunt trauma

Tumor (rare)

Pancreatic and periampullary tumors, intraductal papillary mucinous neoplasms, lymphoma

Steroids Mumps Autoimmune Scorpions Hyperlipidemia/ hypercalcemia ERCP Drugs

ACE = angiotensin converting enzyme; ERCP = endoscopic retrograde cholangiopancreatography; HAART = highly active antiretroviral therapy.


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Diagnostic Testing All patients should undergo abdominal US to evaluate for gallstones and labs including lipase, amylase, triglycerides, calcium, and liver function tests. • Contrasted radiographic studies should only be performed when there is diagnostic uncertainty or lack of clinical improvement in the first 48 h • If autoimmune pancreatitis is suspected, antinuclear antibodies and serum IgG4 levels should be obtained • In the absence of other risk factors, consider evaluation for malignancy in patients >40 yr

Treatment All patients with severe acute pancreatitis should be admitted to the ICU with treatment as indicated for the underlying etiology. • IVF resuscitation: aggressive volume resuscitation ≤250-500 mL/h during first 12-24 h reduces morbidity and mortality. There is no evidence to support aggressive resuscitation beyond 24 h • Nutrition: address within 72 h of admission ◦◦ Enteral feeding is preferred until nutrition can be provided orally ◦◦ Parenteral feeding should be avoided whenever possible • Antibiotics: routine use of empiric antibiotics is not recommended • ERCP: early (20 mm Hg in setting of new onset organ failure. In setting of pancreatitis, abdominal tissue edema develops secondary to inflammation and initial resuscitation, ascites, and ileus. Supportive management +/− surgical intervention as per other causes of abdominal compartment syndrome. SYSTEMIC COMPLICATIONS—Acute pancreatitis is associated with acute

respiratory distress syndrome and hyperglycemia. Additionally, patients with chronic diseases such as chronic obstructive pulmonary disease, coronary disease, etc., are at risk for exacerbations of their underlying condition.

►►GALLBLADDER ►ACUTE ► CHOLECYSTITIS Acute cholecystitis is inflammation of the gallbladder accompanied by RUQ pain, leukocytosis, and fever. It most often occurs in the setting of gallstone disease but may also occur when gallstones are not present.

►ACUTE ► CALCULOUS CHOLECYSTITIS Acute calculous cholecystitis is the most common cause of acute cholecystitis and occurs when gallstones migrate from gallbladder and obstruct the cystic duct, leading to gallbladder inflammation.

key fact Infected pancreatic tissue necrosis is most commonly caused by enteric organisms such as E coli, Klebsiella, Pseudomonas, and Enterococcus.

flash card Q. Mr. S. was admitted to the ICU 5 d ago with severe acute pancreatitis and is increasingly difficult to ventilate, with high peak and plateau pressures noted on the ventilator. A CXR shows mild pulmonary edema and reduced lung volumes. What is the most likely etiology?

A. Elevated abdominal pressure due to tissue edema and possible third spacing of fluids.

key fact Patients are at increased risk for acalculous cholecystitis in the setting of: • Critical illness • Total parenteral nutrition • Bone marrow transplantation • Major surgery (eg, cardiac, aortic reconstruction) • Acute Epstein Barr virus infection


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►ACALCULOUS ► CHOLECYSTITIS Acalculous cholecystitis accounts for 10% of all cases of acute cholecystitis and is mostly seen in patients in the ICU. Presentation is often nonspecific, and complications may occur before a diagnosis is made. Acalculous cholecystitis should be considered in any critically ill patient with unexplained fever, jaundice, or signs of sepsis.

Diagnosis Table 5-13. Diagnosis of Acute Cholecystitis Acalculous Cholecystitis

Calculous Cholecystitis

Physical exam

Fever, vague abdominal pain, RUQ mass or crepitus, jaundice

Fever, severe persistent RUQ or epigastric pain, jaundice

Laboratory findings

Leukocytosis, mild elevations in aminotransferases and alkaline phosphatase, hyperbilirubinemia

Leukocytosis and mild elevations in aminotransferases and hyperbilirubinemia; if marked elevation in bilirubin or ALP, consider presence of choledocholithiasis or cholangitis

Radiographic findings

US: gallbladder wall thickening is most common sign

US: same as acalculous cholecystitis + presence of gallstones

HIDA: much less sensitive than ultrasound but may be useful if diagnosis remains unclear; lack of gallbladder opacification considered a positive test

Same as for acalculous cholecystitis.

Abdominal CT: same findings as US

Abdominal CT: findings same as US but often does not visualize stones as well ERCP/MRCP: more sensitive than US for detecting cystic duct stones

ALP = alkaline phosphatase; CT = computed tomography; ERCP = endoscopic retrograde cholangiopancreatogram; HIDA = hepatic iminodiacetic acid; MRCP = magnetic resonance cholangiopancreatogram; RUQ = right upper quadrant; US = ultrasound.

Treatment Early recognition and treatment is important to prevent complications such as gallbladder gangrene/perforation. Patients should have blood cultures and broadspectrum antibiotics, as secondary infection with enteric pathogens may occur. Antifungal coverage should be considered in immunosuppressed patients. CHOLECYSTOSTOMY vs CHOLECYSTECTOMY—Cholecystectomy should be

performed in all patients with calculous cholecystitis, but perioperative risk may be prohibitive in many cases. In those situations, cholecystotomy drainage should be performed until cholecystectomy can be safely accomplished. Patients with acalculous cholecystitis should undergo cholecystostomy drainage, and most will not ultimately require cholecystectomy.

Complications Patients are at risk for gallbladder gangrene, which may lead to perforation,


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particularly in cases of acalculous cholecystitis. Perforation is more common in patients with emphysematous cholecystitis (Figure 5-19).

Figure 5-19. Emphysematous cholecystitis (arrows), with resulting significant pneumoretroperitoneum.

(Reproduced. Yagi Y, Sasaki S, Terada I, et al. Massive pneumoretroperitoneum arising from emphysematous cholecystitis: a case report and the literature review. BMC Gastroenterol. 2015;15:114.)

key fact

►ACUTE ► CHOLANGITIS Also known as ascending cholangitis, acute cholangitis is a bacterial infection of the normally sterile biliary tract, with significant associated morbidity and mortality. When infection occurs, it is most often caused by translocation of duodenal bacteria due to obstruction, bile stasis, or disruption of barrier mechanisms caused by procedures such as stent placement or sphincterotomy. The classic presentation of Charcot's triad: fever, abdominal pain, and jaundice is very specific (95%) but has poor sensitivity, with only ~50% of patients presenting with all three.

Ultrasound findings of acalculous cholecystitis include: • Gallbladder thickening of >3-5 mm • Intramural or intraluminal gas • Pericholecystic fluid • Mucosal sloughing • Gallbladder distension >5 cm

flash card

Diagnosis Table 5-14.

Q. A patient in the ICU

Diagnosis of Acute Cholangitis Symptom Group


Group 1: Systemic inflammation

Fever (temp >38⁰C) and chills Lab findings showing inflammation (WBC 10, elevated CRP ≥1, etc)

Group 2: Cholestasis

Jaundice Total bilirubin ≥2 ALP >1.5× ULN γ-GGT >1.5× ULN AST >1.5× ULN ALT >1.5× ULN

undergoes cholecystostomy drainage for acalculous cholecystitis but fails to improve over the next 48 h. What is the next step in managing this patient?

A. Patients with acute cholecystitis, regardless of the etiology, should undergo cholecystectomy when gallbladder drainage does not result in clinical improvement within 24–48 h.


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Diagnosis of Acute Cholangitis Group 3: Imaging

Biliary dilatation (Figure 5-20) Obstructive etiology identified on imaging (mass, stone, stent, stricture, etc)

Suspected diagnosis: one item from group A and an item from B or C Definite diagnosis: one item from each group ALP = alkaline phosphatase; CRP (C-reactive protein) = mg/L; ULN = upper limit of normal; WBC (white blood cell) = × 109/L.; GGT = glutamyltransferase; Total bilirubin = mg/dL

key fact Figure 5-20. Cholangiography demonstrating biliary dilatation with multiple stones impacted in the common bile duct. (Reproduced. Frossard JL, Bonvin F. Charcot’s triad. Int J Emerg Med. 2011;4:18.)

Treatment • Supportive care with volume resuscitation and hemodynamic support • Blood and bile cultures, initiation of broad-spectrum antibiotics aimed at enteric organisms • Urgent drainage of biliary system ◦◦ ERCP to allow removal of stones or stent insertion as needed ◦◦ Cholecystostomy should be performed if drainage is not accomplished by ERCP or if ERCP is not readily available or contraindicated


Biliary calculi, benign bile duct stenosis, and malignancy are the most common causes of bile duct obstruction leading to acute cholangitis.

key fact Reynolds' pentad is said to occur when fever, abdominal pain, and jaundice are associated with hypotension and altered mental status. The presence of encephalopathy predicts a poor outcome.


surgery, trauma, and transplantation Anthony Arredondo, MD; Ayodeji Adegunsoye, MD

►►PATIENT RISK ASSESSMENT Patient risk assessment and improved perioperative management have reduced morbidity and mortality associated with surgical procedures. Surgical patients with high perioperative risk are characterized by limited physiological reserve to respond to the increased oxygen demand and stress of surgery and are at greater risk for tissue hypoxia, organ failure, postoperative complications, and death. Chronic medical conditions (particularly cardiac, pulmonary, and hepatic disease) and severity of acute illness increases surgical risk. Early identification of high-risk surgical patients permits directed therapies to reduce adverse outcomes.

►PREDICTORS ► OF INCREASED MORBIDITY/ MORTALITY Factors that increase perioperative risk and postoperative complications may be related to the surgical procedure or patient factors. These factors may be related to risk for respiratory complications, cardiac complications, or both. SURGICAL RISK FACTORS for complications are outlined in Table 6-1. Examples

of high-risk surgical factors: complex GI surgery for carcinoma with anastomotic repair, surgical management of acute abdomen, massive hemorrhage with >2.5 L blood loss.


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Table 6-1. Surgical Risk Factors for Surgical Complications Risk Factor

Cardiac Risk

Respiratory Risk

Peripheral arterial surgery

Abdominal aortic aneurysmal repair

Emergency surgery

Airway surgery

Thoracic surgery

Upper abdominal surgery

Duration > 3 h

PATIENT-RELATED FACTORS for complications are outlined in Table 6-2. Examples

of high-risk patient factors: active sepsis, age >70 with multi-organ impairment. Table 6-2. Patient Risk Factors for Surgical Complications Risk Factor

Cardiac Risk

Respiratory Risk

AF history

Cardiac ischemia history

Renal insufficiency/failure


American Society of Anesthesiologists Class

Heart failure

Pulmonary hypertension

Active smoking



AF = atrial fibrillation; COPD = chronic obstructive pulmonary disease; OSA = obstructive sleep apnea.

Acute or chronic liver disease also has a significant effect on surgical risk. Elective surgery is contraindicated in patients with acute or chronic severe hepatitis or cirrhosis with Child-Pugh class C or Model for End-stage Liver Disease (MELD) >15.

Preoperative Strategies for Risk Assessment Although patient-associated clinical criteria may be useful, risk stratification based on an objective assessment of cardiopulmonary status is of greater value in identifying patients with mortality risk that exceeds 5%. • Stress echocardiography ◦◦ Occurrence of ischemia at 7 mg/dL (higher targets in ischemic heart disease), using noninvasive ventilation strategies in specific patient populations (eg, COPD or postcardiac surgery), and using IVF and vasopressors as needed to optimize cardiac output and improve tissue perfusion.

key fact In high-risk surgical patients, strategies that optimize tissue perfusion and increase delivery of oxygen index >600 mL/min/m2 reduce risk of morbidity and mortality.

►►SURGICAL CRITICAL CARE Surgical critical care involves the care of patients with acute, life-threatening, or potentially life-threatening surgical conditions. Any perioperative patient is a candidate for the ICU. This chapter will highlight common scenarios in which cardiovascular, genitourinary, obstetric, or transplant patients require ICU care.

►CARDIOVASCULAR ► SURGERY Most cardiovascular surgery patients, including those undergoing coronary artery bypass graft (CABG) and mitral valve replacement, require ICU level of care postoperatively.

Cardiac Surgery Recipients of cardiac surgery are subject to both cardiac and noncardiac complications. Cardiopulmonary bypass is often required to perform cardiac surgery and results in greater risk for the patient involved.


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Figure 6-1. Cardiopulmonary bypass simplified schematic representation. (Reproduced courtesy of Wikipedia.)

CARDIOPULMONARY BYPASS (CPB) extracts deoxygenated blood into a reservoir

(blue arrows in diagram above). Blood flows into the oxygenator, which in turn "pumps" oxygenated blood into the systemic circulation (red arrows). This method is used to arrest the heart and provide a bloodless, stable surgical field while perfusing the rest of the body. • Common indications ◦◦ ◦◦ ◦◦ ◦◦ ◦◦ ◦◦ ◦◦

CABG Cardiac valve repair/replacement Repair of large septal defects Repair of congenital heart defects Repair of thoracic aneurysms Heart and lung transplant Pulmonary thrombectomy or thromboendarterectomy

• Adverse effects of CPB result from: ◦◦ ◦◦ ◦◦ ◦◦ ◦◦ ◦◦

Hypothermia Full anticoagulation Ischemia, emboli, and hypoperfusion Cannulation and cross-clamping of major vessels Exposure to CPB circuit Exposure to blood products

GENERAL CARDIAC COMPLICATIONS of cardiac surgery include mechanical

complications specific to the surgery, reduced cardiac output, dysrhythmias, and myocardial infarction (MI).


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• Mechanical complications ◦◦ Bypass graft vessel spasm or occlusion ◦◦ Prosthetic valve paravalvular regurgitation ◦◦ Systolic anterior motion of mitral valve with left ventricular outflow obstruction ◦◦ Cardiac tamponade ◦◦ Hematoma ◦◦ Diagnosis: clinical scenario and echocardiography ◦◦ Treatment: typically surgical re-exploration and correction • Reduced cardiac output ◦◦ Intravascular hypovolemia ◦◦ Excessive left ventricular afterload ◦◦ Reduced inotropy ◦◦ Diagnosis: echocardiography and invasive hemodynamic monitoring ◦◦ Treatment: specific to underlying physiologic derangement and may include volume resuscitation, afterload reduction, and inotropic support (eg, inotrope or intra-aortic balloon pump) • Dysrhythmias ◦◦ Atrial fibrillation (AF) ◦◦ Ventricular arrhythmias ◦◦ Bradyarrhythmias • MI CARDIAC COMPLICATIONS OF CABG—CABG is the most common cardiac

surgery and complications specific to this surgery include:

• MI ◦◦ Risk factors: cardiomegaly, time on CPB, repeat CABG, or CABG with other cardiac surgery ◦◦ Diagnosis: elevation of cardiac enzymes >5× the upper limit of normal (ULN) + new pathologic Q wave on postoperative EKG OR new bundle branch block OR angiographically proven graft or native vessel occlusion ◦◦ Treatment: revascularization with percutaneous coronary intervention (PCI) or redo CABG • Early graft occlusion ◦◦ A subcategory of MI usually occurring within first 30 d of surgery ◦◦ Usually thrombotic and related to technical problems at anastomosis (poor distal perfusion after grafting of the more proximal coronary arteries) ◦◦ Treatment: revascularization with PCI or redo CABG • AF and flutter ◦◦ AF more common than atrial flutter ◦◦ Risk factors: age, prior AF, mitral disease, COPD, withdrawal of β-blockers or angiotensin-converting enzyme inhibitor (ACEi) before


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◦◦ ◦◦ ◦◦ ◦◦ ◦◦

surgery, hypokalemia, hypomagnesemia, obesity, white race Incidence: CABG 15–40%, valve 37–50%, CABG + valve 60% Presentation: within 48 h postop, 80% self-resolve within 24 h if no prior history of AF Treatment: β-blockers, sotalol, or amiodarone given preoperatively reduces postop AF by 52–65% (β-blockers typically favored as fewer adverse events), electrical cardioversion if hemodynamically unstable Complications of amiodarone: bradycardia, need for temporary pacing, and QT prolongation Complications of sotalol: torsades de pointes and bradycardia, limited use despite being more effective in reducing postop AF compared with β-blockers

• Ventricular tachyarrhythmia (VT) ◦◦ Presentation: nonsustained VT common (17–97%), lower incidence of sustained VT, polymorphic VT, or ventricular fibrillation (VF) ◦◦ Risk factors: age >65, female, BMI 30 d) exudates ◦◦ Early: bloody with high eosinophilic count and neutrophil predominance ◦◦ Late: yellow exudates with lymphocytic predominance

Postpericardiotomy syndrome

◦◦ Fever, pleuritic chest pain, pericardial rub

Heart failure

◦◦ Typically transudate and bilateral ◦◦ Can be exudative in setting of diuretics


◦◦ New focal infiltrate with exudative parapneumonic effusion

Pulmonary embolism

◦◦ Effusion small and almost always exudative


◦◦ Bloody effusion with pleural fluid hematocrit ≥50% of peripheral blood hematocrit


◦◦ Surgical disruption of thoracic duct ◦◦ Milky or opalescent fluid with triglyceride >110 mg/dL and/or chylomicron-positive

Infectious mediastinitis

◦◦ Bilateral pleural effusions with CT evidence of mediastinal soft tissue swelling

CVC erosion

◦◦ Pleural effusion in setting of mediastinal widening in patient with CVC

CT = computed tomography; CVC = central venous catheter.


repaired by open or endovascular techniques. Historically, endovascular repair was reserved for higher-risk patients meeting technical criteria for deployment of stents, but there are no clear guidelines in choosing open vs endovascular repair (case-by-case basis). In asymptomatic aneurysms, repair is recommended for diameters 6-7 cm OR 5-6 cm if it is the result of a genetic condition (eg, Marfan or Turner syndrome). Repair is indicated for symptomatic patients with/without aneurysmal dissection or rupture. • Descending thoracic aortic aneurysm ◦◦ Involves any portion of the thoracic aorta distal to left subclavian • Thoracoabdominal aneurysms ◦◦ May extend from left subclavian artery to different portions of the abdominal aorta, involving visceral arteries, such as the celiac axis, superior mesenteric artery, and renal arteries ◦◦ Crawford classification is used to describe the extent of the aneurysm ◦◦ Open repair is gold standard for treatment ◦◦ Mortality 2-10% for open repair ◦◦ Mortality up to 40% in emergent setting (ie, acute dissection or rupture) CRAWFORD CLASSIFICATION—The extent of the thoracoabdominal aneurysm can

be classified using the modified Crawford classification, which distinguishes each type by the start and endpoints of the aneurysm.


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Table 6-5. Complications for Descending Thoracic and Thoracoabdominal Aneurysm: Open Repair Complication

Risk Factors

Clinical Features


◦◦ Atelectasis ◦◦ COPD ◦◦ Clinical and ◦◦ Pleural effusion ◦◦ Surgical division radiographic diagnosis ◦◦ Pneumonia of diaphragm ◦◦ Postoperative ◦◦ Prolonged oneventilation >48 h lung ventilation ◦◦ ARDS (left lung collapse) ◦◦ Massive transfusion of blood products


◦◦ AKI


◦◦ Preoperative renal ◦◦ ATN secondary dysfunction to hypotension, ◦◦ Significant hypovolemia, atherosclerosis atheromatous ◦◦ Nephrotoxembolization, renal ins (contrast, ischemia, and/or NSAIDs, aminorhabdomyolysis glycosides) ◦◦ Spinal cord ◦◦ Size of aneurysm ◦◦ Onset from immediate ischemia (rate ◦◦ Aortic dissection to weeks later 2–8%): anterior ◦◦ Emergent surgery ◦◦ Lower extremity spinal syndrome ◦◦ Length of paraparesis to flaccid ◦◦ Stroke (3–10%) cross-clamp time paralysis ◦◦ Proprioception and vibratory sensation may be preserved ◦◦ Compromised spinal cord perfusion (anterior spinal artery)


◦◦ MI ◦◦ CHF ◦◦ AF ◦◦ HTN ◦◦ Hypotension


◦◦ Hemorrhage ◦◦ Thrombocytopenia


◦◦ Mesenteric ischemia (2%) ◦◦ Ileus ◦◦ Pancreatitis ◦◦ Cholecystitis ◦◦ Ischemic colitis

◦◦ Prior comorbid conditions

◦◦ Uncontrolled HTN can exacerbate postop bleeding, compromise suture lines, and increase risk for MI and ventricular dysfunction ◦◦ Prolonged hypotension may compromise organ perfusion ◦◦ Extensive surgical ◦◦ Postop hemorrhage dissection may require re◦◦ Massive exploration (2%–5%) transfusion ◦◦ Thrombocytopenia ◦◦ Mesenteric typically from platelet ischemia consumption or ◦◦ Hypothermia sequestration by graft material ◦◦ HIT ◦◦ Hypoperfusion and ischemia from embolic, thrombotic, or mechanical obstruction of arterial flow

Management ◦◦ Optimize preop ◦◦ Avoid allogeneic blood products ◦◦ Conservative transfusion threshold (Hgb 7g/dL) ◦◦ Lung-protective ventilation ◦◦ Avoid phrenic nerve damage ◦◦ Early extubation ◦◦ Maintain adequate intravascular volume and renal perfusion ◦◦ Avoid nephrotoxins ◦◦ Minimize renal ischemic time ◦◦ Avoid transection of major anterior spinal arteries ◦◦ Hypothermia ◦◦ Optimize spinal cord perfusion pressure: MAP >90, CSF drainage acutely if neuro deficits (CSF 10 g/dL ◦◦ Aggressive physical therapy ◦◦ Target SBP within 20% of baseline ◦◦ Fluid management to avoid third-spacing ◦◦ Postop β-blockers, statins, and aspirin

◦◦ Blood products based on coagulation factors and TEG ◦◦ Hgb >7 g/dL

◦◦ Abdominal pain with ◦◦ Serial abdominal exams lactic acidosis ◦◦ General surgery ◦◦ Can trigger SIRS with consultation end organ damage and coagulopathy

AF=atrial fibrillation; AKI=acute kidney injury; ARDS=acute respiratory distress syndrome; ATN=acute tubular necrosis; CHF=congestive heart failure; COPD=chronic obstructive pulmonary disease; CSF=cerebrospinal fluid; Hgb=hemoglobin; HIT=heparin-induced thrombocytopenia; HTN=hypertension; MAP=mean arterial pressure; MI=myocardial infarction; NSAID=nonsteroidal anti-inflammatory drug; SBP=systolic blood pressure; SIRS=systemic inflammatory response syndrome; TEG=thromboelastography.

flash card Q. What equation determines spinal cord perfusion pressure (SCPP), and how can you optimize SCPP during acute spinal cord ischemia?

A. SCPP=MAP – CSF pressure. SCPP can be optimized by increasing MAP >90, ensuring adequate oxygen delivery, decreasing CSF pressure to 20 mm Hg + end organ damage

◦◦ IC: ex-lap with bowel resection for transmural colonic necrosis; bowel rest for reversible ischemia ◦◦ AACS: medical vs surgical management


◦◦ AKI

◦◦ Suprarenal cross-clamping

◦◦ Infrarenal aortic cross-clamping reduces renal blood flow by 45%; suprarenal by 80%

◦◦ Avoid nephrotoxins, hypovolemia, and hypotension

AACS=acute abdominal compartment syndrome; AKI=acute kidney injury; CAD=coronary artery disease; ex-lap=exploratory laparotomy; IAP=intra-abdominal pressure; IC=ischemic colitis; IVF=intravenous fluids; MI=myocardial infarction.


flash card Q. What AAA surgical complication portends the highest mortality?

A. Ischemic colitis with an estimated mortality of 40–65%.

key fact In AAA open repair, suprarenal aortic cross-clamping increases the incidence of acute kidney injury from 5% to 15%.

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applies to both thoracic endovascular aortic repair (TEVAR) and abdominal endovascular aortic repair (EVAR).

• TEVAR ◦◦ Used for elective and emergent repair of thoracoabdominal aortic aneurysms, pseudoaneurysms, complicated type B aortic dissections, and traumatic aortic injuries ◦◦ Percutaneous arterial access via femoral artery to deliver ≥1 self-expanding aortic grafts under fluoroscopic guidance ◦◦ Can be combined with open surgery by creating an extra-anatomical bypass when the graft covers the ostium at an arterial branch ◦◦ Avoids extensive aortic dissection and aortic cross-clamping ◦◦ Reduced 30-d mortality, stroke, and cardiopulmonary complications compared with open surgery ◦◦ Less postoperative pain, blood loss, and recovery time ◦◦ Endovascular repair comes with both immediate- and long-term complications (Table 6-7) • EVAR ◦◦ Used for elective and emergent repair of AAAs ◦◦ In the U.S., 60% of AAAs are electively repaired by EVAR ◦◦ Associated with lower 30-d mortality and stroke than open repair

key fact Endovascular repair of thoracoabdominal aneurysms is associated with a significant reduction in perioperative mortality and stroke but does not portend long-term mortality benefit compared to open repair.

Table 6-7. Complications of Endovascular Repair Early


Vascular access injury (15–20%)

Stent graft migration, infolding, or collapse

◦◦ Iliofemoral laceration and rupture ◦◦ Pseudoaneurysm ◦◦ Retroperitoneal bleed ◦◦ Ischemia to limb, pelvic, or visceral organs

◦◦ Device infolding or collapse more common in young trauma patients ◦◦ Present with symptoms of acute aortic occlusion

Stroke (2–8%)

Endoleak with possible aneurysm expansion, dissection, and rupture

◦◦ Typically embolic from atherosclerotic aorta ◦◦ RF: duration of wire instrumentation, prior stroke, CKD, proximal descending aorta coverage

Spinal cord ischemia (3–10%)

◦◦ Persistent blood flow outside the lumen of endograft and within aneurysm sac ◦◦ More common in AAA repair ◦◦ CTA with contrast for diagnosis

key fact The incidence of spinal cord ischemia is significantly higher in TEVAR compared with EVAR, given a higher chance of impairing spinal artery blood flow. Intercostal arteries at T6-T12 may be occluded, leading to compromise of spinal artery blood flow.

Stent graft infection

◦◦ Immediate or delayed presentation ◦◦ RF: length of thoracic aorta coverage, prior AAA repair, pelvic occlusive atherosclerosis AKI (2%)

GI tract erosion

◦◦ Etiology: embolic disease, hypoperfusion, contrast ◦◦ RF: prior renal failure, blood transfusion, length of aortic disease

◦◦ Aortoesophageal fistula ◦◦ Aortoenteric fistula ◦◦ May present as GI bleed

Postimplantation syndrome ◦◦ Leukocytosis, fever, elevated CRP ◦◦ Likely endothelial activation by endograft AAA=abdominal aortic aneurysm; AKI=acute kidney injury; CKD=chronic kidney disease; CRP=C-reactive protein; CTA=computed tomography angiogram; GI=gastrointestinal; RF=risk factor.


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ARTERIAL OCCLUSIVE DISEASE—Extracranial internal carotid artery (ICA) and

peripheral artery occlusive atherosclerosis require revascularization to prevent stroke and limb ischemia. • Carotid endarterectomy (CEA) ◦◦ ~66% of strokes are caused by thromboembolic events and atherosclerosis of extracranial ICA ◦◦ CEA is recommended for all patients with ICA stenosis of 60–99% and symptomatic patients with 50–99% stenosis ◦◦ Carotid artery stenting is less invasive and reserved for high-risk patients with ICA stenosis of 50–99%

Table 6-8. Complications of CEA Type of Complication


Stroke (0.25–7%)

◦◦ Onset: immediate to 24 h postop ◦◦ Mechanism: embolism, thrombosis, hemorrhage, hypoperfusion ◦◦ Intervention: evaluate patency of carotid artery (duplex US, CTA brain, arteriography) ◦◦ May require re-exploration ◦◦ Expected stroke management

Cerebral hyperperfusion syndrome (1–2%)

◦◦ Onset: 3–7 d post-CEA ◦◦ Presentation: AMS, headache, and seizures ◦◦ Mechanism: cerebral and intracranial edema from elevated cerebral perfusion pressure after surgical correction of stenosis ◦◦ RF: high-grade stenosis, bilateral stenosis, postop hypertension ◦◦ Intervention: CT head, control BP and seizures

Cranial nerve injury

◦◦ Etiology: retraction trauma or nerve transection ◦◦ Nerves: recurrent laryngeal, hypoglossal, marginal mandibular ◦◦ Intervention: speech/swallow evaluation before oral intake; if vocal cord dysfunction, proceed with fiber-optic exam ◦◦ Resolution within 26 mo if from retraction injury during surgery

Myocardial ischemia (2%)

◦◦ RF: CAD, HTN, history of angina ◦◦ Presentation: open CEA more likely to be symptomatic, have EKG changes, or have elevated enzymes

Postoperative hypertension

◦◦ Mechanism: impaired baroreceptor function from carotid sinus damage during dissection or local anesthetic infiltration

Postoperative hypotension

◦◦ Mechanism: hypersensitivity of carotid sinus baroreceptor after plaque removal and usually resolves within 12–24 h ◦◦ Management: IVF resuscitation, vasopressors, and/or inotropes


◦◦ Upper airway compromise from expanding wound/neck hematoma requiring intubation ◦◦ Chemoreceptor dysfunction leading to absence of CNS response mechanisms and reduction in respiratory drive

AMS=altered mental status; CEA=carotid endarterectomy; CAD=coronary artery disease; CNS=central nervous system; CT=computed tomography; EKG=electrocardiogram; HTN=hypertension; RF=risk factors; US=ultrasound.

• Peripheral arterial disease ◦◦ Critical limb ischemia results from progressive chronic atherosclerotic disease


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◦◦ Acute presentation of severe pain and cool, pale, pulseless extremity can result from atherosclerotic embolism or plaque rupture ◦◦ Clinical suspicion needed for early treatment and can be confirmed by duplex arterial evaluation ◦◦ Repair can be endovascular or surgical bypass, depending on location, morphology, and surgeon preference ◦◦ Complications: MI, graft thrombosis, reperfusion syndrome presenting as compartment syndrome (hourly monitoring with possible need for fasciotomy)

►GENITOURINARY ► SURGERY Urologic emergencies and perioperative surgical complications are common reasons for ICU admission.

Urologic Emergencies Urologic emergencies include both surgical and nonsurgical entities. The range of urologic emergencies is broad and includes complications related to trauma, infection, vascular disease, and acute urinary tract obstruction. UROGENITAL TRAUMA—Blunt and penetrating trauma can cause renal,

ureteral, bladder, and urethral injuries. Urogenital trauma accounts for 10% of traumatic injuries. • Renal injury ◦◦ Mostly related to blunt trauma ◦◦ Severity measured by American Association for the Surgery of Trauma (AAST) Organ Injury Severity Scores for the Kidney • Indications for radiographic imaging for renal trauma ◦◦ Adult penetrating abdominal trauma ◦◦ Adult blunt abdominal trauma and gross hematuria ◦◦ Adult blunt abdominal trauma, microhematuria, and shock SBP 300 mg/d or protein/creatinine ratio ≥0.3 mg protein/mg creatinine), hypertension (>140/90 mm Hg), and edema. Patients may also present with symptoms of headache, visual changes, stroke, abdominal pain, or shortness of breath. RISK FACTORS • Previous history of preeclampsia • Nulliparity • Pregestational diabetes • Chronic hypertension • Obesity • Family history • Multiple gestation DIAGNOSIS—1) New onset hypertension after 20 wk and proteinuria OR 2) New onset hypertension after 20 wk + presence of end organ damage (preeclampsia with severe features)

• End organ damage: ◦◦ Severe hypertension (SBP >160 mm Hg or DBP >110 mm Hg) ◦◦ Cerebral or visual symptoms ◦◦ Pulmonary edema ◦◦ Platelets 1.1 mg/dL or doubling of serum creatinine ◦◦ Severe right upper quadrant pain or aminotransferase elevation >2× normal


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TREATMENT • Seizure prevention with magnesium sulfate (MgSO4) • Antihypertensive therapy when SBP >160 mm Hg or DBP ≥110 mm Hg ◦◦ Labetalol, nicardipine, and hydralazine preferred; avoid prolonged use of nitroprusside given potential fetal cyanide toxicity; ACEi contraindicated ◦◦ Goal BP 140-160/90-105 mm Hg (SBP >160 mm Hg associated with hemorrhagic stroke) • Glucocorticoids for fetal lung development if 160/110 mm Hg) despite two antihypertensives ◦◦ Eclampsia (generalized tonic-clonic seizures) ◦◦ Persistent, severe headaches, or visual changes ◦◦ End-organ damage

HELLP Syndrome HELLP syndrome is a constellation of hemolysis, elevated liver enzymes, and low platelets, which typically presents between 28-36 wk gestation but can present as late as 7 d postpartum. Although many believe this to be a severe form of preeclampsia, it is important to note that hypertension and proteinuria are NOT necessary for diagnosis, and one will be absent in up to 15% of patients. DIAGNOSIS • Prevalence: 2× normal) ◦◦ Platelets 34 wk gestation ◦◦ Glucocorticoids for fetal lung development if 24-48 h; large volume resuscitation Clinical features: pulmonary edema within 24-48 h of therapy Supportive care: discontinue tocolytics, supplemental oxygen, diuresis Symptoms usually resolve 12-24 h after stopping therapy; if symptoms persist, look for alternative diagnosis

Pulmonary edema is also associated with administration of MgSO4 tocolysis as well.


flash card Q. What is the biggest risk factor for the development of tocolytic-associated pulmonary edema?

A. Prolonged tocolytic therapy >24-48 h.

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Cardiogenic Pulmonary Edema Cardiogenic pulmonary edema during pregnancy or the postpartum period can be the result of preexisting or new cardiac disease. PERIPARTUM CARDIOMYOPATHY—New onset cardiomyopathy (left ventricular

ejection fraction 10% within an hour post-injury strongly

indicates smoke inhalation. Inhalation injury induces upper airway edema (often exacerbated by IVF for comorbid burns), often leading to airway compromise. Oral intubation is preferred, but advanced airway techniques, including the ability to perform a cricothyroidotomy, are critical, given injury to the upper airway. Securing the airway to orally intubated patients with significant facial burns may be challenging, and the endotracheal tube may be secured to the maxillary teeth using dental wires. Laryngeal mask airways are often unhelpful in this scenario, as edema frequently involves the vocal cords. Risk factors for airway compromise requiring early intubation in patients with burns include: • • • • • • •

Burns in an enclosed space Facial burns History of unconsciousness Presence of hoarseness or sensation of "lump in throat" Production of carbonaceous sputum Stridor/respiratory distress Carboxyhemoglobin >10% in first hour

Although upper airway injury may be induced by thermal or chemical exposure, lower airway injury usually is the result of chemical injury (unless steam is involved). Resultant airway inflammation and sloughing can cause cough and airflow obstruction sufficient to induce respiratory failure. Care involves mechanical ventilation, bronchodilation, cautious consideration of mucolytics (as may cause bronchospasm), and chest physiotherapy for airway clearance. LUNG PARENCHYMA—Inhalation injury may be sufficient to induce ARDS, and

a protective ventilator strategy should be used. Airway injury may predispose to atelectasis and pneumonia (up to 70% may develop ventilator-associated pneumonia), and clinicians should have a high index of suspicion for the development of these complications.

key fact SYSTEMIC TOXICITY Carbon monoxide poisoning is a common and potentially fatal complication of inhalation injury, progressing from mild headache and weakness to vision loss and GI symptoms to cardiopulmonary collapse and death. Co-oximetry or blood gas analysis is necessary for diagnosis. Treatment involves high concentrations of inhaled oxygen and in severe cases (CO level >20–25%), hyperbaric oxygen.

Cyanide toxicity is difficult to diagnose and less common than CO poisoning yet must be a consideration in severe inhalation injury. Presentation is nonspecific, including decreased mentation and cardiovascular effects (hypotension,


The Parkland formula is the most widely used guideline for initial resuscitation: • 4 mL of IV crystalloid × kg × % TBSA burned = total IVF in first 24 h • Give half in the first 8 h • Give other half in following 16 h

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bradycardia, and dysrhythmias in severe toxicity). Suspected toxicity should prompt therapy with hydroxocobalamin and sodium thiosulfate or inhaled amyl nitrite, sodium nitrite, and sodium thiosulfate (cyanide antidote kit).

Burn Shock CIRCULATION—Combined hypovolemic and distributive shock frequently

occurs, necessitating effective IVF resuscitation through large-bore IVs, with strict monitoring of urinary output (goal 0.5 mL/kg/h). Resuscitation of burn patients using crystalloid solution (such as Lactated Ringers) is crucial in initial management and is based on total body surface area (TBSA) involved.

key fact Mortality is increased when IVF resuscitation is delayed beyond 2 h from the time of burn injury.

Table 6-12. Pathophysiology of Burn Shock Physiologic Impairment


Depressed cardiac output

Increased afterload, decreased preload, decreased contractility

Intravascular volume depletion

Loss of vessel wall integrity in microcirculation, loss of intravascular oncotic pressure

Elevated systemic vascular resistance

Increase in neurohumoral responses and plasma levels of vasopressin

Wound Care Excision of full-thickness burns should occur within first 7 d. Immediate autografting should occur when feasible; otherwise, allografts, xenografts, or other temporary dermal replacement therapies may be required. Daily cleansing with soap and water and topical antibiotic therapy are effective in mitigating the risk of systemic infection. NUTRITION IN BURNS—In moderate-to-severe burns, optimal nutritional

key fact Patients with burns exceeding 20% TBSA who receive a high-protein diet through a transpyloric feeding tube have improved wound healing.

support is essential to meet the ensuing energy demands resulting from the hypermetabolic response to burn injury. Parenteral nutrition should be avoided if possible, as it is associated with increased mortality. Nutritional support via an enteric feeding tube should be initiated within the first 2 d of injury in the stable patient if oral caloric intake is insufficient. Daily assessment of clinical course, wound healing, total body weight, indirect calorimetry, and laboratory results (nitrogen balance/urinary urea nitrogen) are vital to evaluate the adequacy of the nutrition given. PAIN CONTROL—Although multimodal pain management is advocated, NSAIDs

impair wound healing, increase risk of bleeding and renal impairment, and should be avoided. First-line analgesics are the longer-acting IV opioids, and anxiolytics may be helpful for procedures. Physical therapy and early mobilization improve outcomes.


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►HYPOTHERMIA ► Hypothermia refers to a state in which core body temperature is 10 min


flash card Q. Which test is most useful in the diagnosis of HACE? (a) Pulse oximetry (b) CXR (c) CT scan of brain (d) MRI of brain A. Correct answer is "D." Increased T2 signal intensity within white matter of the corpus callosum splenium is characteristic for HACE. CT demonstrates no changes specific to HACE, pulse oximetry values do not correlate with disease severity, and CXR is indicated only with coexistent HAPE.

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• • • • •

Resuscitation duration >25 min Age >14 yr Glasgow Coma Scale 10Gy; (hematopoietic, GI, and cerebrovascular syndromes)

◦◦ Infertility and thyroid dysfunction ◦◦ Cataracts, organ dysfunction, and vasculopathy ◦◦ Carcinogenesis and genetic mutations


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Table 6-17. Management of Radiation Injury Radiation Injury

Recommended Management

All patients

◦◦ Ensure scene safety for responder entry ◦◦ Stabilize medical and surgical conditions ◦◦ Remove patient from further radiation contamination ◦◦ Obtain history and vitals and perform complete physical exam ◦◦ Bilateral nasal swab and perform count with radiation detector ◦◦ Diagnostic imaging and labs (CBC, serum amylase for involvement of head and neck, CRP, urinalysis, and stool studies for enteric pathogens and fat) ◦◦ Type and screen/cross-match

Localized irradiation with cutaneous injury

◦◦ Institute similar treatment as in thermal burns

Internal ingestion or contamination

◦◦ Consider specific therapies to decrease absorption (eg, gastric lavage or activated charcoal) ◦◦ Saturated solution of potassium iodide for radioactive iodine ◦◦ Chelating agents may be used for specific radioactive metals (eg, penicillamine, ferric hexacyanoferrate)

Whole-body radiation exposure (large-dose)

◦◦ Supportive care, IVF, anti-emetics, analgesics ◦◦ Antibiotics (for infection prophylaxis) and transfusion therapy if >5 Gy exposure ◦◦ Filgrastim increases survival in hematopoietic syndrome

key fact High-voltage electrical injuries differ primarily from lightning injuries in their duration of exposure to the electrical current.

key fact Filgrastim increases survival in radiation exposure presenting with hematopoietic syndrome.

key fact A standard CXR delivers a radiation dose of 6-11 mrad (0.06-0.11 mGy) while a typical chest CT delivers a dose of 700 mrad (7 mGy).

►BIOTERRORISM ► Bioterrorism refers to the use of pathogenic microbes or toxins for inflicting harm on a large population. POTENTIAL BIOTERRORISM AGENTS include:

• Agents that are easily disseminated, result in high mortality, and require special preparedness due to their potential public health impact ◦◦ Ebola, Marburg, Lassa, Bacillus anthracis, Clostridium botulinum toxin, Yersinia pestis, variola major • Agents with moderate ease of dissemination, low mortality, and require enhanced laboratory diagnostic capacity and disease surveillance ◦◦ Ricinus communis, Rickettsia prowazekii, Staphylococcus aureus, Brucella spp., Clostridium perfringens, Salmonella spp, E coli O157:H7, Shigella, Chlamydia psittaci, Coxiella burnetii, Western equine encephalitis, Vibrio cholerae • Agents that could be engineered for widespread dissemination due to their availability and potentially high public health morbidity and mortality ◦◦ Multidrug-resistant tuberculosis, yellow fever, tick-borne encephalitis viruses


key fact In management of anthrax exposure, administration of anthrax immunoglobulin should accompany early antibiotic therapy.

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Table 6-18. Therapy After Exposure to Bioterrorism Agents Bioterrorism Agent

Clinical Presentation


B anthracis

◦◦ Inhalation anthrax (woolsorter's disease): HA, malaise, myalgia, fever +/− dry cough. Sudden respiratory distress with chest/neck edema. Widened mediastinum + pleural effusion on CXR. May progress to septic shock and death within 36 h ◦◦ Cutaneous anthrax: Small papule that progresses to a vesicle and ruptures, resulting in painless necrotic ulcer with black eschar. GI anthrax and anthrax meningitis may also occur

◦◦ Early antibiotic treatment with penicillin, doxycycline, or ciprofloxacin ◦◦ Anthrax immunoglobulin (Anthrasil) or monoclonal antibodies (obiltoxaximab or raxibacumab) may be administered

Y pestis

◦◦ Primary bubonic plague: malaise, HA, vomiting, chills, AMS, cough, abdominal/chest pain ◦◦ Primary septicemic plague: fever, vomiting, diarrhea, purpura, DIC, acrocyanosis, and necrosis. ◦◦ Primary pneumonic plague: cough, hemoptysis, CXR with bilateral alveolar infiltrates

◦◦ Isolate patient and treat with streptomycin; add IV chloramphenicol if hemodynamically unstable or meningitis

F tularensis

◦◦ Ulceroglandular form: fever, HA, cough, sore throat, vomiting, diarrhea, myalgia, chest pain, arthralgia, dyspnea, back pain, neck stiffness ◦◦ Typhoidal form: enlarged lymph nodes typically 40°C and consequent neurologic dysfunction. Classic heat stroke, or nonexertional hyperthermia, occurs when environmental heat exposure limits the ability of the body to dissipate heat. Exertional heat stroke occurs in a similar hot and humid environment but is also driven by heat production from exercise. Severe hyperthermia is also a commonly encountered adverse drug effect (see Chapter 3) and manifestation of endocrine disease (see Chapter 1) whose pathophysiology and treatment are discussed elsewhere.

Treatment Management should focus on early diagnosis, resuscitation, and initiation of rapid cooling techniques. Hypotension should be treated with boluses of IV crystalloids and not α-adrenergic agonists, as these decrease heat dissipation. Benzodiazepines may improve core body cooling, suppress agitation, and treat seizures. Both evaporative and convective cooling methods are acceptable. Common methods of cooling: • Spraying patient with water after removing their clothes, with a fan blowing on them • Ice packs • Cool IV fluids • Ice water immersion (often used in exertional heatstroke but impractical in the inpatient setting secondary to monitoring equipment) Occasionally, multi-organ failure can ensue with renal failure, DIC, and acute liver failure that may warrant transfer to a liver transplant center.


key fact As the pathophysiology of heatstroke does not involve an alteration in the hypothalamic set point, antipyretics (eg, acetaminophen, NSAIDs) have no role in management and may exacerbate lifethreatening complications such as hepatic injury or DIC.

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►►THORACIC TRAUMA Injury from trauma can be minor (eg, focal isolated wounds) or complex (with multisystem involvement). Although traumatic torso injuries are frequently viewed separately as thoracic and abdominal trauma, any trauma should be considered as a single composite entity requiring a systematic approach to management.

►GENERAL ► APPROACH TO MANAGEMENT Primary Evaluation and Management (per ATLS) AIRWAY—Initial assessment involves asking the patient his or her name, as the

ability to answer suggests mentation, phonation, and airway protection. Assess the face, mouth, oropharynx, neck, and chest for injury that may be causing airway compromise. Patients with blunt thoracic trauma should be assumed to have C-spine injury, and an immobilizing collar or manual in-line stabilization performed. If the airway is threatened, expedite airway management in a controlled fashion while assessing potential for difficult intubation and neurologic injury. Necessary equipment may include: • Video laryngoscope • Endotracheal tube introducers • Cricothyroidotomy equipment

mnemonic Assessing for difficult airway— LEMON Look – for facial or neck injury Evaluate – intraoral, mandibular, and hyoid-tothyroid distances Mallampati – calculation Obstruction/Obesity – assessment (eg, hematomas/ soft tissue edema) Neck mobility – should be limited to in-line stabilization

Figure 6-8. Anatomy for cricothyroidotomy. The vertical red line marks the correct location for the procedure. (Reproduced. By Olek Remesz (wiki-pl: Orem, commons: Orem) (Larynx external en.svg) [GFDL (http:// or CC BY-SA 3.0 (], via Wikimedia Commons)


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• • • • •

Inspect chest wall for injury Palpate for crepitus and deformity Ascultate for bilateral breath sounds CXR and bedside US Low threshold for needle decompression with large-bore angiocath (≥14 G) and/or chest tube placement as indicated for suspected pneumothorax


• • • •

Assess pulses Establish access with 2 large-bore IVs, CVC, or intraosseous line Type and cross-match blood Search for evidence of hemorrhage, and treat with transfusion, reversal of anticoagulation if relevant, and source control • Consider emergency thoracotomy if central pulses absent • Assess for nonhemorrhagic causes of shock (cardiac tamponade, tension pneumothorax) DISABILITY/NEUROLOGIC

• Glasgow Coma Scale assessment • Evaluate gross motor function and sensation to assess for spinal cord injury • Spinal immobilization with appropriate imaging as necessary EXPOSURE AND ENVIRONMENTAL CONTROL The trauma patient should be completely undressed and examined thoroughly for injury in the primary survey. Prevent hypothermia and treat if present.

Definitive Therapies Prioritize intervention based on severity of life-threatening injuries, with ability to explore chest/abdomen surgically as needed. In unresponsive/unstable patients with potential for benefit, consider emergent thoracotomy. Ultrasound, peritoneal lavage, and CT are important adjuncts in assessing need for laparotomy. Consider specific measures targeting correction of thoracic causes of hypoxemia and hypoperfusion.

►FLAIL ► CHEST Flail chest results from fracture of multiple adjacent ribs (two sites on each rib) or on both sides of the sternum, resulting in paradoxical movement of the freefloating portion of the chest wall during spontaneous breathing.


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Table 6-20. Management of Flail Chest Severity


Large flail + severe hypoxemia

◦◦ Intubation and mechanical ventilation ◦◦ Ipsilateral chest tube placement to prevent tension pneumothorax ◦◦ Initiate ventilator weaning at resolution of gas exchange abnormalities from pulmonary contusion

Flail, no hypoxemia

◦◦ Supplemental oxygen ◦◦ Analgesia: IV opiates, consider epidural/intercostal blockade ◦◦ If thoracotomy needed, consider concurrent fracture reduction and plating

mnemonic Evaluation of trauma patient— ABCDE Airway and appropriate c-spine stabilization Breathing and ventilation Circulation and control hemorrhage Disability Exposure and environmental control

Figure 6-9. Flail chest. (a) shows a 3-D reconstruction of a CT scan with red arrows pointing to rib fractures; (b) shows the paradoxical motion of respirations in the setting of flail chest; (c) chest x-ray shows flail chest with associated right sided pulmonary contusion and subcutaneous emphysema. (Reproduced, James Heilman, MD (Own work) [CC BY-SA 4.0 ( by-sa/4.0)], via Wikimedia Commons; Lyman A. Brewer III, M.D., and Thomas H. Burford, M.D. [Public domain], via Wikimedia Commons; Karim ( [CC BY-SA 3.0 (https://], via Wikimedia Commons)


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►PULMONARY ► CONTUSION Pulmonary contusion is characterized by lung hemorrhage and edema after substantial blunt or penetrating chest trauma, without any obvious pulmonary laceration (Figure 6-10 and Table 6-21).

Figure 6-10. Chest CT depicting pulmonary contusion in right lung.

(Reproduced, for the original image [CC BY-SA 3.0 (], via Wikimedia Commons)

Table 6-21. Pulmonary Contusion Clinical/Physiologic Manifestations ◦◦ Hypoxemia +/− hypercarbia ◦◦ Respiratory distress ◦◦ Alveolar hemorrhage/ hemoptysis ◦◦ Bronchospasm ◦◦ Reduced surfactant production and mucus clearance ◦◦ Lung parenchymal destruction ◦◦ V/Q mismatch ◦◦ Loss of lung compliance




◦◦ Chest CT: shows opacification and subpleural sparing ◦◦ If CT not possible, US/ DPL may help exclude concurrent abdominal injury ◦◦ TEE helps exclude aortic injuries

◦◦ Supportive care ◦◦ ATLS trauma protocols ◦◦ Early selective bronchial intubation/ bronchial blocker may be needed ◦◦ Pulmonary toilet ◦◦ Regional analgesia ◦◦ Mechanical ventilation as needed ◦◦ Consider ECMO in refractory hypoxemia

◦◦ Pneumonia ◦◦ ARDS ◦◦ Long-term sequelae (eg, disabling dyspnea, PFT impairment)

ARDS = acute respiratory distress syndrome; DPL = diagnostic peritoneal lavage, ECMO = extracorporeal membrane oxygenation; PFT = pulmonary function test; TEE = transesophageal echocardiography; US = ultrasound; V/Q = ventilation/perfusion.


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►HEMOTHORAX ► AND GREAT VESSEL INJURY Blunt or penetrating traumatic injury with disruption of great vessels or laceration of an intrathoracic systemic artery may result in hemothorax and should be diagnosed promptly and treated.

Clinical Features of Massive Hemothorax • • • •

Hypotension from blood loss Hypoxemia from lung compression and collapse Dullness to percussion, reduced air entry, and mediastinal shift Central venous pressure (CVP) usually low due to hemorrhage but may be high if obstruction to venous return (tension physiology)

DIAGNOSIS—Drainage of blood ~2L or 100 mL/h via large-bore chest tube

confirms diagnosis of massive hemothorax and should prompt surgical intervention. SPECIFIC THERAPY

• • • •

Surgical intervention (usually via posterolateral incision) Evacuation of pleural space and identification of bleeding vessel Lung resection may be necessary Clamping aorta and bypassing the laceration with a graft prosthesis or preheparinized shunt to facilitate aortic repair may be necessary

►PNEUMOTHORAX, ► TRACHEOBRONCHIAL LACERATION, RUPTURE, AND AIRWAY INJURY Tension Pneumothorax Tension pneumothorax results from traumatic chest wall or lung injury with gas entry into the pleural space that is unable to exit. This leads to an increase in thoracic pressures that can result in both respiratory failure and cardiovascular collapse. PATHOPHYSIOLOGY

• • • • •

Initial ipsilateral lung atelectasis Impairment of gas exchange/ventilation Mediastinal shift Contralateral lung compression with ventilatory compromise Impairment of venous return, leading to impaired cardiac output


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• • • • • • • •

History of thoracic trauma Dyspnea/tachypnea Ipsilateral reduction in air entry Contralateral tracheal shift Hypoxemia Elevated jugular venous pressure (JVP) Hypoperfusion Pulsus paradoxus


• Immediate large-bore needle decompression of pleural cavity (typically second intercostal space, mid-clavicular line) • Chest tube connected to suction

Figure 6-11. Graphical illustration of pneumothorax.

Reproduced courtsey of staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. (Own work) [CC BY 3.0 ( by/3.0)], via Wikimedia Commons


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Open Pneumothorax In open pneumothorax, traumatic chest wall injury causes pleural space to communicate freely with the external environment, permitting gas entry into pleural space with respiration. PATHOPHYSIOLOGY

• • • •

key fact In massive hemothorax, the CVP is usually low but may be high if obstruction to venous return exists.

Mediastinal shift with initial ipsilateral lung compression Impairment of gas exchange Blood flow obstruction from vascular kinking Contralateral lung compression with ventilatory compromise


• • • • • • • • •

History of thoracic trauma Visible chest wall injury Audible noise as air enters pleural cavity Dyspnea/tachypnea Ipsilateral reduction in air entry Hypoxemia Contralateral tracheal shift Elevated JVP Hypoperfusion


• Occlude open wound with impermeable dressing • If open wound occlusion not feasible, consider intubation and positive pressure ventilation • Surgical repair of site of injury • Large-bore chest tube (32-36Fr) through separate site and connect to suction

Massive Pneumothorax, Tracheobronchial Laceration, Rupture, and Airway Injury Traumatic pneumothorax refractory to chest tube drainage with persistent hypoxemia, hypotension, and hemoptysis suggests tracheobronchial laceration. TREATMENT

• • • • •

Respiratory support with 100% FiO2 and mechanical ventilation Ensure chest tubes are fully functional Consider bronchoscopy to identify laceration site Consider single-lung ventilation of contralateral lung Prompt transfer to OR for thoracotomy and direct repair of laceration or lung resection


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►FOREIGN ► BODY ASPIRATION Aspiration of foreign bodies into the tracheobronchial tree can be associated with significant morbidity and mortality. Risk factors include traumatic injury with loss of consciousness, dental procedures, older age, neurological dysfunction, altered mental status, impaired airway reflexes, and use of alcohol or sedatives. CLINICAL FEATURES

• • • • • •

Choking sensation Persistent cough Chest discomfort Fever Dyspnea Focal wheezing


• Respiratory support for severe cases (bag valve mask ventilation vs intubation with mechanical ventilation) • Consider emergent tracheotomy or cricothyroidotomy (if ventilation unsuccessful due to asphyxiation from proximal airway obstruction) • Diagnostic evaluation with CXR +/− CT may reveal foreign body, atelectasis, hyperlucency, or consolidation • Flexible bronchoscopy can be diagnostic and therapeutic • Rigid bronchoscopy if flexible bronchoscopy is unsuccessful

►BLUNT ► MYOCARDIAL INJURY Blunt cardiac injuries occur commonly after chest trauma and range in severity from mild arrhythmia to myocardial rupture. Common causes include traffic accidents, crush injuries, falls, and traumatic injuries from contact sports. CLINICAL FEATURES

• Potentially asymptomatic • Chest pain • Beck’s triad (muffled heart sounds, hypotension, elevated JVP), suggesting cardiac tamponade • Pallor from hemorrhage • Shock TREATMENT

• • • • • •


Supportive care Serial clinical assessment and imaging of effusions Emergent pericardiocentesis for tamponade Pericardial window Surgical suturing of myocardium (cardiorrhaphy) to repair cardiac chambers Mechanical support such as balloon pump (if hemodynamically unstable)

key fact A traumatic blow to the heart that occurs just before the onset of the T wave in a healthy individual often results in catastrophic ventricular fibrillation (Commotio cordis) and may be prevented by using chestprotective gear during contact sports.

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►►ABDOMINAL TRAUMA Similar to thoracic trauma, patients with obvious abdominal trauma must be evaluated for injury to the abdominal structures but must also undergo a survey for nonabdominal injuries. Abdominal bleeding is common and must be considered in any trauma patient, regardless of symptoms. This evaluation is emergent in patients with hemodynamic instability despite management of cardiothoracic disease.

►BLUNT ► ABDOMINAL INJURY Table 6-22. Pathophysiologic Mechanisms of Blunt Abdominal injury Type of Injury



Rupture of hollow viscus

Sudden elevation in intraabdominal pressure

Transverse colon injury from lap-belt use without shoulder attachment in vehicular passenger injury

Crushed abdominal viscera

Blunt force to anterior abdominal wall, resulting in sudden visceral compression

Hepatic/splenic laceration/ fracture; delayed splenic rupture

Solid organ laceration at peritoneal attachments or vascular pedicles

Sudden deceleration causing shear forces

Renovascular injury

Laceration of abdominal or pelvic viscus

Bony injury from fractured ribs or bony pelvis

Splenic laceration, bladder perforation

Evaluation and Management of Blunt Abdominal Injury Patients at risk for intra-abdominal injury should be evaluated with an approach that has a high level of suspicion (assume there is an injury), focuses on diagnosis simultaneous with preparation for intervention, and accounts for the patient’s overall clinical status. EVALUATION—Exam findings concerning for injury include the nature of injury

(pelvic fracture, seatbelt sign), rebound, guarding, rigidity, ecchymosis, and persistent hypotension.

Labs suggesting intra-abdominal injury include hematocrit 20 cm H2O, peak airway pressures > 40 cm H20, SaO2 8 h or unknown duration ◦◦ Uncooperative/unconscious—compartment pressure >30 mm Hg ◦◦ Hypotensive—compartment pressure >20 mm Hg

►►TRANSPLANT CRITICAL CARE Solid organ transplant recipients often need ICU care, especially in the postoperative period. Complications may be surgical (mechanical), infectious, related to graft rejection, or related to adverse effects of antirejection medications.

►POSTOPERATIVE ► COURSE The postoperative course for solid organ transplant is variable and depends on the type of organ transplanted and severity of illness of the recipient before surgery.

Liver Transplant

key fact Normal myocyte metabolism requires a 5–7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4–6 mm Hg.

key fact Urgent surgical intervention is required when compartmental pressures are >30 mm Hg, as nerve injury and muscle infarction can occur if left untreated for more than 6–10 h.

key fact Tibial fractures are the most common cause of acute compartment syndrome.


• Length of stay usually related to severity of illness before surgery • Bleeding risk is highest postop because of residual coagulopathy • Signs of functioning graft ◦◦ Golden-brown bile production ◦◦ Clotting factors normalize within 3 d ◦◦ Encephalopathy resolves ◦◦ Liver enzymes decrease


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• Extubated in recovery area and sent to non-ICU bed

Kidney-Pancreas Transplant ICU COURSE

• • • •

Tight glucose control and electrolyte monitoring Metabolic acidosis from pancreatic HCO3 secretion into bowel or bladder Pancreatic rest with insulin drip May take days for pancreatic graft to fully function

Heart Transplant ICU COURSE

• Depressed cardiac function requiring inotropic support • Denervated heart may require pacing or isoproterenol for 2-3 d • Extubation typically within 24 h

Lung Transplant ICU COURSE

• Complications related to cardiopulmonary bypass if used • Single vs bilateral lung transplant ◦◦ Typically more postop complications with bilateral lung transplant ◦◦ Native lung may hyperventilate after single-lung transplant for COPD • Pulmonary toilet important given loss of cough reflex • Pulmonary edema common due to vascular manipulation and disruption of lymphatic drainage • Primary graft dysfunction (see below) • Extubation typically within 24-48 h

►IMMUNOSUPPRESSION ► Immunosuppression is needed to prevent rejection of the transplanted organ. Most solid organ transplants rely on a combination of immunosuppressive medications to prevent high doses and toxicity from a single agent.


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Table 6-29. Transplant Immunosuppression Agent

Mechanism of Action

Adverse Effects


Polyclonal antibodies against T and B cells

Leukopenia, thrombocytopenia, serum sickness, infusion reactions (cytokine release syndrome, anaphylaxis)

IL-2 RAs (basiliximab/daclizumab)

Antagonize IL-2-induced T-cell proliferation

Relatively well tolerated, with rare infusion reactions


Decreases T-cell activation and proliferation via inhibition of calcineurin-dependent induction of IL-2 expression

Nephrotoxic, neurotoxic, TMA, HLD, HTN, hypomagnesemia, hyperkalemia, GI disturbance, gingival hyperplasia, hypertrichosis


Decreases T-cell activation and proliferation via inhibition of calcineurin-dependent induction of IL-2 expression

Nephrotoxic, neurotoxic, TMA, HLD, HTN, hypomagnesemia, hyperkalemia, GI disturbance, hyperglycemia


Antagonizes purine metabolism and DNA synthesis

Pancytopenia, hepatotoxicity, pancreatitis


Inhibits the de novo pathway of purine synthesis

Pancytopenia, diarrhea, abdominal pain, nausea


Decreases inflammation through multiple mechanisms

Hyperglycemia, weight gain, hyperlipidemia, osteoporosis, myopathy, insomnia, cataracts


Decreases cell cycle progression via inhibition of mTOR-dependent cyclin D1 synthesis

Pancytopenia, anastomotic dehiscence/ poor wound healing, interstitial pneumonitis, HLD, arthralgia, LE edema, acne, stomatitis



ALG = anti-lymphocyte globulin; ATG = anti-thymocyte globulin; GI = gastrointestinal; HLD = hyperlipidemia; HTN = hypertension; IL-2 = interleukin 2; LE = lower extremity; MMF = mycophenolate mofetil; mTOR = mammalian target of rapamycin; RA = receptor agonist; TMA = thrombotic microangiopathy.

►COMPLICATIONS ► OF SOLID ORGAN TRANSPLANT Surgical Complications Table 6-30. Surgical Complications of Solid Organ Transplant Solid Organ Transplanted Lung

Mechanical Complication Hemorrhage ◦◦ Mediastinum or pleural ◦◦ CF with higher rate of bleeding Anastomoses ◦◦ Airway dehiscence, stenosis, bronchomalacia Vascular ◦◦ Primary graft dysfunction (ischemia reperfusion injury)


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Surgical Complications of Solid Organ Transplant Liver

Hemorrhage ◦◦ First 2 d related to persistent coagulopathy ◦◦ Necrosis of vascular anastomosis ◦◦ GI: stress ulcers or portal hypertension Vascular ◦◦ HAT, HVT, PVT Biliary ◦◦ Bile leaks (ischemic injury to bile duct with subsequent sepsis) ◦◦ Bile obstruction (kinked bile duct or drainage tube, strictures, dysfunction of sphincter of Oddi)


◦◦ Renal artery thrombosis, renal vein thrombosis, urine leaks, and lymphoceles (all rare)


◦◦ Urethral stricture ◦◦ Hematuria ◦◦ Duodenal perforation ◦◦ Vascular thrombosis


See complications of cardiac surgery


Hemorrhage ◦◦ Mediastinum or pleural ◦◦ CF with higher rate of bleeding Anastomoses ◦◦ Airway dehiscence, stenosis, bronchomalacia Vascular ◦◦ Primary graft dysfunction (ischemia reperfusion injury)

CF = cystic fibrosis; GI = gastrointestinal; HAT = hepatic artery thrombosis; HVT = hepatic vein thrombosis; PVT = portal vein thrombosis.


dysfunction is measured by a grading system. Primary graft dysfunction is characterized by worsening hypoxemia with diffuse pulmonary opacities in the transplanted lung that develops in first 72 h posttransplant. Table 6-31. Primary Graft Dysfunction Grade


Radiographic Evidence of Pulmonary Edema











100 mm Hg

◦◦ IV nitroglycerin ◦◦ Nitropaste β-blockers: ◦◦ Metoprolol

Titrate to heart rate of 55-60 bpm, contraindicated in decompensated HF

flash card Q. ST-segment elevation in leads I, aVL, V5, and V6 are associated with occlusion of which coronary artery or arteries? A. Circumflex or left anterior descending artery

flash card Q. ST-segment elevation in leads aVF, II, and III are associated with occlusion of which coronary artery or arteries? A. Right coronary artery most commonly, circumflex artery less commonly

flash card Q. Which leads on the EKG provide the best assessment of posterior wall ischemia? A. V7, V8, and V9, additional leads not commonly performed in a standard 12lead EKG

◦◦ 5 mg IV q5min × 3, then 25 mg po q6h

GP IIB/IIIa inhibitors:

Best data for eptifibatide and tirofaban

◦◦ Abciximab (ReoPro®) ◦◦ Eptifibatide (Integrilin®) ◦◦ Tirofiban (Aggrastat®)

◦◦ 0.25 mg/kg IV, then 0.125 µg/kg/min ◦◦ 180 µg/kg IV, then 2 µg/kg/min ◦◦ 0.4 µg/kg/min × 30 min, then 0.1 µg/kg/min

bid = twice a day; GP = glycoprotein; HF = heart failure; IV = intravenous; po = per os (by mouth); PTT = partial thromboplastin time; q5min = every 5 minutes; q6h = every 6 hours; qd = every day; SBP = systolic blood pressure; SC = subcutaneous.

mnemonic "MONA greets chest pain at the door" Morphine Oxygen Nitrates

Following acute medical therapy, treatment is focused on reducing risk for recurrence via chronic medical management and lifestyle modifications (Table 7-2).



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Table 7-2. Post-ACS Risk Reduction Strategies Intervention



75 to 160 mg daily, indefinitely


75 mg daily for 30 d to 1 yr Indicated for 1 yr after drug-eluting stent


Indicated for all patients post-MI

ACE inhibitor

Indicated for all patients post-MI, especially if LVEF 110 mm Hg) ◦◦ Traumatic or prolonged (>10 min) CPR ◦◦ Major surgery within 3 wk ◦◦ Recent internal bleeding or active peptic ulcer disease ◦◦ Pregnancy ◦◦ Noncompressible vascular puncture sites ◦◦ Current use of anticoagulants

CPR = cardiopulmonary resuscitation; DBP = diastolic blood pressure; HTN = hypertension; SBP = systolic blood pressure.

EVIDENCE—The Fibrinolytic Therapy Trialists’ Collaborative Group combined

analysis of >60,000 patients in 22 trials of fibrinolytic therapy vs medical management. They reported the following reductions in mortality in patients receiving fibrinolytics: • 30 deaths per 1000 patients when administered in first 6 h • 20 deaths per 1000 patients when administered within 7-12 h • 10 per 1000 when administered within 13-18 h

The estimated risk for hemorrhagic stroke in patients receiving fibrinolytics is 4 per 1000 patients treated, including two likely deaths and one severely disabling event.


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• Alteplase: 100 mg over 90 min, followed by unfractionated heparin bolus 60 U/kg (max 4000 U), then 12 U/kg/h drip • Tenecteplase: 30-50 mg bolus, followed by enoxaparin 30 mg bolus, then 1 mg/kg q12h • Reteplase: 10 mg bolus × 2, followed by unfractionated heparin bolus 60 U/kg (max 4000 units), then 12 U/kg/h drip

Rescue PCI Rescue PCI refers to early angiography with possible intervention in patients who have already received fibrinolytic therapy. It is indicated in patients who fail to reperfuse with fibrinolytics alone, as evidenced by persistent symptoms and STsegment elevation. Rescue PCI is also indicated in patients with high-risk features, including: • • • • •

Anterior myocardial infarction Right ventricular (RV) infarction Cardiogenic shock Decompensated congestive heart failure (CHF) Recurrent ventricular arrhythmias

Additional Medical Therapies In addition to reperfusion, a number of medical therapies are indicated for the treatment of STEMI. ANTITHROMBINS—Patients undergoing reperfusion with fibrinolytics should receive subsequent anticoagulant therapy for a minimum of 48 h. Anticoagulant regimens with established efficacy:

• Unfractionated heparin • Enoxaparin • Fondaparinux THIENOPYRIDINES are selective, irreversible adenosine diphosphate receptor/ P2Y12 inhibitors used for their antiplatelet activity, including:

• Clopidogrel • Prasugrel • Ticlopidine The CLARITY TIMI-28 trial randomly assigned patients with STEMI treated with fibrinolytic therapy to 300 mg load of clopidogrel vs placebo. Clopidogrel load resulted in significant reduction in thrombolysis in myocardial infarction (TIMI) 0/1 flow, death, and re-infarction, with no increase in major bleeding.


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β-BLOCKERS—Oral β-blocker therapy should be initiated in the first 24 h for all patients except patients with:

• Signs of CHF/low cardiac output • Increased risk for cardiogenic shock • Relative contraindication to administration, including active heart block or uncontrolled reactive airway disease ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS should be initiated in all patients with STEMI with left ventricular ejection fraction (LVEF) 3 risk factors for CAD Prior coronary stenosis >50% ST deviation on admission EKG >2 anginal episodes within 24 h Elevated cardiac biomarkers ASA use in last 7 d


Rate of Composite End Point, %

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50 40 30 20 10 0

0/1 Test Cohort No. (%)

2 3 4 5 No. of Risk Factors 85













ASA = aspirin; CAD = coronary artery disease; EKG = electrocardiogram.

Figure 7-4. Rate of all-cause mortality, MI, and need for urgent revascularization through 14 d, based on TIMI risk score.

(Reproduced with permission from Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/ non-ST elevation MI: A method for prognostication and therapeutic decision-making. JAMA. 2000;284:835-842.)

Management Options Early invasive strategy • Planned coronary angiography (day 1-2) • Revascularization (PCI or coronary artery bypass graft [CABG]) Conservative strategy • Optimal medical therapy • Stress testing • Angiography if recurrent ischemia or high-risk stress test The TACTICS TIMI 18 trial randomly assigned patients to an early invasive strategy vs an early conservative strategy. The early invasive strategy reduced cardiac events at 30 d and 6 mo in intermediate- and high-risk patients. The results of this trial have been used to guide choice of management strategy (Table 7-4).


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Table 7-4. Invasive Strategy

Conservative Strategy

◦◦ Recurrent/refractory ischemia ◦◦ Elevated troponin/ST segment deviation ◦◦ CHF/MR ◦◦ Hemodynamic instability ◦◦ Recent PCI/prior CABG ◦◦ LVEF 40% of myocardium involved • Patients with preexisting cardiac dysfunction The SHOCK trial compared early PCI or CABG to a strategy of aggressive initial medical stabilization (fibrinolytics, inotropes, vasopressors, and intra-aortic balloon pump [IABP]) in patients presenting with cardiogenic shock and found: • 30-d survival not significantly different • Significantly increased 6-mo survival in revascularized patients

Mechanical Complications FREE WALL RUPTURE is a devastating complication leading to tamponade and death. It typically occurs within 3 wk of initial infarction, with most ruptures occurring within 3-5 d. ACUTE VENTRICULAR SEPTAL DEFECT (VSD)

• Presentation: sudden deterioration (hypotension, pulmonary edema, new harsh murmur) in a previously stable patient 3-7 d post-MI • Risk factors: first infarct, large left anterior descending artery infarct, single-vessel disease • Characterized by classic step-up in oxygenation on cardiac catheterization

flash card Q. A 67-yr-old man is postop day 4 following primary PCI of a 90% LAD lesion. His course was uncomplicated, but he now has mean arterial pressure (MAP) of 47 mm Hg and is requiring 5 L nasal cannula to maintain an oxygen saturation >90%. An oxygen saturation run of his pulmonary artery catheter yields a step-up of 7 between the right atrium (RA) and PA. What is the recommended management? A. Surgical consultation for repair of a ventricular septal defect.


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(high PA saturation compared with superior vena cava [SVC] saturation) • Surgical emergency, mortality >70% ACUTE MITRAL REGURGITATION (MR)—Risk increased with inferior-posterior MI. It presents with new pansystolic murmur and pulmonary edema. Treatment is afterload reduction and surgical repair of ruptured papillary muscle(s). RV INFARCTION is a complication of inferior and inferoposterior MI. It presents with triad of hypotension, elevated jugular venous pressure (JVP), and clear lungs. Treatment is fluid resuscitation, inotropic agents, and avoidance of preloadreducing agents.

►COCAINE-RELATED ► ISCHEMIA ACS is the most common cardiac complication of cocaine use and can occur regardless of route of ingestion. Cocaine inhibits norepinephrine uptake and promotes thrombus formation, resulting in: • Increased myocardial oxygen demand • Coronary artery vasoconstriction and spasm • Coronary artery thrombosis Most cocaine-associated MIs occur in the absence of high-grade coronary artery disease.

►►ARRHYTHMIAS Arrhythmias are common in the ICU, occurring in up to 75% of patients in some series. Approximately 12% of patients in the ICU develop sustained arrhythmias.

►CARDIAC ► CONDUCTION SYSTEM Figure 7-5 depicts the cardiac conduction system. Electrical signals arise in the sinoatrial (SA) node and stimulate the atria to contract. They then travel to the atrioventricular (AV) node, which is located in the interatrial septum. After a delay, the stimulus diverges and conducts through the left and right bundles of His to the respective Purkinje fibers on each side of the heart.


flash card Q. A patient with a history of cocaine use presents with chest pain and is diagnosed with an NSTEMI. The management of this patient differs from the management of other ACS due to the avoidance of which drug class? A. Beta-blockers. The management of ACS with recent cocaine use is managed with morphine, oxygen, nitrates, aspirin, and benzodiazepines to control BP and heart rate. Beta-blockers are avoided due to the risk of unopposed α-adrenergic stimulation.

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Figure 7-5. Conduction system of the heart. (Reproduced courtesy of Wikicommons.)

►NEURAL ► AND HUMORAL REGULATION Cardiac activity is regulated by both neural and humoral factors: • Neural factors (Table 7-5): sympathetic adrenergic and parasympathetic cholinergic branches of the autonomic nervous system • Humoral factors: ◦◦ Catecholamines ◦◦ Renin-angiotensin-aldosterone system (RAAS) ◦◦ Vasopressin (antidiuretic hormone) ◦◦ Atrial natriuretic peptide ◦◦ Endothelin Table 7-5. Neural Regulation of Cardiac Conduction System Vagus Nerve (Parasympathetic)

Sympathetic Nerves

◦◦ Slows pacemaker cells ◦◦ Slows sinus node ◦◦ Slows AV node ◦◦ Minimal effect on His Purkinje system

◦◦ Accelerate pacemaker cells ◦◦ Facilitate AV node conduction ◦◦ Minimal effect on His Purkinje system

AV = atrioventricula.

►BRADYARRHYTHMIAS ► Many causes of bradycardia are considered "benign," as they are generally well tolerated (eg, sinus arrhythmia and sinus bradycardia with junctional escape); however, even "benign" bradycardia has the potential to cause hemodynamic instability in critically ill patients.


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Sinus Node-Mediated Bradycardia Table 7-6 lists causes of sinus node-mediated bradycardia. Table 7-6. Causes of Sinus Node-Mediated Bradycardia Intrinsic


◦◦ Sinus node dysfunction ◦◦ Athletic heart ◦◦ MI (SA node usually supplied by RCA or LCx) ◦◦ Fibrodegenerative changes: surgery, collagen vascular disease, infiltrative disease

◦◦ Vagal-mediated ▪▪ Situational: micturition, cough ▪▪ Positional ▪▪ Carotid sinus hypersensitivity ◦◦ Metabolic ▪▪ Hypoxemia ▪▪ Hypothermia ▪▪ Electrolyte abnormalities ◦◦ Sepsis ◦◦ Elevated ICP

ICP = intracranial pressure; LCx = left circumflex artery; MI = myocardial infarction; RCA = right coronary artery; SA = sinoatrial.

Atrioventricular (AV) Block Atrioventricular (AV) block is an unexpected delay or block of an impulse traveling from the atrium to the ventricle. Atrioventricular block seen during premature atrial contractions or atrial tachycardia is common and may not represent nodal disease. • First-degree AV block: PR interval is greater than upper limits of normal for age • Second-degree AV block, Mobitz I: progressive lengthening of the PR interval followed by a nonconducted P wave (Figure 7-6) • Second-degree AV block, Mobitz II: non-conducted P wave with no progressive lengthening of the PR in preceding beats (Figure 7-6); pacemaker indicated • Third-degree AV block (complete AV block): absence of communication of electrical activity between atria and ventricles (Figure 7-7); pacemaker indicated


key fact Carotid sinus hypersensitivity is characterized by dizziness or syncope with head turning or while wearing tight collars. It can be assessed by performing carotid sinus massage (after checking for bruits). If a pause of >3 sec occurs, the test is positive.

ATS Review of the Critical Care Boards | CHAPTER 7

Figure 7-6. Second-degree AV block. Mobitz I is characterized by progressive lengthening of PR segment followed by a nonconducted P wave (top tracing). Mobitz II is characterized by a consistent PR interval with intermittent nonconducted P waves (middle tracing). Mobitz I cannot be distinguished from Mobitz II in cases of 2:1 block (bottom tracing). (Reproduced courtesy of Wikicommons.)

Figure 7-7. Complete AV block with junctional escape. There is no consistent PR interval, as the P waves are not conducted. The QRS complexes are the result of junctional escape activity. (Reproduced courtesy of Wikicommons.)


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AV Block vs His Bundle Block Cardiac conduction may also be disrupted below the AV node at the level of the His bundle. Table 7-7 compares characteristics of AV node block and His bundle block. Table 7-7. AV Node vs His Bundle Block AV Node





Exercise response



Atropine response



Carotid massage response



Isoproterenol response



AV = atrioventricular.

►TREATMENT ► OF BRADYCARDIA Treatment of bradycardia depends on presence of symptoms and hemodynamic stability. • Asymptomatic patients: treatment not indicated • Hemodynamically unstable patients: ◦◦ Atropine 0.5 mg IV q3-5min (max 3 mg) ▪▪ Use with caution in setting of MI, as increased heart rate may worsen ischemia ▪▪ In heart transplant, may be ineffective (denervated heart) or may cause paradoxical worsening of bradycardia or heart block ◦◦ If bradycardia and symptoms persist, IV infusions (Table 7-8) and/or temporary pacing indicated • Hemodynamically stable patients: evaluate for systemic conditions associated with bradyarrhythmias In addition, the following recommendations apply to all patients with bradycardia: • Remove offending medications • Correct metabolic derangements • Avoid triggers with vagal mediated responses Table 7-8. Infusions to Treat Bradycardia Medication



2-10 µg/min


2-10 µg/min


3 mg IV followed by 3 mg/h


2-10 µg min

*Used in setting of β-blocker or calcium channel overdose.


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►BRADYCARDIA ► AFTER ACUTE MYOCARDIAL INFARCTION (AMI) A variety of bradyarrhythmias may occur following AMI, including: • Sinus bradycardia—due to increased vagal tone in acute period following inferior MI • First-degree AV block • Second-degree AV block ◦◦ Majority type I ◦◦ Type II usually infranodal ◦◦ Associated with wide QRS • Third-degree AV block ◦◦ May be transient with inferior MI ◦◦ Not a risk factor for mortality Atropine and/or temporary pacing should be considered for: • • • •

Symptomatic bradycardia Hypotension Sinus pauses >3 sec Heart rate 100 QRS < 0.12

QRS > 0.12

R-R Intervals

R-R Intervals

Irregular MAT A-fibrillation


Sinus Tachycardia A-flutter or fibrilation with fixed AV block


Regular VTach

SVT with prolonged AV conduction

Irregular SVT with prolonged AV conduction

AVNRT AV = atrioventricular; AVNRT = atrioventricular nodal reentrant tachycardia; MAT = multifocal atrial tachycardia; R-R = R wave to R wave; SVT =supraventricular tachycardia.

Figure 7-8. Classification of tachyarrhythmias. (Courtsey of Dr. Jason Poston)


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►NARROW ► COMPLEX TACHYARRHYTHMIAS Atrial Fibrillation (AF) EKG shows classic fibrillation or F waves (Figure 7-9). TREATMENT—Acute treatment of atrial fibrillation (AF) is rate control or cardioversion. Rate- and rhythm-control strategies improve symptoms, but neither has been conclusively shown to improve survival compared with the other. Patients with AF may also benefit from anticoagulation.

Figure 7-9. Atrial fibrillation at a rate of 150 bpm. Note the irregular R-R intervals and absence of regular P waves. (Reproduced courtsey of James Heilman, MD. via Wikicommons)

RATE CONTROL—Choice of rate control agent depends on presence of underlying

heart failure (HF) or accessory pathways.

• No HF or accessory pathway: β-blockers, calcium channel blockers, +/− digoxin • HF: amiodarone, digoxin (not as effective in critically ill patients) • Accessory pathway present: amiodarone, procainamide, ibutilide RHYTHM CONTROL (CARDIOVERSION) can be achieved by pharmacologic or

nonpharmacologic means.

• Pharmacologic ◦◦ Amiodarone ◦◦ Ibutilide (note: 4% risk for torsades de pointes; avoid in patients with low LVEF) ◦◦ Procainamide • Synchronized direct current cardioversion (DCCV): indicated for symptomatic or hemodynamically unstable patients when pharmacologic management is ineffective


key fact In the ARISTOTLE trial, patients with AF taking digoxin had an increased risk for death, whether or not they had HF, and the risk increased with higher levels of digoxin in the bloodstream.

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◦◦ Start with 200 J (mono or biphasic), synchronized ◦◦ Pretreatment with antiarrhythmic may increase success ◦◦ Contraindicated in digoxin toxicity ANTICOAGULATION—Patients with new-onset (or unknown duration) AF may benefit from anticoagulation, as AF lasting >48 h is associated with an increased risk for thromboembolism due to thrombus formation in the left atrium.

For AF lasting >48 h • Three weeks of oral anticoagulation prior to attempt at cardioversion; continue anticoagulation for an addition 4 wk if cardioversion is successful OR • Transesophageal echocardiogram to exclude thrombus prior to attempt at cardioversion; continue anticoagulation for an additional 4 wk if cardioversion is successful For AF lasting 3 P-wave morphologies (Figure 7-11) RISK FACTORS—Cor pulmonale, coronary artery disease, history of MI,

hypokalemia, digoxin toxicity.

TREATMENT—Address underlying cause. In decompensated patients, rate control

or pharmacologic cardioversion can be attempted. Direct current cardioversion is not effective.

Figure 7-11. Multifocal atrial tachycardia. Arrows indicate different P-wave morphologies. (Reproduced courtesy of Wikicommons.)

Atrioventricular Node-Dependent Tachycardia Atrioventricular Nodal Reentrant Tachycardia (AVNRT)—Narrow-complex tachycardia resulting from abnormal electrical conduction through dual electrical pathways in the AV node (Figure 7-12). The most common form of AVNRT involves anterograde conduction through the slow AV nodal pathway followed by immediate retrograde conduction through the fast AV nodal pathway. Uncommonly, the reentry circuit can be reversed such that the fast AV nodal pathway is the anterograde limb and the slow AV nodal pathway is the retrograde limb.


ATS Review of the Critical Care Boards | CHAPTER 7


ATRIA ALPHA PATHWAY • Slow Conduction • Short Prefactory Period |

BETA PATHWAY • Fast Conduction • Long Prefactory Period

Time to be able to conduct agan


Figure 7-12. Dual electrical pathways in the AV node provide the substrate for AVNRT. In the most common form of AVNRT, anterograde conduction occurs down the slow (α) pathway followed by retrograde conduction up the fast (β) pathway. In "uncommon AVNRT," the reentry circuit is reversed. (Reproduced from Open Osmosis website. Accessed August 15, 2017.)

EKG (see Figure 7-13)

• Heart rate =150-200 bpm • P wave buried in or following the QRS complex (retrograde P waves)

Figure 7-13. EKG tracing showing AVNRT. Retrograde P waves are highlighted in yellow. (Reproduced courtesy of Wikicommons.)


• • • •

Vagal maneuvers AV nodal blockers (adenosine) Calcium channel blockers β-blockers


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• Antiarrhythmics (digoxin, amiodarone, procainamide) • DCCV • Atrial or ventricular pacing ATRIOVENTRICULAR REENTRANT TACHYCARDIA (AVRT)—In contrast to AVNRT

(which involves a reentrant circuit within the AV node itself), AVRT is caused by a reentrant circuit involving the normal AV conduction system and a pathologic AV accessory pathway. Differences in the conduction time and refractory period between the two circuits can lead to reentry and subsequent tachycardia. • In orthodromic AVRT, anterograde conduction occurs down the normal AV pathway, resulting in a narrow QRS complex. Treatment is similar to that of AVNRT • In antidromic AVRT, anterograde conduction occurs down an accessory pathway and results in a widened QRS complex. Nodal blocking agents should be avoided in these patients, as they can make the tachyarrhythmia worse. Treatment of choice is procainamide EKG findings include a heart rate of 150-250 bpm (slightly faster than AVNRT) and evidence of pre-excitation with δ wave. WOLFF-PARKINSON-WHITE (WPW) SYNDROME—Congenital syndrome in which

patients have an accessory pathway that bypasses the normal AV node.

• Associated with congenital heart disease • Patients at risk for a variety of tachyarrhythmias, including AVRT and AF with rapid ventricular conduction • Risk for sudden death is 1 per 1000 patient-yr: often due to AF with a rapid ventricular response exceeding 200 bpm Treatment of tachyarrhythmias associated with WPW syndrome includes: • • • •

DCCV (when unstable) Chemical cardioversion with amiodarone or ibutilide Rate control with procainamide plus β-blockers Avoidance of AV nodal blockers (digoxin, calcium channel blockers, or β-blockers), as single agents as this can worsen arrhythmias • Definitive treatment of choice is radiofrequency catheter ablation of accessory pathway

Differential Diagnosis of Narrow-Complex Tachyarrhythmias A number of characteristics can be helpful in distinguishing narrow-complex tachyarrhythmias (Table 7-9).


key fact Single-agent AV nodal blockers should be avoided in the management of tachyarrhythmias associated with WPW syndrome, as they may stimulate conduction down accessory pathways.

key fact Antidromic AVRT in WPW syndrome mimics ventricular tachycardia and should be treated as such in an emergent situation unless the diagnosis of WPW is known.

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Table 7-9. Differentiating Narrow-Complex Tachyarrhythmias Characteristic


Mode of initiation ◦◦ Warm up, cool down ◦◦ Sudden onset, termination

◦◦ Sinus tachycardia, EAT, junctional ectopic ◦◦ AVNRT, AVRT, atrial flutter


AVNRT, AVRT, atrial flutter



Response to vagal maneuver/adenosine ◦◦ Abrupt termination ◦◦ Gradual slowing/no response

◦◦ AVNRT, AVRT ◦◦ Sinus tach, EAT/MAT, AF, atrial flutter

AF = atrial fibrillation; AVNRT = atrioventricular nodal reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; EAT = ectopic atrial tachycardia; MAT = multifocal atrial tachycardia.

►WIDE ► COMPLEX TACHYARRHYTHMIAS Diagnosis The differential diagnosis for wide complex tachycardia includes ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrant conduction (aberrancy). Table 7-10 describes characteristics that can help distinguish between the two. Table 7-10. Differentiating VT From SVT With Aberrancy Supports VT

Supports Aberrancy

◦◦ Fusion/capture beats ◦◦ AV dissociation ◦◦ Compensatory pause1 ◦◦ QRS >140 msec, RBBB ◦◦ QRS >160 msec, LBBB ◦◦ Left axis deviation

◦◦ Terminates with vagal maneuver or adenosine ◦◦ Onset with P wave ◦◦ Long-short initiation sequence2 ◦◦ Critical rate3 ◦◦ Alternating bundle branch block

AV = atrioventricular; LBBB = left bundle branch block; RBBB = right bundle branch block; SVT = supraventricular tachycardia; VT = ventricular tachycardia. 1 A compensatory pause allows the ventricular conduction system to recover partially and reveal P waves that are partially obscured by the T waves during tachycardia. 2 The initiation of the tachycardia is pause-dependent, with a late, coupled, premature ventricular contraction. 3 Impaired intraventricular conduction occurs as the heart attains a specific critical rate, resulting in the appearance and disappearance of aberrancy with very small changes in cycle length. Aberrancy often appears at relatively slow rates, frequently 100 msec in one precordial lead 3. Concordance of QRS complexes in precordial lead 4. QRS morphology favoring VT

Note: an exception to the Brugada criteria is antidromic AVRT in WPW syndrome


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• • • • • • • •

DCCV Pharmacologic agents Lidocaine Amiodarone Procainamide β-blockers (stable VT with normal EF) Treat underlying metabolic abnormalities Evaluate for myocardial ischemia


• • • •

Generally asymptomatic and diagnosed incidentally during cardiac monitoring Risk factor for overall mortality but does not predict sudden cardiac death Definition: ≥3 consecutive ventricular beats at a rate of >120 bpm lasting