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PRINCIPLES OF SURGERY
ABSITE and Board Review
Associate Editors
Dana K. Andersen, MD, FACS Lisa Dresner, MD, FACS
Senior Scientific Advisor Program Director and Vice Chair for Education
Division of Digestive Diseases and Nutrition Associate Professor of Surgery
National Institute of Diabetes and Digestive and Kidney Disease Department of Surgery
National Institutes of Health College of Medicine, SUNY Downstate Health and Sciences University
Bethesda, Maryland Brooklyn, New York
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CONTENTS
17 Breast 137
This 11th edition of Schwartz’s Principles of Surgery: ABSITE and Contributors of the primary book have updated the questions
Board Review marks a new milestone of excellence in surgical for each chapter since the last edition in an effort to continue to
education for the betterment of craft, quality of care, and the edification provide a high level of review on the most up-to-date information
of surgical students and colleagues alike. With 870 questions and techniques currently taught and employed in the operating
spanning the 54 updated chapters of this edition, including five new theater. We have maintained the proven format of providing the
chapters, Optimizing Perioperative Care: Enhanced Recovery and answer-bearing portion of the text immediately following the
Chinese Medicine, Understanding, Evaluating and Using Evidence question and answer as an efficient method for reinforcement and
for Surgical Practice, Ambulatory Surgery, Skills and Simulation, recall. The user may read the question followed by the answer as a
and Web-Based Education and Implications of Social Media, this is form of review, or by covering the right-hand column of the page,
the comprehensive companion text for reviewing and assessing the the user can complete the questions in a more authentic test format
information compiled in the main textbook and for preparation for and uncover the answers for review/scoring.
the American Board of Surgery In-Training Examination (ABSITE)
and Board Review.
ix
To Jason Malley, Peter Boyle, Catherine Saggese, and all at McGraw We wish to thank Katie Elsbury for her dedication to the
Hill, we are thankful for the continued belief in and support for organization and editing of this book.
this book. F. Charles Brunicardi, MD, FACS
xi
of medical errors. Which of the following statements is tion due to hierarchical differences, concerns with upward
FALSE regarding communication? influence, conflicting roles and role ambiguity, and interper-
A. To Err Is Human, a publication by the US Institute sonal conflict. (See Schwartz 11th ed., p. 8.)
of Medicine, identified medical errors as the eighth
leading cause of death in the United States, causing
100,000 deaths annually.
Leadership
CHAPTER 1
and development of mentoring, presentation skills, and level of the medical school application pool, which in turn is
networking? caused by educational deficiencies at the primary, secondary,
A. Community outreach and collegiate levels. As an attempted solution, the University
B. “Pipeline” of Michigan developed a “pipeline” program that pairs grade-
C. Physician teacher school and high-school students with physicians for experien-
D. Bottleneck tial learning and the development of mentoring, presentation
Leadership
skills, and networking. It is important for departments of sur-
gery to develop a diversity program for recruitment of resi-
dents and faculty. Multi-institutional blinded studies indicate
that the implementation of formal leadership and diversity
training improves diversity leadership and strategic human
resource management. (See Schwartz 11th ed., p. 12.)
molecular pattern (DAMP) molecules, detectable in associated inflammatory response is high-mobility group
the circulation within 30 minutes of trauma. protein B1 (HMGB1), which is rapidly released into the circu-
B. Is a protein secreted by immune-competent cells lation within 30 minutes following trauma. Subsequent studies
stimulated by pathogen-associated molecular patterns have proven, however, that HMGB1 is actively secreted from
(PAMPs) or inflammatory cytokines. immune-competent cells stimulated by PAMPs (eg, endotoxin)
C. Is also secreted by endothelial cells, platelets, and also or by inflammatory cytokines (eg, tumor necrosis factor and
Systemic Response to Injury and Metabolic Support
5. The most abundant amino acid in the human body is: Answer: C
A. Carnitine Glutamine is the most abundant amino acid in the human
B. Arginine body, comprising nearly two-thirds of the free intracellular
C. Glutamine amino acid pool. (See Schwartz 11th ed., Ch. 2, p. 69.)
D. Methionine
CHAPTER 2
tachycardia, hypotension, weakness, nausea, vomiting, and
fever. (See Schwartz 11th ed., Ch. 2, p. 35.)
11. Which of the following statements best describes the role Answer: B
of IL-10 in the immune response to injury or stress? IL-10 plays an important role in the immune response in
A. Proinflammatory mediator that is rapidly mobilized that it acts in an anti-inflammatory role in order to rees-
and is one of the first cytokines released following tablish immune homeostasis. It regulates the duration and
trauma, mediates coagulation, cell migration, and magnitude of the inflammatory response. IL-10 is secreted
macrophage phagocytosis. by both myeloid and lymphoid immune cells, and its syn-
B. Anti-inflammatory mediator that is secreted from a thesis is upregulated during stress and inflammation. IL-10
variety of immune cells and acts to inhibit secretion inhibits the secretion of proinflammatory cytokines IL-1 and
of proinflammatory cytokines, such as TNF and IL-1. TNF through downregulation of NF-kB signaling. Answer A
C. Proinflammatory mediator that is secreted from a describes TNF-α, Answer C describes IL-6, and Answer D
variety of immune cells, promotes B cell maturation, describes IL-8. (See Schwartz 11th ed., Ch. 2, p. 46.)
induces Th17 development and inhibits Treg differ-
entiation, promotes angiogenesis, and increases vas-
cular permeability.
D. Proinflammatory mediator that is secreted primarily
by macrophages and monocytes, and acts as a che-
moattractant for neutrophils, basophils, eosinophils,
and lymphocytes.
A. Over 80% of cellular functions and pathways in leu- trauma in circulating leukocytes from human patients dem-
kocytes demonstrate a shift in gene expression fol- onstrated a significant shift in the leukocyte transcriptomic
lowing blunt trauma. with >80% of cellular functions and pathways demonstrating
B. Changes in gene expression take 3 to 5 days to alterations. These pathways included those involved in innate
develop. and adaptive immunity, and compensatory anti-inflammatory
C. Changes in gene expression occur rapidly and are mechanisms. Transcriptomic alterations occurred rapidly
Systemic Response to Injury and Metabolic Support
transient, present for only 1 to 2 days. (4–12 hours) and persisted for days to weeks. Different
D. Patterns of gene expression varied widely when injury patterns (blunt, burn, endotoxemia) demonstrated
blunt trauma, burn injury, and endotoxemia were similar patterns of gene expression. (See Schwartz 11th ed.,
compared. Ch. 2, p. 52.)
CHAPTER 2
sion. (See Schwartz 11th ed., Ch. 2, p. 55.)
TABLE 2-1 Caloric adjustments above basal energy expenditure (BEE) in hypermetabolic conditions
Grams of Protein/kg Nonprotein Calories:
Condition kcal/kg per day Adjustment above BEE per day Nitrogen
Normal/moderate malnutrition 25–30 1.1 1.0 150:1
Mild stress 25–30 1.2 1.2 150:1
Moderate stress 30 1.4 1.5 120:1
Severe stress 30–35 1.6 2.0 90–120:1
Burns 35–40 2.0 2.5 90–100:1
13
Ch. 3, p. 90.)
CHAPTER 3
tion of body weight as water than elderly or obese individuals.
An average young adult male will have 60% of his total body
weight as TBW, while an average young adult female’s will be
50%. The lower percentage of TBW in women correlates with
a higher percentage of adipose tissue and lower percentage of
muscle mass in most. Estimates of TBW should be adjusted
12. The free water deficit of a 70-kg man with serum sodium Answer: D
of 154 is: This is the formula used to estimate the amount of water
A. 0.1 L required to correct hypernatremia
B. 0.7 L serum sodium − 140
C. 1 L Water deficit L = × TBW
140
D. 3.5 L
Estimate TBW (total body water) as 50% of lean body mass in
men and 40% in women. (See Schwartz 11th ed., Ch. 3, p. 94.)
13. A patient with serum calcium of 6.8 and albumin of 1.2 Answer: D
has a corrected calcium of: When measuring total serum calcium levels, the albumin
A. 7.7. concentration must be taken into consideration.
B. 8.0. Adjust total serum calcium down by 0.8 mg/dL for every
C. 8.6. 1 g/dL decrease in albumin. (See Schwartz 11th ed., Ch. 3,
D. 9.0. p. 90.)
17. A patient who has spasms in the hand when a blood Answer: B
pressure cuff is blown up most likely has: Asymptomatic hypocalcemia may occur with hypoproteinemia
A. Hypercalcemia (normal ionized calcium), but symptoms can develop with
B. Hypocalcemia alkalosis (decreased ionized calcium). In general, symptoms
C. Hypermagnesemia do not occur until the ionized fraction falls below 2.5 mg/dL,
D. Hypomagnesemia and are neuromuscular and cardiac in origin, including pares-
thesias of the face and extremities, muscle cramps, carpopedal
spasm, stridor, tetany, and seizures. Patients will demonstrate
hyperreflexia and positive Chvostek sign (spasm resulting from
tapping over the facial nerve) and Trousseau sign (spasm result-
ing from pressure applied to the nerves and vessels of the upper
extremity, as when obtaining a blood pressure). Decreased
cardiac contractility and heart failure can also accompany
hypocalcemia. (See Schwartz 11th ed., Ch. 3, p. 90.)
18. The actual anion gap (AG) of a chronic alcoholic with Answer: D
Na 133, K 4, Cl–101, HCO3– 22, albumin of 2.5 mg/dL is: The normal AG is <12 mmol/L and is due primarily to the
A. 6. albumin effect, so that the estimated AG must be adjusted for
B. 10. albumin (hypoalbuminemia reduces the AG).
C. 14.
Corrected AG = actual AG + [2.5(4.5 – albumin)]
D. 15.
(See Schwartz 11th ed., Ch. 3, p. 92.)
19. The effective osmotic pressure between the plasma and Answer: D
interstitial fluid compartments is primarily controlled by: The dissolved protein in plasma does not pass through the
A. Bicarbonate. semipermeable cell membrane, and this fact is responsible
B. Chloride ion. for the effective or colloid osmotic pressure. (See Schwartz
C. Potassium ion. 11th ed., Ch. 3, p. 83.)
D. Protein.
CHAPTER 3
A. Hypochloremic, hypokalemic metabolic alkalosis. from isolated loss of gastric contents in infants with pyloric
B. Hypochloremic, hypokalemic metabolic acidosis. stenosis or in adults with duodenal ulcer disease. Unlike vom-
C. Hypochloremic, hyperkalemic metabolic alkalosis. iting associated with an open pylorus, which involves a loss
D. Hypochloremic, hyperkalemic metabolic acidosis. of gastric as well as pancreatic, biliary, and intestinal secre-
tions, vomiting with an obstructed pylorus results only in the
loss of gastric fluid, which is high in chloride and hydrogen,
A. 7.52. the lungs, and the body pH will increase. Within reasonable
B. 7.40. physiologic ranges a 15 mm Hg fall in Paco2 should produce
C. 7.32. a 0.12 change from the normal body pH of 7.4. (See Schwartz
D. 7.28. 11th ed., Ch. 3, p. 91.)
CHAPTER 3
95 mm Hg; Pco2, 25 mm Hg; HCO3–, 15 mEq/L. The of a metabolic acidosis early in the postresuscitative period is
patient’s metabolic acidosis would be treated best with: indicative of tissue hypoxia due to persistent inadequate tis-
A. Ampule of sodium bicarbonate. sue perfusion. Attempts to correct this problem by admin-
B. Sodium bicarbonate infusion. istering an alkalizing agent will not solve the basic problem.
C. Lactated Ringer solution. However, proper volume replacement by means of a balanced
D. Hyperventilation. salt solution such as Lactated Ringer solution will restore per-
31. Three days after surgery for gastric carcinoma, a 50-year- Answer: A
old alcoholic male exhibits delirium, muscle tremors, Magnesium deficiency should be suspected in any mal-
and hyperactive tendon reflexes. Magnesium deficiency nourished patient who exhibits disturbed neuromuscular or
is suspected. All of the following statements regarding cerebral activity in the postoperative period. Laboratory con-
this situation are TRUE EXCEPT: firmation often is not reliable, and the syndrome may exist in
A. A decision to administer magnesium should be based the presence of a normal serum magnesium level. Hypocalce-
on the serum magnesium level. mia often coexists, particularly in patients who have clinical
B. Adequate cellular replacement of magnesium will signs of tetany. Intravenous magnesium can be adminis-
require 1 to 3 weeks. tered safely to a well-hydrated patient for initial treatment
C. A concomitant calcium deficiency should be of a severe deficit, but concomitant electrocardiographic
suspected. monitoring is essential. The electrocardiographic changes
D. Calcium is a specific antagonist of the myocardial associated with acute hypermagnesemia resemble those of
effects of magnesium. hyperkalemia, and calcium chloride or gluconate should be
readily available to counteract any adverse myocardial effects
of excess magnesium ions. Partial or complete relief of symp-
toms may follow the initial infusion of magnesium, although
continued replacement for a period of 1 to 3 weeks is neces-
sary to replenish cellular stores. (See Schwartz 11th ed., Ch. 3,
pp. 19, 95.)
32. Refeeding syndrome can be associated with all of the fol- Answer: B
lowing EXCEPT: With refeeding, a shift in metabolism from fat to carbohy-
A. Respiratory failure. drate substrate stimulates insulin release, which results in
B. Hyperkalemia. the cellular uptake of electrolytes, particularly phosphate,
C. Confusion. magnesium, potassium, and calcium. However, severe hyper-
D. Cardiac arrhythmias. glycemia may result from blunted basal insulin secretion.
(See Schwartz 11th ed., Ch. 3, p. 98.)
CHAPTER 4
similar clinical course. pathic thrombocytopenic purpura (ITP). In children, it is
B. Includes HIT as a subtype of drug-induced ITP. usually acute at the onset, short-lived, and typically follows
C. is also known as thrombotic thrombocytopenic pur- a viral illness. In contrast, ITP in adults is gradual in onset,
pura (TTP). chronic in nature, and has no identifiable cause. Because the
D. is a disease of impaired platelet production of circulating platelets in ITP are young and functional, bleeding
unknown etiology. is less for a given platelet count than when there is failure of
surgery patients, with rapid reversal, these complications cant increase in morbidity and mortality in acutely injured
can be reduced: Which is NOT TRUE about rapid rever- and emergency surgery patients, with rapid reversal, these
sal of warfarin effect? complications can be reduced. There are several reversal
A. Vitamin K should be given to sustain the effects options that include vitamin K administration, plasma,
of plasma and prothrombin complex concentrate cryoprecipitate, recombinant factor VIIa, and factor con-
(PCC). centrates. The 2012 CHEST guidelines for the Manage-
Hemostasis, Surgical Bleeding, and Transfusion
12. What is the best laboratory test for determine degree of Answer: D
anticoagulation with direct oral anticoagulants such as Direct oral anticoagulants (DOACs) include direct throm-
dabigatran and rivaroxaban? bin inhibitors and factor Xa inhibitors and have no readily
A. Prothrombin time/International normalized ratio available method of detection of the degree of anticoagula-
(PT/INR) tion. More concerning is the difficulty in the reversal of these
B. Partial thromboplastin time (PTT) new anticoagulants. Recently, idarucizumab, a humanized
C. Bleeding time monoclonal antibody fragment that binds dabigatran, has
D. None of the above been approved for use for reversal of the thrombin inhibitor,
dabigatran, and dabigatran-related coagulopathy. (Schwartz
11th ed., p. 113.)
CHAPTER 4
anemia, fever, neurological symptoms, and renal insuffi-
ciency. Schistocytes, fragmented red blood cells, are seen on
peripheral blood smear. Plasma exchange with replacement
of fresh frozen plasma (FFP) is the treatment of acute TTP.
Additionally, Rituxamab, a monoclonal antibody against the
CD20 protein of B lymphocytes is indicated in refractory or
19. In patients with significant blood loss, which of the fol- Answer: C
lowing is incorrect? In the Pragmatic Randomized Optimal Platelet and Plasma
A. Resuscitation with whole blood Ratios (PROPPR) trial patients were resuscitated with packed
B. Resuscitation with packed red blood cells, platelet, red blood cells, platelets, and plasma in various ratios. In
and FFP in a 1:1:1 ratio this trial, the 1:1:1 group had significantly decreased mor-
C. Packed red blood cells with transfusion of FFP and tality due to hemorrhage at 24 hours (9% vs 15%) and more
platelets as needed (when the measured INR > 2 and patients achieving hemostasis (86% vs 78%). Whole blood
PLT# is <75,000) transfusion appears to have similar outcome, as whole blood
D. Resuscitation with crystalloid and artificial colloid contains plasma and platelets in a similar ratio. Waiting for
to avoid transfusion reactions until hemorrhage is INR and platelet count appears to delay achieving hemostasis.
controlled. (Schwartz 11th ed., p. 119.)
CHAPTER 4
B. Noncardiogenic pulmonary edema. monary edema related to transfusion. It can occur with the
C. Fever and rigors. administration of any plasma-containing blood product.
D. Bilateral pulmonary infiltrates. Symptoms are similar to circulatory overload with dyspnea
and associated hypoxemia. However, TRALI is characterized
as noncardiogenic and is often accompanied by fever, rigors,
and bilateral pulmonary infiltrates on chest X-ray. It most
A. The r-value represents the clotting factor activity and r-value (reaction time) represents the time between the start
initial fibrin formation and is increased with factor of the assay and initial clot formation. This reflects clotting
deficiency or severe hemodilution. factor activity and initial fibrin formation and is increased
B. K time is prolonged with hypofibrinogenemia and with factor deficiency or severe hemodilution. The k-time
significant factor deficiency. (clot kinetics) is the time needed to reach specified clot
C. Decreased (alpha) or ∝ angle is treated with cryopre- strength and represents the interactions of clotting factors and
Hemostasis, Surgical Bleeding, and Transfusion
cipitate transfusion or fibrinogen administration. platelets. As such, the k-time is prolonged with hypofibrino-
D. All of the above. genemia and significant factor deficiency. Prolonged r-value
and k-time are commonly addressed with plasma transfu-
sions. The alpha or angle (∝) is the slope of the tracing and
reflects clot acceleration. The angle reflects the interactions
of clotting factors and platelets. The slope is decreased with
hypofibrinogenemia and platelet dysfunction. Decreased
angles are treated with cryoprecipitate transfusion or fibrin-
ogen administration. The maximal amplitude (mA) is the
greatest height of the tracing and represents clot strength. Its
height is reduced with dysfunction or deficiencies in plate-
lets or fibrinogen. Decreased mA is addressed with platelet
transfusion and, in cases where the angle is also decreased,
with cryoprecipitate (or fibrinogen) as well. The G-value is a
parametric measure derived from the mA value and reflects
overall clot strength or firmness. An increased G-value is
associated with hypercoagulability, whereas a decrease is seen
with hypocoagulable states. Finally, the LY30 is the amount
of lysis occurring in the clot, and the value is the percentage
of amplitude reduction at 30 minutes after mA is achieved.
The LY30 represents clot stability and presence of increased
fibrinolysis. (Schwartz 11th ed., p. 124.)
29
with reduction in left atrial pressure. ation of adaptive responses to shock. Volume receptors, sensi-
B. Receptors in the aortic arch and carotid bodies inhibit tive to changes in both chamber pressure and wall stretch, are
the autonomic nervous system when stretched. present within the atria of the heart. They become activated
C. When baroreceptors are stretched, they induced with low-volume hemorrhage or mild reductions in right
increased autonomic nervous system output and pro- atrial pressure. Receptors in the aortic arch and carotid bod-
duce constriction of peripheral vessels. ies respond to alterations in pressure or stretch of the arterial
Shock
CHAPTER 5
shock are associated with vasodilation of larger arterioles? lating cellular perfusion and is significantly influenced in
A. Septic shock response to shock. The microvascular bed is innervated by
B. Cardiogenic shock the sympathetic nervous system and has a profound effect on
C. Neurogenic shock the larger arterioles. Following hemorrhage, larger arterioles
D. A and C vasoconstrict; however, in the setting of sepsis or neurogenic
shock, these vessels vasodilate. Additionally, a host of other
Shock
vasoactive proteins, including vasopressin, angiotensin II,
and endothelin-1, also lead to vasoconstriction to limit organ
perfusion to organs such as skin, skeletal muscle, kidneys,
and the gastrointestinal (GI) tract to preserve perfusion of
the myocardium and central nervous system (CNS). (See
Schwartz 11th ed., p. 136.)
CHAPTER 5
lost; loss of 40% of circulating volume (2 L) is immediately
life-threatening, and generally requires operative control of
bleeding. (See Schwartz 11th ed., p. 141.)
Shock
to constrict due low levels of catecholamines. is the typical physiologic response to the decreased arterial
B. Leads to suppression of the renin-angiotensin system. pressure and tissue perfusion with hemorrhage, hypovolemia,
C. Can also be caused by carbon monoxide poisoning. or acute heart failure. This is not the characteristic response
D. Is similar to early cardiogenic shock. in vasodilatory shock. Vasodilatory shock is the result of dys-
function of the endothelium and vasculature secondary to
circulating inflammatory mediators and cells or as a response
to prolonged and severe hypoperfusion. Thus, in vasodila-
tory shock, hypotension results from failure of the vascular
smooth muscle to constrict appropriately. Vasodilatory shock
is characterized by peripheral vasodilation with resultant
hypotension and resistance to treatment with vasopressors.
Despite the hypotension, plasma catecholamine levels are
elevated, and the renin-angiotensin system is activated in
vasodilatory shock. The most frequently encountered form of
vasodilatory shock is septic shock. Other causes of vasodi-
latory shock include hypoxic lactic acidosis, carbon monox-
ide poisoning, decompensated and irreversible hemorrhagic
shock, terminal cardiogenic shock, and postcardiotomy
shock. Thus, vasodilatory shock seems to represent the final
common pathway for profound and prolonged shock of any
etiology. (See Schwartz 11th ed., p. 145.)
congestive heart failure. failure leading to diminished forward flow and subsequent
B. Is secondary to inadequate intravascular volume. tissue hypoxia, in the setting of adequate intravascular vol-
C. Confers a mortality rate of 50%–80%. ume. Hemodynamic criteria include sustained hypotension
D. Permissive hypotension reduces afterload resulting (ie, SBP < 90 mmHg for at least 30 minutes), reduced cardiac
in improved cardiac perfusion. index (<2.2 L/min per square meter), and elevated pulmo-
nary artery wedge pressure (>15 mm Hg). Mortality rates for
cardiogenic shock are 50% to 80%. Acute, extensive MI is the
most common cause of cardiogenic shock; a smaller infarc-
tion in a patient with existing left ventricular dysfunction
also may precipitate shock. Cardiogenic shock complicates
5% to 10% of acute myocardial infarction (MIs). Conversely,
cardiogenic shock is the most common cause of death in
patients hospitalized with acute MI. Although shock may
develop early after MI, it typically is not found on admission.
Seventy-five percent of patients who have cardiogenic shock
complicating acute MIs develop signs of cardiogenic shock
within 24 hours after onset of infarction (average 7 hours).
(See Schwartz 11th ed., p. 148.)
CHAPTER 5
nal fracture, your patient becomes increasingly hypo- clinical examination. The classic findings include respira-
tensive in route to the emergency department with no tory distress (in an awake patient), hypotension, diminished
response to 2 L of fluid administration. What signs and breath sounds over one hemithorax, hyperresonance to per-
symptoms indicate obstructive shock from a right-sided cussion, jugular venous distention, and shift of mediastinal
tension pneumothorax? structures to the unaffected side with tracheal deviation.
A. Hypotension, tachycardia, jugular venous distension, Cardiac tamponade also may be associated with dyspnea,
Shock
leftward tracheal deviation orthopnea, cough, peripheral edema, chest pain, tachycardia,
B. Hypotension, tachycardia, jugular venous distension, muffled heart tones, jugular venous distention, and elevated
muffled heart sounds central venous pressure. Beck’s triad consists of hypotension,
C. Hypotension, tachycardia, rightward tracheal devia- muffled heart tones, and neck vein distention. (See Schwartz
tion, absent right sided breath sounds 11th ed., p. 150.)
D. Hypotension, tachycardia, pulsus paradoxus
B. Is representative of perfusion status, but not the risk required to titrate 1 L of whole blood to a pH of 7.40 with
of death. the sample fully saturated with O2 at 37°C (98.6°F) and a par-
C. Which is persistently elevated is evidence of hospital- tial pressure of CO2 of 40 mm Hg. It usually is measured by
acquired infection following a traumatic event. arterial blood gas analysis in clinical practice as it is readily
D. Does not provide additional information in clinical and quickly available. The mortality of trauma patients can
resuscitation when serum lactates can be assessed. be stratified according to the magnitude of base deficit mea-
Shock
37
B. An increase of score in ≥2 is correlated with 10% count, mean arterial pressure (MAP), Glasgow Coma Scale
in-hospital mortality risk. (GCS) score, creatinine level, and urine output. An increase
C. Does not depend on lab tests. in SOFA score of ≥2 is correlated with a 10% in-hospital mor-
D. All of the above. tality risk, which is suggestive of the life-threatening nature
of sepsis. An abbreviated version of the scoring system, the
quick SOFA (qSOFA) is recommended as a screening and
Surgical Infection
CHAPTER 6
agent provides additional benefit, and this practice should be
discouraged, as it is costly and is associated with increased
rates of microbial drug resistance. (Schwartz 11th ed., p. 164.)
Surgical Infection
A. Duration of procedure surgeons during performance of an invasive procedure. SSIs
B. Degree of microbial contamination of the wound are classified into incisional and organ/space infections, and
C. Malnutrition the former are further subclassified into superficial (limited
D. General anesthesia to skin and subcutaneous tissue) and deep incisional cat-
egories. The development of SSIs is related to three factors:
(a) the degree of microbial contamination of the wound during
surgery; (b) the duration of the procedure; and (c) host factors
such as diabetes, malnutrition, obesity, immune suppression,
and a number of other underlying disease states. Table 6-1
lists risk factors for development of SSIs. By definition, an
incisional SSI has occurred if a surgical wound drains puru-
lent material or if the surgeon judges it to be infected and
opens it. (Schwartz 11th ed., p. 169.)
(not colon)
Clean/contaminated Colorectal surgery 4%–14%
(class II)
Contaminated Penetrating abdominal 3.4%–13.2%
(class III) trauma, large tissue
injury, enterotomy
during bowel
obstruction
Dirty (class IV) Perforated diverticulitis, 3.1%–12.8%
necrotizing soft tissue
infections
CHAPTER 6
inhaled oxygen to perioperative patients reduces the rate of
SSI. Although an initial study provided evidence that patients
who received high levels of inhaled oxygen during colorec-
tal surgery developed fewer SSIs, a later meta-analysis sug-
gested that the overall benefit is small and may not warrant
use. The 2017 CDC guidelines, however, support administra-
Surgical Infection
tion of increased FiO2 during surgery and after extubation
in patients with normal pulmonary function receiving gen-
eral anesthesia as there has been some evidence of benefit.
Further evaluation via multicenter studies is needed prior to
implementation of hyperoxia as standard therapy, but it is
clear that intraoperative hypothermia and hypoxia should be
prevented. (Schwartz 11th ed., p. 170.)
B. Pancreatic necrosis is an indication for early opera- 15% of patients who develop severe pancreatitis with necro-
tive debridement. sis. The surgical treatment of this disorder was pioneered
C. Open necrosectomy with repeated debridements by Bradley and Allen, who noted significant improvements
should occur in the first 2 weeks after illness. in outcome for patients undergoing repeated pancreatic
D. Early enteral feeding via a nasal-jejunal tube passed debridement of infected pancreatic necrosis. Care of patients
beyond the ligament of Treitz is associated with with severe acute pancreatitis includes staging with dynamic,
decreased development of infected pancreatic contrast-enhanced helical CT scan to evaluate the extent of
necrosis. pancreatitis (unless significant renal dysfunction exists, in
which case one should forego the use of contrast material)
coupled with the use of one of several prognostic scoring sys-
tems. Patients who exhibit clinical signs of instability (eg, oli-
guria, hypoxemia, large-volume fluid resuscitation) should be
carefully monitored in the ICU and undergo follow-up con-
trast CT examination when renal function has stabilized to
evaluate for development of local pancreatic complications.
Routine use of prophylactic antibiotics to prevent infected
pancreatic necrosis is not indicated. Early enteral feeding
using nasojejunal feeding tubes placed past the ligament of
Treitz has been associated with decreased development of
infected pancreatic necrosis, possibly due to a decrease in gut
translocation of bacteria (Schwartz 11th ed., p. 172.)
CHAPTER 6
operative surgical patients should have indwelling urinary
catheters removed as quickly as possible, typically within 1 to
2 days, as long as they are mobile, to avoid the development of
a urinary tract infections (UTI).
Surgical Infection
A. Are not associated with duration of catheter use. Infection associated with indwelling intravascular catheters
B. Single lumen and multilumen have similar infection is a common problem among hospitalized patients. Because
rates. of the complexity of many surgical procedures, these devices
C. Are always associated with purulence at the insertion are increasingly used for physiologic monitoring, vascular
site. access, drug delivery, and hyperalimentation. Among the sev-
D. Can be asymptomatic, with rising white blood cells eral million catheters inserted each year in the United States,
(WBCs) and positive blood culture. approximately 25% will become colonized, and approxi-
mately 5% will be associated with bacteremia. Duration of
catheterization, insertion or manipulation under emergency
or nonsterile conditions, use for hyperalimentation, and the
use of multilumen catheters increase the risk of infection. Use
of a central line insertion protocol that includes full barrier
precautions and chlorhexidine skin prep has been shown to
decrease the incidence of infection. Although no random-
ized trials have been performed, peripherally inserted central
venous catheters have a catheter-related infection rate similar
to those inserted in the subclavian or jugular veins.
Many patients who develop intravascular catheter infec-
tions are asymptomatic, often exhibiting solely an elevation
in the blood white blood cell (WBC) count. Blood cultures
obtained from a peripheral site and drawn through the cath-
eter that reveals the presence of the same organism increase
the index of suspicion for the presence of a catheter infec-
tion. Obvious purulence at the exit site of the skin tunnel,
severe sepsis syndrome due to any type of organism when
other potential causes have been excluded, or bacteremia due
to gram-negative aerobes or fungi should lead to catheter
removal. (Schwartz 11th ed., p. 174.)
16. Sepsis incidence and survival in the United States are: Answer: B
A. Increasing incidence and decreased survival due to The treatment of sepsis has improved over the last decade,
increasing age of the population. with mortality rates dropping to under 30%. Factors con-
B. Increased incidence with improved survival due to tributing to this improvement relate both to recent random-
improvements in care, including Surviving Sepsis ized prospective trials demonstrating improved outcomes
Campaign. with new therapies, and to improvements in the process of
C. Decreasing incidence and improved survival due to care delivery to the sepsis patient. The “Surviving Sepsis
proper use of perioperative antibiotics. Campaign,” a multidisciplinary group that develops treat-
D. Improved survival is due to delay in starting antibiot- ment recommendations, published guidelines incorporating
ics until source of sepsis is clear. evidence-based sepsis treatment strategies most recently in
2016. (Schwartz 11th ed., p. 174.)
17. Which of the following is Not TRUE about the risk of Answer: A
human immunodeficiency virus (HIV) transmission The risk of HIV transmission from patient to surgeon is low.
from patient to surgeon? As of May 2011, there had been six cases of surgeons with HIV
A. Risk from a needlestick is 3% and 1% from mucous seroconversion from a possible occupational exposure, with
membrane exposure. no new cases reported since 1999. Of the numbers of health
B. Transmission can be minimized by observation of care workers with likely occupationally acquired HIV infec-
universal precautions. tion (n = 200), surgeons were one of the lower risk groups
C. Postexposure prophylaxis is most effective if initiated (compared to nurses at 60 cases and nonsurgeon physicians
within hours. at 19 cases). The estimated risk of transmission from a needle-
D. Is decreased where patients have low viral load. stick from a source with HIV-infected blood is estimated
20. A patient in the ICU has been on ventilator support for Answer: B
3 weeks. He has new onset elevated white blood cells Prolonged mechanical ventilation is associated with noso-
(WBCs) count, fever, and consolidation seen on chest comial pneumonia. These patients present with more severe
x-ray. What is an appropriate next step? disease, are more likely to be infected with drug-resistant
A. Exchange endotracheal tube and change respiratory pathogens, and suffer increased mortality compared to
circuit. patients who develop community-acquired pneumonia. The
B. Obtain bronchoalveolar lavage. diagnosis of pneumonia is established by presence of a puru-
C. Start treatment with empiric penicillin G. lent sputum, elevated leukocyte count, fever, and new chest
D. Obtain chest CT. x-ray abnormalities such as consolidation. The presence of
CHAPTER 6
ation should be given to perform bronchoalveolar lavage to
obtain samples for Gram’s stain and culture. Some authors
advocate quantitative cultures as a means to identify a thresh-
old for diagnosis. Surgical patients should be weaned from
mechanical ventilation as soon as feasible, based on oxygen-
ation and inspiratory effort, as prolonged mechanical ventila-
Surgical Infection
tion increases the risk of nosocomial pneumonia. (Schwartz
11th ed., p. 174.)
25. The first step in the evaluation and treatment of a patient Answer: D
with an infected bug bite on the leg with cellulitis, bullae, The diagnosis of necrotizing infection is established solely
thin grayish fluid draining from the wound, and pain out upon a constellation of clinical findings, not all of which
of proportion to the physical findings is: are present in every patient. Not surprisingly, patients often
A. Obtain C-reactive protein. develop sepsis syndrome or septic shock without an obvious
B. Computed tomographic scan of the leg. cause. The extremities, perineum, trunk, and torso are most
C. Magnetic resonance imaging of the leg. commonly affected, in that order. Careful examination should
D. Operative exploration. be undertaken for an entry site such as a small break or sinus
in the skin from which grayish, turbid semipurulent material
(“dishwater pus”) can be expressed, as well as for the presence
of skin changes (bronze hue or brawny induration), blebs, or
crepitus. The patient often develops pain at the site of infec-
tion that appears to be out of proportion to any of the physical
manifestations. Any of these findings mandates immediate
surgical intervention, which should consist of exposure and
direct visualization of potentially infected tissue (including
deep soft tissue, fascia, and underlying muscle) and radi-
cal resection of affected areas. Radiologic studies should be
undertaken only in patients in whom the diagnosis is not
seriously considered, as they delay surgical intervention and
frequently provide confusing information. Unfortunately,
surgical extirpation of infected tissue frequently entails
amputation and/or disfiguring procedures; however, incom-
plete procedures are associated with higher rates of morbidity
and mortality. (See Schwartz 11th ed., p. 174.)
CHAPTER 6
other vascular access site exists. Use of systemic antibacterial
or antifungal agents to prevent catheter infection is of no util-
ity and is contraindicated. (See Schwartz 11th ed., p. 174.)
Surgical Infection
antibiotics, will result in a wound infection in what per- minant of the propensity to develop a surgical site infec-
centage of patients? tion (SSI). In healthy individuals, class I and II wounds
A. 3%–4% may be closed primarily, while skin closure of class III and
B. 8%–12% IV wounds is associated with high rates of incisional SSIs
C. 15%–18% (~25% to 50%). The superficial aspects of these latter types
D. 22%–25% of wounds should be packed open and allowed to heal by sec-
ondary intention, although selective use of delayed primary
closure has been associated with a reduction in incisional
SSI rates. It remains to be determined whether National
Nosocomial Infections Surveillance System (NNIS)-type
stratification schemes can be employed prospectively in
order to target specific subgroups of patients who will ben-
efit from the use of prophylactic antibiotic and/or specific
wound management techniques. One clear example based
on cogent data from clinical trials is that class III wounds
in healthy patients undergoing appendectomy for perforated
or gangrenous appendicitis can be primarily closed as long
as antibiotic therapy directed against aerobes and anaerobes
is administered. This practice leads to SSI rates of approxi-
mately 3% to 4%. (See Schwartz 11th ed., p. 170.)
49
tension and tachycardia respond marginally to volume patient. Neither external fixation nor the use of medical anti-
replacement. Once it is evident that her major problem shock trousers control free intra-abdominal hemorrhage
is free intraperitoneal bleeding and a pelvic hematoma in regardless of its source. In the unstable patient, celiotomy is
association with the fracture, appropriate management mandatory. If there is a ruptured retroperitoneal hematoma
would be: bleeding into the peritoneal cavity, control is a major prob-
A. Application of medical antishock trousers with infla- lem. Internal iliac artery ligation has been abandoned as it
Trauma
tion of the extremity and abdominal sections. is rarely effective. Angiography and arterial embolization
B. Arterial embolization of the pelvic vessels. may be effective with an arterial bleeding problem, but most
C. Celiotomy and ligation of the internal iliac arteries severe pelvic hemorrhage is venous in origin. If the hema-
bilaterally. toma is stable, it is best to leave it undisturbed. However, if
D. Celiotomy and pelvic packing. the hematoma has ruptured into the peritoneal cavity, pelvic
E. External fixation application to stabilize the pelvis. packing offers the best hope of control. (See Schwartz 11th ed.,
Ch. 7, p. 234.)
CHAPTER 7
A. An elevation in WBC to 20,000/mm3 and platelets to rhage may be due to an improperly ligated or unrecognized
300,000/mm3 on postoperative day 7 is a common short gastric artery, or recurrent bleeding from the splenic
benign finding in postsplenectomy patients. parenchyma if splenic repair was used. An immediate post-
B. Delayed rebleeding or rupture will typically occur splenectomy increase in platelets and WBCs is normal;
within 48 hours of injury. however, beyond postoperative day 5, a WBC count above
C. Common complications after splenectomy include 15,000/mm3 and a platelet/WBC ratio of <20 are associated
Trauma
subdiaphragmatic abscess, pancreatic tail injury, and with sepsis and should prompt a thorough search for underly-
gastric perforation. ing infection. A common infectious complication after sple-
D. Postsplenectomy vaccines against encapsulated bac- nectomy is a subphrenic abscess, which should be managed
teria are optimally administered preoperatively or with percutaneous drainage. Additional sources of morbidity
immediately postoperative. include a concurrent or unrecognized iatrogenic injury to the
pancreatic tail during rapid splenectomy resulting in pancre-
atic ascites or fistula, or gastric perforation during short gas-
tric vessel ligation. Enthusiasm for splenic salvage was driven
by the rare, but often fatal, complication of overwhelming
postsplenectomy sepsis. Overwhelming postsplenectomy
sepsis is caused by encapsulated bacteria, Streptococcus pneu-
moniae, Haemophilus influenzae, and Neisseria meningitidis,
which are resistant to antimicrobial treatment. In patients
undergoing splenectomy, prophylaxis against these bacteria
is provided via vaccines administered optimally at >14 days
postinjury. (See Schwartz 11th ed., Ch. 7, p. 227.)
CHAPTER 7
A. Exploratory laparotomy and bypass of the duodenum. tomas, perforation (blunt blow-outs, lacerations from stab
B. Exploratory laparotomy and evacuation of the wounds, or blast injury from gunshot wounds), and com-
hematoma. bined pancreaticoduodenal injuries. The majority of duode-
C. Exploratory laparotomy to rule out associated nal hematomas are managed nonoperatively with nasogastric
injuries. suction and parenteral nutrition. Patients with suspected
D. Observation. associated perforation, suggested by clinical deterioration or
Trauma
imaging with retroperitoneal free air or contrast extravasa-
tion, should undergo operative exploration. A marked drop in
nasogastric tube output heralds resolution of the hematoma,
which typically occurs within 2 weeks; repeat imaging to con-
firm these clinical findings is optional. If the patient shows
no clinical or radiographic improvement within 3 weeks,
operative evaluation is warranted. (See Schwartz 11th ed.,
Ch. 7, p. 229.)
CHAPTER 7
for the uninjured side, termed the A-A index. If the pressures
are within 10% of each other, a significant injury is unlikely
and no further evaluation is performed. If the difference is
>10%, computed tomography angiogram (CTA) or arteriog-
raphy is indicated. Others argue that there are occult injuries,
such as pseudoaneurysms or injuries of the profunda femo-
Trauma
ris or peroneal arteries, which may not be detected with this
technique. If hemorrhage occurs from these injuries, com-
partment syndrome and limb loss may occur. Although busy
trauma centers continue to debate this issue, the surgeon who
is obliged to treat the occasional injured patient may be bet-
ter served by performing CTA in selected patients with soft
signs. (See Schwartz 11th ed., Ch. 7, p. 206.)
CHAPTER 7
lateral lung is compressed and the heart rotates about the
superior and inferior vena cava; this decreases venous return
and ultimately cardiac output, which culminates in cardiovas-
cular collapse. (See Schwartz 11th ed., Ch. 7, p. 186.)
Trauma
FIG. 7-2. A. Tube thoracostomy is performed in the midaxillary
line at the fourth or fifth intercostal space (inframammary
crease) to avoid iatrogenic injury to the liver or spleen. B. Heavy
scissors are used to cut through the intercostal muscle into the
pleural space. This is done on top of the rib to avoid injury to the
intercostal bundle located just beneath the rib. C. The incision is
digitally explored to confirm intrathoracic location and identify
pleural adhesions. D. A 28Fr chest tube is directed superiorly and
posteriorly with the aid of a large clamp.
20. Patients who are conscious, without tachypnea, and have Answer: D
a normal voice are unlikely to require air intervention. Patients who are conscious, without tachypnea, and have a
Additional findings that should prompt airway interven- normal voice are unlikely to require early airway interven-
tion include all of the following EXCEPT: tion. Exceptions are penetrating injuries to the neck with
A. Penetrating injury to the neck with expanding an expanding hematoma; evidence of chemical or thermal
hematoma. injury to the mouth, nares, or hypopharynx; extensive sub-
B. Evidence of chemical or thermal injury to mouth, cutaneous air in the neck; complex maxillofacial trauma; or
nares, or hypopharynx. airway bleeding. Although these patients may initially have
C. Extensive subcutaneous air in the neck. an adequate airway, it may become compromised if soft tissue
D. Right pneumohemothorax. swelling, hematoma formation, or edema progresses. In these
E. Airway bleeding. cases, preemptive intubation should be performed before air-
way access becomes challenging. Simple pneumohemotho-
rax is NOT an indication for airway intervention during
the primary survey.
22. Which of the following does NOT describe flail chest? Answer: A
A. Fracture of greater than at least three ribs on both Flail chest occurs when three or more contiguous ribs are
sides of the chest. fractured in at least two locations. Paradoxical movement
B. Three of more ribs fractured in at least two locations of this free-floating segment of chest wall is usually evident
C. Paradoxical movement of a free floating segment of in patients with spontaneous ventilation, due to the negative
chest wall intrapleural pressure of inspiration. The additional work of
D. High likelihood of associated pulmonary contusion breathing and chest wall pain caused by the flail segment is
rarely sufficient to compromise ventilation. Instead, it is the
decreased compliance and increased shunt fraction caused by
the associated pulmonary contusion that is the source of acute
respiratory failure. Pulmonary contusions often progress dur-
ing the first 12 hours. Resultant hypoventilation and hypox-
emia may require intubation and mechanical ventilation. The
patient’s initial chest radiograph often underestimates the
extent of the pulmonary parenchymal damage; close moni-
toring and frequent clinical reevaluation are warranted. (See
Schwartz 11th ed., Ch. 7, p. 186.)
CHAPTER 7
A. Occurring within 3 cm of the mainstem bronchus injuries are those occurring within 2 cm of the carina. These
B. Likely to cause a pneumothorax may not be associated with a pneumothorax due to the envel-
C. A distal bronchial injury opment in the mediastinal pleura. Type II injuries are more
D. Occurring within 2 cm of the carina distal injuries within the tracheobronchial tree and hence
manifest with a pneumothorax. Bronchoscopy confirms the
extent of the injury and its location, and directs management.
Trauma
(See Schwartz 11th ed., Ch. 7, p. 187.)
24. Which of the following is NOT one of the four injuries Answer: B
that should be identified during the “circulation” section During the circulation section of the primary survey, four life-
of the primary survey? threatening injuries must be identified promptly: (a) massive
A. Massive hemothorax hemothorax, (b) cardiac tamponade, (c) massive hemoperi-
B. Extremity vascular injury toneum, and (d) mechanically unstable pelvic fractures with
C. Cardiac tamponade bleeding. Critical tools used to differentiate these in the mul-
D. Massive hemoperitoneum tisystem trauma patient are the chest and pelvis radiographs,
and extended focused abdominal sonography for trauma
(eFAST). Identification of one of these injuries during the
primary surgery necessitates immediate intervention. (See
Schwartz 11th ed., Ch. 7, p. 188.)
25. For motor vehicle collisions, which of the following vari- Answer: A
ables are NOT among those strongly associated with life- Patients who have sustained blunt trauma can be separated
threatening injuries? into categories according to their risk for multiple injuries:
A. Head on impact those sustaining high-energy transfer injuries and those sus-
B. Death of another occupant in the vehicle taining low-energy transfer injuries. Injuries involving high-
C. Extrication time >20 minutes energy transfer include auto-pedestrian accidents, motor
D. Change in velocity of >20 MPH vehicle collisions in which the car’s change of velocity (ΔV)
E. Lack of restraint use exceeds 20 mph or in which the patient has been ejected,
motorcycle collisions, and falls from heights >20 ft. In fact,
for motor vehicle collisions the variables strongly associ-
ated with life-threatening injuries, and hence reflective
of the magnitude of the mechanism, are death of another
occupant in the vehicle, extrication time of >20 minutes,
ΔV >20 mph, lack of restraint use, and lateral impact. Low-
energy trauma, such as being struck with a club or falling from
a bicycle, usually does not result in widely distributed inju-
ries. However, potentially lethal injuries of internal organs can
occur because the net energy transfer to any given location
may be substantial. (See Schwartz 11th ed., Ch. 7, p. 196.)
DPA
FIG. 7-3. Algorithm for the initial evaluation of a patient with suspected blunt abdominal trauma. CT = computed
tomography; DPA = diagnostic peritoneal aspiration; FAST = focused abdominal sonography for trauma; Hct = hematocrit.
CHAPTER 7
definitive repair done through the supraclavicular incision.
Emergent median sternotomy is optimal for anterior stab
wounds to the heart. Typically, these patients have pericar-
dial tamponade and may undergo placement of a pericardial
drain before a semiurgent median sternotomy is performed.
Patients in extremis, however, should undergo anterolateral
Trauma
thoracotomy. (See Schwartz 11th ed., Ch. 7, p. 210.)
CHAPTER 7
A. Admission Glasgow Coma Score (GCS) score after bles after the age of 55 years. Moreover, 25% of patients with
severe head injury is a good predictor of outcome. a normal GCS score of 15 had intracranial bleeding, with an
B. Rib fractures are associated with pulmonary contu- associated mortality of 50%. Just as there is no absolute age
sion in 35% of patients, and complicated by pneumo- that predicts outcome, admission GCS score is a poor predic-
nia in 10% to 30% of patients. tor of individual outcome. Therefore, the majority of trauma
C. Approximately 10% of patients older than 65 years centers advocate an initial aggressive approach with reevalu-
Trauma
will sustain a rib fracture from a fall <6 ft. ation at the 72-hour mark to determine subsequent care. Sec-
D. Chronologic age older than 65 years is associated ondly, one of the most common sequelae of blunt thoracic
with higher morbidity and mortality after trauma. trauma is rib fractures. In fact, in one study, 50% of patients
older than 65 years sustained rib fractures from a fall of <6 ft,
compared with only 1% of patients younger than 65 years.
Concurrent pulmonary contusion is noted in up to 35% of
patients, and pneumonia complicates the injuries in 10% to
30% of patients with rib fractures. (See Schwartz 11th ed.,
Ch. 7, p. 243.)
2. What percentage burn does a patient have who has suf- Answer: C
fered partial-thickness burns to their anterior right leg Most burn resuscitation formulas estimate fluid require-
and anterior chest and abdomen as well as superficial ments based on burn size measured as a percentage of total
burns to their right arm? body surface area (TBSA) (%TBSA). The “rule of nines” is a
A. 18% crude but quick and effective method of estimating burn size
B. 27% (Fig. 8-1). In adults, the anterior and posterior trunk each
C. 36% account for 18%, each lower extremity is 18%, each upper
D. 45% extremity is 9%, and the head is 9%. In children under 3 years
of age, the head accounts for a larger relative surface area and
should be taken into account when estimating burn size. For
smaller or odd-shaped burns, the “rule of the palm” where the
palmar surface of the hand, including the digits, is 1% TBSA
is useful. Diagrams such as the Lund and Browder chart give
a more accurate accounting of the true burn size in children
and adults. The importance of an accurate burn size assess-
ment cannot be overemphasized. Superficial or first-degree
burns should not be included when calculating burn size, and
thorough cleaning of soot and debris is mandatory to avoid
confusing soiled skin with burns. Examination of referral
65
9% 9% 9%
18%
1%
1%
FIG. 8-1. The “rule of nines” can be used as a quick reference for estimating a patient’s burn size by dividing the
body into regions to which total body surface area is allocated in multiples of 9.
CHAPTER 8
A. All extremity compartments should be evaluated and have special concerns, including cardiac arrhythmia and com-
a baseline ECG should be obtained. partment syndrome with concurrent rhabdomyolysis. A base-
B. A full neurologic assessment including ophthal- line ECG is recommended in all patients with an electrical
mologic is required to evaluate acute intraocular injury, and a normal ECG in a low-voltage injury (<1000 V)
pathology. may preclude hospital admission. Because compartment syn-
C. A Foley catheter should be placed to allow for titra- drome and rhabdomyolysis are common in high-voltage elec-
Burns
tion of fluid administration. trical injuries, vigilance must be maintained for neurologic or
D. Workup should include an echocardiogram to evalu- vascular compromise, and fasciotomies should be performed
ate ventricular wall motion. even in cases of moderate clinical suspicion. For patients with
rhabdomyolysis, a Foley catheter and monitoring of elec-
trolytes may be aid in renal function monitoring, but fluid
administration and urine output is not prioritized as highly in
electrical when compared to external burns. Long-term neuro-
logic symptoms and cataract development are not uncommon
with high-voltage electrical injuries, and neurologic and oph-
thalmologic consultation should be obtained to define base-
line patient function. However, acute intraocular pathology is
unlikely to be uncovered. (See Schwartz 11th ed., p. 252.)
second-degree burn to his right arm, and third-degree formula, consists of 3 to 4 mL/kg per % burn of Lactated
burns to his torso and right leg. What is the rate of initial Ringer’s, of which half is given during the first 8 hours after
fluid resuscitation? burn and the remaining half is given over the subsequent
A. 4.5 L over 8 hours, followed by 4.5 L over 16 hours 16 hours. The most recent American Burn Association con-
B. 4.5 L over 8 hours, followed by 6 L over 16 hours sensus formula recommends 2 mL/kg per % burn of Lactated
C. 6 L over 8 hours, followed by 6 L over 16 hours Ringers given the tendency toward excessive fluid adminis-
Burns
D. 6 L over 8 hours, followed by 9 L over 16 hours tration with the traditional formulas. The concept behind
continuous fluid requirements is simple. The burn (and/
or inhalation injury) drives an inflammatory response that
leads to capillary leak; as plasma leaks into the extravascular
space, crystalloid administration maintains the intravascular
volume. Therefore, if a patient receives a large fluid bolus in
a prehospital setting or emergency department, the fluid has
likely leaked into the interstitium, and the patient still requires
ongoing burn resuscitation according to the estimates. Con-
tinuation of fluid volumes should depend on the time since
injury, urine output, and mean arterial pressure (MAP). As
the capillary leak closes, the patient will require less volume to
maintain these two resuscitation endpoints. Children under
20 kg have the additional requirement that they do not have
sufficient glycogen stores to maintain an adequate glucose
level in response to the inflammatory response. Specific pedi-
atric formulas have been described, but the simplest approach
is to deliver a weight-based maintenance IV fluid with glu-
cose supplementation in addition to the calculated resuscita-
tion with lactated Ringer’s. (See Schwartz 11th ed., p. 254.)
9. What is the indication for the topical therapy which can Answer: A
cause neutropenia when applied to burns? Silver sulfadiazine is one of the most widely used in clinical
A. Primarily as prophylaxis against burn wound infec- practice. Silver sulfadiazine has a wide range of antimicrobial
tions with a wide range of antimicrobial activity activity, primarily as prophylaxis against burn wound infec-
B. Primarily as antimicrobial prophylaxis against eschar tions rather than treatment of existing infections. It has the
and newly grafted areas added benefits of being inexpensive, being easily applied,
C. MRSA culture-positive burn wound infections and having soothing qualities. It is not significantly absorbed
D. To improve patient comfort while reducing the need systemically and thus has minimal metabolic derangements.
for daily dressing changes Silver sulfadiazine has a reputation for causing neutropenia,
CHAPTER 8
True allergic reactions to the sulfa component of silver sul-
fadiazine are rare, and at-risk patients can have a small test
patch applied to identify a burning sensation or rash. Silver
sulfadiazine destroys skin grafts and is contraindicated on
burns or donor sites in proximity to newly grafted areas. Also,
silver sulfadiazine may retard epithelial migration in healing
Burns
partial-thickness wounds. (See Schwartz 11th ed., p. 257.)
A. Tangential excision consists of tangential slices of hemodynamically stable, attention should be turned to excis-
burn tissue until bleeding tissue is encountered. ing the burn wound. Burn excision and wound coverage
Thus, excision can be associated with potentially sig- should ideally start within the first several days, and in larger
nificant blood loss. burns, serial excisions can be performed as patient condition
B. Xenographs are a permanent alternative to split allows. Excision is performed with repeated tangential slices
thickness skin grafts when there is insufficient donor using a Watson or Goulian blade until viable, diffusely bleed-
Burns
CHAPTER 8
A. Do not include exposure to radioactive materials. involved due to the sudden nature of the event, the difficulty
B. Should be coordinated by local hospital systems, of managing personnel and resources, a deficit of staff expe-
regionalization and national plans inappropriately rience in burn management, and relatively small resource
allocate resources. availability for a potentially large number of patients. The
C. Thirty percent of patients in mass casualty incidents American Burn Association has estimated that up to 30% of
suffer from burn injury. patients in mass casualty incidents suffer from burn injury.
Burns
D. Globally, they occur most commonly in the United A recent review of the literature between 1990 and 2016 iden-
States. tified 752 burn disasters worldwide, defined as an incident
with ≥50 burn injuries and/or ≥30 burn-related deaths. The
majority occurred in Asia and the Middle East and are thought
to be secondary to rapid industrialization, inadequate fire-
prevention strategies, and poor building codes. There was a
significant increase in terrorist-related incidences from 2000
to 2015. Finally, the authors demonstrated that international
adoption of the US Health and Human Services guidelines
on bed availability for burns and trauma dramatically under-
estimated the number of beds needed for burn disasters.
(See Schwartz 11th ed., p. 261.)
Inflammation
0 2 4 6 8 10 12 14 16 months
Relative number of cells
Neutrophils
Macrophages
Fibroblasts
Lymphocytes
0 2 4 6 8 10 12 14 16
Relative amount of
matrix synthesis
Collagen I
Fibronectin
Collagen III
Wound-breaking
strength
FIG. 9-1. The cellular, biochemical, and 0 2 4 6 8 10 12 14 16
mechanical phases of wound healing. Days postwounding
73
glandins, complement factors, IL-1, TNFα, GF-β, of bacteria and tissue debris. PMNs are also a major source
platelet factor 4, or bacterial products. of cytokines early during inflammation, especially TNF-α,
D. PMNs are the first cells to infiltrate the wound, peak- which may have a significant influence on subsequent angio-
ing at 24 to 48 hours. genesis and collagen synthesis. PMNs also release proteases
E. Neutrophils release cytokines that later assist with such as collagenases, which participate in matrix and ground
collagen deposition and epithelial closure. substance degradation in the early phase of wound healing.
Other than their role in limiting infections, these cells do not
appear to play a role in collagen deposition or acquisition of
mechanical wound strength. On the contrary, neutrophil fac-
tors have been implicated in delaying the epithelial closure of
wounds. (See Schwartz 11th ed., p. 273.)
CHAPTER 9
fibers found in connective tissue. Scar remodeling continues
for many (6 to 12) months postinjury, gradually resulting in a
mature, avascular, and acellular scar. The mechanical strength
of the scar never achieves that of the uninjured tissue. (See
Schwartz 11th ed., p. 275.)
Wound Healing
5. The most common causes of Ehler-Danlos syndrome
are: Ehlers-Danlos syndrome (EDS) is a group of 10 disorders
A. An acquired collagen deficit. that present as a defect in collagen formation. Over half of the
B. Genetic defects encoding α-chains of collagen type V. affected patients manifest genetic defects encoding α-chains
C. Genetic defect in platelet-derived growth factor of collagen type V, causing it to be either quantitatively or
(PDGF). structurally defective. (See Schwartz 11th ed., p. 278.)
D. Type I and type III collagen genetic defect.
TABLE 9-1 Comparison of wound healing in the gastrointestinal tract and skin
GI Tract Skin
Wound environment pH Varies throughout GI tract in accordance with Usually constant except during sepsis or local
local exocrine secretions infection
Microorganisms Aerobic and anaerobic, especially in the colon Skin commensals rarely cause problems;
and rectum; problematic if they contaminate infection usually results from exogenous
the peritoneal cavity contamination or hematogenous spread
Shear stress Intraluminal bulk transit and peristalsis exert Skeletal movements may stress the suture
distracting forces on the anastomosis line but pain usually acts as a protective
mechanism preventing excess movement
Tissue oxygenation Dependent on intact vascular supply and Circulatory transport of oxygen as well as
neocapillary formation diffusion
Collagen synthesis Cell type Fibroblasts and smooth muscle cells Fibroblasts
Lathyrogens d-Penicillamine has no effect on collagen Significant inhibition of cross-linking with
cross-linking decreased wound strength
Steroids Contradictory evidence exists concerning Significant decrease in collagen accumulation
their negative effect on GI healing; increased
abscess in the anastomotic line may play a
significant role
Collagenase activity — Increased presence throughout GI tract after Not as significant a role in cutaneous wounds
transection and reanastomosis; during
sepsis, excess enzyme may promote
dehiscence by decreasing suture-holding
capacity of tissue
Wound strength — Rapid recovery to preoperative level. Less rapid than GI tissue
Scar formation Age Definite scarring seen in fetal wound sites Usually heals without scar formation in the
fetus
CHAPTER 9
of healing, as it occurs as the bone at the frac- at the site of injury to restore structural and functional integ-
ture site is degraded and normal bone undergoes rity. Most of the phases of healing resemble those observed in
revascularization. dermal healing, but some notable individual characteristics
B. Erythema and swelling occur during formation of apply to bone injuries. The initial stage of hematoma formation
soft callus. consists of an accumulation of blood at the fracture site, which
C. Callus mineralization is complete in 1 week. also contains devitalized soft tissue, dead bone, and necrotic
Wound Healing
D. Erythema, swelling, and pain usually take 5 days to marrow. The next stage accomplishes the liquefaction and deg-
resolve. radation of nonviable products at the fracture site. The normal
bone adjacent to the injury site can then undergo revascular-
ization, with new blood vessels growing into the fracture site.
This is similar to the formation of granulation in soft tissue.
The symptoms associated with this stage are characteristic of
inflammation, with clinical evidence of swelling and erythema.
Three to four days following injury, soft tissue forms a
bridge between the fractured bone segments in the next
stage (soft callus stage). The soft tissue is deposited where
neovascularization has taken place and serves as an internal
splint, preventing damage to the newly laid blood vessels and
achieving a fibrocartilaginous union. The soft callus is formed
externally along the bone shaft and internally within the mar-
row cavity. Clinically, this phase of healing is characterized by
the cessation of pain and inflammatory signs.
The next phase consists of mineralization of the soft cal-
lus and conversion to bone (hard callus stage). This may take
up to 2 to 3 months and leads to complete bony union. (See
Schwartz 11th ed., p. 281.)
12. Fetal wound healing differs from adults wound healing Answer: D
in a number of ways. Which is TRUE? Although early fetal wound healing is characterized by
A. Fetal wound healing is slower. the absence of scarring and resembles tissue regeneration,
B. All fetal wounds heal without a scar. there is a phase of transition during gestational life when
C. Fetal wounds continue to be scarless and look like a more adult-like healing pattern emerges. This so-called
regeneration throughout gestation until birth. “transition wound” occurs at the beginning of the third
D. Fetal wounds in late third trimester resemble an adult trimester, and during this period, there is scarless healing;
wound healing pattern. however, there is a loss of the ability to regenerate skin append-
ages. Eventually a classic, adult-patterned healing with scar
formation occurs exclusively, although overall healing contin-
ues to be faster than in adults. (See Schwartz 11th ed., p. 282.)
B. Decreasing platelet plug integrity. phase of wound healing (angiogenesis, neutrophil and macro-
C. Increasing release of lysosomal enzymes. phage migration, and fibroblast proliferation) and the release
D. Increasing fibrinolysis. of lysosomal enzymes. The stronger the anti-inflammatory
effect of the steroid compound used, the greater the inhibi-
tory effect on wound healing. Steroids used after the first 3 to
4 days postinjury do not affect wound healing as severely as
Wound Healing
CHAPTER 9
nutrition in wound healing? wound complications and increased wound failure following
A. Adequate protein and calorie intake is needed for diverse surgical procedures. This reflects impaired healing
wound healing. response as well as reduced cell-mediated immunity, phago-
B. Brief periods of starvation, or absence of nutrient cytosis, and intracellular killing of bacteria by macrophages
intake has no impact on wound healing. and neutrophils during protein-calorie malnutrition.
C. Arginine supplementation is associated with First, the degree of nutritional impairment need not be
Wound Healing
improved outcome. long-standing in humans, as opposed to the experimental
D. Brief nutritional interventions can correct collagen situation. Thus, patients with brief preoperative illnesses or
deposition deficits seen in malnutrition and postop- reduced nutrient intake in the period immediately preced-
erative starvation. ing the injury or operative intervention will demonstrate
impaired fibroplasias. Second, brief and not necessarily
intensive nutritional intervention, either via the parenteral or
enteral route, can reverse or prevent the decreased collagen
deposition noted with malnutrition or with postoperative
starvation.
The possible role of single amino acids in enhanced wound
healing has been studied for the last several decades. Arginine
appears most active in terms of enhancing wound fibropla-
sia. Arginine deficiency results in decreased wound-breaking
strength and wound-collagen accumulation in chow-fed rats.
Rats that are given 1% arginine HCl supplementation, and
therefore are not arginine-deficient, have enhanced wound-
breaking strength and collagen synthesis when compared to
chow-fed controls. Studies have been carried out in healthy
human volunteers to examine the effect of arginine supple-
mentation on collagen accumulation. Young, healthy, human
volunteers (age 25–35 years) were found to have significantly
increased wound-collagen deposition following oral supple-
mentation with either 30 g of arginine aspartate (17 g of free
arginine) or 30 g of arginine Hall (24.8 g of free arginine)
daily for 14 days. (See Schwartz 11th ed., p. 284.)
17. Vitamins most closely involved with wound healing are: Answer: D
A. Vitamin C only. The vitamins most closely involved with wound healing are
B. Vitamin C and vitamin D. vitamin C and vitamin A. Scurvy or vitamin C deficiency
C. Vitamin C and vitamin E. leads to a defect in wound healing, particularly via a failure
D. Vitamin C and vitamin A. in collagen synthesis and cross-linking. Biochemically, vita-
min C is required for the conversion of proline and lysine to
hydroxyproline and hydroxylysine, respectively. Vitamin C
deficiency has also been associated with an increased inci-
dence of wound infection, and if wound infection does occur,
it tends to be more severe. These effects are believed to be
due to an associated impairment in neutrophil function,
decreased complement activity, and decreased walling-off of
bacteria secondary to insufficient collagen deposition. The
recommended dietary allowance is 60 mg daily. This provides
a considerable safety margin for most healthy nonsmokers. In
severely injured or extensively burned patients, this require-
ment may increase to as high as 2 g daily. There is no evidence
that excess vitamin C is toxic; however, there is no evidence
that supratherapeutic doses of vitamin C are of any benefit.
Vitamin A deficiency impairs wound healing, while sup-
plemental vitamin A benefits wound healing in nondeficient
humans and animals. Vitamin A increases the inflammatory
response in wound healing, probably by increasing the lability
of lysosomal membranes. There is an increased influx of mac-
rophages, with an increase in their activation and increased
CHAPTER 9
the predilection to keloid formation appears to be autosomal
dominant with incomplete penetration and variable expres-
sion. (See Schwartz 11th ed., p. 292.)
Wound Healing
FIG. 9-2. Recurrent keloid on the neck of
a 17-year-old patient that had been revised
several times. (Reproduced with permission from
Cohen IK, Diegelmann RF, Lindblad WJ: Wound
Healing: Biochemical and Clinical Aspects.
Philadelphia, PA: WB Saunders/ Elsevier; 1992.)
83
CHAPTER 10
A. Prognostic biomarkers predict response to specific Tumor markers are substances that can be detected in higher
treatments. than normal amounts in the serum, urine, or tissues of patients
B. Predictive biomarkers predict likelihood of survival with certain types of cancer. The term “prognostic marker”
for specific tumors. generally is used to describe molecular markers that predict
C. Results of multigene assays can be linked together to disease-free survival, disease-specific survival, and overall
provide optimal survival predictability. survival, whereas the term “predictive marker” often is used in
D. Circulating free DNA is more informative as solid the context of predicting response to certain therapies. Multi-
Oncology
tumor biomarkers than circulating free proteins. gene profiles to predict prognosis are in validation phase for
many solid tumor types. (See Schwartz 11th ed., pp. 334–335.)
2. In humans: Answer: C
A. Antigen encoding genes are located on chromosome 8. The main antigens responsible for this process are part of the
B. Major histocompatibility complex (MHC) system in MHC. In humans, these antigens make up the human leuko-
humans is called the human histocompatibility com- cyte antigen (HLA) system. The antigen-encoding genes are
plex (HHC). located on chromosome 6. Two major classes of HLA anti-
C. Class I antigens (HLA-A, HLA-B, HLA-C) are expressed gens are recognized. They differ in their structure, function,
on all nucleated cells. and tissue distribution. Class I antigens (HLA-A, HLA-B,
D. Class II antigens are expressed on all nucleated cells. and HLA-C) are expressed by all nucleated cells. Class II anti-
gens (HLA-DR, HLA-DP, and HLA-DQ) are expressed by
antigen-presenting cells (APCs) such as B lymphocytes, den-
dritic cells, macrophages, and other phagocytic cells. (See
Schwartz 11th ed., p. 358.)
87
CHAPTER 11
Other Medications That Other Medications That Other Medications That
Common Side Effects Increase Blood Levels Decrease Blood Levels Potentiate Toxicity
Cyclosporine (CSA) Hypertension, nephrotoxicity, Verapamil, diltiazem, Isoniazid, carbamazepine, Nephrotoxicity: ganciclovir,
hirsutism, neurotoxicity, clarithromycin, azithromycin, phenobarbital, phenytoin, aminoglycosides, NSAIDs,
gingival hyperplasia, erythromycin, azole rifampin, St. John’s wort ACE-Is, and ARBs
hypomagnesemia, antifungals, protease
hyperkalemia inhibitors, grapefruit juice
Transplantation
Tacrolimus (FK506) Hypertension, nephrotoxicity, Verapamil, diltiazem, Isoniazid, carbamazepine, Nephrotoxicity: ganciclovir,
alopecia, hyperglycemia, clarithromycin, azithromycin, phenobarbital, phenytoin, aminoglycosides, NSAIDs,
neurotoxicity, erythromycin, azole rifampin, St. John’s wort ACE-Is, and ARBs
hypomagnesemia, antifungals, protease
hyperkalemia inhibitors, grapefruit juice
Sirolimus Thrombocytopenia and Verapamil, diltiazem, Isoniazid, carbamazepine, —
neutropenia, elevated clarithromycin, azithromycin, phenobarbital, phenytoin,
cholesterol, extremity edema, erythromycin, azole rifampin, St. John’s wort
impaired wound healing antifungals, protease
inhibitors, grapefruit juice
Mycophenolate Leukopenia, — Cholestyramine, antacids Bone marrow suppression:
mofetil thrombocytopenia, GI upset valganciclovir, ganciclovir,
TMP-SMX
Corticosteroids Hyperglycemia, osteoporosis, — — —
cataracts, myopathy, weight
gain
Azathioprine Leukopenia, anemia, — — Bone marrow suppression:
thrombocytopenia, neoplasia, allopurinol, sulfonamides
hepatitis, cholestasis
ACE-I = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; NSAID = nonsteroidal anti-inflammatory drug; TMP-SMX = trimethoprim-sulfamethoxazole
CHAPTER 11
cardiac death (DCD): Given the severe shortage of donor organs, DCD—also known
A. Most patients meet the criteria for brain death. as donation by non–heart-beating donors (NHBDs)—was
B. Is associated with increased warm ischemia time. reintroduced to the transplant community in the 1990s. The
C. In both procurement surgeons wait until cessation of category of DCD (Maastricht classification) was initially
cardiac activity. proposed at an international workshop and is now widely
D. Transfer to the operating room occurs after cessation adopted for organ procurement. Currently, most NHBDs in
of cardiac activity. the United States meet Maastricht classification III; that is, they
Transplantation
have suffered a devastating injury with no chance of a mean-
ingful recovery but do not meet the criteria for brain death.
After consent for donation is obtained from the next of kin,
the donor’s life support is removed. After the cessation of car-
diac and respiratory function, organ procurement commences.
DCD procurement protocols vary between states; religious and
cultural differences need to be taken into consideration. The
surgical team must be familiar with, and respect, the local pro-
tocol. With cardiac death (as opposed to brain death), warm
ischemic injury to organs can occur during the period between
circulatory cessation and rapid core cooling through perfu-
sion of preservation solution. However, the difference in long-
term outcomes is negligible for recipients of organs from either
type of donor. Still, a significant percentage of liver grafts pro-
cured after cardiac death, especially those with >25 minutes of
warm ischemic time, develop devastating ischemic cholangi-
opathy and fail. (See Schwartz 11th ed., p. 365.)
11. The most common cause of renal failure in the United Answer: C
States is: Diabetes and hypertension are the leading causes of chronic
A. Chronic glomerulonephritis. renal disease. Concomitant cardiovascular disease (CVD)
B. Chronic pyelonephritis. is a common finding in this population. An estimated 30%
C. Diabetes mellitus. to 42% of deaths with a functioning kidney graft are due to
D. Obstructive uropathy. CVD. Therefore, assessment of the potential kidney trans-
plant candidate’s cardiovascular status is an important part of
the pretransplant evaluation. (See Schwartz 11th ed., p. 369.)
A B
FIG. 11-1. Vascular anastomoses of kidney transplant. A. Arterial anastomosis: donor renal artery with Carrel patch to recipient external
iliac artery, end-to-side. B. Venous anastomosis: donor renal vein with caval extension conduit to recipient external iliac vein, end-to-side.
CHAPTER 11
antiplatelet treatments, the threshold for surgical exploration
is lower. Small unligated vessels at the donor’s renal hilum or
recipient’s retroperitoneum are likely sources of bleeding.
One of the most devastating postoperative complications
in kidney recipients is graft thrombosis. It is rare, occur-
ring in fewer than 1% of recipients. The recipient risk factors
include a history of recipient hypercoagulopathy and severe
Transplantation
peripheral vascular disease; donor-related risk factors include
the use of en bloc or pediatric donor kidneys, procurement
damage, technical factors such as intimal dissection or tor-
sion of vessels, and hyperacute rejection. Graft thrombosis
usually occurs within the first several days posttransplant.
Acute cessation of urine output in recipients with brittle post-
transplant diuresis and the sudden onset of hematuria or graft
pain should arouse suspicion of graft thrombosis. Doppler
ultrasound may help confirm the diagnosis. In cases of graft
thrombosis, an urgent thrombectomy is indicated; however, it
rarely results in graft salvage. (See Schwartz 11th ed., p. 373.)
CHAPTER 11
mus, sirolimus, and IL-2 receptor antibody induction. Those
results were replicated at other experienced transplant cen-
ters, but the rates of long-term (>5 year) insulin indepen-
dence remained poor, well below those of whole-pancreas
transplants. Still, despite the low rates of long-term insulin
independence, most islet recipients were C-peptide positive
and retained hypoglycemia awareness, indicating residual
Transplantation
islet function and benefit. In fact, at 9 years posttransplant,
15% remained insulin-independent, and 73% had hypogly-
cemia awareness and corrected hemoglobin Aic levels. (See
Schwartz 11th ed., p. 378.)
19. The most common diagnosis leading to heart transplant is: Answer: C
A. COPD. The most common diagnosis leading to a heart transplant is
B. Congenital heart disease. ischemic dilated cardiomyopathy, which stems from coronary
C. Ischemic dilated cardiomyopathy. artery disease, followed by idiopathic dilated myopathy and
D. Idiopathic dilated cardiomyopathy. congenital heart disease. About 3000 patients are added to the
waiting list each year. (See Schwartz 11th ed., p. 389.)
20. The best method for monitoring the development of acute Answer: C
rejection in a patient after cardiac transplantation is: The goal of immunosuppression is to prevent rejection,
A. Dipyrimidole thallium study. which is assessed by immunosuppressive levels and, early
B. Electrocardiogram. on, by endomyocardial biopsy. Both T-cell–mediated (cellu-
C. Endomyocardial biopsy. lar) and B-cell–mediated (antibody-mediated) rejection are
D. Echocardiography (ultrasound of heart). monitored. Most of the immunosuppression used is aimed at
T-cells; however, if the recipient has many preformed anti-
bodies or develops donor-specific antibodies, other strategies
(such as plasmapheresis or rituximab) are used to reduce the
antibody load. Immunosuppressive regimens can vary by cen-
ter, but most often consist of three categories of medications: a
calcineurin inhibitor (usually tacrolimus or cyclosporine),
an antiproliferative agent (mycophenolate mofetil [MMF] or
azathioprine [AZA]), and a corticosteroid (prednisone). Other
immunosuppressive agents can be used, depending on the
needs of individual recipients. (See Schwartz 11th ed., p. 390.)
22. Which of the following patients with hepatic failure ben- Answer: D
efit from liver transplantation? The MELD was originally developed to assess risk for tran-
A. Model for End-Stage Liver Disease (MELD) > 18 sjugular intrahepatic portosystemic shunt (TIPS) placement.
B. All patients with MELD < 18 Later analysis revealed it to be an excellent model to predict
C. MELD 15–18 if they have significant morbidity from survival among patients with cirrhosis, especially those on
cirrhosis the waiting list for a liver transplant. In 2002, liver graft allo-
D. A and C only cation was restructured to be based on the MELD score.
Although the historic indication for a liver transplant is
decompensated cirrhosis, a landmark analysis comparing
waiting list mortality with posttransplant mortality estab-
lished that a minimum MELD score of 18 is necessary to have
a survival benefit posttransplant. A MELD score between 15
and 18 does not confer a survival advantage, but a transplant
may be justified if the patient has significant morbidity from
cirrhosis. (See Schwartz 11th ed., p. 381.)
97
fies all of the following as main types of improvements The Donabedian model of measuring quality identifies three
EXCEPT: main types of improvements: changes to organizational struc-
A. Changes to structure ture, changes in organizational processes, and changes in
B. Changes to process outcomes. Structure refers to the physical and organizational
C. Changes to culture tools, equipment, and policies that improve safety. Structural
D. Changes to outcomes measures ask, “Do the right tools, equipment, and policies
exist?” Process is the application of these tools, equipment, and
Patient Safety
CHAPTER 12
A. Is essentially the same as Surgical Care Improvement The National Surgical Quality Improvement Program
Project (SCIP). (NSQIP) is a measurement program that allows hospitals to
B. Collects data on individual surgeon outcomes. sample their rates of postoperative events and compare them
C. Was created by the Institute of Medicine. to similar hospitals. Created by the Veterans Health Admin-
D. Allows hospitals to compare their rates of postopera- istration (VA) in 1991, NSQIP has been credited with mea-
tive events and compare them to similar hospitals. suring and improving morbidity and mortality outcomes at
the VA, reducing 30-day mortality rate after major surgery by
Patient Safety
31%, and 30-day postoperative morbidity by 45% in its first
decade. Beta testing at 18 non-VA sites from 2001 to 2004
demonstrated the feasibility and utility of the program in the
private sector. The program was subsequently expanded to
the private sector in 2004. (See Schwartz 11th ed., p. 407.)
A. Pneumothorax occurs in 10%. Pneumothorax occurrence rates from both subclavian and
B. Pneumothorax is eliminated using ultrasound when internal jugular vein approaches are 1% to 6%. Prevention
placing the line. requires proper positioning of the patient and correct inser-
C. Central line infections are associated with significant tion technique. A postprocedure chest X-ray is recommended
mortality and increased hospital costs. to confirm the presence or absence of a pneumothorax,
D. Frequent line changes are recommended to decrease regardless of whether a pneumothorax is suspected. Recent
infection risk. reports have questioned whether a chest X-ray is required
Patient Safety
CHAPTER 12
reasons other than acute respiratory failure. The beneficial
effects of PEEP for ARDS were confirmed in this study as
well. (See Schwartz 11th ed., p. 420.)
Patient Safety
• Predisposing condition
• Pao2:Fio2 <200 (regardless of positive end-expiratory pressure)
• Bilateral infiltrates
• Pulmonary artery occlusion pressure <18 mm Hg
• No clinical evidence of right heart failure
Fio2 = fraction of inspired oxygen; Pao2 = partial pressure of arterial oxygen.
14. Which of the following have been shown to decrease the Answer: D
time of postoperative ileus? Postoperative ileus is related to dysfunction of the neural reflex
A. Cyclooxygenase-1 inhibitors axis of the intestine. Excessive narcotic use may delay return
B. Morphine patient-controlled analgesia of bowel function. Epidural anesthesia results in better pain
C. Nasogastric drainage until full return of bowel control, and there is an earlier return of bowel function and
function a shorter length of hospital stay. The limited use of nasogas-
D. Alvimopan, a μ -opioid receptor antagonist tric tubes and the initiation of early postoperative feeding are
associated with an earlier return of bowel function. The use
of chewing gum and other oral stimulants to minimize ileus
remains controversial. Pharmacologic agents commonly used
to stimulate bowel function include metoclopramide and
erythromycin. Metoclopramide’s action is limited to the stom-
ach and duodenum, and it may help primarily with gastropa-
resis. Erythromycin is a motilin agonist that works throughout
the stomach and bowel. Several studies demonstrate significant
benefit from the administration of erythromycin in those suf-
fering from an ileus. Alvimopan, a newer agent and a μ-opioid
receptor antagonist, has shown some promise in many studies
for earlier return of gut function and subsequent reduction in
length of stay. Neostigmine has been used in refractory pan-
ileus patients (Ogilvie’s syndrome) with some degree of success.
It is recommended for patients receiving this type of therapy to
be in a monitored unit. (See Schwartz 11th ed., p. 421.)
CHAPTER 12
copy may also be helpful for irrigation and drainage of the
infection. Refractory empyemas require specialized surgical
approaches. (See Schwartz 11th ed., p. 425.)
Patient Safety
B. Hematoma from trauma. hyperbilirubinemia, but other mechanisms of hyperbiliru-
C. Cholestasis. binemia include reabsorption of blood (eg, hematoma from
D. Increased unconjugated bilirubin due to hemolysis. trauma), decreased bile excretion (eg, sepsis), increased
unconjugated bilirubin due to hemolysis, hyperthyroidism,
and impaired excretion due to congenital abnormalities
or acquired disease. Errors in surgery that cause hyper-
bilirubinemia largely involve missed or iatrogenic injuries.
(See Schwartz 11th ed., p. 422.)
Supply-dependent Supply-independent
oxygen consumption oxygen consumption
Oxygen utilization, VO2
105
enced by an underdamped or overdamped intra-arterial If the system is underdamped, then the inertia of the system,
blood pressure monitoring system? which is a function of the mass of the fluid in the tubing and
A. Systolic blood pressure the mass of the diaphragm, causes overshoot of the points
B. Mean arterial blood pressure of maximum positive and negative displacement of the dia-
C. Diastolic blood pressure phragm during systole and diastole, respectively. Thus, in an
D. Pulse pressure underdamped system, systolic pressure will be overestimated
and diastolic pressure will be underestimated. In an over-
Physiologic Monitoring of the Surgical Patient
CHAPTER 13
preload is not linear, but rather is exponential (Fig. 13-2A,B).
This fact limits the utility of EDP as a surrogate marker at
extremes of EDV. (See Schwartz 11th ed., p. 436-7.)
Changing preload
Left ventricle pressure-volume loop
(end-diastolic volume)
End-systolic
El
nc
e
volume
lin
e
Stroke volume
e
li n
li n
R R
PV PV
line
line
ED ED
VR
VR
ESP
ESP
Left ventricular volume (mm Hg) Left ventricular volume (mm Hg)
FIG. 13-2 A-B. Left ventricular pressure-volume loops constructed for various clinically relevant
scenarios. For further information refer to the text. A. Standard left ventricular pressure-volume
loop, with stroke volume, end-systolic volume, and end-diastolic volume highlighted for reference.
Note the directionality of the pressure-volume loop, which is not annotated in the figure B for
clarity. B. Demonstration of the effect of changing preload.
CHAPTER 13
to evaluate the broad applicability of the RI and similar
measures, the evidence to date is compelling. (See Schwartz
11th ed., p. 436.)
Balloon
inflated
FIG. 13-3. Representative pressure traces at different stages of insertion of the PAC. In the
central venous circulation, the pressure remains low, with characteristic waves from atrial filling
and tricuspid valve closing. Upon entry into the right ventricle, the pressure increases sharply,
with the broadest range between systole and diastole. When in the main pulmonary artery,
the systolic pressure remains elevated to the same degree, but the diastolic pressure is now
significantly elevated due to the closure of the pulmonic valve during the cardiac cycle. Upon
further advancement with the balloon inflated, the pressure differences become smaller and the
magnitude of the mean pressure drops, reflecting an estimate of the left atrial pressure.
saturation of hemoglobin in venous blood (SvO2)? Oxygen saturation can replace oxygen content, yielding the
A. Anemia final clinically valuable equation:
B. Fever
C. Age VO2
S v O 2 = Sa O 2 −
D. Heart failure (Q T × Hgb × 1.36)
PPmin
Time
FIG. 13-4. Calculation of pulse pressure variation as it would appear on bedside monitor. This
provides a helpful and rapid assessment of fluid responsiveness in the critically ill mechanically
ventilated patient.
CHAPTER 13
uration of hemoglobin in arterial blood) in mechanically DO2 is dependent to a greater degree on the oxygen satura-
ventilated patients? tion of hemoglobin (Hgb) in arterial blood (SaO2) than on the
A. Mean airway pressure partial pressure of oxygen in arterial blood (PaO2). DO2 also
B. FiO2 (fraction of inspired oxygen) is dependent on QT and Hgb. As discussed earlier and illus-
C. SvO2 (oxygen saturation of hemoglobin in venous trated mathematically by previous equations, the dissolved
blood) oxygen in blood makes only a negligible contribution to DO2.
D. Respiratory rate SaO2 in mechanically ventilated patients depends on the mean
13. Which of the following regarding Ppeak (peak airway pres- Answer: A
sure) is true? Airway pressures are routinely monitored in mechanically
A. Ppeak is measured at the end of inspiration. ventilated patients. The peak airway pressure measured at
B. To measure Ppeak, the expiratory valve must be closed. the end of inspiration (Ppeak) is a function of the tidal volume,
C. Ppeak is independent of airway resistance, chest wall the resistance of the airways, lung/chest wall compliance, and
compliance, and peak inspiratory flow. peak inspiratory flow. The airway pressure measured at the
D. Ppeak is not routinely measured in mechanically venti- end of inspiration when the inhaled volume is held in the
lated patients. lungs by briefly closing the expiratory valve is termed the pla-
teau airway pressure (Pplateau). As a static parameter, plateau
airway pressure is independent of the airway resistance and
peak airway flow and is related to the lung/chest wall com-
pliance and delivered tidal volume. Mechanical ventilators
monitor Ppeak with each breath and can be set to trigger an
alarm if the Ppeak exceeds a predetermined threshold. Pplateau
is not measured routinely with each delivered tidal volume
but rather is measured intermittently by setting the ventilator
to close the exhalation circuit briefly at the end of inspira-
tion and record the airway pressure when airflow is zero. (See
Schwartz 11th ed., p. 446.)
D. Fulminant hepatic failure with coma and cerebral hemorrhage with coma or neurologic deterioration, intracra-
edema on CT nial hemorrhage with intraventricular blood, ischemic mid-
dle cerebral artery stroke, fulminant hepatic failure with coma
and cerebral edema on CT scan, and global cerebral ischemia
or anoxia with cerebral edema on CT scan. The goal of ICP
monitoring is to ensure that cerebral perfusion pressure (CPP)
is adequate to support perfusion of the brain. CPP is equal to
the difference between MAP and ICP: CPP = MAP – ICP.
(See Schwartz 11th ed., pp. 447–8.)
CHAPTER 13
ate the diagnosis. In practice, transurethral bladder pressure
measurement reflects IAP and is most often used to confirm
the presence of ACS. After instilling 50 to 100 mL of sterile
saline into the bladder via a Foley catheter, the tubing is con-
nected to a transducing system to measure bladder pressure
in the supine position at end-expiration.
Intra-abdominal hypertension is defined as an IAP ≥ 12 mm
115
CHAPTER 14
Minimally Invasive Surgery
FIG. 14-1. Robotic instruments and hand controls. The
surgeon is in a sitting position, and the arms and wrists
are in an ergonomic and relaxed position.
119
single amino acid. this case, random combinations of the four bases form 4 ×
B. More than one triplet codes for the same amino acid. 4 × 4, or 64 codes. Because 64 codes are more than enough
C. Codons are mRNA sequentially recognized by tRNA for 20 amino acids, most amino acids are coded by more than
adaptor proteins. one codon. The start codon is AUG, which also corresponds
D. Protein synthesis proceeds in the carboxy-to-amino- to methionine; therefore, almost all proteins begin with this
terminus direction. amino acid. The sequence of nucleotide triplets that follows
the start codon signal is termed the reading frame. The codons
on mRNA are sequentially recognized by tRNA adaptor pro-
teins. Specific enzymes termed aminoacyl-tRNA synthetases
link a specific amino acid to a specific tRNA. The translation
of mRNA to protein requires the ribosomal complex to move
stepwise along the mRNA until the initiator methionine
sequence is identified. In concert with various protein initia-
tor factors, the methionyl-tRNA is positioned on the mRNA
and protein synthesis begins. Each new amino acid is added
sequentially by the appropriate tRNA in conjunction with
proteins called elongation factors. Protein synthesis proceeds
in the amino-to-carboxy-terminus direction. (See Schwartz
11th ed., p. 484.)
Nucleus Cytoplasm
DNA mRNA Protein
turnover turnover
Nuclear envelope
Transcription RNA Protein
degradation degradation
RNA RNA Posttranslational Active
transcript mRNA mRNA Translation Protein
processing modification protein
RNA
transport
FIG. 15-1. Four major steps in the control of eukaryotic gene expression. Transcriptional and posttranscriptional control determine the level
of messenger RNA (mRNA) that is available to make a protein, while translational and posttranslational control determine the final outcome
of functional proteins. Note that posttranscriptional and posttranslational controls consist of several steps.
CHAPTER 15
A. 35,000 to 40,000 genes. The human genome has an estimated 25,000 to 30,000 genes,
B. 20,000 to 25,000 genes. and overall it is 99.9% identical in all people. Approximately
C. 25,000 to 30,000 genes. 3 million locations where single-base DNA differences exist have
D. 30,000 to 35,000 genes. been identified and termed single nucleotide polymorphisms.
Single nucleotide polymorphisms may be critical determinants
of human variation in disease susceptibility and responses to
environmental factors. (See Schwartz 11th ed., p. 485.)
Mitosis
M
G2
G1
FIG. 15-2. The cell cycle and its control system. M is the mitosis
phase, when the nucleus and the cytoplasm divide; S is the phase
when DNA is duplicated; G1 is the gap between M and S; G2 is the A/CDK1 S
gap between S and M. A complex of cyclin and cyclin-dependent
DNA replication D/CDK4
kinase (CDK) controls specific events of each phase. Without cyclin, D/CDK6
CDK is inactive. Different cyclin/CDK complexes are shown around
the cell cycle. A, B, D, and E stand for cyclin A, cyclin B, cyclin D, and
cyclin E, respectively. A/CDK2 E/CDK2
vates the: See Figure 15-3. (See Schwartz 11th ed., Figure 15-8, p. 487.)
A. FAS receptor.
B. A membrane bound death receptor.
C. Tumor necrosis factor (TNF) receptor.
D. Caspase cascade.
Death signal
(e.g., TNF or Fas)
Death Plasma
receptor membrane
Mitochondrion
Death
receptor
signaling Cytochrome c
FIG. 15-3. A simplified view of the pathway release
apoptosis pathways. Extracellular death
receptor pathways include the activation
Activation of
of Fas and tumor necrosis factor (TNF) caspase cascade
receptors and consequent activation
of the caspase pathway. Intracellular
death pathway indicates the release of Apoptotic target cell
Nucleus
cytochrome c from mitochondria, which
also triggers the activation of the caspase
cascade. During apoptosis, cells undergo
DNA fragmentation and nuclear and cell
membrane breakdown and are eventually
digested by other cells. Normal target cell
CHAPTER 15
survival/apoptosis. Dysregulation (particularly mutations) of
these receptors is thought to underlie conditions of abnor-
mal cellular proliferation in the context of cancer. The fol-
lowing sections will further review two examples of growth
factor signaling pathways and their connection with human
diseases. (See Schwartz 11th ed., p. 488.)
11. Dysregulation of transforming growth factor-β (TGF-β) Answer: B
A. In normal cells, oncogenes promote cell growth by There are two classes of cancer genes in which alteration has
activating cell cycle progression. been identified in human and animal cancer cells: oncogenes,
B. In cancer cells, oncogenes promote cell growth by with dominant gain-of-function mutations, and tumor sup-
activating cell cycle progression. pressor genes, with recessive loss-of-function mutations. In
C. Tumor suppressors enhance oncogene function. normal cells, oncogenes promote cell growth by activating
D. Oncogenes do not play an important role in main- cell cycle progression, whereas tumor suppressors counteract
taining controlled state of cell growth. oncogenes’ functions. Therefore, the balance between onco-
genes and tumor suppressors maintains a well-controlled
state of cell growth. (See Schwartz 11th ed., p. 490.)
14. All of the following are correct about human embryonic Answer: D
stem cells (hESCs) EXCEPT: hESCs are derived from early preimplantation embryos
A. They are derived from early preimplantation called blastocysts (5 days postfertilization) and are capable of
embryos. generating all differentiated germ layers in the body by chi-
B. They are derived from blastocysts. mera assays or 2-D/3-D differentiation in a dish—ectoderm,
C. They can generate all differential germ layers. mesoderm, and endoderm—and therefore are considered
D. They are considered multipotent. pluripotent. There are two pluripotent states associated with
hESCs, one of which is the classic culture with basic fibroblast
growth factor (bFGF) and knock out replacer (KSR), termed
as “primed” pluripotent state. More recently, “naive” hESC
culture methods have been introduced based on mouse stud-
ies, by supplementing 2i inhibitors (MEK1 and GSK3β inhib-
itors) into the medium in addition to bFGF. (See Schwartz
11th ed., p. 492.)
CHAPTER 15
notherapy that targets an oncogene? One of the most exciting applications of immunotherapy has
A. Trastuzumab come from the identification of certain tumor targets called
B. Methotrexate antigens and the aiming of an antibody at these targets. This
C. Adriamycin was first used as a means of localizing tumors in the body
D. Gleevec for diagnosis and was more recently used to attack cancer
cells. Trastuzumab (Herceptin) is an example of such a drug.
Trastuzumab is a monoclonal antibody that neutralizes the
129
CHAPTER 16
The Skin and Subcutaneous Tissue
FIG. 16-2. Nodular melanoma seen in the leg of
a 55-year-old man.
A B
CHAPTER 16
part of the skin’s adaptive immunity. (See Schwartz 11th ed.,
p. 515.)
B. Irrigation with normal saline for 30 minutes acidic burns and 2 hours for alkaline injuries. Attempting to
C. Irrigation with normal saline for 120 minutes neutralize the offending agent is typically discouraged, as it
D. Immediate coverage with light compressive dressing does not offer an advantage over dilution and the neutraliza-
tion reaction could be exothermic, increasing the amount of
tissue damage. After removal of the caustic agent, the burn
is treated like other burns and is based on the depth of tissue
injury. (See Schwartz 11th ed., p. 521.)
The Skin and Subcutaneous Tissue
17. How long does it take to get irreversible tissue damage Answer: B
with external pressure greater than double capillary per- The average perfusion pressure of the microcirculation is
fusion pressure? about 30 mm Hg, and pressures greater than that cause local
A. 1 hour tissue ischemia. In animal models, pressure greater than twice
B. 2 hours the capillary perfusion pressure produces irreversible tissue
C. 3 hours necrosis in just 2 hours. Tissues with a higher metabolic
D. 4 hours demand are typically susceptible to insult from tissue hypo-
perfusion more rapidly than tissues with a lower metabolic
demand. Because of this, it is possible to have muscle necrosis
beneath cutaneous tissue that has yet to develop signs of irre-
versible damage. (See Schwartz 11th ed., p. 523.)
CHAPTER 16
ferring low risk, and types 16, 18, 31, and 33 conferring a high
risk. The recently developed quadrivalent HPV vaccine, tar-
geting HPV types -6, -11, -16, and -18, is now available to
both males and females age 9 to 26 and is associated with an
up to 90% reduction of infections from those HPV types. (See
Schwartz 11th ed., p. 526.)
22. What subtype of basal cell carcinoma (BCC) is the most Answer: D
common, characterized by raised, pearly pink papules There are multiple variants of BCC, and presentation can
with telangiectasias and occasionally a depressed tumor range from red, flesh-colored, or white macule or papule
center with raised borders? to nodules and ulcerated lesions. Growth patterns of these
A. Micronodular lesions can either be well-circumscribed or diffuse and
B. Infiltrating the most common types of BCC are nodular and micronodu-
C. Superficial spreading lar, superficial spreading, and infiltrative. The most com-
D. Nodular mon subtype is the nodular variant, characterized by raised,
pearly pink papules with telangiectasias and occasionally a
depressed tumor center with raised borders giving the clas-
sic “rodent ulcer” appearance. Superficial spreading BCC is
confined to the epidermis as a flat, pink, scaling or crusting
lesion, often mistaken for eczema, actinic keratosis, fungal
infection, or psoriasis. This subtype typically appears on the
trunk or extremities and the mean age of diagnosis is 57 years.
The infiltrative form appears on the head and neck in the late
60s, often at embryonic fusion lines, with an opaque yellow-
white color that blends with surrounding skin and has no
raised edges. The morpheaform subtype represents 2% to 3%
of all BCC and is the most aggressive subtype. It usually pres-
ents as an indurated macule or papule with the appearance of
an enlarging scar. The clinical margins are often indistinct,
and the rate of positive margins after excision is high. There
is also a pigmented variant of BCC that can be difficult to
distinguish from certain melanoma subtypes. (See Schwartz
11th ed., pp. 528–529.)
9. Patients not suitable for sentinel node biopsy include all Answer: D
of the following EXCEPT: Clinical situations where sentinel lymph node (SLN) dissec-
A. Inflammatory carcinoma of the breast tion is not recommended include patients with inflammatory
B. Prior axillary surgery breast cancers, those with palpable axillary lymphadenopathy
CHAPTER 17
C. Biopsy proven distant metastases and biopsy proven metastasis, DCIS without mastectomy, or
D. Breast lower inner quadrant carcinoma prior axillary surgery. Although limited data are available, SLN
dissection appears to be safe in pregnancy when performed
with radioisotope alone. (See Schwartz 11th ed., p. 590.)
Breast
A. Metastases to lymph nodes occurs in approximately axillary lymph node metastases are present in up to 75% of
75% of these patients. these women. Less than 25% of the breast nodules developing
B. Approximately 50% of breast nodules developing during pregnancy and lactation will be cancerous. Mammog-
during pregnancy are malignant. raphy is rarely indicated because of its decreased sensitivity
C. Mammography is especially useful in localizing small during pregnancy and lactation; however, the fetus can be
lesions. shielded if mammography is needed. Chemotherapy admin-
D. There is risk of chemotherapy teratogenicity if used istered during the first trimester carries a risk of spontaneous
during the second, but not the third, trimester of abortion and a 12% risk of birth defects. There is no evidence
pregnancy. of teratogenicity resulting from administration of chemo-
therapeutic agents in the second and third trimesters. (See
Schwartz 11th ed., p. 600.)
A. Most common organism is Escherichia coli. isms most frequently recovered from nipple discharge from
B. Operative drainage is the most common therapeutic an infected breast. Previously almost all breast abscesses were
approach. treated by operative incision and drainage, but now the initial
C. Fungal infections of the breast are most commonly approach is antibiotics and repeated aspiration of the abscess,
initiated by nursing infants. usually ultrasound-guided aspiration. Intraoral fungi that are
D. Bilateral Mondor disease is more common than uni- introduced into the breast tissue by the suckling infant can
lateral disease. initiate infection which presents as mammary abscesses in
Breast
CHAPTER 17
D. Radical mastectomy removes all breast tissue, nipple- and Ill axillary lymph nodes. The Halsted radical mastectomy
areola complex, and levels I, II, and III axillary lymph removes all breast tissue and skin, the nipple-areola complex,
nodes, the pectoralis major muscle, and internal the pectoralis major and pectoralis minor muscles, and the
mammary lymph nodes sampling. levels I, II, and Ill axillary lymph nodes. (See Schwartz 11th ed.,
p. 591.)
Breast
143
Inferior
thyroid a.
3
2
1
Lateral longitudinal
Branch from anastomosis
internal thoracic a.
Superior bronchial a.
Middle bronchial a.
FIG. 19-1. Arterial blood supply to the larynx and upper
trachea. a. = artery.
145
Internal
laryngeal n.
CHAPTER 19
Aryepiglottic m.
Transverse, oblique
arytenoid mm.
Lateral
Thyroepiglottic m.
cricoarytenoid m.
Chest Wall, Lung, Mediastinum, and Pleura
Posterior
Thyroarytenoid m.
cricoarytenoid m.
Thyroid cartilage
facet
Recurrent
FIG. 19-2. Anatomy of the larynx and upper trachea. laryngeal n. Cricothyroid m.
m. = muscle; n. = nerve. (cut)
3. All of the following increase the risk for tracheal stenosis Answer: C
EXCEPT: Intubation-related risk factors include: prolonged intubation;
A. Age > 70 years. high tracheostomy through the first tracheal ring or crico-
B. Radiation. thyroid membrane; transverse rather than vertical incision
C. Male gender. on the trachea; oversized tracheostomy tube; prior tracheos-
D. Excessive corticosteroid therapy. tomy or intubation; and traumatic intubation. Stenosis is also
more common in older patients, in females, after radiation,
or after excessive corticosteroid therapy, and in the setting of
concomitant diseases such as autoimmune disorders, severe
reflux disease, or obstructive sleep apnea and the setting of
severe respiratory failure. However, even a properly placed
tracheostomy can lead to tracheal stenosis because of scar-
ring and local injury. Mild ulceration and stenosis are fre-
quently seen after tracheostomy removal. Use of the smallest
tracheostomy tube possible, rapid downsizing, and a vertical
tracheal incision minimize the risk for posttracheostomy ste-
nosis. (See Schwartz 11th ed., p. 663.)
CHAPTER 19
without alveoli). The tracheobronchial tree is normally lined
by pseudostratified ciliated columnar cells and mucous (or
goblet) cells, which both derive from basal cells (Fig. 19-3).
Ciliated cells predominate. Goblet cells, which release mucus,
can significantly increase in number in acute bronchial
injury, such as exposure to cigarette smoke. The normal bron-
chial epithelium also contains bronchial submucosal glands,
C. Adenocarcinoma in-situ --> Lepidic predominate ized criteria and terminology for diagnosis in cytologic and
adenocarcinoma --> Minimally invasive adenocarci- small biopsy specimens, and routine molecular testing for
noma --> Invasive adenocarcinoma known mutations, such as estimated glomerular filtration rate
D. Minimally invasive adenocarcinoma --> Lepidic pre- (EGFR) and KRAS mutations. The new classification system
dominate adenocarcinoma --> Adenocarcinoma in- delineated a stepwise pathologic progression, from Atypical
situ --> Invasive adenocarcinoma adenomatous hyperplasia (AAH) to invasive adenocarci-
noma based on the predominant histologic growth patterns;
Chest Wall, Lung, Mediastinum, and Pleura
CHAPTER 19
monary hilum. Tumors at the medial lung surface or anterior
hilum can directly invade the nerve; symptoms include referred
shoulder pain, hiccups, and dyspnea with exertion because of
diaphragm paralysis. Radiographically, unilateral diaphragm
elevation on chest radiograph is present. The diagnosis can be
confirmed by fluoroscopic examination of the diaphragm with
paradoxical motion with breathing and sniffing, also known as
Classic morphology:
ADC SQCC marker +ve
ADC marker –ve/or
ADC marker STEP 2 Mucin –ve
and/or
Mucin +ve; Apply ancillary panel of
SQCC One SQCC and one ADC marker
marker –ve +/OR Mucin
(or weak in
same cells)
NSCLC, NOS,
Molecular analysis: possible
eg, EGFR mutation† adenosquamous ca
STEP 3
FIG. 19-4. Algorithm for adenocarcinoma diagnosis in small biopsies and/or cytology. Step 1: When positive biopsies (fiberoptic
bronchoscopy [FOB], transbronchial [TBBx], core, or surgical lung biopsy [SLBx]) or cytology (effusion, aspirate, washings, and brushings)
show clear adenocarcinoma (ADC) or squamous cell carcinoma (SQCC) morphology, the diagnosis can be firmly established. If there is
neuroendocrine (NE) morphology, the tumor may be classified as small cell carcinoma (SCLC) or non-small-cell lung carcinoma (NSCLC),
probably large cell neuroendocrine carcinoma (LCNEC) according to standard criteria (+ = positive, − = negative, and ± = positive or
negative). If there is no clear ADC or SQCC morphology, the tumor is regarded as NSCLC -not otherwise specified (NOS). Step 2: NSCLC-NOS
can be further classified based on (a) immunohistochemical stains, (b) mucin (DPAS or mucicarmine) stains, or (c) molecular data. If the stains
all favor ADC-positive ADC marker(s) (ie, TTF-1 and/or mucin positive) with negative SQCC markers, then the tumor is classified as NSCLC,
favor ADC. If SQCC markers (ie, p63 and/or CK5/6) are positive with negative ADC markers, the tumor is classified as NSCLC, favor SQCC. If
the ADC and SQCC markers are both strongly positive in different populations of tumor cells, the tumor is classified as NSCLC-NOS, with a
comment it may represent adenosquamous carcinoma. If all markers are negative, the tumor is classified as NSCLC-NOS. †EGFR mutation
testing should be performed in (1) classic ADC, (2) NSCLC, favor ADC, (3) NSCLC-NOS, and (4) NSCLC-NOS, possible adenosquamous carcinoma.
In NSCLC-NOS, if EGFR mutation is positive, the tumor is more likely to be ADC than SQCC. Step 3: If clinical management requires a more
specific diagnosis than NSCLC-NOS, additional biopsies may be indicated. CD = cluster designation; CK = cytokeratin; DPAS = diastase-periodic
acid Schiff; DPAS +ve = periodic-acid Schiff with diastase; EGFR = epidermal growth factor receptor; IHC = immunohistochemistry; NB = of note;
TTF-1 = thyroid transcription factor-1; -ve = negative; +ve = positive. (Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al:
Diagnosis of lung cancer in small biopsies and cytology: implications of the 2011 International Association for the Study of Lung Cancer/American
Thoracic Society/European Respiratory Society classification, Arch Pathol Lab Med. 2013;137(5):668–684.)
CHAPTER 19
had a sensitivity of 88% and a specificity of 91%, whereas CT
scanning had a sensitivity of 63% and a specificity of 76%.
Combining CT and PET scanning may lead to even greater
accuracy. In one study of CT, PET, and mediastinoscopy in
68 patients with potentially operable NSCLC, CT correctly
identified the nodal stage in 40 patients (59%). It understaged
the tumor in 12 patients and overstaged it in 16 patients. PET
CHAPTER 19
these infections are caused by purely anaerobic bacteria, 25%
are caused by mixed aerobes and anaerobes, and 25% or fewer
are caused by aerobes only. In nosocomial pneumonia, 60% to
70% of the organisms are gram-negative bacteria, including
Klebsiella pneumoniae, Haemophilus influenzae, Proteus spe-
cies, Pseudomonas aeruginosa, Escherichia coli, Enterobacter
cloacae, and Eikenella corrodens. Immunosuppressed patients
17. The population most at risk for developing active tuber- Answer: D
culosis is: Epidemiology. Tuberculosis is a widespread problem that
A. Elderly. affects nearly one-third of the world’s population. Between
B. Minorities. 8.3 and 9 million new cases of tuberculosis and 12 million
C. Urban residents. prevalent cases (range 10–13 million) were estimated world-
D. HIV infection. wide in 2011 according to the World Health Organization.
Only 10,521 new cases were reported to the World Health
Organization in the United States in 2011. HIV infection is
the strongest risk factor for developing active tuberculosis.
The elderly, minorities, and recent immigrants are the most
common populations to have clinical manifestations of infec-
tion, yet no age group, sex, or race is exempt from infection.
In most large urban centers, reported cases of tuberculosis are
more numerous among the homeless, prisoners, and drug-
addicted populations. Immunocompromised patients addi-
tionally contribute to an increased incidence of tuberculosis
infection, often developing unusual systemic as well as pul-
monary manifestations. (See Schwartz 11th ed., p. 710.)
18. The fungi associated with the highest mortality rate due Answer: A
to invasive mycoses in the United States is: Aspergillosis. The genus Aspergillus comprises over 150 species
A. Aspergillus. and is the most common cause of mortality due to invasive
B. Cryptococcus. mycoses in the United States. It is typically acute in onset
C. Candidia. and life-threatening and occurs in the setting of neutropenia,
D. Mucor. chronic steroid therapy, or cytotoxic chemotherapy. It can also
occur in the general intensive care unit population of critically ill
patients, including patients with underlying chronic obstructive
pulmonary disease (COPD), postoperative patients, patients
with cirrhosis or alcoholism, and postinfluenza patients, with-
out any of these factors present. The species most commonly
responsible for clinical disease include A. fumigatus, A. flavus,
A. niger, and A. terreus. Aspergillus is a saprophytic, filamen-
tous fungus with septate hyphae. Spores (2.5–3 μm in diameter)
are released and easily inhaled by susceptible patients; because
the spores are microns in size, they are able to reach the distal
bronchi and alveoli. (See Schwartz 11th ed., p. 711.)
Answer: A
CHAPTER 19
22. Desmoid tumors are associated with which of the follow- Answer: D
ing gene? Desmoid tumors. Soft tissue neoplasms arising from fascial
A. KRAS or musculoaponeurotic structures, desmoid tumors consist
B. RET of proliferations of benign appearing fibroblastic cells, abun-
C. P53 dant collagen, and few mitoses. Desmoid tumors possess
D. Adenomatous polyposis coli (APC) alterations in the APC/β-catenin pathway. Cyclin D1 dys-
regulation is thought to play a significant role in their patho-
genesis. Associations with other diseases and conditions are
well documented, especially those with similar alterations in
the APC pathway, such as familial adenomatous polyposis
(Gardner syndrome). Other conditions with increased risk of
desmoid tumor formation include increased estrogen states
(pregnancy) and trauma. Surgical incisions (abdominal and
thorax) have been the site of desmoid development, either in
or near the scar. (See Schwartz 11th ed., p. 722.)
CHAPTER 19
eosinophilic granulomas, 7% involve multiple eosinophilic
granulomas, and 14% belong to other forms of more systemic
LCH. Isolated single eosinophilic granulomas can occur in the
ribs or skull, pelvis, mandible, humerus, and other sites. They
are diagnosed primarily in children between the ages of 5 and
15 years. Because of the associated pain and tenderness, they
may be confused with Ewing sarcoma or with an inflamma-
27. All of the following are associated with increased risk of Answer: B
CHAPTER 19
1. The most common form of atrial septal defect (ASD) is: Answer: C
A. Sinus venosus defect. ASDs can be classified into three different types (Fig. 20-1):
B. Ostium primum defect. (a) ostium secundum type defect (Fig. 20-1B,C) (deficiency
C. Ostium secundum defect. of septum primum), which are the most prevalent subtype,
D. Combined primum and secundum defect. comprising 80% of all ASDs; (b) ostium primum defects
(Fig. 20-1A), which may also be described as partial or tran-
sitional AV canal defect; and (c) sinus venosus type defects,
comprising approximately 5% to 10% of all ASDs. (See
Schwartz 11th ed., p. 752.)
A B
157
CHAPTER 20
4. The most common location for a coarctation of the aorta Answer: B
is: Coarctation of the aorta (COA) is defined as a luminal nar-
A. Aortic arch. rowing in the aorta that causes an obstruction to blood flow.
B. Distal to the left subclavian artery. This narrowing is most commonly located distal to the left
C. At the diaphragm. subclavian artery. The embryologic origin of COA is a sub-
D. At the level of the renal arteries. ject of some controversy. One theory holds that the obstruct-
CHAPTER 20
C. At 10 kg of weight. ity to pump against systemic afterload. In patients presenting
D. In adolescence. later than 2 weeks, the LV can be retrained with preliminary
pulmonary artery banding and aortopulmonary shunt fol-
lowed by definitive repair. Alternatively, the unprepared LV
can be supported following arterial switch with a mechanical
assist device for a few days while it recovers ability to manage
systemic pressures. Echocardiography can be used to assess
13. During left thoracotomy for repair of patent ductus arte- Answer: B
riosus the blood pressure is 70/22. Immediately after The hemodynamic consequences of an unrestrictive ductal
placement of a clip across the duct the blood pressure is: shunt are left ventricular volume overload with increased left
A. 70/22. atrial and pulmonary artery pressures and right ventricular
B. 70/40. strain from the augmented afterload. These changes result
C. 90/22. in increased sympathetic discharge, tachycardia, tachypnea,
D. 90/40. and ventricular hypertrophy. The diastolic shunt results in
lower aortic diastolic pressure and increases the potential for
myocardial ischemia and underperfusion of other systemic
organs, while the increased pulmonary flow leads to increased
work of breathing and decreased gas exchange. Unrestrictive
ductal flow may lead to pulmonary hypertension within the
first year of life (See Schwartz 11th ed., pp. 759–760.)
CHAPTER 20
C. Aortic 1-patch repair (Doty procedure) imparted by the subvalvular stenosis may affect leaflet mor-
D. Aortoventriculoplasty phology and valve competence.
Diffuse subvalvular AS results in a long, tunnel-like obstruc-
tion that may extend to the left ventricular apex. In some
individuals, there may be difficulty in distinguishing between
hypertrophic cardiomyopathy and diffuse subaortic stenosis.
Operation for subvalvular AS is indicated with a gradient
CHAPTER 20
tic position, reimplantation of the coronary arter- pulmonary artery continuity. Over the next 20 years, improved
ies, and right ventricular outflow tract (RVOT) survival rates led to uniform adoption of complete repair even
reconstruction in the youngest and smallest infants. Surgical correction entails
D. Mobilization of the pulmonary arteries, patch repair the use of cardiopulmonary bypass (CPB). Repair is com-
of the aorta and ventricular septal defect (VSD), and pleted by separation of the pulmonary arteries from the aorta,
extracardiac reconstruction of the RVOT closure of the aortic defect (occasionally with a patch) to
minimize coronary flow complications, placement of a valved
20. Which of the following factors confers the highest post- Answer: C
operative mortality after total anomalous pulmonary The most significant postoperative complication of TAPVC
venous connection (TAPVC) repair? repair is pulmonary venous obstruction (Fig. 20-5), which
A. Postoperative atrial arrythmias occurs 9% to 11% of the time, regardless of the surgical tech-
B. Patient age at operation nique employed. Mortality varies between 30% and 45%,
C. Pulmonary venous sclerosis and alternative catheter interventions do not offer definitive
D. Postoperative left ventricular (LV) dysfunction solutions. Recurrent pulmonary venous obstruction can be
localized at the site of the pulmonary venous anastomosis
(extrinsic), which usually can be cured with patch enlarge-
ment or balloon dilatation, or it may be secondary to endo-
cardial thickening of the pulmonary venous ostia frequently
resulting in diffuse pulmonary venous sclerosis (intrinsic),
which carries a 66% mortality rate because few good solutions
exist. More commonly, post repair left ventricular dysfunc-
tion can occur as the noncompliant LV suddenly is required
to handle an increased volume load from redirected pulmo-
nary venous return. This can manifest as an increase in pul-
monary artery pressure but is distinguishable from primary
CHAPTER 20
Congenital Heart Disease
FIG. 20-6. CT angiogram showing the four artery sign classic of FIG. 20-7. MRI showing a double aortic arch.
double aortic arch.
FIG. 20-8. Unilateral hyperinflation of the left lung associated with FIG. 20-9. CT angiogram showing a PA sling. Note the LPA
a rare vascular ring: left ascending aorta and right-sided descending wrapping around behind the trachea.
aorta.
CHAPTER 20
to increase coronary blood flow cyanotic. Reestablishing ductal patency (with PGE1) restores
pulmonary blood flow and stabilizes patients for surgical
intervention. Pulmonary hypertension is unusual in tricus-
pid atresia. However, occasional patients have a large VSD
between the LV and the infundibular portion of the RV (just
below the pulmonary valve). If there is no obstruction at the
level of this VSD or at the valve, these infants may actually pres-
FIG. 20-12. EKG of a newborn with Ebsteins anomaly and WPW syndrome. Note the pre-excitation (arrow).
25. After accounting for size and location of the accompa- Answer: D
nying ventricular septal defect (VSD), which additional Patients with DORV typically present with one of the follow-
Congenital Heart Disease
factor is a critical determinant of the clinical presenta- ing three scenarios: (a) those with doubly committed or sub-
tion and management of double-outlet right ventricle aortic VSD present with congestive heart failure and a high
(DORV)? propensity for pulmonary hypertension, much like infants
A. Left ventricular hypertrophy with a large single VSD; (b) those with a subaortic VSD and
B. Posterior location of the aorta pulmonary stenosis present with cyanosis and hypoxia, much
C. Anterior location of the aorta like infants with tetralogy of Fallot; and (c) those with sub-
D. Presence of right ventricular outflow tract (RVOT) pulmonic VSD present with cyanosis, much like those with
obstruction D-TGA, because streaming directs desaturated systemic
venous blood to the aorta and oxygenated blood to the pul-
monary artery. Thus, the three critical factors influencing the
clinical presentation and subsequent management of infants
with DORV are the size and location of the VSD, the presence
or absence of important RVOT obstruction, and the presence
of other anomalies (especially associated hypoplasia of left-
sided structures sometimes seen with subpulmonic VSD).
(See Schwartz 11th ed., p. 783.)
171
CHAPTER 21
tive strategy. (See Schwartz 11th ed., p. 804.)
5. The bypass conduit with the highest patency rate is the: Answer: B
A. Radial artery. Bypass Conduit Selection. The most important criterion in
B. Internal thoracic artery. conduit selection is graft patency. The conduit with the high-
C. Greater saphenous vein. est patency rate (98% at 5 years and 85%–90% at 10 years)
D. Radial artery. is the internal thoracic artery which is most commonly left
attached proximally to the subclavian artery (although occa-
sionally used as a free graft) and anastomosed distally to
the target coronary artery. The use of both internal thoracic
arteries has been shown to increase event-free survival in a
number of studies. (See Schwartz 11th ed., p. 811.)
D. Bioprosthetic valves have similar rates of thrombosis togenic potential. Conversely, patients with other indications
compared to mechanical valves. for systemic anticoagulation, such as other risk factors for
thromboembolism (ie, atrial fibrillation), or the presence of
a mechanical prosthetic valve in place in another position,
may benefit from mechanical valve replacement. Current
ACC/AHA guidelines recommend a shared-decision-making
process between patient and physician when determining the
Acquired Heart Disease
CHAPTER 21
10. Patients undergoing mechanical mitral valve Answer: B
replacement: Although mechanical valves necessitate systemic anticoagula-
A. Have a target INR of 4 to 5 times normal. tion, careful monitoring of the international normalized ratio
B. Have increased left atrial size. (INR) reduces the risk of thromboembolic events andhemor-
C. Have atrial fibrillation. rhagic complications, and improves overall survival. Patients
D. Are at lower risk for thromboembolism. undergoing mechanical aortic valve replacement generally
CHAPTER 21
left atria and long-standing persistent AF. In most cases, the right atrial lesion set performed on the
beating heart, whereas the left atrial lesions are performed
during cardioplegic arrest (Fig. 21-1). (See Schwartz 11th ed.,
p. 838.)
A B
C. Constrictive pericarditis. sive testing. Central venous pressure (CVP) is often elevated
D. Primary pulmonary artery hypertension. 15 to 20 mm Hg or higher. Electrocardiogram (ECG) com-
monly demonstrates nonspecific low voltage QRS complexes
and isolated repolarization abnormalities. Chest X-ray may
demonstrate calcification of the pericardium, which is highly
suggestive of constrictive pericarditis in patients with heart
failure, but this is present in only 25% of cases. Cardiac CT
Acquired Heart Disease
CHAPTER 21
cardiac index and decreases both preload and myocardial
oxygen consumption. (See Schwartz 11th ed., p. 835.)
181
CHAPTER 22
therapy has made syphilitic aneurysms a rarity in developed
nations. In other parts of the world, however, syphilitic aneu-
rysms remain a major cause of morbidity and mortality. The
spirochete Treponema pallidum causes an obliterative end-
arteritis of the vasa vasorum that results in medial ischemia
and loss of the elastic and muscular elements of the aortic
wall. The ascending aorta and arch are the most commonly
12. The primary modes to study for thoracic aorta disease Answer: C
is/are: Although catheter-based contrast aortography was previously
Thoracic Aneurysms and Aortic Dissection
A. Invasive aortography. considered the gold standard for evaluating thoracic aortic
B. Cardiac catheterization. disease, cross-sectional imaging (ie, CT and MRA) has largely
C. Cross-sectional imaging (computed tomography replaced this modality. Technologic improvements have
[CT] and magnetic resonance angiography [MRA]). enabled CT and MRA to provide excellent aortic imaging
D. Abdominal ultrasound. while causing less morbidity than catheter-based studies do,
so CT and MRA are now the primary modes for evaluating
thoracic aortic disease. Today, the use of invasive aortography
in patients with thoracic aortic disease is generally limited to
those undergoing endovascular therapies or when other types
of studies are contraindicated or have not provided satisfac-
tory results. (See Schwartz 11th ed., p. 859.)
CHAPTER 22
Thoracic Aneurysms and Aortic Dissection
FIG. 22-1. Illustration of the classification schemes for aortic dissection based on which portions of the aorta are involved. Dissection
can be confined to the ascending aorta (left) or the descending aorta (middle), or it can involve the entire aorta (right). (Reproduced with
permission from Baylor College of Medicine.)
16. Endoleaks:
A. Type I and Type IV generally require early and Another significant complication of descending thoracic
aggressive intervention. aortic stent grafting is endoleak. An endoleak occurs when
B. Are uncommon. there is a persistent flow of blood (visible on radiologic imag-
C. Can during the initial procedure or over time. ing) into the aneurysm sac, and it may occur during the
D. Are categorized by leak site. initial procedure or develop over time. Although endoleaks
are a relatively common complication, they are not benign,
because they lead to continual pressurization of the sac,
which can cause expansion or even rupture. These compli-
cations are categorized (Table 22-1) according to the site
of the leak. Although all endoleaks may progress such that
they can be considered life-threatening, type I and type III
CHAPTER 22
19. Delay of emergency repair of ascending aortic dissection Answer: D
should be considered in: Because of the risk of aortic rupture, acute ascending aortic
A. Patients who present with severe acute stroke or mes- dissection is usually considered an absolute indication for
enteric ischemia. emergency surgical repair. However, specific patient groups
B. Dissections that occur in the first 3 weeks after car- may benefit from nonoperative management or delayed
diac surgery. operation. Delayed repair should be considered for patients
189
A. The cuff is inflated to above systolic pressure to detect determine the underlying arterial occlusive disease. Pressure
pulse volume changes. measurement in such patients is not accurate because of non-
B. Brisk upstroke of the waveform in the pulse volume compressibility. Capsule placed at different levels on the leg
recording is suggestive of proximal disease. detect changes in blood volume and he produced a graft. To
C. When compared with angiography, PVR has an accu- obtain accurate PVR waveforms, the cuff is inflated to a pres-
racy of 30%. sure of 60 to 65 mm Hg, so as to detect volume changes without
D. Its best application is in patients with noncompress- causing arterial occlusion. Pulse volume tracings are suggestive
Arterial Disease
ible vessels that would interfere with accurate mea- of proximal disease of the upstroke of the pulse is not brisk,
surement of segmental pressures. the peak of the wave tracing is rounded, and there is disap-
pearance of the dicrotic notch. Although isolated segmental
limb pressures and PVR measurements are 85% accurate when
compared with angiography in detecting and localizing signifi-
cant atherosclerotic lesions, when using combination, accuracy
reaches 95%. (See Schwartz 11th ed., p. 900.)
CHAPTER 23
ischemia. geon must decide whether intraoperative cerebral monitoring
D. Stump pressure measurement is the most sensitive is necessary or intra-arterial carotid shunting would be used.
test for potential cerebral ischemia. In general, if the patient is awake, then his or her abilities to
respond to commands during carotid clamp determine the
adequacy of cerebral perfusion to the ipsilateral hemisphere.
On the other hand, intraoperative EEG or transcranial power
Doppler (TCD) has been used to monitor for adequate cere-
Arterial Disease
bral perfusion during the clamp. For patients undergoing
surgery under general anesthesia, focal ipsilateral decreases
in amplitude and slowing of EEG waves are indicative of cere-
bral ischemia. Similarly, a decrease to <50% of baseline veloc-
ity in the ipsilateral middle cerebral artery is a sign of cerebral
ischemia. For patients with poor collateral flow exhibiting
signs of cerebral ischemia, intra-arterial carotid shunting
with removal of the clamp will restore cerebral flow for the
remaining part of the surgery. Stump pressures have been
used to determine the need for intra-arterial carotid shunt-
ing. Some surgeons prefer to shunt all patients on a routine
basis and not use intraoperative cerebral monitoring. (See
Schwartz 11th ed., pp. 912–913.)
C. External iliac artery diameter >7 mm. site and the access vessels, respectively. The requirements
D. Aortic neck angle < 60 degrees. for proximal aortic neck are diameter of 18 to 28 mm and
the minimum length of 15 mm. Usually, multiple measure-
ments of the diameter are taken along the length of the neck
to assess its shape. All diameter measurements are made from
mid wall to mid wall of the vessel. Secondary considerations
include the mural calcification < 50% circumference, luminal
Arterial Disease
CHAPTER 23
natural history of untreated chronic mesenteric ischemia may
justify revascularization in some minimally symptomatic or
asymptomatic patients if the operative risks are acceptable,
since the first clinical presentation may be acute intestinal
ischemia in as many as 50% of patients, with a mortality
rate that ranges from 15% to 70%. Mesenteric angioplasty
and stenting is particularly suited for this patient subgroup
Arterial Disease
given its low morbidity and mortality. (See Schwartz 11th ed.,
pp. 928–933.)
CHAPTER 23
D. Applying rings to the graft to improve patency tal anastomosis to get the benefit obtained with vein cuffs
and covalently binding agents onto the luminal surface with
anticoagulant, anti-inflammatory, and antiproliferative char-
acteristics. A comparison of precuffed PTFE versus PTFE
with a vein cuff showed a 1 year and 2 years primary patency
rates were 52% and 49% in the precuffed group and 62% and
44% in the vein cuff group, respectively. Another approach
Arterial Disease
for improving outcomes using prosthetic for bypass grafts
involves binding anticoagulants to the conduit. The Gore pro-
paten graft has heparin-bonded into the luminal surface of
the PTFE graft using Carmeda bioactive surface technology.
The heparin-binding does not alter the micro structure and
handling characteristic of the PTFE. A prospective random-
ized trial suggested that heparin-bonded Dacron or PTFE
was superior to plain PTFE for above-knee popliteal bypass.
The 3-year primary patency rate for the heparin-bonded graft
was 55% compared with 42% for the PTFE. But both of these
patency rates are inferior to greater saphenous vein grafts.
(See Schwartz 11th ed., p. 967-968.)
197
CHAPTER 24
Venous and Lymphatic Disease
FIG. 24-1. Characteristic hyperpigmentation
of chronic venous insufficiency.
5. All of the following are acquired risk factors for venous Answer: B
thromboembolism (VTE) EXCEPT: The more common acquired VTE risk factors include older
A. Nephrotic syndrome. age (>40 years), hospitalization and immobilization, hor-
B. Factor V Leiden. mone replacement and oral contraceptive therapy, pregnancy
C. Malignancy. and the recently postpartum state, prior VTE, malignancy,
D. Pregnancy. major surgery, obesity, nephrotic syndrome, trauma and spi-
E. Obesity. nal cord injury, long-haul travel (>6 hours), varicose veins,
F. Varicose veins. antiphospholipid syndrome, myeloproliferative disorders,
and polycythemia. Heritable risk factors include male sex,
factor V Leiden mutation; prothrombin 20210A gene variant;
antithrombin, protein C, and protein S deficiencies; and dys-
fibrinogenemias. In some patients, the cause of the thrombo-
philia may have both a heritable and an acquired component.
These mixed causes include homocysteinemia; factors VII,
VIII, IX, and XI elevation; hyperfibrinogenemia; and acti-
vated protein C resistance in the absence of factor V Leiden.
There may be a synergistic effect when particular multiple
inherited and acquired risk factors are present in the same
patient.
Other patient-specific factors associated with venous
thrombosis include the traditional cardiovascular risk fac-
tors of obesity, hypertension, and diabetes. VTE is more
common in whites and African Americans than Asians and
Native Americans. Certain gene variants (single nucleotide
polymorphisms) are also associated with a mildly increased
risk for VTE, and their presence may interact with other risk
factors to increase the overall risk for venous thrombosis.
(See Schwartz 11th ed., Figure 24-3, p. 984.)
CHAPTER 24
D. A rapidly expanding hemangioma
• Asymptomatic and no risk factors for progression Serial imaging in 2 weeks, if progression VKA
for 3 months
Second episode DVT/unprovoked VKA for extended therapy
DVT and cancer LMWH for extended therapy over VKA
LMWH = low molecular weight heparin; VKA = vitamin K antagonist.
Data from Kearon C, Akl EA, Comerota AJ, et al: Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention
of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012;
141(2 Suppl): e419S-e496S.
CHAPTER 24
A
11. All of the following are appropriate therapies for suppu- Answer: C
rative thrombophlebitis (SVT) EXCEPT: Treatment of SVT is quite variable. A Cochrane Review
A. Nonsteroidal anti-inflammatory medications. reported that low molecular weight heparin (LMWHs) and
B. Antibiotics. nonsteroidal anti-inflammatory drugs both reduce the rate of
C. Systemic steroid therapy. SVT extension or recurrence. Topical medications appear to
D. Removal of existing indwelling venous catheters. improve local symptoms. Surgical treatment, combined with
the use of graduated compression stockings, is associated with
a lower rate of venous thromboembolism (VTE) and SVT
progression. The treatment is individualized and depends on
the location of the thrombus and the severity of symptoms. In
patients with SVT not within 1 cm of the saphenofemoral junc-
tion, treatment consists of compression and administration
of an anti-inflammatory medication such as indomethacin.
In patients with suppurative SVT, antibiotics and removal of
any existing indwelling catheters are mandatory. Excision of
the vein may be necessary but is usually reserved for patients
with systemic symptoms or when excision of the involved vein
is straightforward. If the SVT extends proximally to within
1 cm of the saphenofemoral junction, extension into the com-
mon femoral vein is more likely to occur. In these patients,
anticoagulation therapy for 6 weeks and GSV ligation appear
equally effective in preventing thrombus extension into the
deep venous system. (See Schwartz 11th ed., p. 994.)
R FVP R FVP
CHAPTER 24
heparin be monitored periodically in patients receiving continuous
D. Minimal association with thrombotic complications heparin therapy.
HIT is diagnosed based on previous exposure to heparin,
platelet count < 100,000, and/or platelet count decline of
50% following exposure. All heparin must be stopped and
alternative anticoagulation initiated immediately to avoid
thrombotic complications, which may approach 50% over
207
Esophageal branch
Inferior thyroid
artery
Superior left
Right bronchial bronchial artery
artery Inferior left
CHAPTER 25
bronchial artery
Aortic esophageal
arteries
The Esophagus and Diaphragmatic Hernia
CHAPTER 25
(See Schwartz 11th ed., p. 1035.)
CHAPTER 25
the approach. Lesions of the proximal and middle esopha-
gus require a right thoracotomy, whereas distal esophageal
lesions require a left thoracotomy. Videothoracoscopic and
laparoscopic approaches are now frequently used. The mor-
tality rate associated with enucleation is low, and success in
relieving the dysphagia is near 100%. Large lesions or those
involving the gastroesophageal junction (GEJ) may require
Recurrent
laryngeal
nerves
Right vagus nerve
Right recurrent
laryngeal nerve
Left recurrent
laryngeal nerve
Anterior esophageal
Thoracic chain
plexus
Left or anterior
vagal trunk
CHAPTER 25
metastasize: The lymphatics located in the submucosa of the esophagus are
A. In the submucosal lymph plexus. so dense and interconnected that they constitute a single plexus
B. Into regional nodes. (Fig. 25-3). There are more lymph vessels than blood capillar-
C. In a transverse direction. ies in the submucosa. Lymph flow in the submucosal plexus
D. Directly into the muscle layer. runs in a longitudinal direction, and, on injection of a contrast
E. In a hematogenous fashion. medium, the longitudinal spread is seen to be about six times
that of the transverse spread. In the upper two-thirds of the
Paratracheal
nodes
Pulmonary hilar
nodes Subcarinal nodes
Inferior paraesophageal
nodes
Parahiatal nodes
Splenic artery
nodes
Left gastric artery nodes
Hepatic artery
nodes
A B
FIG. 25-4. Complications of reflux disease as seen on endoscopy. A. Linear erosions of LA grade B esophagitis. B. Uncomplicated Barrett
mucosa. C. High-grade dysplasia in Barrett mucosa. D. Early adenocarcinoma arising in Barrett mucosa. (Continued)
CHAPTER 25
The Esophagus and Diaphragmatic Hernia
C D
FIG. 25-4. (Continued)
19. The most direct method of measuring gastric juice expo- Answer: C
sure in the esophagus is: The most direct method of measuring increased esophageal
A. Esophageal motility study. exposure to gastric juice is by an indwelling pH electrode,
B. High resolution manometry. or, more recently, via a radiotelemetric pH monitoring cap-
C. 24-hour ambulatory pH monitoring. sule that can be clipped to the esophageal mucosa. The lat-
D. Esophageal impedance. ter consists of an antimony pH electrode fitted inside a small,
E. Esophageal transit scintigraphy. capsule-shaped device accompanied by a battery and elec-
tronics that allow 48-hour monitoring and transmission of
the pH data via transcutaneous radio telemetry to a waist-
mounted data logger. The device can be introduced either
transorally or transnasally, and it can be clipped to the
esophageal mucosa using endoscopic fastening techniques. It
passes spontaneously within 1 to 2 weeks. Prolonged moni-
toring of esophageal pH is performed by placing the pH
probe or telemetry capsule 5 cm above the manometrically
measured upper border of the distal sphincter for 24 hours.
It measures the actual time the esophageal mucosa is exposed
to gastric juice, measures the ability of the esophagus to clear
refluxed acid, and correlates esophageal acid exposure with
the patient’s symptoms. A 24- to 48-hour period is necessary
so that measurements can be made over one or two complete
circadian cycles. This allows measuring the effect of physi-
ologic activity, such as eating or sleeping, on the reflux of gas-
tric juice into the esophagus (Fig. 25-5). (See Scwartz 11th ed.,
p. 1029–1030.)
pH sp
8
CHAPTER 25
6
4
2
CHAPTER 25
length can be surgically augmented over preoperative values,
and that the change in the former is a function of the degree
of gastric wrap around the esophagus (Fig. 25-7). However,
the aim of any fundoplication is to create a loose wrap and to
maintain the position of the gastric fundus close to the distal
intra-abdominal esophagus, in a flap valve arrangement. The
efficacy of this relies on the close relationship between the
Distention
15
10
0 240 360
Degree of wrap
FIG. 25-7. The relationship between the augmentation of
sphincter pressure over preoperative pressure (ΔP) and the degree
of gastric fundic wrap in three different antireflux procedures.
(Reproduced with permission from O’Sullivan GC, DeMeester
TR, Joelsson BE, et al. Interaction of lower esophageal sphincter
pressure and length of sphincter in the abdomen as determinants of
gastroesophageal competence, Am J Surg. 1982;143(1):40–47.)
mediastinum and (c) the combined sliding-rolling or mixed hernia, type III,
characterized by an upward dislocation of both the cardia and
the gastric fundus (Fig. 25-8C). The end stage of type I and
type II hernias occurs when the whole stomach migrates up
into the chest by rotating 180° around its longitudinal axis,
with the cardia and pylorus as fixed points. In this situation,
the abnormality is usually referred to as an intrathoracic stom-
The Esophagus and Diaphragmatic Hernia
A B
FIG. 25-8. A. Radiogram of a type I (sliding) hiatal hernia. B. Radiogram of a type II (rolling or paraesophageal) hernia. C. Radiogram of a
type III (combined sliding-rolling or mixed) hernia. D. Radiogram of an intrathoracic stomach. This is the end stage of a large hiatal hernia
regardless of its initial classification. Note that the stomach has rotated 180° around its longitudinal axis, with the cardia and pylorus as fixed
points. (Reproduced with permission from Nyhus LM, Condon RE. Hernia, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1989.) (Continued)
CHAPTER 25
The Esophagus and Diaphragmatic Hernia
C
CHAPTER 25
recent randomized clinical trial, 7% of patients undergoing
Dor fundoplication following lower esophageal sphincter
(LES) myotomy had abnormal 24-hour pH probes, and 42%
of patients with a myotomy only had abnormal reflux profiles.
If an antireflux procedure is used as an adjunct to esophageal
myotomy, a complete 360° fundoplication should be avoided.
Rather, a 270° Belsey fundoplication, a Toupet posterior 180°
28. The top three most common complications (in order of Answer: A
most common to least common) following an minimally The MIS transthoracic two-field esophagectomy is slightly
invasive surgery (MIS) three-field esophagectomy are: different. In this operation, the abdominal portions of the
A. Pneumonia, atrial fibrillation, anastomotic leak. operation are done first, including placement of the feeding
B. Anastomotic leak, pneumonia, deep vein thrombosis tube, the creation of the conduit, and the sewing of the tip of
(DVT). the conduit to the fully dissected gastroesophageal junction
C. Atrial fibrillation, thoracic duct injury, pneumonia. (GEJ). The patient is then rolled into the left lateral decubitus
D. Pneumonia, anastomotic leak, pneumothorax. position and, through right thoracoscopy, the esophagus is
E. Atrial fibrillation, anastomotic leak, pneumonia. dissected and divided 10 cm above the tumor. Once freed, the
specimen is pulled out through the mini-thoracotomy, and
an end-to-end anastomosis stapler is introduced through the
high corner of the gastric conduit and out a stab wound along
the greater curvature. The anvil of the stapler is placed in the
proximal esophagus and held with a purse-string, the stapler
is docked, the anastomosis is created, and a gastrotomy is
then closed with another firing of the gastrointestinal anas-
tomosis (GIA) stapler. The three-field esophagectomy has
the advantage of placing the anastomosis in the neck where
223
p. 1117.)
Because H. pylori induces a strong immunologic response,
serological testing is useful but may not be as accurate as the
urea breath test or the stool antigen test, and a positive serol-
ogy persists after eradication of H. pylori infection, so serology
is not useful to confirm successful treatment of Helicobacter
infection. (See Schwartz 11th ed., p. 1119.)
Stomach
CHAPTER 26
divided into those associated with hyperacidity and those
associated with hypoacidity (see Fig. 26-1). The diagnosis of
ZES is confirmed by the secretin stimulation test. An intra-
venous (IV) bolus of secretin (2 U/kg) is given, and gastrin
levels are checked before and after injection. An increase in
serum gastrin of 200 pg/mL or greater suggests the presence
of gastrinoma. (See Schwartz 11th ed., p. 1137.)
Stomach
Elevated serum gastrin
(off PPI + H2RA)
Yes No
FIG. 26-1. Algorithm for diagnosis and management of hypergastrinemia. BAO = basal acid output; B1 = Billroth 1; B2 = Billroth 2; Bx = biopsy;
ECL = enterochromaffin-like; EGD = esophagogastroduodenoscopy; GJ = gastrojejunostomy; H2RA = histamine 2 receptor antagonist;
insuff = insufficiency; MEN1 = multiple endocrine neoplasia type I; PPI = proton pump inhibitor; R/O = rule out; SB = small bowel; S/P = status
post; TV = truncal vagotomy; TV and A = truncal vagotomy and antrectomy.
CHAPTER 26
injection of 100 mL oral contrast via NG shows extravasa- p. 1134.)
tion from the duodenal bulb, copious-free peritoneal fluid,
and air. BP is now 110/70, serum lactate is normal, and
urine output in the past hour is 20 mL. You strongly suspect
perforated duodenal ulcer and you would recommend:
A. Endoscopy and biopsy.
B. Immediate closure of perforation with Graham patch.
Stomach
C. Nonoperative management.
D. Immediate closure of perforation with definitive
ulcer operation.
E. An additional 8 hours of ICU resuscitation, followed
by laparoscopic patch and highly selective vagotomy.
A B C
FIG. 26-4. A through C. Billroth II antecolic gastrojejunostomy. (Reproduced with permission from
Zinner MJ, Schwartz SI, Ellis H. Maingot’s Abdominal Operations, 10th ed. Vol. I. Stamford, CT: Appleton
& Lange; 1997.)
<50% gastric
remnant
50 to 60 cm
CHAPTER 26
gastrectomy. resented and the absolute benefit of multimodality therapy
D. Subtotal gastrectomy with removal and assess- in this context may not be as great as in the overall cohort
ment of >16 regional lymph nodes and adjuvant of patients with locally advanced disease. Selective omission
chemoradiotherapy. of adjuvant therapy in patients with more favorable surgical
E. Endoscopic resection. pathology may be appropriate. T2 tumors are not well treated
with endoscopic resection given a prohibitive risk of recur-
rence. (See Schwartz 11th ed., pp. 1139–1149.)
Stomach
12. Which of the following is not TRUE of hereditary diffuse Answer: B
gastric cancer (HDGC)? Mutations in the E-cadherin gene (CDH1) are associated with
A. It is associated with a mutation in the E-cadherin HDGC. The lifetime risk of gastric cancer is approximately
gene. 70% in men and 56% in women. Mutation-carrying women
B. Lifetime risk of gastric cancer in affected women is are at increased risk for breast cancer, typically lobular carci-
greater than in men. nomas. Because of the poor prognosis associated with clini-
C. It is associated with an increased risk of lobular breast cal gastric cancer in this setting and limitations of existing
cancer. surveillance protocols, prophylactic gastrectomy is a consid-
D. Presentation with clinically significant gastric cancer eration in individuals with CDH1 mutations. (See Schwartz
is associated with a very poor prognosis. 11th ed., p. 1143.)
D. Adjuvant Sunitinib for at least 3 years. coma Group XV111 trial and there is increasing momentum
E. Adjuvant Imatinib for at least 3 years. for indefinite treatment after resection of high-risk disease.
(See Schwartz 11th ed., pp. 1149–1151.)
16. Which of the following options is the best initial man- Answer: A
agement of a low-grade mucosa-associated lymphoid tis- Low-grade MALT lymphoma, essentially a monoclonal pro-
sue (MALT) lymphoma of the gastric antrum? liferation of B cells, presumably arises from a background of
Stomach
A. Helicobacter pylori eradication chronic gastritis associated with H. pylori. These relatively
B. Chemotherapy +/– radiation therapy innocuous tumors then undergo degeneration to high-grade
C. Wedge resection lymphoma, which is the usual variety seen by the surgeon.
D. Antrectomy Remarkably, when the H. pylori is eradicated and the gastritis
improves, the low-grade MALT lymphoma often disappears.
Thus, low-grade MALT lymphoma is not a surgical lesion.
Careful follow-up is necessary particularly in those lesions
with a t (11:18) translocation, thought to be a risk factor for a
more aggressive MALT lesion. (See Schwartz 11th ed., p. 1149.)
18. In the patient with a normal liver and endoscopic diag- Answer: C
nosis of watermelon stomach (gastric antral vascular The parallel red stripes atop the mucosal folds of the distal
ectasia [GAVE]), chronic blood loss requiring multiple stomach give this rare entity its name. Histologically, gastric
transfusions is best treated by: antral vascular ectasia (GAVE) is characterized by dilated
A. Proton pump inhibitors and Carafate. mucosal blood vessels that often contain thrombi, in the
B. Beta blockers. lamina propria. Mucosal fibromuscular hyperplasia and hya-
C. Distal gastrectomy. linization often are present (Fig. 26-6). The histologic appear-
D. Total gastrectomy. ance can resemble portal hypertensive gastropathy, but the
latter usually affects the proximal stomach, whereas water-
melon stomach predominantly affects the distal stomach.
CHAPTER 26
plasma coagulator. Antrectomy may be required to control
blood loss, and this operation is quite effective but carries
increased morbidity in this elderly patient group. Patients
with portal hypertension and antral vascular ectasia should
be considered for transjugular intrahepatic portosystemic
shunt (TIPSS). (See Schwartz 11th ed., p. 1154.)
Stomach
19. Treatment for severe early dumping after gastrectomy Answer: C
that is persistent despite an antidumping diet and fiber is: A variety of hormonal aberrations have been observed in
A. Expectant management. early dumping, including increased serum levels of vasoactive
B. Oral glucose for symptoms. intestinal polypeptide (VIP), cholecystokinin (CCK), neuro-
C. Octreotide. tensin, peripheral hormone peptide YY, renin-angiotensin-
D. Surgical conversion to a Roux-en-Y drainage. aldosterone, and decreased atrial natriuretic peptide. Late
dumping is associated with hypoglycemia and hyperinsu-
linemia. Medical therapy for the dumping syndrome consists
of dietary modification and somatostatin analogue (octreo-
tide). (See Schwartz 11th ed., p. 1157.)
233
gastric remnant. tion are not relevant concerns. (See Schwartz 11th ed., p. 1184.)
A. Very low carbohydrate diet. in some patients, and diazoxide and somatostatin have been
B. Anti-secretory agents such as diazoxide and used in those who fail diet therapy. Recently GLP-1 recep-
somatostatin. tor antagonists have been reported to be successful. Although
C. GLP-1 receptor antagonists. pancreatic resection was initially reported in patients with
D. Pancreatic resection. severe hypoglycemia, it is no longer recommended. Partial
pancreatectomy results in a recurrence of the problem, and
total pancreatectomy exchanges one severe condition for
another. (See Schwartz 11th ed., pp. 1204–1205.)
5. How much fluid normally enters the adult small intes- Answer: D
tine each day? About 8 to 9 L of fluid enters the small intestine daily, of
A. 2 L which over 80% is absorbed. This includes 2 L from oral
B. 4 L intake, 1.5 L of saliva, 2.5 L of gastric juice, 1.5 L of bilio-
C. 6 L pancreatic s ecretions, and 1 L of fluid secreted by the small
D. 8 L intestine. (See Schwartz 11th ed., p. 1222.)
235
sorption in the distal ileum and are reabsorbed in the distal ileum where they enter
D. The secretion of cholecystokinin by the jejunum and the portal venous c irculation and are resecreted in the bile.
its stimulation of bile flow (See Schwartz 11th ed., p. 1225.)
CHAPTER 28
D. Obstruction due to an internal hernia.
Small Intestine
B. Laparoscopic surgery is preferable in cases where a mation. The morbidity risks of laparoscopic surgery are less
single adhesive band is causing the obstruction. than with open surgery and the risk of iatrogenic injury to the
C. Laparoscopic surgery is less likely to produce fur- bowel is similar. (See Schwartz 11th ed., p. 1232.)
ther adhesion formation which may cause recurrent
obstruction.
D. The risk of iatrogenic bowel injury is higher with
laparoscopic surgery.
14. The primary genetic defect associated with Crohn’s dis- Answer: A
ease is a mutation of the NOD2 gene on chromosome 16. The protein product of the NOD2 gene mediates the innate
This gene encodes for a protein product which: immune response to microbial pathogens. A variety of defects
A. Mediates the innate immune response to microbial in immune regulatory mechanisms such as over responsive-
pathogens. ness of mucosal T cells to enteric flora-derived antigens can
B. Activates stellate cells to produce collagen. lead to defective immune tolerance and sustained inflamma-
C. Regulates the rate of crypt-to-villus enterocyte tion. (See Schwartz 11th ed., p. 1236.)
migration.
D. Mediates the production of enterocyte alkaline
phosphatase.
CHAPTER 28
the following EXCEPT: In adults, the common etiologies of short bowel syndrome
A. Mesenteric ischemia. include mesenteric ischemia, malignancy, and Crohn dis-
B. Malignancy. ease. In pediatric patients, common causes include intestinal
C. Crohn disease. atresias, volvulus, and necrotizing enterocolitis. Radiation
D. Radiation enteritis. enteritis usually involves isolated segments of small bowel of
<50% of total small intestinal length. (See Schwartz 11th ed.,
p. 1254.)
Small Intestine
24. After an emergency operation for bowel infarction in Answer: D
which more than half of the small intestine was removed Reducing gastric secretion with proton pump inhibitors or
and a jejunostomy created, high-volume ostomy losses histamine-2 receptor antagonists, reducing gastro-entero-
cause recurrent dehydration. Initial management of this pancreatic secretions with octreotide, and inhibiting motility
condition includes all of the following EXCEPT: with agents such as loperamide or diphenoxylate are useful
A. Proton pump inhibitors or histamine-2 receptor approaches to prevent dehydration as the short gut adapts to
antagonists. its new length. Small intestinal transplantation would be con-
B. Octreotide. sidered only after other therapies including total parenteral
C. Loperamide. nutrition (TPN) fail. (See Schwartz 11th ed., p. 1255.)
D. Small bowel transplantation.
B. Ultrasound can reliably distinguish between most integrity of the submucosal layer. Ultrasound can also differ-
benign and malignant rectal polyps. entiate superficial T1-T2 from deeper T3-T4 tumors. Overall,
C. Ultrasound is useful for determining depth of rectal the accuracy of ultrasound in detecting depth of mural inva-
cancer invasion. sion ranges between 81% and 94%. This modality also can
D. Identification of involved perirectal lymph nodes via detect enlarged perirectal lymph nodes, which may suggest
ultrasound is possible in most cases.
Mucosal surface
Mucosa/Muscularis mucosa
Submucosa
Muscularis propria
Serosa/Perirectal fat
Chapter 29
tion, when compared to open surgery? laparoscopically, with hand-assisted laparoscopy (HAL), or
A. Improved cosmetic results robotically. Potential advantages of minimally invasive sur-
B. Decreased postoperative pain gery include improved cosmetic result, decreased postop-
C. Earlier return of bowel function erative pain, and earlier return of bowel function. Moreover,
D. Less expensive some experimental data suggest that minimally invasive oper-
E. All of the above ations have less immunosuppressive impact on the patient
F. A-C and thus might improve postoperative outcome and even
Chapter 29
A
rate of incisional infection, even when a mechanical solutions are generally better tolerated but are more likely to
bowel prep is not used. cause fluid and electrolyte abnormalities. Both are equally
C. Routine postoperative intravenous (IV) antibiotics efficacious in bowel cleansing. Preparatory formulations
have no role in an uncomplicated colectomy. have been recently introduced in tablet form in an attempt to
D. Prophylactic IV antibiotics should only be given improve tolerance. However, these methods of bowel cleansing
before incision regardless of the length of the opera- require ingestion of ≥40 tablets with water over several hours.
tion, as additional doses during an operation can lead To date, these formulations have not been proven to be supe-
Colon, Rectum, and Anus
Chapter 29
assessed with a computed tomography (CT) scan for cated diverticulitis will respond to outpatient therapy with
abscess formation. broad-spectrum oral antibiotics and a low-residue diet. Anti-
C. Worsening abdominal pain in a patient hospitalized biotics should be continued for 7 to 10 days. About 10% to
with diverticulitis should be addressed with broaden- 20% of patients with more severe pain, tenderness, fever, and
ing of antibiotics. leukocytosis are treated in the hospital with parenteral anti-
D. Most patients with uncomplicated diverticulitis will biotics and bowel rest. Most patients improve within 48 to
never have another episode. 72 hours. Failure to improve may suggest abscess formation.
cer specimen. The cancer was noted to invade through Staging. Colorectal cancer staging is based on tumor depth
the bowel wall into the subserosa. There was one involved and the presence or absence of nodal or distant metastases.
lymph node. Assuming there was no distant metastatic Older staging systems, such as the Dukes’ Classification and
disease noted on preoperative imaging, what is the cor- its Astler-Coller modification, have been replaced by the TNM
rect tumor-node-metastasis (TNM) classification and staging system described by the American Joint Committee
stage? on Cancer (AJCC). The AJCC TNM classification has recently
A. T3N1M0, stage II been updated to reflect survival outcomes based upon the
B. T4N1M0, stage II Surveillance Epidemiology and End Results (SEER) registry.
C. T3N1M0, stage III Stage I disease includes adenocarcinomas that are invasive
D. T4N1M0, stage III through the muscularis mucosa but are confined to the sub-
mucosa (T1) or the muscularis propria (T2) in the absence
of nodal metastases. Stage II disease consists of tumors that
invade through the bowel wall into the subserosa or non-
peritonealized pericolic or perirectal tissues (T3) or into
other organs or tissues or through the visceral peritoneum
(T4) without nodal metastases. Stage III disease includes any
T stage with nodal metastases, and stage IV disease denotes
distant metastases. (See Schwartz 11th ed., p. 1296.)
Chapter 29
14. Which of the following statements about total mesorec- Answer: C
tal excision (TME) for rectal cancer is TRUE? Total mesorectal excision (TME) is a technique that uses sharp
A. TME improves local recurrence but not long-term dissection along anatomic planes to ensure complete resection
survival. of the rectal mesentery during low and extended low anterior
B. TME is not necessary for rectosigmoid tumors. resections. For upper rectal or rectosigmoid resections, a partial
C. TME is associated with less blood loss than a blunt mesorectal excision of at least 5 cm distal to the tumor appears
dissection. adequate. TME both decreases local recurrence rates and
Chapter 29
promise occurs early in the course of cecal volvulus, surgical
exploration is necessary when the diagnosis is made. Right
hemicolectomy with a primary ileocolic anastomosis can
usually be performed safely and prevents recurrence. Simple
detorsion or detorsion and cecopexy are associated with a
high rate of recurrence. (See Schwartz 11th ed., p. 1307.)
21. In which way do small and large bowel ischemia differ? Answer: C
A. Small bowel ischemia is more common overall. Intestinal ischemia occurs most commonly in the colon.
B. Large bowel ischemia is typically due to major arte- Unlike small bowel ischemia, colonic ischemia rarely is asso-
rial or venous occlusion, whereas small bowel isch- ciated with major arterial or venous occlusion. Instead, most
emia is more frequently seen in low flow states. colonic ischemia appears to result from low flow and/or small
C. Large bowel ischemia is managed nonoperatively vessel occlusion. Risk factors include vascular disease, dia-
more frequently than small bowel ischemia. betes mellitus, vasculitis, hypotension, and tobacco use. In
addition, ligation of the inferior mesenteric artery during
aortic surgery predisposes to colonic ischemia. Occasionally,
thrombosis or embolism may cause ischemia. Although the
splenic flexure is the most common site of ischemic colitis,
any segment of the colon may be affected. The rectum is rela-
tively spared because of its rich collateral circulation.
Chapter 29
cose value of 310 mg/dL in the emergency room (ER) the patient is immunocompromised, has diabetes mellitus, or
D. A 30-year-old woman with a well-drained abscess has valvular heart disease. Antibiotics alone are ineffective at
and no cellulitis, though this is her third episode of treating perianal or perirectal infection. (See Schwartz 11th
perianal abscess in the last decade ed., p. 1314.)
Probe in
rectovaginal
fistula
Flap of mucosa
and internal
sphincter muscle
Chapter 29
Excess flap of
mucosa excised
Chapter 29
body 3 days ago, which remains in place. He is hemody- cause damage to the rectum, rectosigmoid, or descending
namically stable and without peritonitis on examination. colon. Generalized abdominal pain suggests intraperitoneal
What is the next best step in management? perforation. Evaluation of the patient includes inspection of
A. Upright abdominal X-ray to evaluate for free air the perineum and a careful abdominal examination to detect
B. CT abdomen/pelvis to locate foreign body any evidence of perforation. Plain films of the abdomen are
C. Removal of foreign body in the ER mandatory to detect free intra-abdominal air.
D. Proceed to operating room (OR) for laparotomy Foreign bodies lodged low in the rectum may often be
Should she have any further colon screening? vitamin C) will produce a false-positive result. Any positive
A. No, vitamin C can produce a false positive result. FOBT mandates further investigation, usually by colonos-
B. Yes, all positive FOBT requires further investigation copy. (See Schwartz 11th ed., p. 1293.)
with a colonoscopy.
C. Yes, all positive FOBT requires further investigation
with FOBT in 1 year.
D. No, she has no risk factors for colon cancer and
should follow the United States Preventive Ser-
vices Task Force (USPSTF) screening guidelines for
colorectal cancer.
Chapter 29
serpiginous ulcers colon; rectal sparing or skip lesions suggest a diagnosis of
C. Atrophic mucosa, noncaseating granulomas, stric- Crohn disease. Crohn disease is a transmural inflammatory
tures, “cobblestone” appearance on endoscopy process that can affect any part of the gastrointestinal tract
D. Mucosal ulcerations, crypt abscesses, inflammatory from mouth to anus. Mucosal ulcerations, an inflammatory
pseudopolyps, continuous involvement of colon and cell infiltrate, and noncaseating granulomas are characteristic
rectum pathologic findings. Chronic inflammation may ultimately
result in fibrosis, strictures, and fistulas in either the colon or
D. Adjuvant chemotherapy. of metastases. For lesions that are <1 cm (95% of all lesions),
a negative margin appendectomy is adequate. For tumors
≥2 cm, a right hemicolectomy is recommended. For lesions
1 to 2 cm in size, there is no consensus on a completion col-
ectomy. A right colectomy is often performed for mesenteric
invasion, enlarged nodes, or positive or unclear margins.
Measurement of serum chromogranin A is recommended.
The Appendix
CHAPTER 30
surgery, you noticed the appendix base is perforated and is retrieved through the midline port in a specimen bag,
appeared nonviable (Fig. 30-1). What is the most appro- especially if an appendiceal lesion is suspected. If a peri-
priate management? appendiceal phlegmon is encountered or if the operation is
A. Place a drain and close the abdomen being performed for perforated appendicitis, careful sweeping
B. Place an endoloop around the site of perforation and of the bowel with a blunt dissector can release the appendix. It
divide the appendix is important to carefully separate adjacent bowel, which can
C. Resect the appendix at the site of perforation and be friable in such settings. (See Schwartz 11th ed., p. 1336.)
The Appendix
suture the base
D. Perform appendectomy using a stapling device, with
staple line through the healthy cecum
Diaphragm
Right triangular
ligament
Left triangular
ligament
Falciform
ligament
Round
ligament
Liver in situ
Gastrohepatic
ligament
Foramen of
Winslow Open hepato-
duodenal ligament
II
IVa III
VIII
VII
CHAPTER 31
IVb
V
VI
Liver
V
IVb
VI
III
LHA
CHAPTER 31
artery Splenic artery
Common hepatic artery
Gastroduodenal artery
Liver
FIG. 31-4. Arterial anatomy of the upper abdomen and liver, including the celiac trunk and
hepatic artery branches. a. = artery; LHA = left hepatic artery; RHA = right hepatic artery.
FIG. 31-5. Common hepatic artery anatomic variants. SMA = superior mesenteric artery.
structures hepatic
v.
Right HV
Left lobe
Middle HV
Liver
Medial
segment
structures
Falciform
ligament
Hepatic a.
Anterior
segment Portal v.
structures
Gallbladder
FIG. 31-6. Confluence of the three hepatic veins (HVs) and the inferior vena cava (IVC). Note that the middle and left HVs drain
into a common trunk before entering the IVC. a. = artery; v. = vein. (Adapted with permission from Cameron JL: Atlas of Surgery.
Vol. I, Gallbladder and Biliary Tract, the Liver, Portasystemic Shunts, the Pancreas. Toronto: BC Decker; 1990.)
A57% B12%
ra ra
C: R anterior (C1, 16%) or R posterior lh
(C2, 4%) duct draining into CHD rp lh
CHAPTER 31
rp
C20% 16% 4%
C1 C2
ra ra
Liver
duct (D2, 1%) draining into the left rp lh
lh
hepatic duct
D6%
5% 1%
D1 D2
III
IV
ra IV III
E: Absence of hepatic duct ra
rp
confluence 3%
II
II
rp
E3% I
I
2% 1%
E1 E2
ra
F: Drainage of R posterior duct into rp
cystic duct 2% lh
F2%
FIG. 31-7. Main variations of hepatic duct confluence. As described by Couinaud in 1957, the bifurcation of
the hepatic ducts has a variable pattern in approximately 40% of cases. CHD = common hepatic duct; lh = left
hepatic; R = right; ra = right anterior; rp = right posterior. (Reproduced with permission from Blumgart LH, Fong Y:
Surgery of the Liver and Biliary Tract, 3rd ed, Vol. I. London: Elsevier; 2000.)
CHAPTER 31
and specificity of ultrasound compared with CT and MRI.
MRI offers advantages over CT in allowing higher soft tissue
contrast and superior depiction of fluid-containing structures
while eliminating the need for ionizing radiation. Develop-
ment of specialized liver-specific contrast agents, including
ferumoxide and gadoxetate, has led to the development of
MRI that allows characterization of both hepatic structure
Liver
and function. While positron emission tomography/com-
puted tomography (PET/CT) is used frequently in the stag-
ing and follow-up of patients with metastatic liver lesions, its
role in the diagnosis and management of primary liver lesions
is uncertain. The reported sensitivity of fluorodeoxyglucose
(FDG)-PET/CT for the detection of hepatocellular carci-
noma is only 50%–65%. While this has been improved with
development of dual-tracer PET/CT, the clinical benefits of
this modality have yet to be clearly defined. Despite advances
in other imaging modalities, intraoperative liver ultrasound
remains the gold standard. This technique has the ability to
identify 20%–30% more lesions than preoperative imaging,
and it is estimated that approximately 50% of planned sur-
gical resections are influenced by information gleaned from
intraoperative ultrasound. (See Schwartz 11th ed., p. 1357.)
10. In a patient without prior liver disease, what is the most Answer: D
common cause of hepatic encephalopathy occurring Differences in etiology, management, and patient outcomes
within 26 weeks of severe liver injury? have been described for various regions of the globe. In the
A. Alcohol in developing nations. East and developing portions of the world, the most com-
B. Causes are unknown. mon causes of acute liver failure (ALF) are viral infections,
C. Hepatitis B, A, and E in the United States. primarily hepatitis B, A, and E. In these areas, there are a rela-
D. Drug-/toxin-induced (including acetaminophen) in tively small number of drug-induced cases. In contrast, 65%
the United States. of cases of ALF in the West are thought to be due to drugs
and toxins, with acetaminophen (paracetamol) being the
most common etiologic agent in the United States, Australia,
United Kingdom, and most of Europe. In France and Spain,
where acetaminophen sales are restricted, the rate of acet-
aminophen-induced ALF is quite low. Acetaminophen-
induced ALF is also uncommon in South America. The US
Acute Liver Failure Study Group identified several other
causes of ALF, including autoimmune hepatitis, hypoperfu-
sion of the liver (in cardiomyopathy or cardiogenic shock),
pregnancy-related conditions, and Wilson disease. Even with
exhaustive efforts to identify a cause, approximately 20% of all
cases of ALF remain indeterminate in origin. (See Schwartz
11th ed., p. 1361.)
CHAPTER 31
the wedged hepatic venous pressure (WHVP). The hepatic
venous pressure gradient (HVPG) may then be calculated by
subtracting the FHVP from the WHVP (HVPG = WHVP −
FHVP). Clinically significant portal hypertension is defined
as HVPG > 10 mm Hg. (See Schwartz 11th ed., p. 1365.)
Liver
among patients with cirrhosis? The most significant manifestation and the leading cause
A. Portal hypertension associated variceal bleeding of morbidity and mortality related to portal hypertension is
B. Encephalopathy variceal bleeding. Approximately 30% of patients with com-
C. Development of hepatocellular carcinoma pensated cirrhosis and 60% of patients with decompensated
D. Hepatorenal syndrome cirrhosis have esophageal varices. One-third of all patients
with varices will experience variceal bleeding. Each episode
of bleeding is associated with a 20% to 30% risk of mortality.
If left untreated, 70% of patients who survive the initial bleed
will experience recurrent variceal hemorrhage within 2 years
of the index hemorrhage. (See Schwartz 11th ed., p. 1367.)
CHAPTER 31
appearance with a peripheral zone of edema in the The diagnosis of hydatid disease is based on the findings of
left lobe an enzyme-linked immunosorbent assay (ELISA) for echino-
C. Anteroinferior hypodense lesion with a distinct wall coccal antigens, and results are positive in approximately 85%
and ring-like calcifications in the right lobe of infected patients. Ultrasonography and CT scanning of the
D. Asymmetrical nodular peripheral enhancement that abdomen are both quite sensitive for detecting hydatid cysts.
is isodense with large vessels and exhibit progressive The appearance of the cysts on images depends on the stage
centripetal enhancement fill-in over time in the right of cyst development. Typically, hydatid cysts are well-defined
Liver
lobe hypodense lesions with a distinct wall. Ring-like calcifica-
tions of the pericysts are present in 20% to 30% of cases. As
healing occurs, the entire cyst calcifies densely, and a lesion
with this appearance is usually dead or inactive. Daughter
cysts generally occur in a peripheral location within the main
cyst and are typically slightly hypodense compared with the
mother cyst. Magnetic resonance imaging (MRI) of the abdo-
men may be useful to evaluate the pericyst, cyst matrix, and
daughter cyst characteristics. (See Schwartz 11th ed., p. 1370.)
B. Summation of his creatinine, INR, and bilirubin indi- added to improve sensitivity and specificity.
cates he has a Child-Pugh Score in Class B. The Child-Turcotte-Pugh (CTP) score was originally
C. Based upon clinical and laboratory values, he has a developed to evaluate the risk of portocaval shunt procedures
Child-Pugh Score in Class A. performed for portal hypertension and subsequently has
D. Formulation of his laboratory values indicate his been shown to be useful in predicting surgical risks of other
MELD is 29. intra-abdominal operations on cirrhotic. Numerous studies
have demonstrated overall surgical mortality rates of 10%
Liver
for patients with class A cirrhosis, 30% for those with class
B cirrhosis, and 75% to 80% for those with class C cirrhosis.
Ranging from 5 to 15, the CTP is calculated based upon a
summation of points derived from the presence of ascites and
encephalopathy, serum bilirubin and albumin levels, as well
as INR. Multiple retrospective studies have demonstrated
that perioperative mortality and morbidity rates correlate
well with the CTP score, and for over 30 years, this measure
had been used as the principal predictor of operative risk
(Table 31-1). (See Schwartz 11th ed., Table 31-4, p. 1365.)
CHAPTER 31
potential for malignant degeneration, it is generally recom-
mended that hepatic adenomas be resected once discovered.
(See Schwartz 11th ed., p. 1375.)
Liver
enhancement during arterial phase, isodensity on the that demonstrates enhancement on the arterial phase and
venous phase, and a central scar. In general, what would isointensity on the venous phase. FNH also demonstrates a
be the recommended treatment? characteristic central scar. FNH are solid benign lesions are
A. Reassurance and observation similar to adenomas in that they are more common in women
B. Percutaneous radio frequency ablation of childbearing age. Unlike adenomas, however, they are not
C. Resection prone to malignant degeneration or spontaneous rupture. For
D. Transarterial chemoembolization this reason, asymptomatic FNHs may be managed conserva-
tively unless adenoma or hepatocellular carcinoma (HCC)
cannot be definitively excluded. Gadolinium-enhanced mag-
netic resonance imaging (MRI) may allow better visualization
of the fibrous septa extending from the FNH’s central scar.
While FNH and adenomas ma appear similar on computed
tomography (CT) or standard MRI, new MRI contrast agents
like gadobenate dimeglumine (MultiHance) allow supe-
rior discrimination between these two lesions (Fig. 31-9).
(See Schwartz 11th, Fig. 31-18, p. 1375.)
CHAPTER 31
Given these encouraging results, the paradigm for surgical
evaluation and treatment of these patients has shifted to pri-
marily consider the health of the background liver and volume
of the hepatic remnant, and not tumor characteristics like size
and number. (See Schwartz 11th ed., p. 1378.)
27. Based on the standard Milan criteria, which of the fol- Answer: B
Liver
lowing patients with hepatocellular carcinoma (HCC) Orthotopic liver transplantation (OTL) was first attempted in
would be eligible for transplantation? the 1980s and 1990s, with initial series reporting 5-year sur-
A. One 4.5 cm lesion in segment VI with invasion of the vival rates of 20% to 50%. This led to the introduction of the
right portal vein Milan criteria which limited eligibility to patients with one
B. Three lesions confined to the right lobe, with the tumor <5 cm or up to three tumors <3 cm and no evidence of
largest being 2.5 cm gross intravascular or extrahepatic spread. Adoption of these
C. A single, 5.5 cm lesion in segment II guidelines resulted in significant improvement in 5-year sur-
D. Three lesions spread throughout the liver, with the vival for patients with HCC treated with OTL. (See Schwartz
largest being 3.5 cm 11th ed., p. 1380.)
and calcineurin inhibitors. ing the intrahepatic and extrahepatic biliary tree. It is a
B. Anti-TNF monoclonal antibodies (infliximab). progressive disease which can lead to biliary cirrhosis. Medi-
C. Consideration for transplantation. cal therapy has long been attempted with immunosuppres-
D. Ursodeoxycholic acid. sants, antibiotics, steroids, and ursodeoxycholic acid, and has
E. Excision of the extrahepatic biliary tree (Kasai been disappointing. Surgical management with resection of
procedure). the extrahepatic biliary tree and hepaticojejunostomy has
produced reasonable results in patients with extrahepatic
The Gallbladder and Extrahepatic Biliary System
CHAPTER 32
9. The best initial imaging test for evaluating suspected Answer: C
cholangiocarcinoma includes: The initial tests are usually ultrasound or computed tomog-
A. Percutaneous cholangiography. raphy (CT) scan. A perihilar tumor causes dilatation of the
B. Endoscopic retrograde cholangiopancreatography. intrahepatic biliary tree, but normal or collapsed gallbladder
C. Ultrasound. and extrahepatic bile ducts distal to the tumor. Distal bile
D. Magnetic resonance cholangiopancreatography duct cancer leads to dilatation of the extra- and intrahepatic
pp. 1420–1421.)
13. In the early postoperative period, what is the most com- Answer: D
mon presentation of a patient with a biliary injury? In the early postoperative period, patients present either
A. Fever with progressive elevation of liver function tests due to an
B. Abdominal pain occluded or a stenosed bile duct, or with a bile leak from an
C. Steatorrhea injured duct. (See Schwartz 11th ed., pp. 1419–1420.)
D. Elevated transaminases
E. Nausea
CHAPTER 32
quantity of bile acids produced to have maximal effect. (See
Schwartz 11th ed., Chapter 32, pp. 1396–1397.)
A B
FIG. 32-1. HIDA scanning. A. Normal HIDA scan showing filling of the extrahepatic
biliary tree and gallbladder (white arrow). B. HIDA scan in a patient with acute
cholecystitis showing no filling of the gallbladder.
admission
D. Antibiotics and laparoscopic cholecystectomy after
28 weeks of pregnancy
findings concerning for acute cholecystitis, what is the be treated with antibiotics and biliary decompression with
best course of action? cholecystostomy tube placement, which is usually effective in
A. Antibiotics, endoscopic retrograde cholangiopancrea- stabilizing the patient. For those who do recover after chole-
tography (ERCP), lap chole when stable this admission cystostomy, the tube can be removed once the track is mature
B. Antibiotics, lap chole when stable this admission (approximately 4 weeks) and cholangiography through it
C. Antibiotics, cholecystostomy tube, lap chole this shows a patent cystic duct. Elective laparoscopic cholecystec-
admission tomy can be scheduled within approximately 6 to 8 weeks,
D. Antibiotics, cholecystostomy tube, lap chole in 6 to assuming their medical fitness recovers. Failure to improve
8 weeks if able after cholecystostomy may be due to gangrene of the gallblad-
der or perforation, in which case, damage control surgery
may be unavoidable. (See Schwartz 11th ed., p. 1406.)
CHAPTER 32
The Gallbladder and Extrahepatic Biliary System
FIG. 32-2. Gallstone Ileus. Intraoperative photo showing a
longitudinal enterotomy and extraction of an impacted stone from
the distal small bowel.
FIG. 32-3. Classification of choledochal cysts. Type I, fusiform or cystic dilations of the extrahepatic biliary
tree, is the most common type, making up >50% of the choledochal cysts. Type II, saccular diverticulum of
an extrahepatic bile duct. Rare, <5% of choledochal cysts. Type III, bile duct dilatation within the duodenal
wall (choledochoceles), makes up about 5% of choledochal cysts. Types IVa and IVb, multiple cysts, make
up 5% to 10% of choledochal cysts. Type IVa affects both extrahepatic and intrahepatic bile ducts, whereas
type IVb cysts affect the extrahepatic bile ducts only. Type V (Caroli disease), intrahepatic biliary cysts, is very
rare and makes up 1% of choledochal cysts.
CHAPTER 32
involves the right or left hepatic duct (Bismuth-Corlette types
IIIa or IIIb), right or left hepatic lobectomy, respectively, should
also be performed. Frequently, resection of the adjacent cau-
date lobe is required because of direct extension into caudate
biliary radicals or parenchyma. Type IV Klatskin tumors, those
with more extensive involvement of both hepatic ducts and
intrahepatic spread, are often considered unresectable or only
289
D. Tube feeding is inferior to parenteral nutrition dur- enteral nutrition (within the first 24 hours of admission) is
ing inflammation. not superior to delaying an oral diet until 72 hours. If this is
not tolerated over 48 to 72 hours, then nasogastric tube feed-
ings can be started and increased in step-wise fashion over 2
to 3 days. (See Schwartz 11th ed., p. 1446.)
CFTR
Idiopathic Genetic (14%) CFTR +
(42%) (24%) SPINK1
(3%)
SPINK1
(4%)
Hyperlipidemia, PRSS1
Gallstone / Autoimmune, (3%)
severe AP Obstructive Other (4%)
(3%) (9%)
CHAPTER 33
6. Pain from chronic pancreatitis can be caused by: Answer: D
A. Ductal hypertension. Pain from chronic pancreatitis has been ascribed to three
B. Parenchymal disease. possible etiologies. Ductal hypertension, due to strictures or
C. Obstructive pancreatopathy. stones, may predispose to pain that is initiated or exacerbated
D. All of the above. by eating. Chronic pain without exacerbation may be related
to parenchymal disease or retroperitoneal inflammation with
persistent neural involvement. Acute exacerbations of pain in
Pancreas
the setting of chronic pain may be due to acute increases in duct
pressure or recurrent episodes of acute inflammation in the set-
ting of chronic parenchymal disease. Nealon and Matin have
described these various pain syndromes as being predictive of
the response to various surgical procedures. Pain that is found
in association with ductal hypertension is most readily relieved
by pancreatic duct decompression, through endoscopic stent-
ing or surgical decompression. (See Schwartz 11th ed., p. 1460.)
Parenchymal changes
Inhomogeneous echo pattern Edema
Reduced echogenic foci (1–3 mm) Edema
Enhanced echogenic foci Calcifications
Prominent interlobular septae Fibrosis
Lobular outer gland margin Fibrosis, glandular atrophy
Pancreas
CHAPTER 33
Pancreas
FIG. 33-3. Radioactive octreotide scan
demonstrating pancreatic endocrine
tumor in the body of the pancreas
(arrow).
CHAPTER 33
nal pancreatic duct stents. Some previous studies indicated
that stents might be harmful. A recent multicenter random-
ized trial comparing external to internal pancreatic duct
stents during pancreaticoduodenectomy showed a lower rate
of pancreatic fistula with internal stents, so this controversy is
likely to continue. (See Schwartz 11th ed., p. 1497.)
Pancreas
14. A pancreatic cystic neoplasms that is <3 cm has atypical Answer: D
cells present and has a solid component requires: See Fig. 33-4. (See Schwartz 11th ed., p. 1501, Figure 33-78.)
A. A repeat computed tomography (CT) scan in 3 to 6
months.
B. A repeat CT scan in 1 year.
C. Continued observation.
D. Resection.
Are any of the following high-risk stigmata of malignancy present?
(i) obstructive jaundice in a patient with cystic lesion of the head of the pancreas,
(ii) enhancing solid component within cyst, (iii) main pancreatic duct ≥10 mm in size
Yes
No
FIG. 33-4. Algorithm for management of pancreatic cystic neoplasms. CEA = carcinoembryonic antigen;
CT = computed tomography; ERCP = endoscopic retrograde cholangiopancreatography; EUS = endoscopic
ultrasound; FNA = fine-needle aspiration; Hx = history; IPMN = intraductal papillary mucinous neoplasm of the
pancreas; MCN = mucinous cystic neoplasm; MRCP = magnetic resonance cholangiopancreatography. (Reproduced
with permission from Tanaka M, Adsay V, Chari S, et al. International consensus guidelines 2012 for the management of
IPMN and MCN of the pancreas, Pancreatology. 2012;12(3):183–197.)
297
A. Positive direct Coombs test (See Schwartz 11th ed., pp. 1524–1525.)
B. Negative indirect Coombs test
C. Increased red cell distribution width
D. Increased lactate dehydrogenase
CHAPTER 34
lets. Further medial mobilization of the spleen is achieved by
incising its lateral peritoneal attachments, most notably the
splenophrenic ligament. Then follows individual ligation and
sequential division of the short gastric vessels, steps that if
carefully executed reduce the risk of these vessels’ retracting
and bleeding. Splenic hilar dissection then takes place. When-
ever possible, care should be taken to dissect and individually
The Spleen
ligate the splenic artery and vein (in that order) before divid-
ing them. (See Schwartz 11th ed., pp. 1533–1534.)
Phrenicocolic
ligament
Lesser sac
CHAPTER 34
Sustentaculum
lienis
The Spleen
Splenocolic
ligament
15. All of the following are functions of the spleen EXCEPT: Answer: C
A. Clearance of damaged or aged red blood cells from The spleen has both fast and slow circulation of blood. It is
the blood. during slow circulation that blood travels through the reticu-
B. Extramedullary site for hematopoesis and recycling lar spaces and splenic cords where it is exposed to contact
iron. with splenic macrophages, which remove senescent blood
C. Initiation of adaptive immune response from filtra- cells. Through this process, the spleen is also able to remove
tion of lymph. erythrocyte inclusions such as Heinz bodies without lysing
D. Clearance of encapsulated bacteria from the blood the cells. Through the reticuloendothelial system, the spleen
stream. clears encapsulated bacteria such as pneumococcus and
Haemophilus influenzae, which are poorly opsonized from
the hepatic reticuloendothelial system. In addition to these
functions, the spleen serves as an extramedullary site for
hematopoiesis and plays a functional role in the recycling of
iron. While the white pulp of the spleen is important in the
initiation of the adaptive immune response, material is deliv-
ered to the spleen through the blood and not the lymph. (See
Schwartz 11th ed., pp. 1520–1521.)
CHAPTER 34
atic patients often present with the gradual onset of fatigue,
anorexia, sweating, and left upper quadrant pain and early
satiety secondary to splenomegaly. Enlargement of the spleen
is found in roughly one half of patients with CML. Splenec-
tomy is indicated to ease pain and early satiety. (See Schwartz
11th ed., p. 1528.)
The Spleen
21. Which of the following is an indication for splenectomy Answer: C
in polycythemia vera? Polycythemia vera (PV) is a clonal, chronic, progressive
A. Failure of aspirin to prevent thrombotic complications myeloproliferative disorder characterized by an increase in
B. Frequent need for phlebotomy red blood cell mass, frequently accompanied by leukocyto-
C. Symptoms related to splenomegaly sis, thrombocytosis, and splenomegaly. Patients affected by
D. Prevention of progression to myeloid metaplasia PV typically enjoy prolonged survival compared to others
affected by hematologic malignancies, but remain at risk for
transformation to myelofibrosis or acute myeloid leukemia
(AML). The disease is rare, with an annual incidence of 5
to 17 cases per million population. Although the diagnosis
may be discovered by routine screening laboratory tests in
asymptomatic individuals, affected patients may present with
any number of nonspecific complaints, including headache,
dizziness, weakness, pruritus, visual disturbances, excessive
sweating, joint symptoms, and weight loss. Physical findings
include ruddy cyanosis, conjunctival plethora, hepatomegaly,
splenomegaly, and hypertension. The diagnosis is established
by an elevated red blood cell mass (>25% of mean predicted
value), thrombocytosis, leukocytosis, normal arterial oxygen
saturation in the presence of increased red blood cell mass,
splenomegaly, low serum erythropoietin (EPO) stores, and
bone marrow hypercellularity. Treatment should be tailored to
the risk status of the patient and ranges from phlebotomy and
aspirin to chemotherapeutic agents. As in essential thrombo-
cythemia (ET), splenectomy is not helpful in the early stages
of disease and is best reserved for late-stage patients in whom
myeloid metaplasia has developed and splenomegaly-related
symptoms are severe. (See Schwartz 11th ed., p. 1529.)
B. Size >1.5 cm more likely to be affected than men. The aneurysm usually
C. History of thrombocytopenia arises in the middle to distal portion of the splenic artery. The
D. History of neutropenia risk of rupture is between 3% and 9%; however, once rupture
occurs, mortality is substantial (35%–50%). According to a
recent series, mortality is significantly higher in patients with
underlying portal hypertension (>50%) than in those with-
out it (17%). SAA is particularly worrisome when discovered
The Spleen
25. Which of the following is NOT part of the triad seen with Answer: D
Felty syndrome? The triad of RA, splenomegaly, and neutropenia is called
A. Rheumatoid arthritis (RA) Felty syndrome. It exists in approximately 3% of all patients
B. Splenomegaly with RA, two-thirds of which are women. Immune complexes
C. Neutropenia coat the surface of white blood cells, leading to their seques-
D. Thrombocytopenia tration and clearance in the spleen with subsequent neutro-
penia. This neutropenia (<2000/mm3) increases the risk for
recurrent infections and often drives the decision for splenec-
tomy. The size of the spleen is variable, from nonpalpable in
5% to 10% of patients, to massive enlargement in others. The
spleen in Felty syndrome is four times heavier than normal.
Corticosteroids, hematopoietic growth factors, methotrex-
ate, and splenectomy have all been used to treat the neu-
tropenia of Felty syndrome. Responses to splenectomy have
CHAPTER 34
tion strategy against overwhelming postsplenectomy Asplenic patients have an increased susceptibility to infection
infection? for the remainder of their lives and although the overall life-
A. Vaccination 2 weeks after splenectomy time risk of overwhelming postsplenectomy infection (OPSI)
B. Vaccination 2 weeks before splenectomy is low the consequences can be devastating. Patients under-
C. Daily antibiotic prophylaxis going splenectomy for hematologic or malignant indications
D. Carrying a reserve supply of antibiotics for self- have a greater risk of OPSI than patients undergoing sple-
administration nectomy for trauma or iatrogenic injury and OPSI is more
The Spleen
common in children than adults. Providers need to have a
high index of suspicion when evaluating asplenic patients
for possible infection. Patient education and vaccinations
against encapsulated pathogens is the mainstay of preventa-
tive therapy. Patients should be vaccinated 2 weeks prior to
elective splenectomy in order to optimize antigen recognition
and processing. If splenectomy is performed emergently, vac-
cinations are given postoperatively with an attempt to delay
administration for 2 weeks to avoid the transient immuno-
suppression associated with surgery. There is little evidence
supporting efficacy of prophylactic antibiotics in asplenic
patients and vaccination remains the most effective preven-
tion strategy. (See Schwartz 11th ed., p. 1532.)
B. A 25-year-old who underwent splenectomy for iatro- There is evidence that those who undergo splenectomy for
genic bleeding after a total colectomy hematologic disease are far more susceptible to OPSI than
C. A 3-year-old who underwent splenectomy for hered- patients who undergo splenectomy for trauma or iatrogenic
itary spherocytosis reasons. When taking age into consideration, children who
D. A 4-year-old who underwent splenectomy due to are 5 years of age or younger and adults who are 50 years of
bleeding after a motor vehicle crash age or older seem to be at an elevated risk. The interval since
splenectomy also seems to be a factor with the greatest risk
The Spleen
307
5 years previously presents with a gradually expand- that occur sporadically or in the setting of FAP. The condi-
ing painless 4 cm mass of the anterior abdominal wall. tion can result in mortality due to aggressive local growth, so
A biopsy is returned as “desmoid tumor with no sign of radical excision with confirmation of tumor-free margins of
malignancy.” The correct management is: resection is required.
A. Observation. Medical treatment with an antineoplastic agent such as
B. A course of doxorubicin, dacarbazine, or carboplatin. doxorubicin, dacarbazine, or carboplatin can produce remis-
C. Enucleation. sion but the prognosis of advanced desmoids is poor. (See
D. Wide local excision. Schwartz 11th ed., p. 1557.)
CHAPTER 35
A. Perforated retrocecal appendicitis. retroperitoneal organs such as the duodenum, the pancreas,
B. Infected acute pancreatitis. the retroperitoneal region behind the cecum, or the descend-
C. Crohn’s disease of the small bowel. ing colon. They do not typically complicate Crohn’s disease of
D. Diverticulitis. the small bowel or other intraperitoneal organs. (See Schwartz
11th ed., pp. 1561–1562.)
1. All of the following are TRUE about soft tissue sarcoma Answer: A
EXCEPT: Most primary soft tissue sarcomas originate in an extremity
A. Most common site is trunk and retroperitoneum. (50%–60%); the next most common sites the trunk (19%),
B. There are more than 11,000 new diagnoses of soft tis- retroperitoneum (15%), and head and neck (9%). The overall
sue sarcoma annually in the United States. 5-year survival rate for patients with all stages of soft tissue
C. Most soft tissue sarcoma-specific deaths are due to sarcoma is 50% to 60%. Of the patients who die of sarcoma,
uncontrolled pulmonary metastases. most succumb to lung metastasis; 80% of these occur within 2
D. The overall 5-year survival rate for all stages of soft to 3 years after initial diagnosis. In the United States in 2012,
tissue sarcoma approximates 50%–60%. approximately 11,280 new cases of soft tissue sarcoma were
diagnosed, and 3900 deaths were attributable to this disease.
The incidence rates are declining for most cancer sites, but
they are increasing among both men and women for mela-
noma of the skin, cancers of the liver, sarcoma, and thyroid.
(See Schwartz 11th ed., p. 1567.)
311
313
CHAPTER 37
inguinal hernia.(See Schwartz 11th ed., p. 11604.)
Inguinal Hernias
FIG. 37-1. Varying degrees of closure of the processus
vaginalis (PV). A. Closed PV. B. Minimally patent PV.
C. Moderately patent PV. D. Scrotal hernia.
Williams syndrome
Androgen insensitivity syndrome
Robinow syndrome
Serpentine fibula syndrome
Alport syndrome
Tel Hashomer camptodactyly syndrome
Leriche syndrome
Testicular feminization syndrome
Inguinal Hernias
Rokitansky-Mayer-Küster syndrome
Goldenhar syndrome
Morris syndrome
Gerhardt syndrome
Menkes syndrome
Kawasaki disease
Pfannenstiel syndrome
Beckwith-Wiedemann syndrome
Rubinstein-Taybi syndrome
Alopecia-photophobia syndrome
7. A hernia sac that extends into the scrotum may require: Answer: B
A. extensive dissection and reduction. In cases where the viability of sac contents is in question, the
B. division within the inguinal canal. sac should be incised, and hernia contents should be evalu-
C. amputation of the sac. ated for signs of ischemia. The defect should be enlarged to
D. the sac to be inverted into the preperitoneum. augment blood flow to the sac contents. Viable contents may
be reduced into the peritoneal cavity, while nonviable con-
tents should be resected, and synthetic prostheses should
be avoided in the repair. In elective cases, the sac may be
CHAPTER 37
niform plexus, resulting in testicular atrophy and orchitis.
At this point, the inguinal canal is reconstructed, either
with native tissue or with prostheses. The following sections
describe the most commonly performed types of tissue-based
and prosthetic-based reconstructions. (See Schwartz 11th ed.,
p. 1610.)
Inguinal Hernias
8. The technique indicated for femoral hernias in cases Answer: C
where prosthetic material is contraindicated is: The McVay repair addresses both inguinal and femoral ring
A. The Bassini repair. defects. This technique is indicated for femoral hernias and in
B. The Shouldice repair. cases where the use of prosthetic material is contraindicated
C. The McVay repair. (Fig. 37-2). Once the spermatic cord has been isolated, an
D. Lichtenstein tension-free repair. incision in the transversalis fascia permits entry into the pre-
peritoneal space. The upper flap is mobilized by gentle blunt
dissection of underlying tissue. Cooper’s ligament is bluntly
dissected to expose its surface. A 2- to 4-cm relaxing incision
is made in the anterior rectus sheath vertically from the pubic
tubercle. This incision is essential to reduce tension on the
repair; however, it may result in increased postoperative pain
and higher risk of ventral abdominal herniation. Using either
interrupted or continuous suture, the superior transversalis
flap is then fastened to Cooper ligament, and the repair is con-
tinued laterally along Cooper ligament to occlude the femoral
ring. Lateral to the femoral ring, a transition stitch is placed,
affixing the transversalis fascia to the inguinal ligament. The
transversalis is then sutured to the inguinal ligament laterally
to the internal ring. (See Schwartz 11th ed., p. 1610.)
1
1
2
6
4 3
2
5 7
6 4
8
3 5
FIG. 37-3. The Desarda repair. A. The medial leaf of the external oblique aponeurosis is sutured to the inguinal ligament. 1 Medial leaf,
2 interrupted sutures taken to suture the medial leaf to the inguinal ligament, 3 pubic tubercle, 4 abdominal ring, 5 spermatic cord,
6 lateral leaf. B. Undetached strip of the external oblique aponeurosis forming the posterior wall. 1 Reflected medial leaf after a strip has
been separated, 2 internal oblique muscle seen through the splitting incision made in the medial leaf, 3 interrupted sutures between
the upper border of the strip and conjoined muscle and internal oblique muscle, 4 interrupted sutures between the lower border
of the strip and the inguinal ligament, 5 pubic tubercle, 6 abdominal ring, 7 spermatic cord, 8 lateral leaf.
CHAPTER 37
reduced complication rates with robotic-assisted surgery in
obese patients; however, this was compared against open
inguinal hernia repair (10.8% vs 3.2%, P = 0.047), the two
groups were covariate matched for preoperative risk. Studies
have also shown excellent long-term (36-month) quality of
life indicators in robot-assisted transabdominal preperitoneal
(TAPP), though this was a single surgeon survey. Further ran-
Inguinal Hernias
domized trials will shed more light into cost issues as surgeons
gain more experience with robotic application that would lead
to shorter operative time and minimize additional instrument
use. (See Schwartz 11th ed., p. 1616.)
11. The medical issue NOT associated with hernia recur- Answer: D
rence is: Hernia recurrence: When a patient develops pain, bulging,
A. Malnutrition. or a mass at the site of an inguinal hernia repair, clinical
B. Steroid use. entities such as seroma, persistent cord lipoma, and hernia
C. Smoking. recurrence should be considered. Common medical issues
D. Alcohol use. associated with recurrence include malnutrition, immuno-
suppression, diabetes, steroid use, and smoking. Technical
causes of recurrence include improper mesh size, tissue isch-
emia, infection, and tension in the reconstruction. A focused
physical examination should be performed. As with primary
hernias, ultrasound (US), computed tomography (CT), or
magnetic resonance imaging (MRI) can elucidate ambiguous
physical findings. When a recurrent hernia is discovered and
warrants re-operation, an approach through a virgin plane
facilitates its dissection and exposure. Extensive dissection of
the scarred field and mesh may result in injury to cord struc-
tures, viscera, large blood vessels, and nerves. After an initial
anterior approach, the posterior laparoscopic approach will
usually be easier and more effective than another anterior
dissection. Conversely, failed preperitoneal repairs should
be approached using an open anterior repair. (See Schwartz
11th ed., p. 1618.)
14. Injury to the lateral femoral cutaneous nerve results in: Answer: C
A. Inguinodynia. Other chronic pain syndromes include local nerve entrap-
B. Osteitis pubis. ment, meralgia paresthetica, and osteitis pubis. At greatest
C. Meralgia paresthetica. risk of entrapment are the ilioinguinal and iliohypogastric
D. Nerve entrapment. nerves in anterior repairs and the genitofemoral and lateral
femoral cutaneous nerves in laparoscopic repairs. Clinical
manifestations of nerve entrapment mimic acute neuropathic
pain, and they occur with a dermatomal distribution. Injury
to the lateral femoral cutaneous nerve results in meralgia par-
esthetica, a condition characterized by persistent paresthesias
of the lateral thigh. Initial treatment of nerve entrapment
consists of rest, ice, nonsteroidal anti-inflammatory drugs
(NSAIDs), physical therapy, and possible local corticosteroid
and anesthetic injection. Osteitis pubis is characterized by
inflammation of the pubic symphysis and usually presents as
medial groin or symphyseal pain that is reproduced by thigh
adduction. Avoiding the pubic periosteum when placing
sutures and tacks reduces the risk of developing osteitis pubis.
Computed tomography (CT) scan or magnetic resonance
imaging (MRI) excludes hernia recurrence, and bone scan is
confirmatory for the diagnosis. Initial treatment is identical
to that of nerve entrapment; however, if pain remains intrac-
table, orthopedic surgery consultation should be sought for
possible bone resection and curettage. Irrespective of treat-
ment, the condition often takes 6 months to resolve. (See
Schwartz 11th ed., p. 1619.)
CHAPTER 37
(See Schwartz 11th ed., p. 1620.)
Inguinal Hernias
and is rarely performed. experienced hands, the overall recurrence rate for the Shoul-
C. Compared with mesh repairs, Shouldice operation dice repair is about 1%. Although it is an elegant procedure,
has a lower incidence of recurrence. its meticulous nature requires significant technical expertise
D. Shouldice technique may be reliably replicated by a to achieve favorable outcomes, and it is associated with longer
novice surgeon. operative duration and longer hospital stay. One study found
the recurrence rate for Shouldice repairs decreased from
9.4% to 2.5% after surgeons performed the repair six times.
Compared with mesh repairs, the Shouldice technique
resulted in significantly higher rates of recurrence (OR 3.65,
CI 1.79–7.47); however, it is the most effective tissue-based
repair when mesh is unavailable or contraindicated. (See
Schwartz 11th ed., p. 1621.)
Chapter 38
13. An adolescent patient with a thyroid mass undergoes Answer: D
fine needle aspiration biopsy which returns as medullary MCT can be spontaneous (in 75%) or familial (in 25%) in
carcinoma of the thyroid (MCT). What other diseases multiple endocrine neoplasia syndrome type 2 (MEN2).
should be screened for before treatment is undertaken? MEN2A is associated with pheochromocytoma and hyper-
A. Hyperparathryroidism parathyroidism, whereas MEN2B is associated with pheo-
B. Pheochromocytoma chromocytoma, Marfanoid habitus, and mucocutaneous
C. Mucocutaneous ganglioneuromas ganglioneuromas. (See Schwartz 11th ed., p. 1655.)
local anesthesia
C. Minimally invasive videoscopic parathyroidectomy
from a left axillary approach under general anesthesia
D. Percutaneous alcohol ablation with ultrasound guid-
ance under local anesthesia
calcium and parathyroid hormone levels undergoes The position of the parathyroid glands can be quite vari-
bilateral neck dissection. Two upper pole parathyroid able. In addition to the tracheoesophageal groove adjacent
glands and one lower pole parathyroid gland are found to the posterior capsule of the thyroid, the gland may be
but despite a diligent search, the fourth gland is not intra-thyroidal, intra-thymic, within the carotid sheath, ret-
apparent. What steps are appropriate to locate the fourth roesophageal, or in the posterior mediastinum. (See Schwartz
gland? 11th ed., p. 1675.)
A. The thyrothymic ligament should be mobilized and
the upper end of the thymus gently retracted into the
field for dissection and removal if any mass is found.
B. The carotid sheath should be opened from the bifur-
cation to the base of the neck and explored.
C. Intraoperative ultrasonography can be employed to
examine the thyroid lobe on the side of the missing
parathyroid to detect an intrathyroidal location.
D. All of the above.
Chapter 38
22. A 35-year-old woman undergoes an evaluation for Answer: B
infertility. She has gained almost 100 pounds in the past Cushing’s syndrome refers to any cause of hypercortisolism
year, is hypertensive, and is borderline diabetic. She also caused by either an adrenal source or exogenous administra-
complains of easy bruising. Her serum chemistries are tion of steroids. Cushing’s disease refers only to an adreno-
normal with the exception of an elevated glucose. Imag- corticotropin hormone (ACTH)-secreting adenoma of the
ing studies reveal a unilateral adrenal mass. What is the pituitary gland. Cushing’s syndrome due to an isolated adre-
likely diagnosis? nal adenoma is far less common than hypercortisolism due
B. Percutaneous fine needle aspiration biopsy symptoms associated with adrenal disease, annual follow-up
C. Adrenal venous sampling for cortisol, renin, and of these lesions with imaging and chemical tests seems pru-
angiotensin dent. (See Schwartz 11th ed., pp. 1696–1697.)
D. Laparoscopic adrenalectomy
FIG. 39-1.
329
bone and tract to the pharynx inadequate initial operation. (See Schwartz 11th ed., p. 1710.)
D. Excision of the cyst
bowel with air-fluid levels. What is the most appropriate vomiting is usually the first sign of volvulus, and all infants
next step in management, after resuscitation? with bilious vomiting must be evaluated rapidly to ensure
A. Upper gastrointestinal series that they do not have intestinal malrotation with volvulus.
B. Barium enema The child with irritability and bilious emesis should raise par-
C. Gastrostomy ticular suspicions for this diagnosis. If left untreated, vascular
D. Laparotomy compromise of the midgut initially causes bloody stools, but
eventually results in circulatory collapse. Additional clues to
the presence of advanced ischemia of the intestine include
erythema and edema of the abdominal wall, which progress
to shock and death. It must be reemphasized that the index
of suspicion for this condition must be high, since abdominal
signs are minimal in the early stages. Abdominal films show
a paucity of gas throughout the intestine with a few scattered
air-fluid levels. When these findings are present, the patient
should undergo immediate fluid resuscitation to ensure ade-
quate perfusion and urine output followed by prompt explor-
atory laparotomy. (See Schwartz 11th ed., p. 1725.)
Chapter 39
FIG. 39-2. The five varieties of esophageal atresia and tracheoesophageal fistula. A. Isolated esophageal atresia.
B. Esophageal atresia with tracheoesophageal fistula between proximal segment of esophagus and trachea.
C. Esophageal atresia with tracheoesophageal fistula between distal esophagus and trachea. D. Esophageal atresia
with fistula between both proximal and distal ends of esophagus and trachea. E. Tracheoesophageal fistula without
Pediatric Surgery
esophageal atresia (H-type fistula).
Stage IV: Hematogenous metastases or lymph node involvement outside the abdomino-pelvic region.
Stage V: Bilateral renal involvement.
International Neuroblastoma Staging System
Stage 1: Localized tumor with complete gross resection, with or without microscopic residual disease
Stage 2A: Localized tumor with incomplete gross excision; representative ipsilateral nonadherent lymph nodes negative for tumor
Stage 2B: Localized tumor with or without complete gross excision, with ipsilateral nonadherent lymph nodes positive for tumor. Enlarged contralateral
lymph nodes must be negative microscopically
Stage 3: Unresectable unilateral tumor crossing midline, with or without regional lymph node involvement; or localized unilateral tumor with contralateral
Pediatric Surgery
Chapter 39
onstrates an absent gallbladder, and a technetium-99m fibroproliferative obliteration of the biliary tree, which pro-
iminodiacetic acid scan shows radionuclide that is con- gresses toward hepatic fibrosis, cirrhosis, and end-stage liver
centrated in the liver, but not excreted into the intestine. failure. Surgical treatment is the first-line therapy, consisting
Which of the following statements is TRUE? of creation of a hepatoportoenterostomy (Kasai procedure).
A. This condition is usually managed nonoperatively. Numerous studies suggest that the likelihood of surgical
B. Surgery should be performed within 60 days of life. success is inversely related to the age at the time of porto-
C. Cystoenterostomy provides adequate biliary enterostomy. Infants treated prior to 60 days of life are more
Pediatric Surgery
drainage. likely to achieve successful and long-term biliary drainage
D. Most of these patients will not require transplantation. than older infants. Although the outlook is less favorable for
patients after the 12th week, it is reasonable to proceed with
surgery even beyond this time point, as the alternative is cer-
tain liver failure. Approximately one-third of patients remain
symptom-free after portoenterostomy; the remainder require
liver transplantation due to progressive liver failure. Indepen-
dent risk factors that predict failure of the procedure include
bridging liver fibrosis at the time of surgery and postoperative
cholangitic episodes. (See Schwartz 11th ed., p. 1737.)
Chapter 39
the rectum with irrigations. postnatal period. Under such circumstances, a plastic spring-
D. Proceed with reduction and primary closure. loaded silo can be placed onto the bowel and secured beneath
the fascia or a sutured silastic silo constructed. The silo cov-
ers the bowel and allows for graduated reduction on a daily
basis as the edema in the bowel wall decreases. (See Schwartz
11th ed., p. 1741.)
Pediatric Surgery
14. A 3-year-old patient presents with recurrent lower gas- Answer: C
trointestinal bleeding. What imaging modality is used to A Meckel diverticulum is a remnant of a portion of the embry-
diagnose a bleeding Meckel’s diverticulum? onic omphalomesenteric (vitelline) duct. It is located on the
A. Doppler ultrasound antimesenteric border of the ileum, usually within 2 ft of the
B. Computed tomography ileocecal valve. Ectopic gastric mucosa within a Meckel diver-
C. Technetium pertechnetate scan ticulum may produce ileal ulcerations that bleed and lead
D. Capsule endoscopy to the passage of maroon-colored stools. Pancreatic mucosa
may also be present. Diagnosis may be made by technetium
pertechnetate scans when the patient presents with bleeding.
(See Schwartz 11th ed., p. 1733.)
15. What type of choledochal cyst accounts for 80% to 90% Answer: D
of all cases and has a fusiform dilatation of the common Type I choledochal cyst is characterized by fusiform dila-
bile duct? tation of the bile duct. This is the most common type and
A. Type IV is found in 80% to 90% of cases. Type II choledochal cysts
B. Type III appear as an isolated diverticulum protruding from the wall
C. Type II of the common bile duct. The cyst may be joined to the com-
D. Type I mon bile duct by a narrow stalk. Type III choledochal cysts
arise from the intraduodenal portion of the common bile
duct and are also known as choledochoceles. Type IVA cysts
consist of multiple dilatations of the intrahepatic and extra-
hepatic bile ducts. Type IVB choledochal cysts are multiple
dilatations involving only the extrahepatic bile ducts. Type V
(Caroli disease) consists of multiple dilatations limited to the
intrahepatic bile ducts. (See Schwartz 11th ed., p. 1739.)
337
detect ureteral injury. all devitalized tissues must be debrided to avoid delayed
B. Bladder mobilization is not integral to repair of ure- tissue breakdown and urinoma formation. Ureteral stents
teric injury. should be placed in this situation to facilitate healing with-
C. Kidney mobilization is not integral to repair of ure- out stricture. Midureteral-level injuries can be treated with a
teric injury. uretero-ureterostomy if a spatulated tension-free repair can
D. Use of ureteric stents is not useful in preventing post- be achieved. For longer defects, the bladder can be mobi-
repair strictures. lized and brought up to the psoas muscle (psoas hitch). For
additional length, a tubularized flap of bladder (Boari flap)
can be created and anastomosed to the remaining ureter.
(See Schwartz 11th ed., pp. 1765–1766.)
CHAPTER 40
of the prostate (TURP) remains the mainstay of endoscopic
procedures. (See Schwartz 11th ed., pp. 1763–1764.)
Urology
C. Often polymicrobial. factors for Fournier’s gangrene include perirectal abscesses,
D. Prompt surgical debridement mandatory. diabetes, obesity, and chronic alcoholism. The often polymi-
crobial infection spreads and can dissect along Scarpa and
Colles fascia. Prompt and aggressive surgical debridement of
nonviable tissue and broad spectrum antibiotics are necessary
to prevent further spread. (See Schwartz 11th ed., p. 1769.)
12. All of the following statements are TRUE of renal cell Answer: D
carcinoma (RCC), EXCEPT: Most patients diagnosed with RCC in the modern era typi-
A. Renal CT imaging with contrast is the definitive cally present with an incidentally discovered renal mass
radiologic test. on the abdominal radiographic imaging. Renal computed
B. Risk factors include smoking, obesity, and hypertension. tomography (CT) imaging with intravenous contrast remains
C. Familial syndromes should be suspected in younger the single most important radiographic test to determine the
patients and in patients with bilateral tumors. nature of the mass. Major recognized risk factors for RCC
D. Renal masses of any size, if suspicious for malignancy, include obesity and hypertension. Familial RCC subtypes
require excision as the first therapeutic maneuver. with classical clinical manifestations are also well described.
Management options for small renal masses (<4 cm) include
active surveillance, thermoablative techniques, or surgical
excision. Percutaneous or laparoscopic techniques (cryo-
ablation, radiofrequency ablation, high intensity-focused
ultrasound) have been used to treat small renal masses, but
they are associated with an increased risk of local recurrence.
(See Schwartz 11th ed., pp. 1772–1773.)
Intramural
Intercavitary
Pedunculated
Subserous
Submucous
Prolapsed
341
A. It can be due to lack of urethrovaginal support. vaginal support (urethral hypermobility) or intrinsic sphincter
B. It can be due to intrinsic sphincter deficiency. deficiency (ISD). ISD is a term applied to a subset of stress-
C. Goal of surgical repair is to create a partial urethral incontinent patients who have particularly severe symptoms,
obstruction. including urine leakage with minimal exertion. This condition
D. Urethral rein plantation is sometimes necessary if is often recognized clinically as the low pressure or “drainpipe”
other approaches fail. urethra. The urethral sphincter mechanism in these patients
is severely damaged, limiting cooptation of the urethra.
Gynecology
CHAPTER 41
B. Sequellae include increased risk of ectopic pregnancy. cases, although microorganisms that comprise the vaginal
C. Initial therapy requires intravenous antibiotics. flora (eg, anaerobes, Gardnerella vaginalis, Haemophilus influ-
D. Clinical criteria include an oral temperature >101° F. enza, enteric Gram-negative rods, and Streptococcus agalac-
tiae) have been implicated as well. Because of the psychosocial
complexity associated with a diagnosis of PID; when possible,
additional criteria should be used to enhance the specificity
of the minimum clinical criteria. These include oral temper-
Gynecology
ature >101° F (>38.3° C). Several outpatient parenteral and
oral antimicrobial regimens have been effective in achieving
clinical and microbiologic cure. Hospitalization for intrave-
nous antibiotics may be necessitated in cases where surgical
emergencies cannot be ruled out. (See Schwartz 11th ed.,
pp. 1803–1804.)
3
2
FIG. 42-1. Schematic drawing of brain herniation patterns.
1. Subfalcine herniation. The cingulate gyrus shifts across midline
under the falx cerebri. 2. Uncal herniation. The uncus (medial
temporal lobe gyrus) shifts medially and compresses the midbrain
and cerebral peduncle. 3. Central transtentorial herniation. The
diencephalon and midbrain shift caudally through the tentorial 4
incisura. 4. Tonsillar herniation. The cerebellar tonsil shifts
caudally through the foramen magnum. (Reproduced with
permission from Wilkins RH, Rengachary SS: Neurosurgery,
2nd ed. New York, NY: McGraw Hill; 1996.)
345
CHAPTER 42
A. A single ring with a darker center spot containing drains into the throat. In indeterminate cases, it is important
blood components surrounded by a light halo of CSF to consider radiographic findings on the computed tomogra-
B. A double ring with a darker center spot containing phy (CT) scan near the fracture that suggest CSF leak, such as
blood components surrounded by a light halo of CSF pneumocephalus, subarachnoid, or intraparenchymal blood
C. A single ring with a lighter center spot containing CSF at the fracture site. The “halo” test assesses for a double ring
surrounded by a darker halo of blood components when a drop of the fluid is allowed to fall on an absorbent
D. A double ring with a lighter center spot containing CSF surface, but it has been shown to have poor clinical utility. The
Neurosurgery
surrounded by a darker halo of blood components fluid can be sent for β-2 transferrin testing, a carbohydrate-
free isoform of transferrin exclusively found in the CSF;
however, these tests often take 1 to 2 weeks to result and also
can be difficult to incorporate into clinical practice. (See
Schwartz 11th ed., p. 1835.)
A B
FIG. 42-3. A. Postcontrast T1-weighted axial magnetic resonance imaging demonstrating a ring-enhancing lesion in the anteromedial
right temporal lobe with central necrosis (dark area) consistent with glioblastoma multiforme. B. T2-weighted axial magnetic resonance
imaging with extensive bright signal signifying peritumoral edema seen with glioblastoma multiformes.
CHAPTER 42
be used. Compression stockings or athrombic pumps should
be used when the patient cannot be mobilized rapidly for pro-
phylaxis of deep venous thrombosis. (See Schwartz 11th ed.,
p. 1839.)
Neurosurgery
A. C4–C5. pedicle of the same-numbered vertebra and at the level of the
B. C5–C6. higher adjacent intervertebral disc. For example, the C6 nerve
C. C6–C7. root passes above the C6 pedicle at the level of the C5–C6
D. C7–T1. discs. The cervical nerve roots may be compressed acutely by
disc herniation, or chronically by hypertrophic degenerative
changes of the discs, facets, and ligaments. Table 42-2 sum-
marizes the effects of various disc herniations. Most patients
with acute disc herniations will improve without surgery.
Nonsteroidal anti-inflammatory drugs (NSAIDs) or cervical
traction may help alleviate symptoms. Patients whose symp-
toms do not resolve or who have significant weakness should
undergo decompressive surgery. The two main options for
nerve root decompression are anterior cervical discectomy
and fusion (ACDF) and posterior cervical foraminotomy
(keyhole foraminotomy). ACDF allows more direct access
to and removal of the pathology (anterior to the nerve root).
However, the procedure requires fusion because discectomy
causes a collapse of the interbody space and instability will
likely occur. Figure 42-4 demonstrates a C6–C7 ACDF with
the typical interposed graft and plating system. Keyhole
foraminotomy allows for decompression without requiring
fusion, but it is less effective for removing centrally located
canal pathology. (See Schwartz 11th ed., p. 1862.)
A B
FIG. 42-4. A. Anteroposterior cervical spine X-ray showing the position of an anterior cervical plate used for stabilization after
C6–C7 discectomy. Patient presented with right triceps weakness and dysesthesias in the right fifth digit. Magnetic resonance imaging
revealed a right paracentral C6–C7 herniated disc compressing the exiting C7 nerve root. B. Lateral cervical spine X-ray of the same
patient clearly demonstrates the position of the plate and screws. The allograft bone spacer placed in the drilled-out disc space is
also apparent.
351
C. Spinal cord infarction. astatic disease. (See Schwartz 11th ed., p. 1904.)
D. Metastatic disease.
B. Treatment of these fractures consists of immediate require immediate administration of antibiotics and irri-
antibiotics, irrigation, debridement. gation and debridement of the wound. When the wound is
C. External fixation needed for clean and contaminated contaminated, an external fixator is initially used. Early cov-
wound. erage of the wound is important to avoid infection. Usually
D. Distal tibial wounds can be covered by local muscle a large wound in the proximal or middle third of the tibia
flaps. can be covered using local muscle flaps, while the distal third
of the tibia will require a free flap. (See Schwartz 11th ed.,
pp. 1881–1883.)
CHAPTER 43
10. Management of arthritis includes which of the following? Answer: A
A. Injection Measures to treat arthritis include weight loss, rest, physi-
B. Osteoplasty cal therapy, nonsteroidal antiinflammatory drugs (NSAIDs),
C. Arthroclasty bracing, and assistive devices such as cane or walker. Joint
D. Arthrotomy injections are commonly performed into the knee and
shoulder. Common injections include corticosteroids and
Orthopedic Surgery
hyaluronic acid gels. Corticosteroid injections can decrease
inflammation within the joint. These injections are usually
administered in combination with a local anesthetic, such as
lidocaine, in order to provide more immediate relief for both
diagnostic and therapeutic purposes. (See Schwartz 11th ed.,
pp. 1905–1907.)
1. The median, radial, and ulnar nerves serve the forearm, Answer: A
wrist, and hand. Which of the following statements about Three principal nerves serve the forearm, wrist, and hand: the
these nerves are TRUE? median, radial, and ulnar nerves. The most critical of these from
A. Median nerve receives fibers from C5–T1 and travels a sensory standpoint is the median nerve. The median nerve
through the carpal tunnel. begins as a terminal branch of the medial and lateral cords of
B. The radial nerve receives fibers from C5–T1 and the brachial plexus. It receives fibers from C5–T1. The ulnar
innervates the intrinsic muscles of the hand. nerve is a terminal branch of the medial cord of the brachial
C. The ulnar nerve receives fibers from C5–T1 and plexus. It receives innervation from C8 and T1 roots. The radial
innervates the extrinsic muscles of the hand. nerve is the larger of two terminal branches of the posterior
D. The ulnar nerve with the median nerve travel through cord of the brachial plexus. It receives fibers from C5–T1 nerve
the carpal tunnel. roots. It innervates all of the extensor muscles of the forearm
and wrist. See also Fig. 44-1. (See Schwartz 11th ed., p. 1930.)
Ulnar
FCR A N
TCL
Radial A Median N
3 4
APL 2 5
EPB 5
S 2 3 4
FPL H U
C
EC
EC
RL
/E
CR
B
EP Q
L ED
EIP/EDC
FIG. 44-1. Cross-section of the wrist at the midcarpal level. The relative geography
of the neurologic and tendinous structures can be seen. The transverse carpal
ligament (TCL) is the roof of the carpal tunnel, passing volar to the median nerve
and long flexor tendons. The TCL is also the floor of the ulnar tunnel, or Guyon’s
canal, passing dorsal to the ulnar artery and nerve. The wrist and digital extensor
tendons are also seen, distal to their compartments on the distal radius and
ulna. Bones: C = capitate; H = hamate; P = pisiform; S = scaphoid. Tendons (flexor
digitorum superficialis is volar to flexor digitorum profundus within the carpal
tunnel): 2 = index finger; 3 = middle finger; 4 = ring finger; 5 = small finger. A =
artery; APL = abductor pollicis longus; ECRB = extensor carpi radialis brevis; ECRL =
extensor carpi radialis longus; ECU = extensor carpi ulnaris; EDC = extensor
digitorum communis; EDQ = extensor digiti quinti; EIP = extensor indices proprius;
EPB = extensor pollicis brevis; EPL = extensor pollicis longus; FCR = flexor carpi
radialis; FPL = flexor pollicis longus; N = nerve.
355
Chapter 44
patient should be informed of the severity of the injury, and
exploration is ideally performed within 6 hours of injury. Up
to 50% of such injuries result in loss of the digit, but early rec-
ognition and treatment are associated with increased chance
of digit survival. Early frank discussion with the patient and
initiation of appropriate treatment produce the best results
and medicolegal protection. (See Schwartz 11th ed., p. 1939.)
Chapter 44
11. All of the following are TRUE about felon EXCEPT: Answer: D
A. Abscess of the fingertip that is caused by penetrating A felon is a subcutaneous abscess of the fingertip and is most
trauma. commonly caused by penetrating trauma. S. aureus is the
B. Staphylococcus aureus is the most common infectious most common pathogen. The fingertip contains multiple
agent. septa connecting the distal phalanx to the skin. These septa
C. Incision and drainage should be through a longitudi- are poorly compliant, and presence of an abscess will increase
12. All hand infections EXCEPT the following require surgi- Answer: C
cal management. All hand infections other than cellulitis will require surgical
A. Paronychia. management. Clinical examination, particularly noting the
B. Felon. area of greatest tenderness and/or inflammation, is the single
C. Cellulitis. most useful diagnostic tool to localize any purulence requir-
D. Osteomyelitis. ing drainage. Specific recommendations for differentiating
among the possible locations of hand infection are included
in the diagnostic algorithm shown in Fig. 44-3. (See Schwartz
11th ed., pp. 1947–1948.)
Hand inflammation
Plain X-rays
Localized fluctuance
Ulnar to
No Yes SF MC Hypothenar
Cellulitis Site of fluctuance abscess
Loss of
admit, IV Abx Palm
Chapter 44
palmar
serial exam concavity
Midpalm
No improvement Entire finger Partial finger Distal abscess
in 48 hours
Radial to
MRI if no Kanavel’s Dorsal Centered Between
IF MC Thenar
fluctuance signs present on joint digits
abscess
Pain with
Subcutaneous axial loading
Surgery of the Hand and Wrist
Pyogenic FTS
abscess of joint
Web space
abscess
Pyogenic vs.
crystalline
arthritis
Consider
arthrocentesis
FIG. 44-3. Diagnostic algorithm. Diagnostic workup for a patient with hand inflammation to evaluate for
infection. See text for details about particular infectious diagnoses. Abx = antibiotics; FTS = flexor tenosynovitis;
IF MC = index finger metacarpal; MRI = magnetic resonance imaging; SF MC = small finger metacarpal.
361
363
A. 2 hours after breast milk is 4 hours, after a light meal (small amount
B. 4 hours of easily digestible food such as toast or crackers) or infant
C. 6 hours formula is 6 hours, and after more food intake is 8 hours. In
D. 8 hours this patient, anesthesia can be induced 2 hours after intake of
clear liquids. (See Schwartz 11th ed., p. 2036.)
365
CHAPTER 47
D. All of the above
15. Elderly patients with acute peritonitis may not present Answer: A
with typical symptoms of acute abdominal pain, fever, In elderly patients with acute appendicitis or acute cholecys-
or leukocytosis due to an impaired immune response. A titis, one-third lack symptoms of abdominal pain, one-third
high index of suspicion is needed as the initial clinical are afebrile, and one-third have a normal white blood cell
diagnosis in elderly patients with acute appendicitis is count. Therefore an “unimpressive” abdominal examination
correct in what percent of cases? is irrelevant in the evaluation of the elderly patient whose tol-
A. Less than 50% erance for food has suddenly changed. (See Schwartz 11th ed.,
B. 70%–80% p. 2055.)
C. 90%–95%
D. 100%
of an abdominal aortic aneurysm (AAA) in elderly Randomized controlled trials of EVAR versus open AAA
patients? repair have shown equal or improved survival, fewer compli-
A. A reduction in blood loss and operative time cations, and shorter length of stay. The procedure can be per-
B. A reduction in the need for postoperative intensive formed under epidural anesthesia in patients who are at high
care risk for general inhalational anesthesia and has comparable or
C. The avoidance of abdominal and pulmonary compli- improved outcomes. (See Schwartz 11th ed., p. 2056.)
cations associated with open AAA repair
Surgical Considerations in the Elderly
369
C. The discussion of the options, risks, and possible haz- (See Schwartz 11th ed., pp. 2062–2063.)
ards has been documented.
D. There are witnesses to the discussion who also under-
stand the discussion.
CHAPTER 48
used on more than three patients. required. (See Schwartz 11th ed., p. 2073.)
C. An innovative modification of an existing surgical
instrument or device can be used in patients with IRB
approval.
D. When employing an innovative modification to an
operative procedure, explicit informed consent of the
patient is required.
373
additional disease. capable of reducing the transmission of HIV. The DCP3 adopted
C. Essential surgical procedures rank among the most a working definition of essential surgical conditions as those
cost-effective of all health interventions. that (a) are primarily or extensively treated by surgery; (b) have
D. All of the above. a large health burden; and (c) can be successfully treated by a
surgical procedure that is cost-effective and feasible to promote
globally. Using this definition, the DCP3 identified 44 essen-
tial procedures, most of which can be performed in first-level
Global Surgery
Measles vaccination
Antiviral therapy for HIV
Y
Y
AL
AL
AL
AL
/D
/D
/D
FIG. 49-1. Cost-effectiveness of surgical interventions,
/
$1
00
0
$1
00
$1
DALY = disability-adjusted life year. (Illustration reproduced Range - Cost/DALY (2012 US$)
with permission from Intermountain Healthcare.)
TABLE 49-1 Essential surgical procedures that can be performed in first level (district)
hospitals (DCP3)
Obstetric Complications
Severe postpartum hemorrhage, obstructed labor, prolonged labor, eclampsia, prolapsed cord, fetal distress,
tubal pregnancy, postabortion endometritis/myometritis, postabortion sepsis, intrauterine fetal death
Trauma and Violence
Major limb fracture/injury, joint dislocation, major soft tissue injury, pneumo/hemothorax, ruptured spleen
Acute Surgical Emergencies
Strangulated hernia, intestinal obstruction, intestinal perforation, appendicitis, liver abscess, major wound
infection, osteomyelitis/septic arthritis
Nonacute Surgical Conditions
Congenital hernia, hernia, breast cancer, chronic osteomyelitis, hydrocele, urethral stricture, prostatic
hypertrophy, cataract, eye injury
CHAPTER 49
D. Organ transplantation. maternal health include cesarean section, hysterectomy for
E. Trauma care. postpartum bleeding and uterine rupture, management of
ectopic pregnancy, and dilatation and curettage. In terms
of nonobstetrical acute surgical emergencies, about 90%
could be addressed by developing the capability to care for
the 10 most common acute surgical conditions in any local
region. Even common nonacute conditions can have sig-
Global Surgery
nificant impact on quality of life and socioeconomic status,
such as cleft lip and cleft palate, hernias, and cataracts. Nearly
2 million lives could be saved each year if LMICs could design
and implement simple trauma care initiatives that reduced
the case fatality rates among seriously injured patients to
equal those in high-income countries (HICs) (Fig. 49-2).
Transplantation, though an area of great interest to people
in poor countries, still eludes most of the developing world,
where cultural and legal prohibitions preclude cadaveric and
nonrelated organ donation. (See Schwartz 11th Ed., p. 2095.)
Kumasi,
80 Ghana Monterrey,
Mexico
Seattle,
60
Fatalities (percent)
Washington
United States
(ISS ≥ 9)
40
20
FIG. 49-2. Case fatality rates for severely injured people,
1998. Note: ISS = injury severity score. Income classifications
are based on status at the time of the study. Ghana is 0
now a lower-middle income country, and Mexico is an Low Middle High
upper-middle-income country. (Illustration reproduced with
Country income
permission from Intermountain Healthcare.)
Sophisticated
technology that
simplifies
Regulations and
standards that
Global Surgery
facilitate
change
Low-cost, Economically
innovative coherent value
business models network
377
CHAPTER 50
10. Traditional Chinese medicine techniques such as acu- Answer: C
puncture can be used as an adjunct to Western medicine Acupuncture can be used to both prevent and treat post-
in achieving the goals of enhanced recovery. Which of operative nausea and vomiting, and it is associated with
the following is associated with the use of acupuncture? improved gastrointestinal function and decreased ileus. It can
A. Increased intravenous opioid use also be used for perioperative pain management, and there is
B. Decreased anesthetic requirements evidence that it reduces opioid use. There is no evidence to
RCT
Cohort study
Case series
Case reports
Animal research
In-vitro research
Expert experience/opinion
FIG. 51-1. Evidence-based hierarchy.
381
CHAPTER 51
and procedures to the target population at large. Alternatively,
Internal validity describes the degree to which a study’s causal
conclusion is warranted. Factors such as randomization, blind-
ing, completeness of follow-up, equivalence among groups,
and accuracy of analysis affect the internal validity of a study.
(See Schwartz 11th ed., p. 2146.)
385
1. Virtual reality (VR) simulation has been used for training Answer: C
in laparoscopy, flexible endoscopy, sinuscopic surgery, VR simulators allow for automated performance measure-
and endovascular interventions. Which of the following ment such as time, instrument motion, and electrosurgery
is an advantage of VR simulator–based training as com- use measurements as well as a tally of the occurrence of
pared to physical laparoscopic video trainers? predefined errors. These measurements are not only auto-
A. Significantly improved operative performance mated but also free of observer bias. Both virtual reality and
B. Ability to perform proficiency-based training physical laparoscopic video trainers (“box” trainers) allow
C. Automated performance measurement for proficiency-based training. Good training results can be
D. Lower upfront costs for development obtained with proficiency-based training within a larger cur-
riculum, regardless of training platform. Although there may
be some advantage with the virtual reality trainer, no signifi-
cant difference has been identified. (See Schwartz 11th ed.,
pp. 2169–2171.)
387
simulation-based training program to reduce bile duct While ideally, simulation training should lead to improved
injuries during laparoscopic cholecystectomy. Which of patient outcomes, the incidence of bile duct injury with lapa-
the following would be the most feasible, relevant learner roscopic cholecystectomy is uncommon. Large, unrealistic
metric in assessing the success of this training? sample sizes would be necessary to demonstrate a clinically
A. Perceptions about the training relevant difference. In evaluating the effectiveness of educa-
B. Knowledge about bile duct injuries tional intervention efforts, the Kirkpatrick four-level scale is
C. Skills transfer to the clinical environment often used. The four levels are: Reaction, learning, behavioral
Skills and Simulation
D. Institutional incidence of bile duct injuries change, and institutional impact. Since institutional impact
cannot be assessed in this example, the next highest level
would be behavioral change—did the knowledge, skills, and
attitudes acquired during simulation transfer to the clinical
environment? (See Schwartz 11th ed., p. 2178.)
389
A. Case report of a patient with an unusual complication considerations surrounding patient confidentiality and pri-
B. Email between physician and established patient vacy. Appropriate safeguards must be taken to guard against
C. Online journal club about a published randomized violation of patient confidentiality and privacy. Although
trial patients must consent to participate in a randomized trial,
D. Posting of a photo that does not have the patient’s discussion of an already published and peer-reviewed ran-
face domized trial does not require additional patient consent.
Case reports, whether published in a journal or posted on
social media, require patient consent. Emails or other elec-
tronic communications should only be used by physicians in
an established patient–physician relationship and with patient
consent. Photos should not be posted that have any details that
would result in the patient being identifiable. (See Schwartz
11th ed., pp. 2190–2193.)
INDEX
Aspergillosis, 153 BE. See Barrett esophagus bi-shRNA. See Bifunctional short
Aspergillus sp., 153 Beck’s triad, 49, 55 hairpin
Aspiration pneumonia, 153 Beclin I gene, 84 Bites, human, 133–134
Aspirin, 23 BEE. See Basal energy expenditure Bladder cancer, 337
Asplenia, 298 Belsey fundoplication, 221 Bladder pressure, 112t
Assistant medical officers, 373 Benign calcifications, Blastocysts, 124
Astrocytoma, 348 in hamartomas, 148 Blastomyces dermatitidis, 90
Atherosclerotic aortoiliac occlusive Benign prostatic hyperplasia, 339 Blood loss, 26, 32–33
disease, 193–194 Betel nut chewing, 144 Blood pressure
AT-III. See Antithrombin III Bevacizumab, 149 intra-arterial monitoring
Atresia bFGF. See Basic fibroblast growth system for, 106
biliary, 333 factor pregnancy-related changes, 62
esophageal, 330, 331f Bicarbonate Blood transfusion
Atrial fibrillation, 174, 176 chemoreceptor sensitivity to complications of, 26
Atrial septal defects, 157f, 157–158 levels of, 30 description of, 25
Atrophic gastritis, 229 metabolic acidosis with anion gap diseases not transmitted by, 27
Atypical adenomatous hyperplasia, 148 caused by loss of, 13, 17 indications for, 25–26
Atypical ductal hyperplasia, 137 Bidirectional Glenn procedure, Blood urea nitrogen, 18
Atypical lobular hyperplasia, 137 160, 160f “Blooming artifact,” 189
AUG, 120 Bifunctional RNAi technology, 125 Blotting, 124
Authoritative leader, 4 Bifunctional short hairpin, 125 Blunt trauma
Autoimmune hemolytic anemia, Bile acids to abdomen, 60, 60f
298–300 description of, 236, 268 duodenal hematoma from, 53
Automobile accidents, 50, 59 reabsorption of, 283 to liver, 50
Autophagy, 9 Bile ducts to pancreas, 53
Autotransplant, 87 cancer/carcinoma of, 246, 276 transcriptomic response to, 10
Axillary lymph nodes, 137 common, 279 BMI. See Body mass index
Axillary vein, 198 stricture of, 282 Body mass index, 233
Axonotmesis, 77 Bile leak, 102 Bone healing, 77
AZA. See Azathioprine Bile salts, 268 Bone marrow suppression, 88
Azathioprine, 88, 89t Biliary atresia, 333 Bottleneck, 5
Biliary cancer, 281 Bougie, 234
B Biliary injury, 282 Bovine aortic arch, 182
Back pain, 352 Biliary scintigraphy, 283 Bowel preparation, 246
Balloon valvotomy, 158–159 Biliary stricture, 282 BPH. See Benign prostatic hyperplasia
Balloon-expandable stents, 189 Bilious emesis, 330 Brachiocephalic veins, 198
Bare coronary stent placement, 364 Billroth I gastroduodenostomy, Bradycardia, 115
Bariatric surgery 227, 227f Brain
gastric stasis after, 224 Billroth II gastroduodenostomy, herniation of, 345, 345f
questions regarding, 233–234 227, 228f malignant tumors of, 348
Barium esophagogram Biloma, after laparoscopic traumatic injury of. See Traumatic
of H-type tracheoesophageal cholecystectomy, 102 brain injury
fistula, 331f Biologic mesh, for abdominal wall Brain stem compression, 346
of vascular rings, 168f hernia repair, 307 Branched-chain amino acids, 9
Barium swallow, for eosinophilic Biomarkers, cancer, 85 BRCA1, 140
esophagitis, 220 Biomedical ethics, 369 BRCA2, 140
Baroreceptors, 30 Biopsy Breast
Barotrauma, 112 fine needle aspiration, of thyroid abscess of, 140
Barrett esophagus, 208–209 nodules, 324 anatomy of, 139
Barrett mucosa, 214f–215f primitive neuroectodermal tumor blood supply to, 139
Basal cell carcinoma, 129, 135 diagnosis, 154 Cooper suspension
Basal energy expenditure, 11, 11t sentinel lymph node ligaments of, 139
Base deficit, 36 for breast cancer, 139 hormonal effects on, 139
Basic fibroblast growth factor, 124 for melanoma, 132 infection of, 140
INDEX
thrombosis and, 107 agents used in, 84 Clostridium perfringens, 80
Catheter-based contrast hairy cell leukemia treated Clot
aortography, 184 with, 302 formation of, 21
Catheter-directed thrombolysis, 201 hepatocellular carcinoma treated propagation of, 22
Catheter-related bloodstream with, 277 Clotting factors, 268
infection, 108 Chenodeoxycholic acid, 268 congenital deficiency of, 22
Cauda equina syndrome, 350 Chernobyl disaster, 324 in intrinsic and extrinsic
Cause of death Chest injury, penetrating, 53 pathways, 21
medical errors as, 97 Chest wall tumors, 154 CML. See Chronic myelogenous
in pediatric patients, 333 Children. See Pediatric patients leukemia
Caustic injury, 134 Child-Turcotte-Pugh score, 274, 274t CMS. See Centers of Medicare and
CCK. See Cholecystokinin Chin lift, 58 Medicaid Services
CD117, 249 Chinese medicine, traditional, 379 CMV. See Cytomegalovirus
CD4+ T cells Chlamydia trachomatis, 343 COA. See Coarctation of the aorta
cytokines produced by, 9 Chloroquine, 84 Coaching, 3
helper T cells, 10 Cholangiocarcinoma, 276, 281, Coagulation
CD8+ T cells, 9 286–287 in cardiopulmonary bypass, 25
CDC. See Centers for Disease Cholecystectomy extrinsic pathway of, 21
Control and Prevention indications for, 286 intrinsic pathway of, 21
CDH. See Congenital diaphragmatic laparoscopic Coagulation cascade, 22
hernia acute cholecystitis treated with, 284 Coagulopathy, trauma-induced, 23
Cecal volvulus, 250–251 anesthesia for, 364 Coarctation of the aorta, 159, 163–164
Cell(s) biloma after, 102 Codon, 120
apoptosis of, 84, 122 safety concerns for, 117 Coercive style, of leadership, 4
physiologic alterations of, Cholecystitis, acute, 279–280, 283f, Colectomy
in cancer, 83 283–284 bowel preparation for, 246
tumorigenic transformation of, 83 Cholecystokinin, 279 left, 244
Cell cycle, 83, 121f, 121–122 Choledochal cysts, 281, 285, 286f, 335 right, 243
Cell-free mitochondrial DNA, 8 Cholestasis, 103 sigmoid, 244, 250
Cell-surface receptors, 122–123 Cholic acid, 268 subtotal, 244
Cellulitis, 129 Chondromas, 154 total, 244
Centers for Disease Control and Chondrosarcoma, 154 transverse, 244
Prevention, 100 Chronic allograft nephropathy, 93 Collagen
Centers of Medicare and Medicaid Chronic bacterial prostatitis, 338 in inguinal hernias, 315, 316t
Services, 385 Chronic liver disease, 270 synthesis of, steroid effects on, 78
Central line infections, 100 Chronic lymphedema, 311 in wound healing, 74, 76t
Central transtentorial herniation, 345f Chronic lymphocytic leukemia, 297 Collagen disorders, 315
Central venous pressure, 55, Chronic myelogenous leukemia, 303 Collagenase, 74, 76t
106–107, 178 Chronic pancreatitis, 290f–291f, Colloid osmotic pressure, 16
Cephalic vein, 198 290–292, 292t Colloid resuscitation, 30
Cerebellar stroke, 346f Chronic venous insufficiency, 198, 199f Colocolic anastomosis, 245f
Cerebral perfusion pressure, 53, 112 Chvostek sign, 16 Colon
Cerebrospinal fluid leak/leakage, 144, Chylothorax, 156 hepatic flexure of, 54
346–347 Cingulate gyrus, 345f laparoscopic resection of, 378
Cerebrovascular accident, 190 Cirrhosis, 270–271, 276, 280 layers of, 256
Cervical disc herniation, 349, 349t CKI. See Cyclin-dependent kinase leiomyoma of, 249
Cervical esophagus, 207, 213 inhibitors leiomyosarcoma of, 249
Cervical radiculopathy, 349 Claudication, 196 minimally invasive
Cesarean delivery, 341 Clean wound, 39, 40t resection of, 243
Chagas’ disease, 27 Clean/contaminated wound, penetrating injuries to, 54
Charcot triad, 284 39–40, 40t questions regarding, 241–257
Chemical burns, 134 CLL. See Chronic lymphocytic resection of, 243–244
Chemoprevention, of cancer, 84 leukemia Colonic pseudo-obstruction, 251
Chemoreceptors, 30 Clopidogrel, 22–23 Colonoscopy, 252
INDEX
proinflammatory, 9 Digestion, carbohydrate, 236 adenocarcinoma of, 238
shock-related elevations of, 32 Digit amputation, 356 gastrinoma of, 294
Th1, 9 Direct Coombs test, 298 hematoma of, 53
Cytomegalovirus, 90 Direct oral anticoagulants, 24 obstruction of, 333, 334f
Direct thrombin inhibitors, 24, 205 ulcers of, 226–227
D Dirty wound, 40, 40t Duplex ultrasonography, for venous
Dabigatran, 24 Disability-adjusted life year, 374 thromboembolism, 204, 204f
Dacron patch aortoplasty, for Disasters, 71 Durable power of attorney for health
coarctation of the aorta, 164 Dislocation care, 370
DALY. See Disability-adjusted life year knee, 352 DVT. See Deep vein thrombosis
Damage control resuscitation, 26 shoulder, 352 Dysphagia, 210
Damage-associated molecular Disseminated intravascular
patterns, 7–8, 10, 29, 37 coagulation, 23 E
DAMPs. See Damage-associated Distal aortic aneurysms, 183 EA. See Esophageal atresia
molecular patterns Distal carcinoma in situ, 137–138 Ebstein’s anomaly, 169f
Damus-Kaye-Stansel anastomosis, 160 Distal ischemia, 107 EBV. See Epstein-Barr virus
DCD. See Donation after cardiac death Distal pancreatectomy, 54 E-cadherin gene, 229
DCIS. See Distal carcinoma in situ Distant flaps, 361 Eccrine sweat glands, 133
DCP3, 374, 374t Diversity, in surgery, 5 Echinococcal antigens, 273
DCR. See Damage control resuscitation Diverticulectomy, 220 Echocardiography
Death Diverticulitis, 247 dobutamine-stress, 172
cardiac, organ donation after, 91 Diverticulopexy, 220 transesophageal, 172–173
causes of, 97 Diverticulum transthoracic, 172–173
medical errors as cause of, 97 Meckel, 235, 335 Edmonton protocol, 94
Decompressive laparotomy, 69 Zenker’s, 220 EDP. See End-diastolic pressure
Deep vein thrombosis, 200–202, DKS anastomosis. See Damus-Kaye- EDS. See Ehler-Danlos syndrome
202t, 366 Stansel anastomosis EDV. See End-diastolic volume
Defecation, 241 DLCO. See Carbon monoxide EE. See Eosinophilic esophagitis
Delirium, postoperative, 365–366 diffusion capacity eFAST. See Extended focused
Democratic leadership style, 3–4 DNA abdominal sonography
Dermatitis, 294 eukaryotic, 119 for trauma
Dermoid cysts, 135 replication of, 121–122 EGD. See
DES. See Diffuse esophageal spasm in RNA synthesis, 120 Esophagogastroduodenoscopy
Desarda repair, of inguinal hernias, DO2. See Oxygen delivery EGFR. See Estimated glomerular
318, 318f DOACs. See Direct oral anticoagulants filtration rate
Desmoid tumors Dobutamine, 34 Ehler-Danlos syndrome, 75,
of abdominal wall, 308 Dobutamine-stress 182, 315
description of, 154 echocardiography, 172 Elderly
Desufflation, 115 Donation after cardiac death, 91 abdominal aortic
Diabetes mellitus Donation by non–heart-beating aneurysms in, 368
dermatitis and, 294 donors, 91 anticoagulation in, 367
pancreatic endocrine tumors Donebedian model of measuring appendicitis in, 367
associated with, 294 quality, 98 cardiac function in, 366
questions regarding, 78, 123–124 Dopamine, 34 colon cancer resection in, 367
Roux-en-Y gastric bypass Dor fundoplication, 221 deep venous thrombosis
effects on, 234 Dormancy, 84 prophylaxis in, 366
wound healing affected by, 78 DORV. See Double-outlet right falls in, 367
Diagnostic peritoneal lavage, ventricle frailty in, 365
59–60, 60t Double aortic arch, 167f heart valve replacement in, 367
Diaphragm, penetrating trauma to, 59 “Double bubble” sign, 333, 334f medications in, 366
Diaphragmatic hernia, 218, 329 Double-outlet right ventricle, 170 necrotizing fasciitis in, 80
DIC. See Disseminated intravascular DPL. See Diagnostic peritoneal nutritional status in, 366
coagulation lavage preoperative assessment and
Difficult airway algorithm, 364 Drug metabolism, 268 counseling in, 365
INDEX
Factor XI, 21 normal saline for, 18, 378 cancer of, 276, 280
Factor XII, 21 Fluid volume deficit, 17–18 lesions of, 281
Factor XIII deficiency, Fluorodeoxyglucose-PET/CT, 269 lymphatics of, 280
congenital, 22 FMD. See Fibromuscular dysplasia polyps of, 286
Falciform ligament, 263, 263f FNAB. See Fine needle aspiration wall layers of, 282
Falls, 367 biopsy Gallstone(s)
False aneurysms, 181 FNH. See Focal nodular hyperplasia description of, 280
Familial adenomatous polyposis, FOBT. See Fecal occult blood test ileus, 284, 285f
238, 308 Focal nodular hyperplasia, 275, 275f pancreatitis, 289
FAP. See Familial adenomatous Focused assessment with sonography GALT. See Gut-associated lymphoid
polyposis in trauma, 60 tissue
FAST. See Focused assessment with Fontan repair, 160 Ganglion cyst, 360
sonography in trauma Forced expiratory volume in Gangrenous appendicitis, 261f
Fasting, 364, 366 1 second, 152 Gardner syndrome, 154
FBN-1 gene, 75 Forced-error approach, 387 Gastrectomy
Fecal continence, 241–242 Foreign bodies dumping after, 231
Fecal occult blood test, 256 rectal, 255 partial, 62
Felon, 359, 359f retained, 99 Gastric antral vascular ectasia,
Felty syndrome, 298, 304–305 Fournier’s gangrene, 339 230–231, 231f
Femoral hernia, 313, 317 Fourth-degree hemorrhoids, 252 Gastric banding, adjustable, 233
Ferritin, 270 Fractional inspiration of Gastric bypass
Fetal acidosis, 117 oxygen, 41 hypoglycemia after, 234
Fetal aortic valvotomy, 158 Fractional saturation of Roux-en-Y. See Roux-en-Y gastric
Fetal wound healing, 77 hemoglobin, 110 bypass
α-Fetoprotein, 155 Fractures Gastric cancer, 229
FEV1. See Forced expiratory volume facial, 144 Gastric carcinoid tumors, 230
in 1 second humeral shaft, 352 Gastric emptying, 224t
FFP. See Fresh frozen plasma long bone, 351–352 Gastric injuries, 62
Fibrillin, 75, 181 pelvic, 351–352 Gastric juice, esophageal exposure to,
Fibrin glue fixation, for inguinal reduction of, 351 215, 216f
hernia repair, 319 rib, 63 Gastric sleeve procedure, 234
Fibrinogen, 21 sacral, 352 Gastric stasis, after bariatric
Fibroblastic phase, of wound healing, skull base, 346–347 surgery, 224
73f, 74 Frailty, 365 Gastrin, 208, 223
Fibroids, uterine, 341 Free flaps, 361 Gastrinoma, 225–226, 294
Fibromas, 180 Free water deficit, 15 Gastroduodenal arteries, 279
Fibromuscular dysplasia, 195 Fresh frozen plasma, for thrombotic Gastroesophageal junction, 211, 216
Fibroplasia, 78 thrombocytopenic purpura, 25 Gastroesophageal reflux disease, 214,
Fine needle aspiration biopsy, of FTS. See Flexor tenosynovitis 216, 219, 234
thyroid nodules, 324 Full-thickness burns, 67–68 Gastrografin, 236
First-degree burns, 66, 68 Full-thickness wounds, 75–76 Gastrointestinal anastomosis
First-degree hemorrhoids, 252 Fundoplication stapler, 221
Fistula Belsey, 221 Gastrointestinal bleeding, 238
enterocutaneous, 237 Dor, 221 Gastrointestinal stromal tumors,
pancreatic, 294 goal of, 217 230, 238, 249
rectovaginal, 253–255, 254f Nissen, 116, 216 Gastrointestinal tract, wound healing
tracheoesophageal, 330, 331f Fungi, 153 in, 75–76, 76t
FK506-binding proteins, 89 Furosemide, 18 Gastroschisis, 335
FKBPs. See FK506-binding Gastrosplenic ligament, 300, 301f
proteins G GBM. See Glioblastoma multiforme
Flail chest, 58 G0 phase, of cell cycle, 83 GCS. See Glasgow Coma Scale
Flaps, 361 G1 phase, of cell cycle, 83, 121 GEJ. See Gastroesophageal junction
Flexor tenosynovitis, 359 G2 phase, of cell cycle, 83, 121 Gene expression, 10, 124
Fluid maintenance, 16 Gain-of-function mutations, 121 General anesthesia, 245, 363, 366
INDEX
Herbicide exposure, 311 HS. See Hereditary spherocytosis Hypoparathyroidism, 14
Herceptin. See Trastuzumab HSV. See Herpes simplex virus Hypoplastic left heart syndrome,
Hereditary cancer, 83 HTS. See Hypertrophic scars 160–161, 169
Hereditary diffuse gastric cancer, 229 Human bites, 133–134 Hypoplastic left ventricle, 159
Hereditary hemochromatosis, 270 Human chorionic gonadotropin, 155 Hypotension, in shock, 35
Hereditary nonpolyposis colorectal Human embryonic stem cells, 124 Hypothalamic-pituitary-adrenal axis,
cancer, 247–248 Human genome, 121 8–9
Hereditary spherocytosis, 297, 301 Human immunodeficiency virus Hypothermia, 40–41, 185
Hernia blood transfusion transmission of, 27 Hypovolemic shock, 29, 31–32
abdominal, 270 surgeon-to-patient transmission Hypoxia, intraoperative, 40–41
abdominal wall, 307 of, 43–44
congenital diaphragmatic, 329 transmission of, 27, 43–44 I
diaphragmatic, 218 tuberculosis risks, 153 IABP. See Intra-aortic balloon pump
esophageal, 218, 218f–219f Human leukocyte antigen system, 87, IAP. See Intra-abdominal pressure
femoral, 313, 317 91–92 ICP. See Intracranial pressure, increased
fibrin glue fixation for, 319 Human papillomavirus Idarucizumab, 24
groin, 313, 314t head and neck cancers, 143 Idiopathic thrombocytopenic
hiatal, 218, 218f–219f malignancy risks, 135 purpura, 23, 298, 302
incisional, 307–308 vaccine for, 135, 342 IL-2. See Interleukin-2
inguinal. See Inguinal hernias Humeral shaft fractures, 352 IL-6. See Interleukin-6
Nyhus classification of, 313, 313t Hurley classification, of hidradenitis IL-10. See Interleukin-10
paraesophageal, 218, 218f–219f suppurativa, 133 IL-17. See Interleukin-17
recurrence of, 319, 321 Hydatid disease, 273 Ileocolic anastomosis, 245f
Shouldice repair for, 321 Hydroxocobalamin, for cyanide Ileocolostomy, 54
transabdominal preperitoneal poisoning, 66 Ileum, 235
repair of, 321 Hydroxyethyl starch solutions, 14 Ileus
Herpes simplex virus, 90 Hyperacute rejection in gallstone, 284, 285f
hESCs. See Human embryonic transplantation, 88 postoperative, 101, 378
stem cells Hyperbilirubinemia, 103 IM. See Intestinal metaplasia
Heterotopic ossification, 70 Hypercalcemia, acute, 18 Imatinib, 230, 249
Hiatal hernia, 218, 218f–219f Hyperchloremic metabolic Iminodiacetic acid, 283
HIDA scan. See Hepatobiliary acidosis, 18 Immune response
iminodiacetic acid scan Hypercoagulability, 30 to injury, 9
Hidradenitis suppurativa, 133 Hypergastrinemia, 225, 225f platelet’s role in, 10
High reliability organization Hyperglycemia Immune thrombocytopenia,
theory, 97 in critically ill patients, 33 23, 300, 302
High-mobility group protein B1, 8 postoperative, 40 Immune-based therapies,
High-pressure injection injuries, 357 postoperative fasting as cause of, 377 for cancer, 85
Hirschsprung disease, 334 Hyperkalemia Immunonutrition supplements, 377
Hispanics, 5 signs and symptoms of, 13 Immunosuppression
HIT. See Heparin-induced treatment of, 15–16 cardiac transplantation, 95
thrombocytopenia Hyperreflexia, 16 drugs for, 88–90, 89t
HLA system. See Human leukocyte Hypertonic saline, 14 indications for, 87
antigen system Hypertriglyceridemia, 90 lung abscess secondary to, 153
HLHS. See Hypoplastic left heart Hypertrophic scars, 80–81 tuberculosis secondary to, 153
syndrome Hypoalbuminemia, 16 Immunotherapy, oncogene
HMGB1. See High-mobility group Hypocalcemia, 14 targeting by, 125
protein B1 asymptomatic, 16 IMPDH. See Inosine monophosphate
HNPCC. See Hereditary nonpolyposis hypomagnesemia and, 16, 19 dehydrogenase
colorectal cancer Hypochloremic, hypokalemic Imperforate anus, 336
HO. See Heterotopic ossification metabolic alkalosis, 17 Impingement syndromes, 352–353
Hodgkin disease, 297 Hypocoagulability, 30 In situ cancers, 84
Holosystolic murmur, 175 Hypoglycemia, post-gastric Incisional hernia, 307–308
Horner syndrome, 149 bypass, 234 Incontinence, stress, 342–343
INDEX
transplantation of, 91–93, 92f Large bowel ischemia, 251–252 anatomy of, 263, 263f–264f
Kidney grafts, 91–92, 92f Larynx benign lesions of, 274–275, 275f
Kidney transplant anatomy of, 146, 146f Child-Turcotte-Pugh
in adult recipients, 91–92 cancer of, 144 score of, 274, 274t
complications of, 92–93 fractures of, 56 cholangiocarcinoma of, 276
graft thrombosis in, 93 Lateral femoral cutaneous nerve chronic disease of, 270
living donor, 91 injury, 320 cirrhosis of, 270–271, 276, 280
Kirkpatrick four-level LCGS. See Lancet Commission on colorectal metastases to, 277
scale, 388 Global Surgery drug metabolism in, 268
Klatskin’s tumor, 276, 287 LCH. See Langerhans cell ducts of, 266, 267f
Knee dislocation, 352 histiocytosis failure of, 95
KRAS mutations, 148 LCIS. See Lobular carcinoma in situ falciform ligament of, 263, 263f
K-time, 28 Le Fort fractures, 144 focal nodular hyperplasia of,
Kulchitsky cells, 147, 147f Leadership 275, 275f
Kupffer cells, 283 communication in, 3–4 glucose production by, 267
conflict resolution in, 3t, 4 hemangiomas of, 274–275
L principles of, 3, 3t hemorrhage of, angiography for, 61
Lactated Ringer solution styles of, 3–4 hepatic artery of, 264, 265f
for burns, 68 Leadership skills, 5 hepatocellular carcinoma, 276–277
intravenous colloid solution Learning inflammatory bowel disease
versus, for hemorrhagic experiential, 5 effects on, 246
shock, 30 willingness to learn, 3t lesions of, 268–269, 274–275
for metabolic acidosis, 19 Left atrial pressure, 174 lobes of, 263, 264f
Lactic acid, 17 Left colectomy, 244 Model for End-Stage Liver Disease,
LAMN. See Low-grade appendiceal Left subclavian artery, proximal, 95, 274
mucinous neoplasms 60–61 portal hypertension, 270–271
Lancet Commission on Global Left ventricle pyogenic abscesses of, 41, 272, 272f
Surgery, 375 aneurysms of, 176 transplantation of, 95, 276–277,
Langerhans cell histiocytosis, 155 hypoplastic, 159 280, 287
Langerhans cells, 133 tricuspid atresia and, 168 variceal hemorrhage of, 271
Laparoscopic cholecystectomy Left ventricular assist devices, 179 veins of, 265, 266f
acute cholecystitis treated Left ventricular outflow tract Liver trauma
with, 284 obstruction, 158 bleeding caused by, 61
anesthesia for, 364 Left ventricular pressure-volume description of, 50
biloma after, 102 loops, 107 Living donor kidney transplant, 91
safety concerns for, 117 Left ventricular stroke volume, 110 Living donors, 91
Laparoscopy Leiomyoma Living wills, 370
abdominal compartment of colon, 249 LMICs. See Low- and middle-income
syndrome after, 103 of esophagus, 211 countries
adrenalectomy, 328 of uterus, 341 LMWH. See Low molecular weight
antireflux surgery, 216 Leiomyosarcoma, 249 heparin
appendectomy, 259–261 Lentigo maligna melanoma, 130 Lobular carcinoma in situ, 137
arrhythmia during, 115 LES. See Lower esophageal sphincter Local anesthetic systemic toxicity, 364
cholecystectomy. See Laparoscopic Lesions Local tissue ischemia, 134
cholecystectomy gallbladder, 281 Long bone fractures, 351–352
enterolithotomy, 284 liver, 274–275, 275f Loop colostomy, 54
gangrenous appendicitis on, 261f Leukoplakia, vocal cord, 143 Low- and middle-income countries,
hand-assisted, 243 Life-threatening injuries, 49, 59 373–375
ileus after, 378 Ligament of Treitz, 42 Low glycemic index diets, 377
Nissen fundoplication, 116 Limb amputation, 356 Low molecular weight heparin,
in pregnancy, 117 Linitis plastica, 229 203, 366
robotic surgery versus, 116–117, Lip cancer, 143 Lower esophageal sphincter, 208,
117f, 319 Lipid metabolism, 11 212, 214, 217f, 221
skills training in, 375–376 Lipodermatosclerosis, 198 Lower extremity veins, 197
Luminal peptides, 223 Magnetic resonance imaging ABCDE initialism for, 130
Lumpectomy, 138, 140 computed tomography versus, 269 acral lentiginous, 130–131
Lund and Browder chart, 66 of double aortic arch, 167f advanced, 131f
Lung glioblastoma multiforme on, 348f anorectal, 250
abscess of, 152, 152t hernia recurrence evaluations, 319 cutaneous, 130, 132
adenocarcinoma of, 148–149, 150f mesenteric vein thrombosis on, 206 description of, 130
histology of, 147f pheochromocytomas on, 327 excision of, 132
Lung cancer Major adverse cardiac events, 172 lentigo maligna, 130
algorithm for, 150f Major histocompatibility complex, 87 metastasis of, 130
computed tomography of, 148 Malaria, 27 nodular, 130, 131f
management of, 149 Malignant hyperthermia, 363 sentinel lymph node biopsy for, 132
non-small-cell, 151 Malignant mesothelioma, 156 superficial spreading, 130, 130f
pathologic progression of, 148 Malignant wounds, 80 MELD. See Model for End-Stage
predictive markers for, 149 Mallory-Weiss tears, 211 Liver Disease
prognostic markers for, 149 Malnutrition/malnourished patients MEN2A, 325
pulmonary function magnesium deficiency in, 19 MEN2B, 325
studies in, 152 total body water in, 15 Ménétrier disease, 231, 231f
signs and symptoms of, 149 wound healing, 79 Mentees, 5
staging of, 152 Maloney dilator, 220 Mentoring, 5
TNM staging of, 152 MALT lymphoma. See Mucosa- Mentors, 5
LVADs. See Left ventricular associated lymphoid tissue Meralgia paresthetica, 320
assist devices lymphoma 6-Mercaptopurine, 88
LVOT. See Left ventricular outflow Mammalian target of rapamycin Mesenteric circulation, 192–193
tract obstruction inhibitors, 90 Mesenteric ischemia, 192–193
LVSV. See Left ventricular Mammography, 138 Mesenteric vein thrombosis, 206
stroke volume Marfan syndrome, 75, 175, 181, 183 Mesothelioma, 156
LY30, 28 Marginal artery of Drummond, 243 Meta-analyses, 381
Lymph nodes Marijuana smoking, 144 Metabolic acidosis
axillary, 137 Marjolin’s ulcer, 80 diagnosis of, 17
breast cancer metastasis to, 139 Mass casualty incidents, 71 in hemorrhagic shock patients, 19
colorectal cancer metastasis to, Massive resuscitation, 69 hyperchloremic, 18
248–249 Mastectomy, 140–141 laboratory tests for, 14
mediastinal, 151 Maternal hypercarbia, 117 Lactated Ringer solution for, 19
metastases, 139, 148 Matrix metalloproteinases, 74, 84 metabolic alkalosis versus, 17
Lymphatic drainage Mayo protocol, 276 with normal anion gap, 13, 17
of anorectal region, 241 May-Thurner syndrome, 201 Metabolic alkalosis
of gallbladder, 280 MCT. See Medullary carcinoma of diagnosis of, 17
Lymphatic massage, 205 the thyroid hypochloremic, hypokalemic, 17
Lymphedema, 205–206, 311 McVay Cooper ligament repair, metabolic acidosis versus, 17
Lynch syndrome, 247–248 317, 317f Metabolic support, 7–11
Mechanical bowel preparation, 246 Metabolism
M Mechanical valve replacement, drug, 268
M phase, of cell cycle, 121 174–175, 268 after injury, 11
MACE. See Major adverse Mechanical ventilation Metastases
cardiac events nosocomial pneumonia Barrett esophagus, 208–209
Macrophages caused by, 44 colorectal cancer, 248–249
microbe response by, 37 peak airway pressure melanoma, 130
questions regarding, 10, 37 monitoring, 111 omental, 308
in wound healing, 79 Meckel diverticulum, 235, 335 questions regarding, 84–85
Mafenide acetate, 69 Medial thyroid anlage, 323 splenic, 298
Magnesium Median nerve, 355, 355f surgical resection of, 85
deficiency of, 19 Mediastinal lymphadenopathy, 151 Methicillin-resistant Staphylococcus
depletion of, 16 Mediastinal mass, 155 aureus, 129, 134
Magnesium citrate, 246 Medical errors, 97 Methionine, 120
INDEX
Warning Score system MSLT-1, 132 NETs. See Neutrophil extracellular
MH. See Malignant hyperthermia mtDNA. See Mitochondrial DNA traps
MHC. See Major histocompatibility mTOR inhibitors. See Mammalian Neurapraxia, 77
complex target of rapamycin inhibitors Neuroendocrine carcinoma, 148
Microbes, macrophage response to, 37 Mucosa-associated lymphoid tissue Neurogenic shock, 29–31, 35
Microbial peritonitis, primary, 41 lymphoma, 230 Neuropathic pain, 320
Microcirculation, 134 Mucosal biopsy, in Ménétrier disease, Neurosurgery, 345–350
Micro-organisms, 45 231, 231f Neurotmesis, 77
MicroRNA, 119 Mucous cells, 147f Neutropenia
Microsatellite instability, 247–249 Multidisciplinary teams, 5 in Felty syndrome, 298, 304–305
Microvascular thrombosis, in Multiple organ dysfunction silver sulfadiazine as cause of, 68–69
thrombotic thrombocytopenic syndrome, 32 Neutropenic enterocolitis, 255
purpura, 24–25 Murmur, holosystolic, 175 Neutrophil(s)
Middle cerebral artery, 112 MVT. See Mesenteric vein thrombosis in phagocytosis, 74
Midface fractures, 144 Mycophenolate acid, 88 polymorphonuclear, 74
Milliosmoles, 15 Mycophenolate mofetil, 88, 89t Neutrophil extracellular traps, 10
Minimally invasive surgery Mycoses, 153 New York Heart Association
colon resection, 243 Mycotic aneurysms, 182–183 Classification, 171, 171f, 179
esophagectomy, 221–222 Myocardial infarction, cardiogenic Newborn
questions regarding, 115–117 shock and, 33 congenital diaphragmatic
resection, 243 Myonecrosis, 358 hernia in, 329
Mismatch repair, 247 Myotomy, 116, 221 emesis in, 330
Mithramycin, 18 Myxomas, cardiac, 179 imperforate anus in, 336
Mitochondrial DNA, 8 intestinal obstruction in, 330
Mitral stenosis, 174–175 N packed red blood cell
Mitral valve replacement, 175 N-acetylcysteine, 336 transfusion in, 336
M&M conferences. See Morbidity Nasojejunal feeding tubes, 42 total body water in, 15
and mortality conferences National Nosocomial Infections NHBDs. See Non–heart-beating
MMF. See Mycophenolate mofetil Surveillance System, 47 donors
MMPs. See Matrix National Surgical Quality NHL. See Non-Hodgkin lymphoma
metalloproteinases Improvement Project, 99, 172 Nikolsky sign, 133
Model for End-Stage Liver Nausea and vomiting, Nissen fundoplication
Disease, 95, 274 postoperative, 378 gastric pressure after, 216
Modified Early Warning Score Near-total thyroidectomy, 324 laparoscopic, 116
system, 108–109 NEC. See Necrotizing enterocolitis; NNISS. See National Nosocomial
Modified Norwood procedure, 160 Neuroendocrine carcinoma Infections Surveillance System
Modified radical mastectomy, 141 Neck Nociceptive pain, 320
MODS. See Multiple organ injuries to, 52, 57 NOD2 gene, 237
dysfunction syndrome questions regarding, 143–144 Nodular basal cell carcinoma, 135
Mohs micrographic surgery, 129 Necrotizing enterocolitis, 332f, Nodular melanoma, 130, 131f
Molecular surgery, 119–125 332–333 Noncardiac surgery, 172
Mondor disease, 140 Necrotizing fasciitis, 80, 339 Non–heart-beating donors, 91
Monocytes, 10 Necrotizing infections, 46, 358 Non-Hodgkin lymphoma, 297, 299
Monopolar coagulation, 116 Necrotizing myositis, 358 Nonseminatous germ-cell
Morbidity and mortality Necrotizing soft-tissue infections, tumors, 155
conferences, 4 42, 134 Non-small-cell lung cancer, 151
Morpheaform basal cell Needle thoracostomy decompression, Nonsteroidal anti-inflammatory
carcinoma, 135 of tension pneumothorax, drugs, 226, 320
mOsm. See Milliosmoles 56, 58 Nontechnical skills, 387
Motilin, 208 Needlesticks, 43–44 Norepinephrine, 31
Motor vehicle collisions, 59 Neisseria gonorrhoeae, 343 Normal saline, 14, 18, 378
MRCP. See Magnetic resonance Nelson syndrome, 328 Normovolemia, 378
cholangiopancreatography Neobladder, orthotopic, 337 Northern blotting, 124
mRNA, 119–120 Neostigmine, 101, 251 Norwood operation, 158
INDEX
transfusion in, 336 Phagocytosis, 74 fundoplication, 116
pneumatosis intestinalis in, 332f, Pheochromocytoma, 327 simple, 56, 58
332–333 Pheromones, 133 tension. See Tension
short bowel syndrome in, 239 Phlegmasia alba dolens, 201 pneumothorax
thyroglossal duct cyst in, 330 Phlegmasia cerulea dolens, 201, 201f Poikilothermia, 194
tracheoesophageal fistula in, Phrenic nerve palsy, 149 Point of critical oxygen delivery, 105
330, 331f Phrenosplenic ligament, 300 Poisoning, cyanide, 66
undescended testes in, 336 Physician authorship, 390 Polycythemia vera, 303
Wilms tumor in, 331, 332t Physicians Polyethylene glycol, 246
Pediatric surgery, 329–336 diversity of, 5 Polymorphonuclear neutrophils, 74
Pedicle flaps, 361 laparoscopic skills training in, Polyps, gallbladder, 286
PEEP. See Positive end-expiratory 375–376 Polytetrafluoroethylene, 195
pressure Physiologic monitoring of surgical Popliteal artery, adventitial cystic
PEG. See Polyethylene glycol patient, 105–113 disease of, 196
Pelvic floor dysfunction, 342 PICO, 382 Portal hypertension, 270–271, 304
Pelvic fractures, 351–352 PID. See Pelvic inflammatory disease Portal hypertensive gastropathy, 231
Pelvic hemorrhage, 50 p15INK4B, 123 Positive end-expiratory pressure,
Pelvic inflammatory disease, 343 “Pipeline” program, 5 for acute respiratory distress
Pemetrexed, 149 Pituitary fossa tumor, 328 syndrome, 100–101
Penetrating trauma Plasma Positron emission tomography, for
to chest, 53 fresh frozen, for thrombotic mediastinal lymph node
to colon, 54 thrombocytopenic purpura, 25 staging, 151
diaphragmatic injury from, 59 interstitial fluid compartments Posterior cervical foraminotomy, 349
to neck, 57 and, 16 Posterior fossa lesions, 346, 346f
to thoracoabdominal region, 59 Plasminogen, 22 Post-gastric bypass hypoglycemia, 234
Pentaxins, 7 Plasminogen activator inhibitor-1, 22 Postoperative period
Peptic ulcer disease Plastic surgery, 361–362 delirium in, 365–366
antrectomy for, 227f–228f, 227–228 Plateau airway pressure, 111 empyema in, 102–103
description of, 223, 226 Platelet(s) hyperglycemia in, 40
primary hyperparathyroidism acquired hemostatic defect, 23 hyponatremia in, 13
associated with, 326 aggregation of, 21, 23, 25 ileus in, 101, 378
Percutaneous tracheostomy, 101 circulating, decreases in, 22 nausea and vomiting in, 378
Perforated appendicitis, 259 drugs that inhibit function of, 23 opioid requirements in, 378
Perianal abscess, 253 endothelial adherence of, 21 urinary tract infection in, 42–43
Pericardial adhesions, 178 in immune response, 10 Postsinusoidal hypertension, 270
Pericardial constriction, 178 life span of, 23 Potassium
“Pericardial knock,” 178 postsplenectomy increase in, 51 alkalosis-related changes in, 15
Pericardial tamponade sequestration of, 22, 25 elevated levels of.
in left subclavian artery trauma, 61 shortened survival of, 22 See Hyperkalemia
traumatic, 55 Platelet-derived growth factor, 74 serum, 15–16
Pericarditis, 178 Plicae circularis, 235 Pouchitis, 256
Pericholangitis, 246 Plummer-Vinson syndrome, 143 Ppeak. See Peak airway pressure
Perihilar cholangiocarcinoma, 287 PN. See Parenteral nutrition PPIs. See Proton pump inhibitors
Perihilar tumor, 281 PNETs. See Primitive Pplateau. See Plateau airway pressure
Perioperative care, 377–379 neuroectodermal tumors PPV. See Patent processus vaginalis;
Peripheral arterial injury, 54–55, 55t Pneumatic tourniquet, 70 Pulse pressure variability
Peritonitis Pneumatosis intestinalis, 332f, 332–333 PRA assay. See Panel-reactive
in elderly, 367 Pneumohemothorax, 57 antibody assay
in pediatric patients, 335 Pneumonia Pragmatic Randomized Optimal
primary microbial, 41 aspiration, 153 Platelet and Plasma Ratios
Permissive hypotension, 26 community-acquired, 44 trial, 26
PET. See Positron emission tomography empyema caused by, 102 Prasugrel, 23
Petco2, 111 nosocomial, 44, 100 pRB, 123
Peyer patches, 235–236 ventilator-associated, 100 Predictive marker, 85
INDEX
Retroperitoneal fibrosis, 309 normal, 14, 18 blood loss percentages, 32–33
Retroperitoneal infections, 309 Salivary gland-type tumors, 147 cardiogenic, 29, 34, 55–56, 56f
Retroperitoneum, 309 Sarcoma categories of, 29
Retropubic urethropexy, 343 breast, 312 compensated, 35
Reverse-transcriptase PCR, 124 Ewing, 154–155 cytokine elevations after, 32
Reynolds pentad, 284 soft tissue, 311–312 hemorrhagic, 19, 30
Rhabdomyomas, 180 Scar hypotension in, 35
Rheumatic disease, 175–176 hypertrophic, 80–81 hypovolemic, 29, 31–32
Rheumatic fever, 174–175 remodeling of, 75 neurogenic, 29–31, 35
RI. See Rothman Index SCC. See Squamous cell carcinoma obstructive, 29, 35
Rib(s) Schatzki ring, 219 questions regarding, 29–36
fractures of, 63 Schwann cell basal lamina, 77 resuscitation for, 35, 62
“onion-peel” appearance of, 154 Scimitar sign, 196 septic, 32–33
Right colectomy, 243 SCIP. See Surgical Care Improvement signs and symptoms of, 32–33
Right hemicolectomy, 260 Project tension pneumothorax as
Right hepatic artery, 282, 289 Sclerosing adenosis, 137 cause of, 29
Right ventricular outflow tract Sclerosing cholangitis, 246, 276, 280 trauma-induced coagulopathy
obstruction, 161, 170 Sclerosing mesenteritis, 309 caused by, 23
Rituximab, 302 Scrotum, 316–317 traumatic, 29
Rivaroxaban, 24 Scurvy, 79 treatment of, 33–34
RNA, 120 Seborrheic keratoses, 136 vasodilatory, 33
RNA gel blot analysis, 124 Second-degree burns, 67 vasogenic, 29
RNA polymerases, 119 Second-degree hemorrhoids, 252 Short bowel syndrome, 239
Robotic prostatectomy, 117 Second-impact syndrome, 347 Shoulder dislocation, 352–353
Robotic surgery Secretin stimulation test, 225–226 Shouldice repair, 321
description of, 243 “Seed and soil” theory, SICU. See Surgical intensive care unit
inguinal hernia repair using, 319 of metastasis, 84 Side-to-side anastomoses, 244, 245f
laparoscopic surgery versus, SEER registry, 248 Sigmoid colectomy, 244, 250
116–117, 117f, 319 Seldinger technique, 109 Sigmoidectomy, 256
transabdominal preperitoneal, 319 Self-expanding stents, 189, 282 Silver sulfadiazine
Rothman Index, 108 Sengstaken-Blakemore tube, 211 for burn wounds, 68–69
Roux-en-Y gastric bypass Sentinel lymph node biopsy neutropenia caused by, 68–69
complications of, 233–234 for breast cancer, 139 Simple pneumothorax, 56, 58
gastric stasis after, 224 for melanoma, 132 Simulation, 387–388
illustration of, 228f Sepsis Simulation training, 388
nutritional deficiencies after, 234 incidence of, 43 Sinus bradycardia, 115
small bowel obstruction after, 234 postsplenectomy, 51, 299 Sirolimus, 89t, 90
Roux-en-Y hepaticojejunostomy, survival rates for, 43 SIRS. See Systemic inflammatory
285, 287 Sepsis syndrome, 46 response syndrome
RT. See Resuscitative thoracotomy Septic shock SJS. See Stevens-Johnson syndrome
Rubber band ligation, for characteristics of, 32 Skin
hemorrhoids, 252 hyperglycemia in, 33 epidermis, 133
“Rule of nines,” 65, 66f insulin resistance in, 33 Langerhans cells of, 133
R-value, 28 treatment of, 33 lesions of, 135–136
RVOT. See Right ventricular outflow Sequential Organ Failure Assessment partial thickness wounds of, 132
tract obstruction score, 38 stratum basale of, 132
RYGB. See Roux-en-Y gastric bypass Serine/threonine kinase receptors, 122 stratum spinosum of, 133
Serotonin, 21 wound healing of, 76t
S Serum calcium, 15 Skin cancer
S phase, of cell cycle, 83, 121 Serum osmolality, 15 basal cell carcinoma, 129, 135
SAA. See Splenic artery aneurysm Serum sodium, 18 melanoma. See Melanoma
Saccular aneurysms, 181 Sestamibi scans, 326 squamous cell carcinoma, 130, 136
Sacral fractures, 352 Sex hormones, 133 Skin-sparing mastectomy, 141
Sacroiliitis, 246 Sexually transmitted infections, 135 Skull base fractures, 346–347
INDEX
in mesenteric ischemia, 192 Surgical intensive care unit, 50, 61 diagnosis of, 35
stenosis of, 192 Surgical palliative care, 367, 370 diagnostic criteria for, 58
Superior thyroid artery, 323 Surgical research, 371 needle thoracostomy
Supernumerary parathyroid Surgical site infections, 39t, decompression of, 56, 58
glands, 325 39–41, 47, 246 obstructive shock versus, 35
Suppurative thrombophlebitis, 203 Surgical wounds, 39–40, 40t, 47 shock caused by, 29
Supracolic injuries, 61 Sustentaculum lienis, 301f signs of, 56, 58
Surface epithelial cells, gastric, 231 SvO2. See Fractional saturation of simple pneumothorax versus, 56, 58
Surgery hemoglobin tube thoracostomy for, 56, 57f
ambulatory, 385–386 SVT. See Suppurative TEP. See Totally preperitoneal repair
anorectal melanoma treated thrombophlebitis Testes, undescended, 336
with, 250 Sweat glands, 133 Testicular cancer, 337, 339
after bare coronary stent Syphilis Tetralogy of Fallot, 161, 170
placement, 364 ascending aortic aneurysms TF. See Tissue factor
bowel preparation for, 246 caused by, 183 TFPI. See Tissue factor pathway
cost-effectiveness of, 374f blood transfusion inhibitor
diversity in, 5 transmission of, 27 TGF-ß. See Transforming growth
in elderly, 365–368 Syphilitic aortitis, 183 factor-ß
genomic, 119–125 Systemic inflammatory response Th1 cells, 10
global, 373–376 syndrome, 37 Th1 cytokines, 9
hand, 355–360 Th2 cells, 10
major adverse cardiac events T Th17 cells, 10
screening, 172 T cells Thalassemia, 302
minimally invasive, 115–117 CD4+, 9 The Joint Commission, 99
molecular, 119–125 CD8+, 9 Thermal wounds, 129
noncardiac, 172 helper, 10 Thermodilution method, for cardiac
obesity treated with, 233–234 T regulatory cells, 9 output, 108
orthopedic, 351–353 TACO. See Transfusion-related Third-degree burns, 67
pediatric, 329–336 circulatory overload Third-degree hemorrhoids, 252
physiologic monitoring during, Tacrolimus, 88–89, 89t Thoracic aorta disease, 184
105–113 Tamoxifen, 138 Thoracic aortic disease, 183
plastic, 361–362 TAPP. See Transabdominal Thoracic compartment syndrome, 68
reconstructive, 361–362 preperitoneal repair Thoracic escharotomies, 68
retained surgical items, 99, 99t, 103 TAPVC. See Total anomalous Thoracoabdominal region,
robotic, 116–117, 117f pulmonary venous penetrating trauma to, 59
women in, 5 connection Thoracotomy
wrist, 355–360 Task sharing, 373 emergency department, 49
wrong-site, 99 TAVI/TAVR. See Transcatheter for empyema, 102
Surgical, anesthetic, and obstetrical aortic valve implantation/ indications for, 53
providers, 375 replacement trap door, 60
Surgical care, globalization of, 376 TBI. See Traumatic brain injury Thrombin, 21–22, 205
Surgical Care Improvement Project, TBSA. See Total body surface area Thrombocytopenia
98, 98t TBW. See Total body water; Total causes of, 22
Surgical excision body weight heparin-induced, 23–24, 173, 205
of basal cell carcinoma, 129 TCD. See Transcranial Doppler; primary immune, 23
of burn wounds, 70 Transcranial power Doppler Thromboelastography, 27–28
of melanoma, 132 T-cell–mediated rejection, 95 Thromboembolism, venous, 200,
Surgical infection TCL. See Transverse carpal ligament 202, 204, 204f, 366
definition of, 37 TEE. See Transesophageal Thrombolytic therapy
intravascular catheters as echocardiography catheter-directed, 201
cause of, 46–47 TEF. See Tracheoesophageal fistula contraindications for, 201
prophylactic antibiotics for, 38, 45 TEG. See Thromboelastography Thrombomodulin, 22
questions regarding, 37–47 Telemanipulation, 243 Thrombopoietin receptor
of retroperitoneum, 309 Temporal bone fracture, 346 antagonists, 302
INDEX
TTE. See Transthoracic Uncomplicated diverticulitis, 247 description of, 161–162
echocardiography Undescended testes, 336 in double-outlet right ventricle, 170
TTP. See Thrombotic Uremia, 23 holosystolic murmur associated
thrombocytopenic purpura Ureteral injuries, 338 with, 175
T-tube, 281 Ureteral stents, 338 tricuspid atresia without, 168
Tube thoracostomy, for tension Urinary incontinence, 343 Vibrio vulnificus, 134
pneumothorax, 56, 57f Urinary tract infection, 42–43, 338 VILI. See Ventilator-induced lung
Tuberculosis, 153 Urolithiasis, 338 injury
Tumor(s) Urology, 337–339 VIPomas, 294
appendiceal, 260 Uterine leiomyoma, 341 Virtual reality simulation, 387
carcinoid, 260 UTI. See Urinary tract infection Vision, 3, 3t
carotid body, 191 UV. See Ultraviolet radiation exposure Visual abstracts, 389
chest wall, 154 Vitamin(s), in wound healing, 79–80
conservative resections, 85 V Vitamin A, 78–80
desmoid, 154 Vaccinations, 135, 298, 342 Vitamin B12 deficiency, 224
esophageal, 209, 213 VADs. See Ventricular assist devices Vitamin C, 79
gastrointestinal stromal, 230, 238, 249 Vaginal cancer, 343 Vitamin K
nonseminatous germ-cell, 155 Vagus nerve, 208 deficiency of, 268
omentum, 308 Validity, external, 383 warfarin reversal using, 24
pancreatic exocrine, 292, 293f Valsalva maneuver, 241 VO2. See Oxygen utilization
pituitary fossa, 328 Valve replacement, 174–175, 268, 367 Vocal cords
salivary gland-type, 147 Valvulae conniventes, 235 anatomy of, 146, 146f
thymic, 155 VAP. See Ventilator-associated leukoplakia of, 143
Tumor markers, 85 pneumonia Volume receptors, 30
Tumor necrosis factor-alpha, 37 Variceal hemorrhage, 271 Volvulus
Tumor suppressor genes, 124 Vascular endothelial growth factor, 84 cecal, 250–251
Tumorigenic transformation of cells, 83 Vascular injuries, of extremities, endoscopy for, 250–251
TURP. See Transurethral resection of 54–55, 55t Vomiting
the prostate Vascular rings, 166, 167f metabolic derangements
TXA. See Tranexamic acid Vascular stents, 189–190 caused by, 17
Type A blood, 25 Vascular-type Ehlers-Danlos postoperative, 378
Type AB blood, 25 syndrome, 182 von Willebrand factor, 21, 24
Type II error, 382 Vasoactive medications, 271 VSD. See Ventricular septal defect
Type O-negative blood, 25 Vasoactive proteins, 31 VTE. See Venous thromboembolism
Typhlitis, 255 Vasodilatory shock, 33 Vulvar carcinoma, 342
Tyrosine kinase inhibitors, 249 Vasogenic shock, 29 vWF. See von Willebrand factor
Tyrosine kinase receptors, 122 Vasopressin, 31, 271
VEGF. See Vascular endothelial W
U growth factor Wallerian degeneration, 77
Ulcer(s) Veins Warfarin, 24, 205, 268
Cushing, 349 anatomy of, 197–198 Warm-antibody autoimmune
duodenal, 226–227 hepatic, 265, 266f hemolytic anemia, 299
malignant transformation of, 80 lower extremity, 197 Wartenberg sign, 358
pressure, 134 Vena cava filters, 202, 203f Water
Ulcerative colitis Venae comitantes, 197 free water deficit, 15
diagnosis of, 257 Venous anastomosis, 92f in total body weight, 14–15
primary sclerosing cholangitis Venous disease, 197–206 Water deficit, 15
and, 246 Venous thromboembolism, 200, 202, Watermelon stomach, 230, 230f
Ulnar nerve, 355, 355f, 358 204, 204f, 366 Water-soluble contrast agents, 236
Ultrasound Ventilator weaning, 101 Weaning, ventilator, 101
cardiac tamponade evaluations, Ventilator-associated pneumonia, 100 Web-based education, 389–390
55, 56f Ventilator-induced lung injury, 112 West Nile virus, 27
endoscopic. See Endoscopic Ventricular assist devices, 179 Whipple procedure, 286
ultrasound Ventricular compliance, 106–107 Whole-pancreas transplantation, 95