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25. If a patient’s arterial P2 is found to be 25 mm Hg,
CHAPTER 3
Fluid and Electrolyte Management of the Surgical Patient
the arterial pH will be approximately:
A. 7.52.
B. 7.40.
C. 7.32.
D. 7.28.
26. Which of the following are NOT characteristic findings
of acute renal failure?
A. BUN >100 mg/dL
B. Hyperkalemia
C. Severe acidosis
D. Uremic pericarditis
E. Uremic encephalopathy
27. An elderly diabetic patient who has acute cholecystitis is
found to have a serum sodium level of 122 mEq/L and
a blood glucose of 600 mg/dL. After correcting the glucose concentration to 100 mg/dL with insulin, the serum
sodium concentration would:
A. Decrease significantly unless the patient also received
3% saline.
B. Decrease transiently but return to approximately
122 mEq/L without specific therapy.
C. Remain essentially unchanged.
D. Increase to the normal range without specific therapy.
Answer: A
A low Pa2 indicates excess elimination of carbon dioxide by
the lungs, and the body pH will increase. Within reasonable
physiologic ranges a 15 mm Hg fall in Pa2 should produce
a 0.12 change from the normal body pH of 7.4. (See Schwartz
11th ed., Ch. 3, p. 91.)
Answer: A
Hyperkalemia, severe acidosis, uremic encephalopathy, and
uremic pericarditis are all indications of life-threatening
problems, and urgent correction is mandatory. Elevation of
BUN is commonly seen as well, but is not itself an indication
for dialysis. (See Schwartz 11th ed., Ch. 3, p. 99.)
Answer: D
A rise in the extracellular fluid concentration of a substance
that does not diffuse passively across cell membranes (eg,
glucose or urea) causes an increase in effective osmotic pressure, a transfer of water from cells, and dilutional hyponatremia. For each 100 mg/dL rise in blood glucose above normal,
the serum sodium level falls approximately to 3 mEq/L.
Alternatively, the serum sodium level would increase by
about 15 mEq/L if the blood glucose level falls from 600 to
100 mg/dL. (See Schwartz 11th ed., Ch. 3, p. 88.)
28. Excessive administration of normal saline for fluid resuscitation can lead to what metabolic derangement?
A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory alkalosis
D. Respiratory acidosis
29. The first step in the management of acute hypercalcemia
should be:
A. Correction of deficit of extracellular fluid volume.
B. Hemodialysis.
C. Administration of furosemide.
D. Administration of mithramycin.
Answer: B
Sodium chloride is mildly hypertonic, containing 154 mEq
of sodium that is balanced by 154 mEq of chloride. The high
chloride concentration imposes a significant chloride load
on the kidneys and may lead to a hyperchloremic metabolic
acidosis. Sodium chloride is an ideal solution, however, for
correcting volume deficits associated with hyponatremia,
hypochloremia, and metabolic alkalosis. (See Schwartz
11th ed., Ch. 3, p. 93.)
Answer: A
Patients with acute hypercalcemia usually have either acute
hyperparathyroidism or metastatic breast carcinoma with
multiple bony metastases. These patients develop severe
headaches, bone pain, thirst, emesis, and polyuria. Unless
treatment is instituted promptly, the symptoms may be
rapidly fatal. Immediate correction of the associated deficit of extracellular fluid volume is the most important step
in treatment. When effective, this results in the lowering of
the serum calcium level by dilution. Once extracellular fluid
volume has been replaced, furosemide is effective treatment. Hemodialysis may also be employed, but its effect is
less rapid. Mithramycin is very useful in controlling metastatic bone disease, but its effect is slow, and it cannot be
depended upon when the patient has acute hypercalcemia.
(See Schwartz 11th ed., Ch. 3, p. 95.)
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30. A victim of a motor vehicle accident arrives in hemorrhagic shock. His arterial blood gases are pH, 7.25; P2,
95 mm Hg; P2, 25 mm Hg; HCO
–
, 15 mEq/L. The
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patient’s metabolic acidosis would be treated best with:
A. Ampule of sodium bicarbonate.
B. Sodium bicarbonate infusion.
C. Lactated Ringer solution.
D. Hyperventilation.
31. Three days after surgery for gastric carcinoma, a 50-yearold alcoholic male exhibits delirium, muscle tremors,
and hyperactive tendon reflexes. Magnesium deficiency
is suspected. All of the following statements regarding
this situation are TRUE EXCEPT:
A. A decision to administer magnesium should be based
on the serum magnesium level.
B. Adequate cellular replacement of magnesium will
require 1 to 3 weeks.
C. A concomitant calcium deficiency should be
suspected.
D. Calcium is a specific antagonist of the myocardial
effects of magnesium.
Answer: C
In patients suffering from hemorrhagic shock, the presence
of a metabolic acidosis early in the postresuscitative period is
indicative of tissue hypoxia due to persistent inadequate tissue perfusion. Attempts to correct this problem by administering an alkalizing agent will not solve the basic problem.
However, proper volume replacement by means of a balanced
salt solution such as Lactated Ringer solution will restore perfusion and correct the metabolic acidosis by ending anaerobic
metabolism. (See Schwartz 11th ed., Ch. 3, p. 92.)
Answer: A
Magnesium deficiency should be suspected in any malnourished patient who exhibits disturbed neuromuscular or
cerebral activity in the postoperative period. Laboratory confirmation often is not reliable, and the syndrome may exist in
the presence of a normal serum magnesium level. Hypocalcemia often coexists, particularly in patients who have clinical
signs of tetany. Intravenous magnesium can be administered safely to a well-hydrated patient for initial treatment
of a severe deficit, but concomitant electrocardiographic
monitoring is essential. The electrocardiographic changes
associated with acute hypermagnesemia resemble those of
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 symptoms may follow the initial infusion of magnesium, although
continued replacement for a period of 1 to 3 weeks is necessary to replenish cellular stores. (See Schwartz 11th ed., Ch. 3,
pp. 19, 95.)
CHAPTER 3
Fluid and Electrolyte Management of the Surgical Patient
32. Refeeding syndrome can be associated with all of the following EXCEPT:
A. Respiratory failure.
B. Hyperkalemia.
C. Confusion.
D. Cardiac arrhythmias.
Answer: B
With refeeding, a shift in metabolism from fat to carbohydrate substrate stimulates insulin release, which results in
the cellular uptake of electrolytes, particularly phosphate,
magnesium, potassium, and calcium. However, severe hyperglycemia may result from blunted basal insulin secretion.
(See Schwartz 11th ed., Ch. 3, p. 98.)
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CHAPTER 4
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Hemostasis, Surgical Bleeding, and Transfusion
1. Which of the following is NOT one of the four major
physiological events of hemostasis?
A. Vasodilation
B. Platelet aggregation
C. Clot Formation
D. Fibrinolysis
2. Which of the following is required for platelet adherence
to injured endothelium?
A. Thromboxane A
B. Glycoprotein (GP) IIb/IIIa
C. Adenosine diphosphate (ADP)
D. Von Willebrand factor (vWF)
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Answer: A
Hemostasis is a complex process, which limits blood loss
from an injured vessel. The four physiologic events of the
hemostatic process include vasoconstriction, platelet aggregation, clot formation, and fibrinolysis. These processes are
the result of two different cascades, the extrinsic pathway and
intrinsic pathway. Both cause the conversion of prothrombin
to thrombin to fibrin, which are essential for clot formation.
(Schwartz 11th ed., p. 103.)
Answer: D
Platelets do not normally adhere to each other or to the vessel wall but can form a plug that aids in cessation of bleeding
when vascular disruption occurs. Injury to the intimal layer
in the vascular wall exposes subendothelial collagen to which
platelets adhere. This process requires vWF, a protein in the
subendothelium that is lacking in patients with von Willebrand’s disease. vWF binds to glycoprotein (GP) I/IX/V on
the platelet membrane. Following adhesion, platelets initiate
a release reaction that recruits other platelets from the circulating blood to seal the disrupted vessel. Up to this point, this
process is known as primary hemostasis. Platelet aggregation
is reversible and is not associated with secretion. Additionally, heparin does not interfere with this reaction, and thus,
hemostasis can occur in the heparinized patient. ADP and
serotonin are the principal mediators in platelet aggregation.
(Schwartz 11th ed., p. 103.)
3. Which of the following clotting factors is the first factor
common to both intrinsic and extrinsic pathways?
A. Factor I (fibrinogen)
B. Factor IX (Christmas factor)
C. Factor X (Stewart-Prower factor)
D. Factor XI (plasma thromboplasma antecedent)
Answer: C
The intrinsic pathway begins with the activation of factor XII
that subsequently activates factors XI, IX, and VIII. In this
pathway, each of the primary factors is “intrinsic” to the circulating plasma, whereby no surface is required to initiate the
process. In the extrinsic pathway, tissue factor (TF) is released
or exposed on the surface of the endothelium, binding to
circulating factor VII, facilitating its activation to VIIa. Each
of these pathways continues on to a common sequence that
begins with the activation of factor X to Xa (in the presence of
VIIIa). Subsequently, Xa (with the help of factor Va) converts
factor II (prothrombin) to thrombin and then factor I (fibrinogen) to fibrin. Clot formation occurs after fibrin monomers
are cross-linked to polymers with the assistance of factor XIII.
(Schwartz 11th ed., p. 105.)
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4. Which of the following factors are NOT involved in pre-
CHAPTER 4
venting clot propagation?
A. Thrombomodulin
B. Tissue plasminogen activator (tPA) release by the
endothelium
C. Nitric oxide release from the endothelium
D. APC complexes with protein S
Hemostasis, Surgical Bleeding, and Transfusion
5. Which of the following congenital factor deficiency often
presents in the first few days of life?
A. Factor VII
B. Factor IX
C. Factor XI
D. Factor XII
Answer: C
Feedback inhibition on the coagulation cascade deactivates
the enzyme complexes leading to thrombin formation.
Thrombomodulin (TM) presented by the endothelium serves
as a “thrombin sink” by forming a complex with thrombin,
rendering it no longer available to cleave fibrinogen. This
then activates protein C (APC) and reduces further thrombin
generation by inhibiting factors V and VIII. Second, tissue
plasminogen activator (tPA) is released from the endothelium
following injury, cleaving plasminogen to initiate fibrinolysis. APC then consumes plasminogen activator inhibitor-1
(PAI-1), leading to increased tPA activity and fibrinolysis.
Building on the anticoagulant response to inhibit thrombin
formation, tissue factor pathway inhibitor (TFPI) is released,
blocking the TF-VIIa complex and reducing the production
of factors Xa and IXa. Antithrombin III (AT-III) then neutralizes all of the procoagulant serine proteases and also inhibits
the TF-VIIa complex. The most potent mechanism of thrombin inhibition involves the APC system. APC forms a complex with its cofactor, protein S, on a phospholipid surface.
This complex then cleaves factors Va and VIIIa so that they
are no longer able to participate in the formation of TF-VIIa
or prothrombinase complexes. (Schwartz 11th ed., p. 106.)
Answer: D
Congenital factor XIII (FXIII) deficiency, originally recognized by Duckert in 1960, is a rare autosomal recessive disease
usually associated with a severe bleeding diathesis. The maleto-female ratio is 1:1. Although acquired FXIII deficiency has
been described in association with hepatic failure, inflammatory bowel disease, and myeloid leukemia, the only significant association with bleeding in children is the inherited
deficiency. Bleeding is typically delayed because clots form
normally but are susceptible to fibrinolysis. Umbilical stump
bleeding is characteristic, and there is a high risk of intracranial bleeding. Spontaneous abortion is usual in women with
factor XIII deficiency unless they receive replacement therapy.
Replacement can be accomplished with FFP, cryoprecipitate,
or a factor XIII concentrate. Levels of 1% to 2% are usually
adequate for hemostasis. (Schwartz 11th ed., p. 107.)
6. Which of the following is NOT a cause of
thrombocytopenia?
A. Immune thrombocytopenia purpura (ITP)
B. Hemolytic uremia syndrome (HUS)
C. B12 deficiency
D. Clopidogrel administration
Answer: D
Decrease in number of circulating platelets can be the
result of (1) failure of production, (2) shortened survival,
and (3) sequestration. Failure of production occurs in bone
marrow disorders, including leukemias, myelodysplastic
syndromes, severe B12 deficiency, folate deficiency, chemotherapy, radiation treatment, alcohol intoxication, and viral
syndromes. Shortened platelet survival is seen in idiopathic
thrombocytopenia purpura, heparin-induced thrombocytopenia (HIT), thrombotic thrombocytopenia purpura
(TTP), and in hemolytic uremia syndrome (HUS). Sequestration occurs with trapping of platelets in enlarged spleen
secondary to portal hypertension, sarcoid, lymphoma, or
Gaucher’s disease. Clopidogrel does not cause a decrease in
platelet number, but irreversibly inhibits platelet function.
(Schwartz 11th ed., p. 108.)
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7. Primary immune thrombocytopenia (ITP):
A. Occurs more often in children with adults, but has a
similar clinical course.
B. Includes HIT as a subtype of drug-induced ITP.
C. is also known as thrombotic thrombocytopenic pur-
pura (TTP).
D. is a disease of impaired platelet production of
unknown etiology.
8. Which of the following is NOT an acquired platelet
hemostatic defect?
A. Massive blood transfusion following Trauma
B. Acute renal failure
C. Disseminated intravascular coagulation (DIC)
D. Polycythemia vera
Answer: B
Primary immune thrombocytopenia is also known as idiopathic thrombocytopenic purpura (ITP). In children, it is
usually acute at the onset, short-lived, and typically follows
a viral illness. In contrast, ITP in adults is gradual in onset,
chronic in nature, and has no identifiable cause. Because the
circulating platelets in ITP are young and functional, bleeding
is less for a given platelet count than when there is failure of
platelet production. The pathophysiology of ITP is believed to
involve both impaired platelet production and T cell–mediated platelet destruction. Heparin-induced thrombocytopenia
(HIT) is a form of drug-induced immune thrombocytopenia.
It is an immunologic event during which antibodies against
platelet factor 4 formed during exposure to heparin affect
platelet activation and endothelial function with resultant
thrombocytopenia and intravascular thrombosis. TTP is a disorder of platelet activation and production of platelet thrombi.
(Schwartz 11th ed., p. 108.)
Answer: C
Impaired platelet function often accompanies thrombocytopenia, but may also occur in the presence of a normal platelet
count. The importance of this is obvious when one considers
that 80% of overall clot strength is related to platelet function.
The life span of platelets ranges from 7 to 10 days, placing them
at increased risk for impairment by medical disorders and prescription and over-the-counter medications. Impairment of
ADP-stimulated aggregation occurs with massive transfusion of
blood products. Uremia may be associated with increased bleeding time and impaired aggregation. Defective aggregation and
platelet dysfunction are also seen in patients with severe trauma,
thrombocythemia, polycythemia vera, and myelofibrosis.
DIC is an acquired syndrome characterized by systemic
activation of coagulation pathways that result in excessive
thrombin generation and diffuse formation of microthrombi.
(Schwartz 11th ed., p. 110.)
CHAPTER 4
Hemostasis, Surgical Bleeding, and Transfusion
9. What drug irreversibly inhibits platelet function by irreversible acetylation of platelet prostaglandin synthase?
A. Aspirin
B. Clopidogrel
C. Dipyridamole
D. Glycoprotein IIB/IIIA inhibitors
10. Which is TRUE about trauma-induced coagulopathy
(TIC)?
A. The acute coagulopathy of trauma is mechanistically
similar to disseminated intravascular coagulation
(DIC).
B. Coagulopathy can develop in trauma patients fol-
lowing acidosis, hypothermia, and dilution of coagulation factors though coagulation is normal on
admission.
C. TIC is caused by shock and tissue injury.
D. Acute coagulopathy of trauma is mainly a dilutional
coagulopathy.
Answer: A
Drugs that interfere with platelet function include aspirin,
clopidogrel, prasugrel, dipyridamole, and GP IIb/IIIa inhibitors. Aspirin, clopidogrel, and prasugrel all irreversibly inhibit
platelet function. Clopidogrel and prasugrel do so through
selective irreversible inhibition of ADP-induced platelet
aggregation. Aspirin works through irreversible acetylation
of platelet prostaglandin synthase. (Schwartz 11th ed., p. 110.)
Answer: C
Traditional teaching regarding trauma-related coagulopathy
attributed its development to acidosis, hypothermia, and dilution of coagulation factors. Recent data, however, have shown
that over one-third of severely injured patients have laboratorybased evidence of coagulopathy at the time of admission, a
phenotype called trauma- TIC. TIC is independent of traditional (iatrogenic) causes of posttraumatic coagulopathy,
such as hemodilution, is precipitated by tissue injury and/or
hemorrhagic shock, and is associated with significantly higher
risk of mortality, especially in the first 24 hours after injury.
Furthermore, TIC is a separate and distinct process from disseminated intravascular coagulopathy with its own specific
components of hemostatic failure. (Schwartz 11th ed., p. 111.)
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11. Warfarin use is often associated with an increased mor-
CHAPTER 4
Hemostasis, Surgical Bleeding, and Transfusion
bidity and mortality in acutely injured and emergency
surgery patients, with rapid reversal, these complications
can be reduced: Which is NOT TRUE about rapid reversal of warfarin effect?
A. Vitamin K should be given to sustain the effects
of plasma and prothrombin complex concentrate
(PCC).
B. PCC is superior to plasma.
C. PCC more rapidly corrects INR but is associated with
excess thromboembolic events.
D. Four-factor PCC’s have more reliable correction of
INR compared to three-factor PCCs.
Answer: B
Although warfarin use is often associated with a significant increase in morbidity and mortality in acutely injured
and emergency surgery patients, with rapid reversal, these
complications can be reduced. There are several reversal
options that include vitamin K administration, plasma,
cryoprecipitate, recombinant factor VIIa, and factor concentrates. The 2012 CHEST guidelines for the Management of Anticoagulant Therapy, Antithrombotic Therapy,
and Prevention of Thrombosis recommends patients with
major life-threatening bleeding due to warfarin receive
reversal with vitamin K and a rapid reversal agent such as
plasma or PCC. Vitamin K is given to sustain the effects of
the plasma or PCC due to their short half-lives. In major
bleeds, vitamin K 10 mg given as a slow IV infusion is utilized for more rapid onset compared to the oral form. Studies have shown that PCC is superior to plasma for speed
of reversal and has decreased risk of fluid overload, but it
is equivalent in adverse and thromboembolic events and
costlier. PCC is available in two forms: three-factor PCC
(factors II, IX, and X) and four-factor PCC (factors II, VII,
IX, and X). Four-factor PCCs have been shown to have a
more reliable correction of INR compared to three-factor
PCCs. (Schwartz 11th ed., p. 112.)
12. What is the best laboratory test for determine degree of
anticoagulation with direct oral anticoagulants such as
dabigatran and rivaroxaban?
A. Prothrombin time/International normalized ratio
(PT/INR)
B. Partial thromboplastin time (PTT)
C. Bleeding time
D. None of the above
13. A 45-year-old man is now postoperative day 6 after colon
resection for perforated diverticulitis, and is noted to
have new bruising at venipuncture sites. Platelet count
is measured at 45,000 platelets per milliliter. You suspect this is due to Heparin-induced thrombocytopenia
(HIT). Which of the following is TRUE?
A. HIT is due to an antibody against platelet factor 4
(PF4).
B. This can only occur with full dose unfractionated
heparin.
C. HIT is avoided by using fractionated heparins only.
D. Anticoagulation with oral warfarin should be initi-
ated immediately.
Answer: D
Direct oral anticoagulants (DOACs) include direct thrombin inhibitors and factor Xa inhibitors and have no readily
available method of detection of the degree of anticoagulation. More concerning is the difficulty in the reversal of these
new anticoagulants. Recently, idarucizumab, a humanized
monoclonal antibody fragment that binds dabigatran, has
been approved for use for reversal of the thrombin inhibitor,
dabigatran, and dabigatran-related coagulopathy. (Schwartz
11th ed., p. 113.)
Answer: A
HIT is a drug-induced immune thrombocytopenia. Antibodies against platelet factor 4 (PL4) cause destruction of
platelets. Platelet count falls on 5 to 7 days after starting
heparin therapy, but sooner, 1 to 2 days after reexposure.
HIT generally occurs after treatment with full-dose unfractionated heparins, but can occur with prophylactic doses or
with low molecular weight (fractionated) heparins. The clinical diagnosis of HIT is confirmed by a positive anti-platelet
factor 4. In addition to thrombocytopenia, HIT is associated
with arterial and venous thrombosis. Heparins are discontinued, and a direct thrombin inhibitor, such as lepirudin,
argatroban, or danaparoid is prescribed. Warfarin therapy
should be started only after anticoagulation it can initially
induce a hypercoagulable state (Schwartz 11th ed., p. 109.)
14. Which findings are not consistent with thrombotic
thrombocytopenic purpura (TTP)?
A. Splenomegaly
B. Fever
C. Schistocytes on peripheral blood smear
D. Platelet activation
Answer: D
In TTP inhibition of a metalloproteinase enzyme, ADAM
S13 allows for unrestrained growth of microthrombi. Von
Willebrand factor (VWF) is secreted as large molecules.
Normally, ADAM S13 cleaves large vWF molecules which
limits thrombi growth and prevents microvascular thrombosis. In TTP, the microvascular thrombosis leads to tissue
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15. Which of the following is FALSE regarding coagulation
during cardiopulmonary bypass (CPB)?
A. Contact with circuit tubing and membranes activates
inflammatory cascades and causes anormal platelet
and clotting factor function.
B. Coagulopathy is compounded by sheer stress.
C. Following bypass, platelet morphology and ability to
aggregate are irreversibly altered.
D. Coagulopathy is compounded by hypothermia and
hemodilution.
ischemia and organ damage. TTP is clinically characterized
by thrombocytopenia as well as microangiopathic hemolytic
anemia, fever, neurological symptoms, and renal insufficiency. 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
relapsing TTP. (Schwartz 11th ed., p. 109.)
Answer: C
Under normal conditions, homeostasis of the coagulation
system is maintained by complex interactions between the
endothelium, platelets, and coagulation factors. In patients
undergoing CPB, contact with circuit tubing and membranes results in abnormal platelet and clotting factor activation, as well as activation of inflammatory cascades, that
ultimately results in excessive fibrinolysis and a combination
of both quantitative and qualitative platelet defects. Platelets
undergo reversible alterations in morphology and their ability
to aggregate, which causes sequestration in the filter, partially
degranulated platelets, and platelet fragments. This multifactorial coagulopathy is compounded by the effects of shear
stress in the system, induced hypothermia, hemodilution, and
anticoagulation. (Schwartz 11th ed., p. 113.)
CHAPTER 4
Hemostasis, Surgical Bleeding, and Transfusion
16. Which of the following facts about transfusion and
crossmatching is FALSE?
A. Universal donor type O-negative red blood cells and
type AB plasma may be transfused to all recipients.
B. Platelets also require crossmatching.
C. The administration of Rh-positive red blood cells is
acceptable if Rh-negative red blood cells blood is not
available.
D. Crossmatched whole blood may be ideal therapy for
resuscitation of trauma patients.
Answer: C
Platelets do not require crossmatching. In emergency situations, universal donor type O-negative red blood cells and
type AB plasma may be transfused to all recipients. Due to
a shortage of type AB plasma, low anti-B titer type A plasma
has become widely adopted for emergency (uncrossmatched)
transfusion. In the United States, 85% of individuals are
type A or type O, making type A plasma compatible with
the vast majority of potential recipients. Uncrossmatched
plasma is routinely transfused as part of platelet transfusions,
with major transfusion reactions reported rarely, and type
AB plasma currently carries a higher risk of TRALI compared to other plasma types. Many centers have transitioned
to low-titer type A plasma for emergency transfusions, with
no increase in adverse events. O negative and type-specific
red blood cells are equally safe for emergency transfusion.
In patients known to have clinically significant cold agglutinins, blood should be administered through a blood warmer.
If these antibodies are present in high titer, hypothermia is
contraindicated. Whole blood as an ideal therapy for acute
traumatic hemorrhagic shock has increased in the last several
years with multiple reports of successful use in military and
civilian trauma patients. However, there is still limited access
in most civilian centers. (Schwartz 11th ed., p. 115.)
17. Following recent abdominal surgery, your patient is
admitted to the ICU with septic shock. Below what level
of hemoglobin would a blood transfusion be indicated?
A. <12 g/dL
B. <10 g/dL
C. <8 g/dL
D. <7 g/dL
Answer: D
A 1988 National Institutes of Health Consensus Report
challenged the dictum that a hemoglobin value of less than
10 g/dL or a hematocrit level <30% indicates a need for
preoperative red blood cell transfusion. This was verified
in a prospective randomized controlled trial in critically ill
patients that compared a restrictive transfusion threshold to
a more liberal strategy and demonstrated that maintaining
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CHAPTER 4
Hemostasis, Surgical Bleeding, and Transfusion
18. Which of the following is not part of damage control
resuscitation (DCR)?
A. Permissive hypotension
B. Resuscitating with large volumes of crystalloid to
limit RBC transfusion
C. Immediate release and administration of a predefined
ration of blood products to mimic whole blood
D. Use of hemostatic adjuncts
hemoglobin levels between 7 and 9 g/dL had no adverse
effect on mortality. In fact, patients with APACHE II scores
of ≤20 or patients age <55 years actually had a lower mortality. SCCM/EAST and AABB guidelines recommend taking
into account patient-specific characteristics and the overall
clinical context when considering RBC transfusions in nonacutely hemorrhaging patients. Patients with symptomatic
anemia should be transfused 1 RBC unit at a time, and isolated asymptomatic anemia in and of itself is rarely an indication for RBC transfusion. (Schwartz 11th ed., p. 117.)
Answer: B
Prior to DCR, resuscitation guidelines advocated volume
replacement with crystalloid, followed by packed red blood cell
and only later plasma or platelets. This conventional massive
transfusion practice was based on a several small uncontrolled
retrospective studies that used blood products containing
increased amounts of plasma, which are no longer available.
Because of the known early coagulopathy of trauma, the current approach to managing the exsanguinating patient involves
early implementation of DCR. Although most of the attention
to hemorrhagic shock resuscitation has centered on higher
ratios of plasma and platelets, DCR is composed of four basic
components: permissive hypotension, minimizing crystalloidbased resuscitation, the immediate release and administration
of predefined balanced blood products (red blood cells, plasma,
and platelets) in ratios similar to those of whole blood, and the
use of hemostatic adjuncts. The Pragmatic Randomized Optimal Platelet and Plasma Ratios (PROPPR) trial randomized
680 bleeding trauma patients across 12 highest-level trauma
centers to resuscitation with 1:1:1 versus 1:1:2 plasma to platelets to RBCs. Although there was no significant difference in
mortality at 24 hours (13% vs 17%) or 30 days (22% vs 26%),
the 1:1:1 group had significantly decreased mortality due to
hemorrhage at 24 hours (9% vs 15%) and more patients achieving hemostasis (86% vs 78%). (Schwartz 11th ed., p. 117.)
19. In patients with significant blood loss, which of the following is incorrect?
A. Resuscitation with whole blood
B. Resuscitation with packed red blood cells, platelet,
and FFP in a 1:1:1 ratio
C. Packed red blood cells with transfusion of FFP and
platelets as needed (when the measured INR > 2 and
PLT# is <75,000)
D. Resuscitation with crystalloid and artificial colloid
to avoid transfusion reactions until hemorrhage is
controlled.
20. Less than 0.5% of transfusions result in a serious
transfusion-related complication. Which of the following is the leading cause of transfusion-related deaths?
A. Transfusion-related acute lung injury (TRALI)
B. ABO hemolytic transfusion reactions
C. Bacterial contamination of platelets
D. Iatrogenic hepatitis C: infection
Answer: C
In the Pragmatic Randomized Optimal Platelet and Plasma
Ratios (PROPPR) trial patients were resuscitated with packed
red blood cells, platelets, and plasma in various ratios. In
this trial, the 1:1:1 group had significantly decreased mortality due to hemorrhage at 24 hours (9% vs 15%) and more
patients achieving hemostasis (86% vs 78%). Whole blood
transfusion appears to have similar outcome, as whole blood
contains plasma and platelets in a similar ratio. Waiting for
INR and platelet count appears to delay achieving hemostasis.
(Schwartz 11th ed., p. 119.)
Answer: A
Transfusion-related complications are primarily related
to blood-induced proinflammatory responses (Table 4-9).
Transfusion-related 149a events are estimated to occur in
approximately 10% of all transfusions, but <0.5% are serious
in nature. Transfusion-related deaths, although exceedingly
rare, do occur and are related primarily to transfusion-related
acute lung injury (TRALI), ABO hemolytic transfusion reactions, and bacterial contamination of platelets. (Schwartz
11th ed., p. 121.)
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21. TRALI does not include:
A. Transfusion-related circulatory overload (TACO).
B. Noncardiogenic pulmonary edema.
C. Fever and rigors.
D. Bilateral pulmonary infiltrates.
Answer: A
The syndrome of TRALI is defined as noncardiogenic pulmonary edema related to transfusion. It can occur with the
administration of any plasma-containing blood product.
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
commonly occurs within 1 to 2 hours after the onset of transfusion but virtually always before 6 hours. Toy et al reported
a decrease in the incidence of TRALI with the reduction of
transfusion of plasma from female donors, due to a combination of reduced transfusion of strong cognate HLA class II
antibodies and HNA antibodies in patients with risk factors
for acute lung injury. TRALI now occurs <1 in 10,000 units
transfused and is usually self-limited with supportive therapy.
Treatment of TRALI entails discontinuation of any transfusion, notification of the transfusion service, and pulmonary
support, which may vary from supplemental oxygen to
mechanical ventilation.
Respiratory compromise may also be associated with
TACO, which is an avoidable complication. It can occur with
rapid infusion of blood, plasma expanders, and crystalloids,
particularly in older patients with underlying heart disease.
(Schwartz 11th ed., p. 121.)
CHAPTER 4
Hemostasis, Surgical Bleeding, and Transfusion
22. Diseases that are not generally transmitted by blood
transfusion include:
A. Malaria, Chagas’ disease.
B. CMV, hepatitis C, and HIV.
C. Zika and West Nile Virus.
D. All of the above.
23. What are the uses of thromboelastography (TEG)?
A. Predicting the need for lifesaving interventions after
resuscitation for trauma
B. Predicting 24-hour and 30-day mortality following
trauma
C. Predicting early transfusion of RBC, plasma, platelet,
and cryoprecipitate
D. All of the above
Answer: A
Malaria, Chagas’ disease, brucellosis, and, very rarely, syphilis
are among the diseases that have been transmitted by transfusion. Transmission of hepatitis C and HIV-1 has been dramatically minimized by the introduction of better antibody
and nucleic acid screening for these pathogens. The residual
risk among allogeneic donations is now estimated to be less
than 1 per 1,000,000 donations. Recent concerns about the
rare transmission of these and other pathogens, such as West
Nile virus, are being addressed by current trials of “pathogen
inactivation systems” that reduce infectious levels of all
viruses and bacteria known to be transmittable by transfusion.
Recently, there is heightened concern of transmission of Zika
virus by blood product transfusion. Studies in endemic areas
have shown rates of Zika infection detected in donor blood as
high as 2.8%. Although no such cases have been reported in
the United States, transmission of Zika virus via platelet products have been reported in Brazil. (Schwartz 11th ed., p. 123.)
Answer: D
Recent trauma data has shown TEG to be useful in predicting early transfusion of red blood cells, plasma, platelets, and
cryoprecipitate. TEG can also predict the need for lifesaving
interventions shortly after arrival, 24-hour and 30-day mortality, and can be used to guide administration of Tranexamic
Acid (TXA) to injured patients with hyperfibrinolysis. Lastly,
some centers have demonstrated that the graphic display
options allow for more rapid return of results and may be less
expensive than standard coagulation panels. Given the strong
association of viscoelastic tests with clinical outcomes, some
centers now use TEG rather than conventional coagulation
tests to evaluate injured patients in the emergency department. (Schwartz 11th ed., p. 124.)
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