Trauma

Question 1

Forty-eight hours after undergoing clipping of a Hunt and Hess grade 3 ruptured aneurysm with
intraoperative lumbar spinal drainage and lamina terminalis fenestration, a 56-year-old woman
becomes somnolent with pinpoint pupils and flexure posturing. Immediately after the procedure,
she was oriented to person and place. CT scan shows small ventricles and crowding of the brain
stem. Which of the following is the most appropriate initial step in management?
Answers:
A. Give mannitol 1g/kg IV over 30 minutes.
B. Initiate HHH therapy.
C. Position patient in Trendelenburg position.
D. Insert a right frontal ventricular drain.
E. Return to OR for decompressive craniotomy

Answer 1

Position patient in Trendelenburg position

Discussion:
This patient is suffering from central herniation syndrome due to over-drainage of spinal fluid from
the lumbar drain. The first step is to put the patient in reverse Trendelenburg position. A ventricular
drain in this setting is used to treat non-communicating hydrocephalus which is unlikely
considering that the ventricles are small and the lamina terminalis has been fenestrated. HHH
therapy is used for the management of vasospasm. Brain swelling requiring mannitol or return to
OR is in the differential but the patient is a bit early for severe vasospasm and a bit late for postoperative edema.
References:
Alaraj A, Munson T, Herrera SR, Aletich V, Charbel FT, Amin-Hanjani S. Angiographic features of
“brain sag”. J Neurosurg. 2011 Sep;115(3):586-91.
Komotar JR, Mocco J, Ransom ER, Mack WJ, Zacharia BE, Wilson DA, et al. Herniation
secondary to critical postcraniotomy cerebrospinal fluid hypovolemia. Neurosurgery 2005 Aug;
57(2): 286-92.

Question 2

An 80-year-old man suffers an acute left subdural hematoma which is evacuated via a craniotomy.
Following surgery, he regains a withdrawal response to painful stimuli in the right arm and leg. Six
hours later, he is found to have new right gaze deviation and has lost this right extremity motor
response. CT scan of the head shows no blood reaccumulation or shift. Which of the following is
the most appropriate course of action?
Answers:
A. Stat EEG
B. MRI with DWI imaging
C. Return to OR for
D. Administer IV lorazepam
E. CT angiogram and CT perfusion

Answer 2

Administer IV lorazepam

Discussion:
Although a forced gaze and hemiparesis can be caused by stroke, the gaze preference of a stroke
is typically opposite the side of paralysis. It would therefore be unlikely that a CTA/P or MRI would
add additional actionable information in the short term. The patient has already had a CT to rule
out post-operative hemorrhage.
The mostly likely diagnosis is non-convulsive status. The onset of the seizure is unknown. A stat
EEG (3) might be useful, but there is enough information start treatment with a benzodiazepines
such as lorapezpam (4 mg IV one time repeated x 1 if seizures persist). A second longer acting
agent such as fosphenytoin, valproate, or levetiracetam should be loaded as soon as feasible.
At times a subdural drain laying on the surface of the brain may be implicated as a source of
seizure, but return to the OR to remove a drain would probably only be done in medically refractory
cases.
References:
Riviello JJ Jr, Claassen J, LaRoche SM, et al. Neurocritical Care Society Status Epilepticus
Guideline Writing Committee. Treatment of status epilepticus: an international survey of experts.
Neurocrit Care. 2013 Apr;18(2):193-200.
Brophy, Gretchen M., Rodney Bell, Jan Claassen, Brian Alldredge, Thomas P. Bleck, Tracy
Glauser, Suzette M. Laroche, et al. 2012. “Guidelines for the Evaluation and Management of
Status Epilepticus.” Neurocritical Care 17 (1): 3–23.

Question 3

A 23-year-old woman is admitted to the intensive care unit following an unrestrained high-speed
motor vehicle collision. Pulse is 44/min and regular, respirations are 16/min, blood pressure is
68/40 mmHg, and central venous pressure is 2 mmHg. Fluid resuscitation is initiated, but the
patient remains hypotensive and bradycardic. Which of the following is the most likely cause of
shock and the most appropriate treatment?
Answers:
A. None of the Above
B. Hypovolemic Shock – fluid resuscitation (balanced crystalloids)
C. Cardiogenic Shock – sympathomimetic vasopressors + fluid replacement
D. Obstructive Shock – immediate causal treatment
E. Distributive Shock – sympathomimetic vasopressors + fluid replacement

Answer 3

Distributive Shock – sympathomimetic vasopressors + fluid replacement

Discussion:
This patient most likely is in a state of neurogenic shock, characterized by bradycardia,
hypotension, and low central venous pressures. Neurogenic shock is a state of imbalance between
sympathetic and parasympathetic regulation of cardiac action and vascular smooth muscle. The
dominant signs are profound vasodilation with relative hypovolemia while blood volume remains
unchanged, at least initially. Neurogenic shock is classified as a type of distributive shock. The
primary treatment of neurogenic/distributive shock is fluid resuscitation (typically balanced
crystalloids) and administration of sympathomimetic (norepinephrine, epinephrine) vasoactive
medications.
Hypovolemic shock is a condition of inadequate organ perfusion caused by loss of intravascular
volume, usually acute. Early hypovolemic shock is typically characterized by tachycardia and
hypotension and low central venous pressures.
Cardiogenic shock is primarily a disorder of cardiac function in the form of a critical reduction of the
heart’s pumping capacity, caused by systolic or diastolic dysfunction leading to a reduced ejection
fraction or impaired ventricular filling. Patients with cardiogenic shock may be either tachycardic or
bradycardic, however, central venous pressures are usually high.
Obstructive shock is a condition caused by the obstruction of the great vessels or the heart itself.
Although the symptoms resemble those of cardiogenic shock, obstructive shock needs to be
clearly distinguished from the latter because it is treated quite differently. The treatment of
obstructive shock is causal – thrombolysis of pulmonary embolism, tension pneumothorax or
cardiac tamponade by thoracic/pericardial drainage. Central venous pressures would be expected
to be high in obstructive shock.
References:
Standl T, Annecke T, Cascorbi I, Heller AR, Sabashnikov A, Teske W. The Nomenclature,
Definition and Distinction of Types of Shock. Dtsch Arztebl Int. 2018;115(45):757-768.
doi:10.3238/arztebl.2018.0757
VanValkinburgh D, Kerndt CC, Hashmi MF. Inotropes And Vasopressors. [Updated 2021 Feb 11].
In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK482411/

Question 4

Acute respiratory distress syndrome is the result of
Answers:
A. Congestive heart disease
B. Pneumonia
C. Atelectasis
D. Pulmonary fibrosis
E. Diffuse alveolar hemorrhage

Answer 4

Pneumonia

Discussion:
ARDS can result from direct or indirect lung injury. Pnuemonia (bacterial, viral, fungal, or
opportunistic) is the most common direct lung-injury leading to ARDS. Aspiration of gastric
contents, pulmonary contusions, inhalation injury, and near drowning can also lead to ARDS.
Sepsis is the most common cause of indirect lung-injury leading to ARDS. ARDS can also be
caused by trauma or hemorrhagic shock, pancreatitis, burn injury, and blood product transfusion.
After direct or indirect lung injury, lung alveolar macrophages are activated, leading to the release
of potent proinflammatory mediators and chemokines promoting the accumulation of neutrophils
and monocytes. This exudative phase of ARDS leads to alveolar and microvascular damage and
loss of barrier function followed by alveolar flooding. Tumor necrosis factor (TNF) mediated
expression of tissue factor promotes platelet aggregation and microthrombus formation, as well as
intra-alveolar coagulation and hyaline membrane formation. The exudative phase is followed by a
proliferative phase. After epithelial integrity has been reestablished, the reabsorption of alveolar
edema in the provisional matrix restores alveolar architecture and function. A final fibrotic phase
has been linked to prolonged mechanical ventilation and increased mortality.
References:
1. N Engl J Med. 2017 Aug 10;377(6):562-572. 2. Crit Care. 2018 Oct 26;22(1):280

Question 5

A 70-year-old woman with a history of poorly controlled hypertension and type 2 diabetes mellitus
presents with a 2-cm left thalamic hemorrhage. She has right hemiparesis but is currently awake
and following commands on the left side. Blood pressure on presentation is 200/100 mmHg.
Immediate management of this patient should include which of the following?
Answers:
A. Blood pressure reduction
B. EEG
C. Emergent intubation
D. MRI brain
E. Administration of steroids

Answer 5

Blood pressure reduction

Discussion:
Patients with acute ICH need close medical attention in the initial 24-48 hours involving airway,
breathing, circulatory support, after which BP control and reversal of coagulopathy is essential.
The role of other diagnostic modalities in the acute settings is then considered based on clinical
history. This patient is awake and alert, not requiring emergent intubation. There is no role for
steroids as a therapeutic modality in spontaneous ICH.
References:
Hemphill JC 3rd, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M, Fung GL,
Goldstein JN, Macdonald RL, Mitchell PH, Scott PA, Selim MH, Woo D; American Heart
Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical
Cardiology. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A
Guideline for Healthcare Professionals From the American Heart Association/American Stroke
Association. Stroke. 2015 Jul;46(7):2032-60; Thabet AM, Kottapally M, Hemphill JC 3rd.
Management of intracerebral hemorrhage. Handb Clin Neurol. 2017;140:177-194.

Question 6

A 67-year-old patient is hospitalized for management of an acute ischemic stroke. In the
emergency department, the patient receives intravenous alteplase (tPA) and then sustains
an intraparenchymal hemorrhage. Which of the following is the most appropriate
pharmacologic reversal agent for this patient?
Answers:
A. Fresh frozen plasma
B. Cryoprecipitate
C. 4-Factor Prothrombin Complex Concentrate
D. Vitamin K
E. Protamine

Answer 6

Cryoprecipitate

Discussion:
The reversal agent of choice for tPA associated hemorrhages is cryoprecipitate which contains
fibrinogen, which is depleted by tPA. If Cryoprecipitate is unavailable, fresh frozen plasma and
tranexamic acid can be considered. There is no role for vitamin K or 4-factor prothrombin complex
concentrate.
References:
Frontera JA, et al. Guideline for reversal of anti-thrombotics in intracranial hemorrhage:
a statement for healthcare professionals from the neurocritical care society and society of critical
care medicine. Neurocrit Care. 2016 Feb;24(1):6-46; Saghi S, Willey JZ, Cucchiara B, Goldstein
JN, Gonzales NR, Khatri P, Kim LJ, Mayer SA, Sheth KN, Schwamm LH; American Heart
Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical
Cardiology; and Council on Quality of Care and Outcomes Research. Treatment and Outcome of
Hemorrhagic Transformation After Intravenous Alteplase in Acute Ischemic Stroke: A Scientific
Statement for Healthcare Professionals From the American Heart Association/American Stroke
Association. Stroke. 2017 Dec;48(12):e343-e361.

Question 7

Which of the following conditions increases the cerebral metabolic rate (CMRO2)?
Answers:
A. Barbiturate coma
B. Fever
C. Brain injury
D. Hyperoxygenation
E. General anesthesia

Answer 7

Fever

Discussion:
The rate of oxygen consumption by the brain is known as the cerebral metabolic rate of oxygen
(CMRO2). The rate of oxygen consumption is decreased by sedatives such as barbiturates and
general anesthesia. Brain injury will also tend to reduce brain metabolism, particularly in the acute
phase. Hyperoxia on its own will not stimulate brain metabolism. Fever has been shown to
increase CMRO2. This is a major reason why prevention of fever is considered important in
patients who are prone to brain ischemia.
References:
Busija, D. W., C. W. Leffler, and M. Pourcyrous. 1988. “Hyperthermia Increases Cerebral Metabolic
Rate and Blood Flow in Neonatal Pigs.” The American Journal of Physiology 255 (2 Pt 2):
H343–46.
Valadka AB, Furuya Y, Hlatky R, et al. Global and regional techniques for monitoring cerebral
oxidative metabolism after severe traumatic brain injury. Neurosurg Focus. 2000 Nov 15;9(5):e3

Question 8

Severe hypomagnesemia is most likely to produce which of the following?
Answers:
A. Hypotension
B. Ventricular arrhythmias
C. Hypercalcemia
D. Hyperkalemia
E. Hypoactive reflexes

Answer 8

Ventricular arrhythmias

Discussion:
Magnesium prevents increases in action potential duration and prolongation of membrane
repolarization. These changes commonly occur after myocardial ischemia and can lead to
ventricular arrhythmias. Atrial fibrillation can also be provoked by hypomagnesemia. Magnesium
causes presynaptic inhibition leading to a depressant effect on the central nervous system.
Hypomagnesemia can lead to seizures, hyperreflexia, tremors, fasciculations, and nystagmus.
Hypomagnesemia results in renal potassium loss and also suppresses parathyroid hormone
release and activity. Hypomagnesemia therefore often occurs in conjunction with hypokalemia and
hypocalcemia. Hypomagnesemia can be associated with hypertension rather than hypotension.
References:
1. Agus MS, Agus ZS. Cardiovascular actions of magnesium. Crit Care Clin. 2001
Jan;17(1):175-86. 2. Handb Clin Neurol. 2017;141:705-713

Question 9

A 42-year-old man with a head injury has clear nasal drainage. Which of the following is the most
useful method to determine the nature of this fluid?
Answers:
A. Endoscopic evaluation
B. CT of the brain and sinuses
C. Send fluid for beta-2 transferrin
D. Lumbar puncture
E. Observation over time

Answer 9

Send fluid for beta-2 transferrin

Discussion:
The patient’s condition is concerning for cerebrospinal fluid (CSF) leakage. The best method to
differentiate CSF from normal discharge is beta-2 transferrin, which would be seen in CSF and not
typical nasal fluid. Endoscopic evaluation, imaging, and observation would be suggestive but not
diagnostic. Lumbar puncture would be useful to rule out meningitis.
References:
Phang SY, Whitehouse K, Lee L, et al. Management of CSF leak in base of skull fractures in
adults. Br J Neurosurg. 2016 Dec;30(6):596-604.
Oh JW, Kim SH, Whang K. Traumatic cerebrospinal fluid leak: Diagnosis and management.
Korean J Neurotrauma. 2017 Oct;13(2):63-67.

Question 10

If a patient on dabigatran presents with a post-traumatic acute subdural hematoma requiring
surgery, which of the following drugs can be used to reverse the anticoagulation of dabigatran?
Answers:
A. Fresh frozen plasma
B. Tranexamic acid
C. Vitamin K
D. Prothrombin complex concentrate
E. Idarucizumab

Answer 10

Idarucizumab

Discussion:
Many agents have been administered for the reversal of dabigatran, but the only effective
medication is idarucizumab. This is a monoclonal antibody fragment specifically designed to
reverse the anticoagulation effects. The other medications may have some effect but are not the
appropriate therapy in an operative intracranial mass lesion.
References:
Pollack CV Jr, Reilly PA, Eikelboom J, et al. Idarucizumab for Dabigatran Reversal. N Engl J Med.
2015 Aug 6;373(6):511-20.2.
Pollack CV Jr, Reilly PA, Bernstein R, et al. Design and rationale for RE-VERSE AD: A phase 3
study of idarucizumab, a specific reversal agent for dabigatran. Thromb Haemost. 2015
Jul;114(1):198-205.3.

Question 11

A 20-year-old man in septic shock has systolic blood pressure of 80 mmHg. Infusion of which of
the following is recommended to increase his blood pressure and improve cardiac output?
Answers:
A. Norepinephrine
B. Amiodarone
C. Dopamine
D. Vasopressin
E. Epinephrine

Answer 11

Norepinephrine

Discussion:
Norepinephrine is the first-line vasopressor in shock and is associated with a lower mortality rate
as well as fewer adverse effects. Dopamine has similar actions but is associated with significantly
more tachydysrhythmias and should be reserved for patients with bradycardia. Epinephrine and
vasopressin are appropriate second-line vasopressors and may enable use of lower doses of
norepinephrine while improving hemodynamics. Inotropes may be added in patients with cardiac
dysfunction.
References:
Colling, Kristin P., Kaysie L. Banton, and Greg J. Beilman. “Vasopressors in sepsis.” Surgical
infections 19.2 (2018): 202-207.
Russell JA. Vasopressor therapy in critically ill patients with shock.
Intensive Care Medicine, 22 Oct 2019, 45(11):1503-1517

Question 12

Inappropriate secretion of antidiuretic hormone can be distinguished from fluid volume overload
most accurately by which of the following?
Answers:
A. Urine osmolality
B. Urine sodium
C. Urine sodium
D. Serum osmolality
E. Clinical examination

Answer 12

Clinical examination

Discussion:
Fluid overload can best be distinguished from SIADH by clinical examination. A diagnosis of
SAIDH requires an examination consistent with euvolemia. Volume overload can be caused by
several conditions such as heart failure, liver failure, nephrotic syndrome, or renal failure. Clinical
features consistent with volume overload include jugular venous distention, peripheral edema,
pulmonary edema, and ascites. Serum osmolality will be low in both SIADH and hypervolemia.
Urine sodium is typically greater than 20 mEq/L and urine osmolality > 10 mOsm in SIADH. While
urine sodium is < 20 mEq/L in heart failure, ascites, and nephrotic syndrome, hypernatremia due to
renal failure may present with urine sodium well in excess of 20 mEq/L.
References:
1. American Family Physician, Management of Hyponatremia. American Family Physician website.
Available at: http://www.aafp.org/afp/2004/0515/p2387.html Accessed February 6, 2015. 2. N Engl
J Med. 2007 May 17;356(20):2064-72

Question 13

Which of the following age groups is at greatest risk for traumatic brain injury?
Answers:
A. >=65
B. 45-54
C. 20-24
D. 25-34
E. 55-64

Answer 13

> =65

Discussion:
Children aged 0 to 4 years, older adolescents aged 15 to 19 years, and adults aged 65 years and
older are most likely to sustain a traumatic brain injury.
References:
1. U.S. Centers for Disease Control. Incidence Rates of Hospitalization Related to Traumatic Brain
Injury — 12 States, 2002. 2. https://www.aans.org/Patients/Neurosurgical-Conditions-andTreatments/Traumatic-Brain-Injury

Question 14

A 38-year-old hypertensive man has a three-day history of neck pain followed by acute onset of
left hemiplegia. Eight hours later, he is obtunded with a poorly reactive 6-mm right pupil. He is
intubated and a CT scan is performed, which identifies a large right hemisphere hypodensity with
mass effect and shift. Which of the following treatments is most likely to optimize this patient’s
outcome?
Answers:
A. Hypertonic saline
B. Stenting of the right carotid artery
C. Mannitol
D. Decompressive hemicraniectomy
E. ICP monitor

Answer 14

Decompressive hemicraniectomy

Discussion:
This patient is likely suffering from a large right hemispheric stroke, possible due to a carotid
dissection. His CT suggests that the stroke is completed and is suffering from mass effect due to
cytotoxic edema. Stenting the carotid artery will not help in the case of a large completed stroke.
Hypertonic saline and mannitol might be considered as temporizing measures, but will not improve
outcome without decompressive surgery. Patients can herniate without an elevated ICP, therefore
placement of an ICP monitor is not indicated. The most likely treatment to optimize this patient’s
outcome is a decompressive craniectomy. A pooled analysis of the Hamlet, Destiny, and Demical
trials suggest that decompressive hemicraniectomy within 48 hours of stroke onset results in lower
mortality and a greater number of patients with a functional outcome.
References:
Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant infarction of the
middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol. 2007
Mar;6(3):215-22.
Neugebauer H, Heuschmann PU, Jüttler E. DEcompressive Surgery for the Treatment of
malignant INfarction of the middle cerebral arterY - Registry (DESTINY-R): design and protocols.
BMC Neurol. 2012 Oct 2;12:115. doi: 10.1186/1471-2377-12-115. PMID: 23031451; PMCID:
PMC3517444.
Hofmeijer J, Kappelle LJ, Algra A, Amelink GJ, van Gijn J, van der Worp HB; HAMLET
investigators. Surgical decompression for space-occupying cerebral infarction (the
Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial
[HAMLET]): a multicentre, open, randomised trial. Lancet Neurol. 2009 Apr;8(4):326-33. doi:
10.1016/S1474-4422(09)70047-X. Epub 2009 Mar 5. PMID: 19269254.

Question 15

A 46-year-old woman is recovering five days after undergoing clipping of a ruptured anterior
communicating artery aneurysm that presented with World Federation of Neurosurgical Societies
(WFNS) grade 1 subarachnoid hemorrhage. She is neurologically intact. Routine management of
this patient in the intensive care unit includes which of the following?
Answers:
A. Maintaining systolic blood pressure < 140 mg Hg.
B. Hemodilution to hematocrit of 33.
C. Daily TCDs.
D. Prophylactic cerebral angioplasty.
E. Oral nimodipine

Answer 15

Oral nimodipine.

Discussion:
Oral nimodipine has been shown in randomized controlled trials to reduce the risk of delayed
ischemic events after aneurysm subarachnoid hemorrhage. It is common practice to keep the
systolic blood pressure below 160 mg Hg prior to securing a ruptured aneurysm. Once the
aneurysm is secured, permissive hypertension rather than anti-hypertensive therapy is common
practice. Patients without vasospasm should be kept euvolemic. Prophylactic angioplasty is not
recommended for patients with aneurysmal subarachnoid hemorrhage, regardless of the grade.
References:
Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical care management of patients following
aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s
Multidisciplinary Consensus Conference. Neurocritical care guidelines. Neurocrit Care. 2011
Sep;15(2):211-40.
Taran S, Trivedi V, Singh JM, English SW, McCredie VA. The Use of Standardized Management
Protocols for Critically Ill Patients with Non-traumatic Subarachnoid Hemorrhage: A Systematic
Review. Neurocrit Care. 2020 Jun;32(3):858-874. doi: 10.1007/s12028-019-00867-5. PMID:
31659678.

Question 16

Which of the following is the most likely explanation for demyelination in multiple sclerosis?
Answers:
A. Hyperactivity of the innate immune system
B. T cell senitization to a component of myelin
C. Development of gray matter plaques.
D. Increased vitamin D
E. Increased sun exposure

Answer 16

T cell senitization to a component of myelin

Discussion:
T cell sensitization to a component of the myelin is thought to trigger demyelination. Prominent
components include myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP). T
cells have been demonstrated to initiate the MS plaques. MS plaques occur in the white matter.
While both B and T cells are involved in the pathophysiology of MS, the innate immune system is
not suspect to play a prominent role in the occurrence of demyelination. Vitamin D deficiency and
decreased sun exposure are thought to contribute to MS and may help to explain why MS is more
prominent in populations living at higher latitudes.
References:
1. Waksman BH, Adams RD: Am J Pathol 33:131, 1957. 2. Neurol Clin. 2011 May; 29(2):
257–278. 3. Adams and Victor’s Principles of Neurology. Chapter 36. Multple Sclerosis and other
Inflammatory and Demyelinating Diseases.

Question 17

ECG changes observed in patients with severe hyperkalemia include which of the following?
Answers:
A. Shortened QT interval and Widened QRS Complex
B. Peaked T-Waves
C. ST-Segment depression and Increased PR Interval
D. All of the above
E. None of the above

Answer 17

All of the above

Discussion:
EKG changes secondary to hyperkalemia include peaked T waves, shortened QT interval, and STsegment depression. These changes are followed by bundle-branch blocks causing a widening of
the QRS complex, increases in the PR interval, and decreased amplitude of the P wave.
References:
Levis JT. ECG diagnosis: hyperkalemia. Perm J. 2013;17(1):69. doi:10.7812/TPP/12-088
Brian T. Montague, Jason R. Ouellette and Gregory K. Buller. Retrospective Review of the
Frequency of ECG Changes in Hyperkalemia. CJASN March 2008, 3 (2) 324-330; DOI:
https://doi.org/10.2215/CJN.04611007

Question 18

A 56-year-old man sustains severe traumatic brain injury in a motor vehicle collision. His
intracranial pressure remains increased despite administration of hyperosmolar agents, CSF
drainage, sedation, and paralysis. A pentobarbital coma is induced. Which of the following is a
potential mechanism of neuroprotection from this intervention?
Answers:
A. Activation of the GABAB receptor.
B. Decreased CSF production.
C. Seizure prevention.
D. Increased blood flow.
E. Reducing metabolic demand.

Answer 18

Reducing metabolic demand

Discussion:
When GABA binds to the GABA-A receptor on a neuron it causes opening of chloride channel that
results in hyperpolarization and reduced synaptic firing. Barbiturates such as pentobarbital also
bind to the GABA-A receptor, but at a different site than the GABA molecule itself. The effect of the
barbiturate is to keep the chloride channel open longer, potentiating the inhibitory effect of the
GABA molecule, a process referred to as allosteric modulation. In high doses, barbiturates result in
a reduction in synaptic firing. As synaptic firing accounts for 50% of brain metabolism, barbiturates
can significantly reduce metabolic demand.
While barbiturates are used for seizure prophylaxis and treatment, seizure prevention is not a
mechanism of neuroprotection. Barbiturates do not affect CSF production. Barbiturates do not bind
to the GABA-B receptor. One criticism regarding the use of barbiturates for neuroprotection is their
tendency to cause hypotension and reduced cerebral perfusion.
References:
Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of
Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain injury. XI.
Anesthetics, analgesics, and sedatives. J Neurotrauma. 2007;24 Suppl 1:S71-6.
Schizodimos T, Soulountsi V, Iasonidou C, Kapravelos N. An overview of management of
intracranial hypertension in the intensive care unit. J Anesth. 2020 Oct;34(5):741-757. doi:
10.1007/s00540-020-02795-7. Epub 2020 May 21. PMID: 32440802; PMCID: PMC7241587

Question 19

Multiple endocrine neoplasia (type I) syndrome is characterized by tumors of the pituitary gland
and the
Answers:
A. Brainstem
B. Heart
C. Pancreas
D. Kidneys
E. Spinal column

Answer 19

Pancreas

Discussion:
MEN type 1 is a hereditary condition that leads to tumors of the endocrine glands. The most
common tumors are of the pituitary gland, pancreas, and parathyroid. The other lesions are not
typically seen in this condition.
References:
Brandi ML, Gagel RF, Angeli A, et al. Guidelines for diagnosis and therapy of MEN type 1 and type
2. J Clin Endocrinol Metab. 2001 Dec;86(12):5658-71.
Thakker RV, Newey PJ, Walls GV, et al. Clinical practice guidelines for multiple endocrine
neoplasia type 1 (MEN1). Clin Endocrinol Metab. 2012 Sep;97(9):2990-3011.

Question 20

A 63-year-old man sustains a hemorrhagic posterior cranial fossa stroke and is taken to the
operating room for emergent surgical evacuation. The patient is placed in the lateral position for
the procedure. Shortly after elevating the bone flap, the end-tidal CO2 and O2 saturation
decrease, leading to a decrease in the patient’s blood pressure. Which of the following is the most
appropriate course of action?
Answers:
A. Immediately close the wound and prepare for reintubation.
B. Immediate place an EVD at Frazier’s point.
C. Resect cerebellar hemisphere to relieve pressure.
D. Increase PEEP.
E. Flood the field with saline.

Answer 20

Flood the field with saline

Discussion:
A drop in ET-CO2 and O2 saturation during posterior fossa surgery likely represents a venous air
embolus due to air entering non-compressed veins such as the dural sinuses and bony venous
lakes during the craniotomy. The first step for the surgeon is to flood the field with saline and/or
cover the field with saline soaked sponges to help seal the veins off from the air.
Posterior fossa swelling requiring tissue resection or a ventricular drain would not likely cause
significant changes in the oxygenation status of a mechanically intubated patient. Increasing PEEP
might be considered initially but is not likely to be effective as the air embolus affects perfusion not
ventilation. Disconnection of the ventilator or dislodgment of the ET tube might result in a drop in
ET-CO2 and O2 sat, but would not likely cause hypotension, at least initially.
References:
Giraldo, Mauricio, Luz María Lopera, and Miguel Arango. 2015. “Venous Air Embolism in
Neurosurgery.” Colombian Journal of Anesthesiology 43 (January): 40–44.
Malhotra SK. Venous Air Embolism in Neurosurgical Patients. Khan Z, eds. In: Challenging Topics
in Neuroanesthesia and Neurocritical Care. Cham, Switzerland: Springer International Publishing;
2017:229-238.

Question 21

Which of the following tests is most appropriate for differentiating between a traumatic lumbar
puncture and pre-existing subarachnoid hemorrhage?
Answers:
A. CSF color
B. CSF cell count
C. CSF glucose
D. CSF protein
E. CSF clarity

Answer 21

CSF color

Discussion:
Xanthochromia refers to the yellow-orange discoloration of CSF, most often caused by lysis of red
blood cells (RBCs). Discoloration begins after RBCs have been in spinal fluid for about two hours.
While it sometimes can be seen visually, detection of xanthochromia via spectrophotometry is the
most reliable method of determining whether a subarachnoid hemorrhage has occurred.
References:
Seehusen DA, Reeves MM, Fomin DA. Cerebrospinal fluid analysis. Am Fam Physician. 2003;
68(6):1103-1109.
Williams A. Xanthochromia in the cerebrospinal fluid. Practical Neurology. 2004;4:174-5

Question 22

A 67-year-old man who receives hemodialysis has acute onset of a large subdural hematoma.
Surgical evacuation is complicated by difficulty controlling bleeding from the scalp and the
contused brain surface. Hemoglobin concentration is 8.0 g/dL, platelet count is 162,000/mm3, and
prothrombin time is 13.2 seconds (N 11.0–13.5). The patient is hemodynamically stable. Which of
the following is the most appropriate next step in management?
Answers:
A. Administer Tranexamic acid
B. Administer Protamine
C. Administer 4-Factor PCC
D. Administer FFP
E. Administer DDAVP

Answer 22

Administer DDAVP

Discussion:
Uremia / renal failure patients develop an acquired deficiency in platelet function caused by
decreased thromboxane A2 function, increased platelet-inhibitory prostaglandin, and excessive
nitric oxide synthesis. In a patient who is hemodynamically stable with difficult to control
intraoperative bleeding, administration of cryoprecipitate or DDAVP would be the best initial step in
management. Postoperative dialysis may be considered as well.
DDAVP increases the plasma levels of factor VIII and vWF and shortens the partial thromboplastin
time and bleeding time. DDAVP has no effect on platelet count or aggregation, but it enhances
platelet adhesion to the vessel wall. A short-lived effect of DDAVP is the release of large amounts
of tissue plasminogen activator into the plasma.
References:
Escolar G, Díaz-Ricart M, Cases A. Uremic platelet dysfunction: past and present. Curr Hematol
Rep. 2005 Sep;4(5):359-67.
Medow JE, Dierks MR, Williams E, et al. The Emergent Reversal of Coagulopathies Encountered
in Neurosurgery and Neurology: A Technical Note. Clin Med Res. 2015; 13(1): 20-31.
Hedges SJ, Dehoney SB, Hooper JS, Amanzadeh J, Busti AJ. Evidence-based treatment
recommendations for uremic bleeding. Nat Clin Pract Nephrol. 2007 Mar;3(3):138-53. doi:
10.1038/ncpneph0421. PMID: 17322926.
Frontera JA, Lewin JJ 3rd, Rabinstein AA, Aisiku IP, Alexandrov AW, Cook AM, del Zoppo GJ,
Kumar MA, Peerschke EI, Stiefel MF, Teitelbaum JS, Wartenberg KE, Zerfoss CL. Guideline for
Reversal of Antithrombotics in Intracranial Hemorrhage: A Statement for Healthcare Professionals
from the Neurocritical Care Society and Society of Critical Care Medicine. Neurocrit Care. 2016
Feb;24(1):6-46. doi: 10.1007/s12028-015-0222-x. PMID: 26714677.

Question 23

A 49-year-old man is brought to the emergency department after being involved in a motor vehicle
collision. Physical examination demonstrates no verbal response, eye opening only to painful
stimuli, and localizing in response to noxious stimuli. Which of the following is the most likely
Glasgow Coma Scale score in this patient?
Answers:
A. 7
B. 8
C. 11
D. 10
E. 6

Answer 23

8

Discussion:
The Glasgow Coma Scale (GCS) score is made up of three components (Eye, Verbal, and Motor)
for a total score of 3 to 15. This particular patient has a score of E2 (eyes open to pain), V1 (no
verbal response), and M5 (localization) for a total score of 8.
References:
The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint
Section on Neurotrauma and Critical Care. Glasgow coma scale score. J Neurotrauma. 2000 JunJul; 17(6-7): 563-571. Review.
Udekwu P, Kromhout-Schiro S, Vaslef S, Baker C, Oller D. Glasgow Coma Scale score, mortality,
and functional outcome in head-injured patients. J Trauma. 2004 May; 56(5): 1084-1089

Question 24

Which of the following is the current “gold standard” for intracranial pressure monitoring and
management?
Answers:
A. Fiberoptic intraparenchymal monitor
B. EVD with fluid coupled pressure transducer.
C. Transcranial doppler
D. Lumbar puncture
E. There is no gold standard for ICP monitoring

Answer 24

EVD with fluid coupled pressure transducer.

Discussion:
The gold standard for ICP monitoring and management is the external ventricular drain with a fluid
coupled pressure transducer. Fiberoptic monitors can also monitor ICP accurately, but do not allow
for removal of spinal fluid. Fiberoptic monitors historically suffer from measurement drift and cannot
be recalibrated unless replaced. Lumbar puncture allows for CSF drainage and pressure
measurements in patients with communicating hydrocephalus. It is not accurate in patients with
non-communicating hydrocephalus.
References:
Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of
Neurological Surgeons; et al. Guidelines for the management of severe traumatic brain injury. VI.
Indications for intracranial pressure monitoring. J Neurotrauma. 2007;24 Suppl 1:S37-44.
Fakhry SM, Trask AL, Waller MA, Watts DD; IRTC Neurotrauma Task Force. Management of
brain-injured patients by an evidence-based medicine protocol improves outcomes and decreases
hospital charges. J Trauma. 2004 Mar;56(3):492-9; discussion 499-500. doi:
10.1097/01.ta.0000115650.07193.66. PMID: 15128118

Question 25

A 36-year-old man has a closed fracture of the femur and a small, focal area of subarachnoid
hemorrhage after being involved in a motor vehicle collision. No other cranial injury is noted, and
neurological examination is normal. After repair of the femur fracture, the patient does not arouse
from anesthesia. A CT scan of the head shows bilateral diffuse, small, hypodense lesions. Which
of the following is the most likely cause of the change in this patient’s clinical status?
Answers:
A. Diffuse axonal injury
B. Fat emboli
C. Diffuse embolic infarcts
D. Watershed infarcts from hypotension
E. Posterior reversible encephalopathy syndrome

Answer 25

Fat emboli

Discussion:
The presence of femur fracture and diffuse hypodense lesions would be indicative of fat emboli.
One would expect diffuse axonal injury to yield an immediate neurological deficit. There is no
reported hypotension that would yield watershed infarcts, and the close proximity to the femur
repair would make diffuse embolic infarcts and PRES less likely.
References:
Akhtar S. Fat Embolism. Anesthesiology Clin. 2009;27:533-50.2. Metting Z, Rödiger LA, Regtien
JG, et al. Delayed coma in head injury: consider cerebral fat embolism. Clin Neurol Neurosurg.
2009 Sep;111(7):597-600.3.
Kellogg RG, Fontes RB, Lopes DK. Massive cerebral involvement in fat embolism syndrome and
intracranial pressure management. J Neurosurg. 2013 Nov;119(5):1263-70.

Question 26

Several days after undergoing endovascular coiling of a ruptured aneurysm with Fisher grade 3
subarachnoid hemorrhage, a patient has hyponatremia. Which of the following findings would
support a diagnosis of cerebral salt-wasting syndrome rather than syndrome of inappropriate
antidiuretic hormone secretion?
Answers:
A. Low serum urate levels
B. Increased urine sodium concentration
C. High urine osmolality
D. Hypovolemic state
E. Low urine output

Answer 26

Hypovolemic state

Discussion:
Hypovolemia is a key distinguishing factor in discerning between cerebral salt-wasting (CSW)
syndrome and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Low urine
output is seen in SIADH but not CSW. High urine osmolality, increased urine sodium concentration,
and low serum urate levels are seen in both CSW and SIADH.
References:
Diringer MN, Bleck TP, Hemphill JC 3rd, et al. Critical care management of patients following
aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s
Multidisciplinary consensus conference. Neurocrit Care. 2011;15:211-40.
Brimioulle S, Orellana-Jimenez C, Aminian A, Vincent JL. Hyponatremia in neurological patients:
cerebral salt wasting versus inappropriate antidiuretic hormone secretion. Intensive Care Med.
2008;34:125–31

Question 27

The Transfusion Requirements in Critical Care (TRICC) trial demonstrated that liberal transfusion
(hemoglobin level is less than 10 g/dL) versus restrictive transfusion (hemoglobin level is 7 g/dL)
protocols are associated with which of the following outcomes in critically ill patients?
Answers:
A. The rate of death within 30 days of admission were similar between the liberal and
restrictive-strategy transfusion groups.
B. Higher rates of multi-organ failure in the liberal-strategy transfusion group
C. Higher rates of multi-organ failure in the restrictive-strategy transfusion group
D. Cardiac events (pulmonary edema, myocardial infarction) were more frequent in the
restrictive-strategy transfusion group in patients in the intensive care unit.
E. The mortality rates during hospitalization were higher in the restrictive-strategy transfusion
group

Answer 27

The rate of death within 30 days of admission were similar between the liberal and
restrictive-strategy transfusion groups.

Discussion:
The primary outcome — the rate of death from all causes in the 30 days after admission to the
intensive care unit — was 18.7 percent in the restrictive-strategy group and 23.3 percent in the
liberal-strategy group (95 percent confidence interval for the difference between the groups, –0.84
percent to 10.2 percent; P=0.11) The mortality rates during hospitalization were lower in the
restrictive-strategy group (22.2 percent vs. 28.1 percent, P=0.05). Other mortality rates including
the mortality rate during the entire stay in the intensive care unit (13.9 percent vs. 16.2 percent,
P=0.29) and the 60-day mortality rate (22.7 percent vs. 26.5 percent, P=0.23) were also lower in
the restrictive-strategy group but not significantly so.
The number of patients with multiorgan failure (more than three organs), which was analyzed as a
dichotomous variable (present or absent) for each of seven organ systems,18 was not significantly
different between the restrictive-strategy and liberal-strategy groups (5.3 percent vs. 4.3 percent,
P=0.36).
Cardiac events, primarily pulmonary edema and myocardial infarction, were more frequent in the
liberal-strategy group than in the restrictive-strategy group during the stay in the intensive care unit
(P<0.01).
The mortality rates during hospitalization were lower in the restrictive-strategy group (22.2 percent
vs. 28.1 percent, P=0.05).
References:
Hébert PC, Wells G, Blajchman MA, Marshall J, Martin C, Pagliarello G, Tweeddale M, Schweitzer
I, Yetisir E. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical
care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group.
N Engl J Med. 1999 Feb 11;340(6):409-17. doi: 10.1056/NEJM199902113400601. Erratum in: N
Engl J Med 1999 Apr 1;340(13):1056. PMID: 9971864.
E. Wesley Ely, M.D., M.P.H., and Gordon R. Bernard, M.D. Transfusions in Criticall Ill patients.
Editorial. February 11, 1999 N Engl J Med 1999; 340:467-468. DOI:
10.1056/NEJM199902113400610

Question 28

A previously healthy 26-year-old man is involved in a motor vehicle collision, resulting in severe
head trauma that is complicated by an anoxic brain injury during extrication from the vehicle. It is
determined that there is no medical or surgical intervention that can help this patient. The patient’s
family would like to move forward with organ donation. Which of the following would prevent organ
donation at this time?
Answers:
A. Alcoholism.
B. Unable to confirm organ donor status on driver’s license.
C. Sepsis.
D. Patient is not brain dead.
E. Professional tattoos.

Answer 28

Sepsis

Discussion:
There are surprisingly few absolute contra-indications to organ donation, but sepsis is one of them.
Alcoholism and (non-prison) tattoos do not typically exclude organ donation. Families can choose
organ donation for family members who do not have their donor status explicitly stated on their
license or proxy documents. Donation after cardiac death (DCD) allows for donation in patients
who are not brain dead.
References:
Wijdicks EF, Varelas PN, Gronseth GS, et al. Evidence-based guideline update: Determining brain
death in adults: report of the Quality Standards Subcommittee of the American Academy of
Neurology. Neurology. 2010 Jun 8;74(23):1911-8.3.
Meyfroidt G, Gunst J, Martin-Loeches I, Smith M, Robba C, Taccone FS, Citerio G. Management
of the brain-dead donor in the ICU: general and specific therapy to improve transplantable organ
quality. Intensive Care Med. 2019 Mar;45(3):343-353. doi: 10.1007/s00134-019-05551-y. Epub
2019 Feb 11. PMID: 30741327; PMCID: PMC7095373.

Question 29

According to the results of prospective, randomized, controlled trials, which of the following best
describes the effect of therapeutic hypothermia in patients with severe traumatic brain injury?
Answers:
A. Attenuation of the release of excitatory neurotransmitters following severe TBI
B. Decreased incidence of myocardial ischemia
C. Insufficient evidence for its utilization in the management of patients with severe TBI
D. Decreased incidence of venous thromboembolic complications
E. Improved GOS-E at 30 days

Answer 29

Insufficient evidence for its utilization in the management of patients with
severe TBI

Discussion:
Despite a large number of studies, there remains no high-quality evidence that hypothermia is
beneficial in the treatment of patients with severe traumatic brain injury.
While hypothermia may be associated with a decreased release of excitatory neurotransmitters
(which, along with reducing cerebral metabolic rate, may explain its mechanism of action), there is
insufficient evidence to show that therapeutic hypothermia improves mortality or long-term
functional outcomes.
The main risks associated with therapeutic hypothermia include increased risk of infectious
complications, coagulation abnormalities, myocardial ischemia, and atrial fibrillation.
References:
Lewis SR, Evans DJ, Butler AR, et al. Hypothermia for traumatic brain injury. Cochrane Database
Syst Rev. 2017 Sep 21;9:CD001048.
Busto R, Globus MY, Dietrich WD, Martinez E, Valdés I, Ginsberg MD. Effect of mild hypothermia
on ischemia-induced release of neuro-transmitters and free fatty acids in rat brain. Stroke
1989;20(7):904-10.
Bering EA Jr. Effect of body temperature change on cerebral oxygen consumption of the intact
monkey. American Journal of Physiology 1961;200:417-9.
Schubert A. Side effects of mild hypothermia. Journal of Neurosurgical Anesthesiology
1995;7(2):139-47

Question 30

Postoperative hypocalcemia is most likely to have which of the following cardiovascular effects?
Answers:
A. Heart Failure
B. Torsades de pointes (Polymorphic Ventricular Tachycardia)
C. Acute cardiac ischemia
D. Prolonged QT interval on EKG
E. Hypotension

Answer 30

Prolonged QT interval on EKG

Discussion:
Hypotension may complicate acute hypocalcemia, particularly when rapidly induced by transfusion
of citrated blood or with use of low calcium dialysate in the patients undergoing renal replacement
therapy. Heart failure has been reported in severe cases but is not the most common occurrence.
Hypocalcemia characteristically causes prolongation of the QT interval on EKG. Hypocalcemia
prolongs phase 2 of the action potential with the impact modulated by the rate of change of serum
calcium concentration and function of the myocyte calcium channels. Torsades de pointes can be
triggered by hypocalcemia but is much less common than with hypokalemia or hypomagnesemia.
References:
Benoit, Stephen R., et al. “Risk factors for prolonged QTc among US adults: third National Health
and Nutrition Examination Survey.” European Journal of Preventive Cardiology 12.4 (2005):
363-368.
Westerdahl J, Lindblom P, Valdemarsson S, Tibblin S, Bergenfelz A. Risk Factors for Postoperative
Hypocalcemia After Surgery for Primary Hyperparathyroidism. Arch Surg. 2000;135(2):142–147.
doi:10.1001/archsurg.135.2.142
Zaloga GP, Chernow B. Hypocalcemia in critical illness. JAMA. 1986 Oct;256(14):124-129.

Question 31

Which of the following treatments is most appropriate for a patient with a hemolytic transfusion
reaction?
Answers:
A. Clinical assessment and hemodynamic support
B. Emergent steroid administration
C. Emergent plasmapheresis
D. Start diuretics
E. Administration of Ringer’s lactate

Answer 31

Clinical assessment and hemodynamic support

Discussion:
Patient’s with transfusion reactions promptly need medical attention, which initially involves
assessment of airway, breathing, circulatory support. First the transfusion should be stopped while
preserving venous access. Patients may respond to oxygen administered by nasal catheter or
mask, but they may need to be intubated for mechanical ventilation. Without signs of volume
overload or cardiogenic pulmonary edema, diuretics and plasmapheresis are not indicated. No
evidence exists that corticosteroids or antihistamines are beneficial. Treat complications with
specific supportive measures.
References:
Delaney M, Wendel S, Bercovitz RS, Cid J, Cohn C, Dunbar NM, et al. Transfusion reactions:
prevention, diagnosis, and treatment. Lancet. 2016 Dec 3. 388 (10061):2825-2836; Tinegate H,
Birchall J, Gray A, Haggas R, Massey E, Norfolk D, et al. Guideline on the investigation and
management of acute transfusion reactions Prepared by the BCSH Blood Transfusion Task Force.
Br J Haematol. 2012 Oct. 159(2):143-53. Friedman T, Javidroozi M, Lobel G, Shander A.
Complications of Allogeneic Blood Product Administration, with Emphasis on Transfusion-Related
Acute Lung Injury and Transfusion-Associated Circulatory Overload. Adv Anesth.
2017;35(1):159-173. doi: 10.1016/j.aan.2017.07.008. PMID: 29103571. Semple JW, Rebetz J,
Kapur R. Transfusion-associated circulatory overload and transfusion-related acute lung injury.
Blood. 2019 Apr 25;133(17):1840-1853. doi: 10.1182/blood-2018-10-860809. Epub 2019 Feb 26.
PMID: 30808638.

Question 32

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is supported by the
findings of decreased serum sodium level accompanied by which of the following?
Answers:
A. High TSH
B. High serum osmolality
C. High Serum Na
D. Low serum osmolality
E. Low Urine osmolality

Answer 32

Low serum osmolality

Discussion:
SIADH is characterized by lab values consistent with low TSH levels, high urine osmolality and low
serum osmolality due to water retention. High Urine Na would be expected in cerebral salt wasting.
SIADH is associated with low serum Na.
References:
Palmer BF. Hyponatremia in a neurosurgical patient: syndrome of inappropriate antidiuretic
hormone secretion versus cerebral salt wasting. Nephrol Dial Transplant. 2000 Feb;15(2):262-8;
Hoorn EJ, Zietse R. Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines. J
Am Soc Nephrol. 2017 May. 28 (5):1340-1349

Question 33

Which of the following best characterizes Cheyne-Stokes respirations?
Answers:
A. Periodic breathing with phases of hyperpnea alternating with apnea
B. Respiratory pause at full inspiration
C. Apnea
D. Sustained hyperventilation
E. Irregular, gasping respiration

Answer 33

Periodic breathing with phases of hyperpnea alternating with apnea

Discussion:
Cheyne-Stokes respiration is characterized by phases of hyperpnea alternating with apnea.
Respiratory depth during the hyperpneic phase increases from breath to breath in a crescendo
until a peak is reached followed by a decrescendo. A period of apnea follows which usually lasts
10-20 seconds. Cheyne-Stokes respiration is seen in metabolic encephalopathies and with lesions
that impair forebrain and diencephalon function. Apnea occurs when lesions affect the ventral
respiratory group in the ventrolateral medulla bilaterally. Irregular gasping breathing characterizes
cluster or ataxic breathing, which is seen with lesions of the pontomedullary junction. A respiratory
pause at full inspiration characterizes apneusis, which is seen with bilateral pontine lesions.
Sustained hyperventilation is seen with metabolic encephalopathies and rarely in cases of high
brainstem tumors.
References:
1. Plum and Posner’s Diagnosis of Stupor and Coma. Chapter 2, examination of the comatose
patient. 2. J Neurol Neurosurg Psychiatry. 2002 May;72(5):595. doi: 10.1136/jnnp.72.5.595.

Question 34

When treating a patient with acute symptomatic hyponatremia with hypertonic saline, the
maximum correction of plasma sodium levels in the first 24 hours is
Answers:
A. No current guidelines
B. 4-8 mEq/L
C. >15 mEq/L
D. 1-4 mEq/L
E. 12-15 mEq/L

Answer 34

4-8 mEq/L

Discussion:
Sodium correction is based on the acuity of hyponatremia and the severity of symptoms. In acute
symptomatic hyponatremia, a correction of 4-6 mEq/L (up to 8mEq/L) is safe and can be achieved
within a few hours, with maintenance of stable sodium levels for up to 24 hours. A more rapid
correction can lead to osmotic demyelination syndrome with neurologic sequelae thereof.
References:
Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol. 2009
May;29(3):282-99; Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier RW, Sterns RH,
Thompson CJ. Diagnosis, evaluation, and treatment of hyponatremia: expert panel
recommendations. Am J Med. 2013 Oct;126(10 Suppl 1):S1-42

Question 35

A 57-year-old woman who had a grade III subarachnoid hemorrhage becomes progressively
obtunded three days after undergoing clipping of an anterior communicating artery aneurysm.
Laboratory studies show a serum sodium level of 119 mEq/L, a serum osmolarity of 260 mOsm/L,
and a urinary sodium level of 40 mEq/L. A postoperative CT scan shows no abnormalities. The
most appropriate treatment is intravenous administration of which of the following agents?
Answers:
A. DDAVP
B. 2% Normal Saline
C. 23% Normal Saline
D. Dextrose 5% water
E. Intravenous Steroids

Answer 35

2% Normal Saline

Discussion:
This patient is experiencing neurologic deterioration due to acute symptomatic hyponatremia. In
this scenario, sodium correction must be promptly, but cautiously, corrected within a few hours
targeting an increase of 4-6 mEq/L (maximum 8 mEq/L ). In acute symptomatic hyponatremia, a
correction of 4-6 mEq/L (up to 8 mEq/L) is safe and well tolerated and can be achieved within a
few hours, with close monitoring and maintenance of levels up to 24 hours. A more rapid
correction can lead to osmotic demyelination syndrome with neurologic sequelae thereof. A slightly
hypertonic saline solution like 2% normal saline can be administered, since iso-osmotic solutions
can worsen hyponatremia by promoting more water retention compared to sodium, potentiating
SIADH. A hypotonic solution like Dextrose 5% can worsen hyponatremia. DDAVP is useful in
diabetes insipidus and thus not in this scenario. A significantly hyperosmolar solution such as 23%
normal saline will over-correct the sodium rapidly, which can be dangerous.
References:
Gross P, Reimann D, Neidel J, Döke C, Prospert F, Decaux G, Verbalis J, Schrier RW. The
treatment of severe hyponatremia. Kidney Int Suppl. 1998 Feb;64:S6-11; Lee, K. (2012). The
neuroICU book. Mcgraw-Hill Medical.

Question 36

The randomized controlled Decompressive Craniectomy in Patients with Severe Traumatic Brain
Injury (DECRA) trial concluded that patients who received a craniectomy for severe traumatic brain
injury experienced which of the following?
Answers:
A. Better functional outcomes
B. Decreased intracranial pressure
C. Higher mortality
D. Fewer complications
E. No benefit

Answer 36

Decreased intracranial pressure

Discussion:
The DECRA trial randomized patients to continued medical management (pentobarbital coma) or
surgical decompression if the patient was refractory to most ICP measures. The study found that
patients who had surgical decompression had fewer episodes of elevated ICP and fewer days in
the intensive care unit. They had similar mortality to the medical group but more unfavorable
outcomes. Criticisms of this trial including failure of randomization as well as too early to
decompression in the surgical group.
References:
Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain
injury. N Engl J Med. 2011 Apr 21;364(16):1493-502.
Kitagawa RS, Bullock MR. Lessons from the DECRA study. World Neurosurg. 2013
Jan;79(1):82-4.

Question 37

A 23-year-old man involved in a motor vehicle collision exhibits a sudden neurological decline from
an initial Glasgow Coma Scale score of 15 to a Glasgow Coma Scale score of 9. He has a new left
hemiparesis with a right dilated pupil. Which of the following is the most appropriate next step in
management of this patient?
Answers:
A. Craniotomy
B. Noncontrast head CT
C. Assessment of respiratory status
D. Administration of mannitol
E. Aspirin for evolving stroke

Answer 37

Assessment of respiratory status

Discussion:
This patient is developing cerebral herniation syndrome with likely expanding intracranial mass
lesion. Although mannitol, imaging, and likely eventual surgical intervention are part of the patient’s
management, the first intervention involves the “ABCs” (airway, breathing, and circulation). This
includes obtaining a secure airway and well as hemodynamic stability prior to the next stage of the
patient’s treatment.
References:
Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of
Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain injury. I.
Blood pressure and oxygenation. J Neurotrauma. 2007;24 Suppl 1:S7-13.2.
Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural hematomas.
Neurosurgery. 2006 Mar;58(3 Suppl):S7-15; discussion Si-iv

Question 38

A 64-year-old woman is evaluated because of a painful, swollen, warm right calf six weeks after
undergoing lumbar laminectomy. Doppler ultrasonography shows extensive deep venous
thrombosis. Which of the following is the most appropriate next step in management?
Answers:
A. Initiation of Intravenous Anticoagulant Therapy
B. Initiation of Oral Anticoagulant therapy
C. No treatment is needed
D. Placement Inferior Vena Cava Filter
E. Initiation of Antiplatelet Medication

Answer 38

Initiation of Oral Anticoagulant therapy

Discussion:
For primary treatment of patients with DVT and/or PE, whether provoked by a transient risk factor
or by a chronic risk factor or unprovoked, the ASH guideline panel suggests using a shorter course
of anticoagulation for primary treatment (3-6 months) over a longer course of anticoagulation for
primary treatment (6-12 months). Oral anticoagulation is the preferred method. These
recommendations apply to patients who are eligible to receive anticoagulation. For patients with a
contraindication to anticoagulation, insertion of a retrievable IVC filter may be indicated, with
retrieval as soon as the patient is able to receive anticoagulation.
References:
Gary H. Lyman et al. American Society of Hematology 2021 guidelines for management of venous
thromboembolism: prevention and treatment in patients with cancer.
Blood Adv (2021) 5 (4): 927–974.
Ortel, Thomas L., et al. “American Society of Hematology 2020 guidelines for management of
venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism.” Blood
advances 4.19 (2020): 4693-4738.

Question 39

A lumbar puncture in a patient with pseudotumor cerebri will show which of the following?
Answers:
A. High protein
B. Elevated opening pressure
C. Low glucose
D. Elevated IgG index
E. Pleocytosis

Answer 39

Elevated opening pressure

Discussion:
Pseudotumor cerebri is a disorder of idiopathic intracranial hypertension. It often affects young,
obese women who present with headache, papilledema, and elevated lumbar puncture opening
pressure. The chemical and cellular composition of the CSF is usually normal. First line treatment
is typically administration of acetazolamide with or without furosemide. If vision is acutely
threatened, temporary CSF drainage by lumbar puncture or lumbar drain may allow a trial of these
diuretics. Options for more permanent treatment are optic nerve sheath fenestration and
ventriculoperitoneal shunting. Although the latter is the gold standard, it is often fraught with
complications over time in this patient population. The venous sinuses and jugular veins should be
imaged as stenting can be considered for stenosis as an alternative to ventriculoperitoneal
shunting.
References:
Kosmorsky G. Neurosurg Clin N Am. 2001; 12(4):775-797.
Johnston PK, Corbett JJ, Maxner CE. Cerebrospinal fluid protein and opening pressure in
idiopathic intracranial hypertension (pseudotumor cerebri). Neurology. 1991; 41(7): 1040-1042.

Question 40

A 35-year-old man comes to the emergency department because of a two-day history of severe
headaches. The CT scan shown is obtained. The patient is awake, alert, and conversing, but when
the patient is returned from the CT scan, he is acutely unresponsive, hypertensive, and has
bradycardia. Which of the following is the most appropriate next step in management?
Answers:
A. Administer atropine
B. Repeat head CT.
C. Have the patient intubated
D. Start IV antihypertensive
E. Place an EVD

Answer 40

Have the patient intubated

Discussion:
The patient has likely suffered rupture (in this case likely rerupture) of a cerebral aneurysm. He is
experiencing Cushing’s triad (unresponsive, hypertensive bradycardic) due to elevated intracranial
pressure. The patient is unresponsive and should be intubated. This will also allow for mild
hyperventilation to help reduce ICP. The next steps include CT scan and placement of an EVD,
and intravenous antihypertensives if blood pressure remains above 160. As the bradycardia is
likely caused by the severe hypertension and the patient is not hypotensive, atropine would not
typically be administered.
References:
Raya AK, Diringer MN. Treatment of Subarachnoid Hemorrhage. Critical Care Clinics. 2014 Oct,
Vol 30(4):719–33.
van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007 Jan
27;369(9558):306-18. doi: 10.1016/S0140-6736(07)60153-6. PMID: 17258671.

Question 41

The American Heart and American Stroke Associations recommend that intravenous tissue
plasminogen activator (tPA) be administered no later than how long after the onset of acute
ischemic stroke?
Answers:
A. 2 hours
B. 4.5 hours
C. 24 hours
D. 6 hours
E. 12 hours

Answer 41

4.5 hours

Discussion:
Administration of intravenous tissue plasminogen activator (tPA) is a mainstay in the management
and treatment of patients with acute ischemic stroke. Initial studies demonstrated benefit for
intravenous tPA given 0-3 hours after stroke onset. A later publication demonstrated utility of tPA
up to 4.5 hours after stroke onset.
Numerous mechanical thrombectomy trials for patients with large vessel occlusion acute ischemic
strokes have demonstrated efficacy in both “early” and “late” windows, expanding the indication for
this intervention to 24 hours. However, this question pertained specifically to recommendations
regarding intravenous tPA administration.
References:
National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue
Plasminogen activator for acute ischemic stroke. New England Journal of Medicine. 1995 Dec;
333(24): 1581-7.
Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute
ischemic stroke. New England Journal of Medicine. 2008 Sept; 359(13): 1317-29.
del Zoppo GJ, Saver JL, Jauch EC, et al. Expansion of the Time Window for Treatment of Acute
Ischemic Stroke With Intravenous Tissue Plasminogen Activator. A Science Advisory From the
American Heart Association/American Stroke Association. Stroke. 2009 Aug; 40(8): 2945–2948.

Question 42

A 20-year-old man exhibits a reduction in his intracranial pressure when his arterial blood pressure
rises. This is an example of which of the following physiologic phenomena?
Answers:
A. Shock
B. Cushing’s response
C. Defective cerebral autoregulation
D. Intact cerebral autoregulation
E. Hypertensive crisis

Answer 42

Intact cerebral autoregulation

Discussion:
Cerebral autoregulation mediates changes to cerebral blood volume and, in turn, changes in
intracranial pressure. If autoregulation is intact, decreases in cerebral perfusion pressure result in
vasodilation. This causes increased cerebral blood volume and increased intracranial pressure.
Conversely, increases in cerebral perfusion pressure result in vasoconstriction at the level of the
largest arterioles which causes decreased cerebral blood volume. This leads to a reduction in
intracranial pressure. Neither Cushing’s response, hypertensive crisis or shock are appropriate
answers for this phenomenon.
References:
Rangel-Castilla L, Gasco J, Nauta HJ, et al. Cerebral pressure autoregulation in traumatic brain
injury. Neurosurg Focus. 2008 Oct;25(4):E7.
Ter Minassian A, Dubé L, Guilleux AM, et al. Changes in intracranial pressure and cerebral
autoregulation in patients with severe traumatic brain injury. Crit Care Med. 2002
Jul;30(7):1616-22

Question 43

Which of the following are the most common findings of cerebral salt wasting syndrome?
Answers:
A. Hypernatremia, Elevated Urine Sodium, Elevated Urine Osmolality, Hypovolemia
B. Hypernatremia, Elevated Urine Sodium, Elevated Urine Osmolality, Hypervolemia
C. Hyponatremia, Decreased Urine Sodium, Elevated Urine Osmolality, Hypovolemia
D. Hyponatremia, Elevated Urine Sodium, Decreased Urine Osmolality, Hypovolemia
E. Hyponatremia, Elevated Urine Sodium, Elevated Urine Osmolality, Hypovolemia

Answer 43

Hyponatremia, Elevated Urine Sodium, Elevated Urine Osmolality,
Hypovolemia

Discussion:
Evaluation for cerebral salt wasting begins with a basic metabolic panel (BMP) to identify the
hyponatremia (serum sodium less than 135 meq/L). Urine studies are commonly checked for urine
sodium and osmolality. Urine sodium is typically elevated above 40 meq/L. Urine osmolality is
elevated above 100 mosmol/kg. The patient must also have signs or symptoms of hypovolemia
such as hypotension, decreased central venous pressure, lack of skin turgor, or elevated
hematocrit.
Syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) will have a similar
laboratory picture as cerebral salt wasting with hyponatremia and increased urine sodium.
However, with SIADH, the patient is euvolemic to hypervolemic from the retained free water as
compared to the hypovolemic picture of cerebral salt wasting.
References:
Tenny, Steven, and William Thorell. “Cerebral Salt Wasting Syndrome.” StatPearls [Internet]
(2020).
Oh JY, Shin JI. Syndrome of inappropriate antidiuretic hormone secretion and cerebral/renal salt
wasting syndrome: similarities and differences. Front Pediatr. 2014;2:146.
Yee AH, Burns JD, Wijdicks EF. Cerebral salt wasting: pathophysiology, diagnosis, and treatment.
Neurosurg Clin N Am. 2010 Apr;21(2):339-52.

Question 44

Which of the following is the normal global cerebral blood flow?
Answers:
A. 60 mL/(100 g/min)
B. 50 mL/(100 g/min)
C. 20 mL/(100 g/min)
D. 70 mL/(100 g/min)
E. 40 mL/(100 g/min)

Answer 44

50 mL/(100 g/min)

Discussion:
Cerebral blood flow (CBF) is defined as the volume of blood that flows per unit mass per unit time
in brain tissue. The normal value of cerebral blood flow in adults is about 50 mL/100 g/min. Lower
values can occur in white matter [approximately 20 mL/(100 g/min)] and greater values can occur
in gray matter [approximately 80 mL/(100 g/min)].
References:
1. Neurophotonics. 2016 Jul; 3(3): 031411, 2. Magnetic Resonance Imaging 18 (2000) 503–51

Question 45

Which of the following complications has been linked to aggressive use of pressors and
intravenous fluids to maintain elevated cerebral blood flow in patients with severe traumatic brain
injury?
Answers:
A. Acute respiratory distress syndrome
B. Progression of intracranial hematoma
C. Acute kidney injury
D. Worsening neurological outcome
E. Refractory elevated intracranial pressure

Answer 45

Acute respiratory distress syndrome

Discussion:
Robertson et al reported a clinical trial comparing intracranial pressure (ICP) directed therapy with
cerebral perfusion pressure (CPP) directed therapy and found that artificially elevating the CPP >
70mmHg led to a five-fold increase in the incidence of acute respiratory distress syndrome. The
other variables, although theoretically possible, were not shown to be true in this trial.
References:
Robertson CS, Valadka AB, Hannay HJ, et al. Prevention of secondary ischemic insults after
severe head injury. Crit Care Med. 1999;27:2086-95.
Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of
Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain injury. I.
Blood pressure and oxygenation. J Neurotrauma. 2007;24 Suppl 1:S7-13.2.

Question 46

Which of the following agents is most likely to partially reverse the effects of enoxaparin?
Answers:
A. Protamine
B. Platelets
C. Tranexamic acid
D. FFP
E. 4-Factor PCC

Answer 46

Protamine

Discussion:
Heparinoids and their low molecular weight derivatives affect the clotting cascade by directly and
indirectly affecting thrombin and factor X. Enoxaparin represents a commonly used low molecular
weight heparin agent which is partially reversible. Protamine allows for reversal of 60-80% of the
effects of enoxaparin.
In order to reverse enoxaparin, it is important to note when the last dose of the medication was
administered. If given within the prior 8 hours, 1mg of protamine must be administered per 1mg of
enoxaparin over 10 minutes, with a maximum dose of 50mg of protamine. If the enoxaparin was
given >8 hours prior, one can give ½ of the calculated protamine dose.
References:
Product Monograph. Available at: http://products.sanofi.ca/en/lovenox.pdf. Published July 2013.
Medow JE, Dierks MR, Williams E, et al. The Emergent Reversal of Coagulopathies Encountered
in Neurosurgery and Neurology: A Technical Note. Clin Med Res. 2015; 13(1): 20-31.
van Veen JJ, Maclean RM, Hampton KK, Laidlaw S, Kitchen S, Toth P, Makris M. Protamine
reversal of low molecular weight heparin: clinically effective? Blood Coagul Fibrinolysis. 2011
Oct;22(7):565-70. doi: 10.1097/MBC.0b013e3283494b3c. PMID: 21959588.
Lauer BR, Nelson RA, Adamski JH, Gibbons J, Janko MR, Ravi G, Barcelona RA. Protamine
sulfate for the reversal of enoxaparin associated hemorrhage beyond 12 h. Am J Emerg Med. 2019
Jan;37(1):174.e5-174.e6. doi: 10.1016/j.ajem.2018.09.043. Epub 2018 Sep 26. PMID: 30274763.

Question 47

A 30-year-old man with a history of alcohol abuse is admitted to the neurointensive care unit with
altered mental status following mild head trauma. Serum sodium level is 109 mEq/L; 3% sodium
chloride is initiated. Over the next 36 hours, sodium level normalizes, but mental status
deteriorates, and the patient becomes dysarthric and quadriparetic. This patient’s deterioration is
most likely due to which of the following?
Answers:
A. Osmotic demyelination
B. Arterial vasospasm
C. Alcohol withdrawal
D. Thiamine deficiency
E. Epileptic seizure

Answer 47

Osmotic demyelination

Discussion:
The patient is experiencing neurologic deterioration due to rapid over-correction of acute
symptomatic hyponatremia, leading to osmotic demyelination syndrome characterized by a
delayed neurologic deterioration after 2-6 days of sodium correction. Symptoms consist of
dysarthria, dysphagia, paraparesis/quadriparesis, seizures, lethargy, coma. In this scenario,
sodium correction must be promptly, but cautiously, corrected up to 4-6 mEq/L (maximum 8mEq/L)
in a 24 hour period. Arterial spasm and epileptic seizures would not be expected in mild TBI, given
the context of sodium correction. Alcohol withdrawal would be associated with tremors,
diaphoresis and hemodynamic instability. Thiamine deficiency is possible but does not follow the
temporal course of the over-correction of hyponatremia and associated neurologic deterioration.
References:
Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid
correction of hyponatremia. Medicine (Baltimore). 1993 Nov;72(6):359-73; Kumar S, Fowler M,
Gonzalez-Toledo E, Jaffe SL. Central pontine myelinolysis, an update. Neurol Res. 2006 Apr.
28(3):360-6.

Question 48

Which of the following is most likely to result from a jugular venous oxygen saturation of less than
50%?
Answers:
A. Global cerebral hypoxia.
B. Barbiturate coma.
C. Posterior fossa ischemia.
D. Hyperperfusion syndrome.
E. ICA-MCA tandem occlusion and stroke.

Answer 48

Global cerebral hypoxia.

Discussion:
Jugular venous oxygen saturation is typically measured using a central line catheter inserted
retrograde in the internal jugular vein with the tip in the jugular bulb. Depending on the equipment
used, intermittent or continuous sampling of the oxygen saturation of the blood exiting the brain via
the jugular vein can be measured. Typical measurements range from 50% to 75%. During global
cerebral hypoxia, decreased oxygen delivery will cause an increase in oxygen extraction in the
capillary bed and a drop in the jugular venous oxygenation below 50%. While an ICA-MCA
occlusion will certainly cause ischemia, complete absence of flow may not cause a measurable
increase in oxygen extraction as there can be no increase in oxygen extraction if flow drops to
zero. Posterior fossa ischemia will often not result in a change jugular venous oxygen saturation
for two reasons. First, the catheter is usually placed on the dominant side which is the side
typically draining the supratentorial space. Second, the posterior circulation only accounts for
15-20% of total brain metabolism so its contribution to overall oxygen extraction is fairly small.
Cerebral hyper perfusion syndrome and barbiturate coma would be expected to result in excess
oxygen delivery and therefore an increase in jugular venous oxygen saturation above 75%.
References:
Ullman JS: Cerebral blood flow and metabolism in Intensive Care in Neurosurgery. Andrews BT,
ed. New York, Thieme, pp29-46, 2003.
Schell, Randall M., and Daniel J. Cole. 2000. “Cerebral Monitoring: Jugular Venous Oximetry.”
Anesthesia & Analgesia 90 (3): 559

Question 49

A patient who has severe asthma requires administration of an antihypertensive drug. Which of the
following drug classes is contraindicated in this patient?
Answers:
A. Angiotensin Receptor Blockers
B. Non-selective Beta-Blockers
C. ACE inhibitors
D. Calcium Channel Blockers
E. Diuretics

Answer 49

Non-selective Beta-Blockers

Discussion:
Non-selective β-blockers should not be prescribed for the management of comorbidities in patients
with asthma while cardio-selective β-blockers, preferably in low doses, may be used when strongly
indicated and other therapeutic options are not available. There are no contraindications to use of
diuretics, ACE inhibitors, or angiotensin receptor blockers in patients with asthma.
References:
Angelica Tiotiu, Plamena Novakova, Krzysztof Kowal, Alexander Emelyanov, Herberto ChongNeto, Silviya Novakova & Marina Labor (2019) Beta-blockers in asthma: myth and reality, Expert
Review of Respiratory Medicine, 13:9, 815-822, DOI: 10.1080/17476348.2019.1649147
The safety of cardioselective β1-blockers in asthma: literature review and search of global
pharmacovigilance safety reports.
Bennett M, Chang CL, Tatley M, Savage R, Hancox RJ.ERJ Open Res. 2021 Mar
1;7(1):00801-2020. doi: 10.1183/23120541.00801-2020. eCollection 2021 Jan.

Question 50

Which of the following is the initial fluid of choice for resuscitation of patients in septic shock?
Answers:
A. Pentastarch
B. Hypertonic saline
C. Lactated ringers
D. Hydroxyethyl starch
E. Concentrated 25% albumin

Answer 50

Lactated ringers

Discussion:
The ideal fluid of choice in the resuscitation of patients in septic shock is a isotonic solution, based
on several clinical trials. There is increasing evidence that normal saline is associated with
increased mortality and kidney injury; balanced isotonic crystalloids may be a safer alternative.
Hyperosmolar solutions have been associated with worse outcomes. Administration of Albumin 5%
can be considered, although controversial, with lesser clinical evidence. There is no evidence for
the efficacy for concentrated Albumin 25%. Hydroxyethyl starches appear to increase mortality and
kidney injury in the critically ill and are no longer indicated in these patients.
References:
Jiang L, Jiang S, Zhang M, Zheng Z, Ma Y. Albumin versus other fluids for fluid resuscitation in
patients with sepsis: a meta-analysis. PLoS One. 2014 Dec 4;9(12):e114666; Asfar P, Schortgen F,
Boisramé-Helms J, Charpentier J, Guérot E, Megarbane B, Grimaldi D, Grelon F, Anguel N,
Lasocki S, Henry-Lagarrigue M, Gonzalez F, Legay F, Guitton C, Schenck M, Doise JM, Devaquet
J, Van Der Linden T, Chatellier D, Rigaud JP, Dellamonica J, Tamion F, Meziani F, Mercat A,
Dreyfuss D, Seegers V, Radermacher P; HYPER2S Investigators; REVA research network.
Hyperoxia and hypertonic saline in patients with septic shock (HYPERS2S): a two-by-two factorial,
multicenter, randomized, clinical trial. Lancet Respir Med. 2017 Mar;5(3):180-190. Chang R,
Holcomb JB. Choice of Fluid Therapy in the Initial Management of Sepsis, Severe Sepsis, and
Septic Shock. Shock. 2016 Jul;46(1):17-26. doi: 10.1097/SHK.0000000000000577. PMID:
26844975; PMCID: PMC4905777

Question 51

Which of the following is most likely to be decreased in a patient who has pulmonary edema?
Answers:
A. Vascular permeability
B. Pulmonary capillary wedge pressure
C. Hydrostatic pressure
D. Central venous pressure
E. PaO2

Answer 51

PaO2

Discussion:
Normal pulmonary physiology favors a small net influx of fluid from the alveolar capillaries into the
lung interstitial space. The amount of fluid leaking from capillaries is dependent on the balance
between hydrostatic and osmotic pressure. Pulmonary edema can occur due to a cardiogenic
etiology characterized by an increased hydrostatic pressure or noncardiogenic etiologies
characterized by increased vascular permeability. In cardiogenic pulmonary edema, pulmonary
capillary wedge pressure (PCWP), which is an estimate of left atrial filling pressure is increased.
Cardiogenic pulmonary edema is also characterized by increased central venous pressures (CVP).
References:
1. N Engl J Med. 2005 Dec 29;353(26):2788-96. 2. Crit Care Clin. 2015 Oct;31(4):803-21

Question 52

A 25-year-old man is brought to the emergency department for a left parasternal stab wound.
Blood pressure is 70/50 mmHg, neck veins are distended, and heart sounds are muffled. Which of
the following is the most likely diagnosis?
Answers:
A. Pericardial tamponade
B. Acute blood loss anemia
C. Vasovagal syncope
D. Pneumothorax
E. Disruption of sympathetic fibers

Answer 52

Pericardial tamponade

Discussion:
The patient has shock related to his stab wound. Beck’s triad of hypotension, elevated systemic
venous pressure (neck vein distension), and muffled heart sounds is present and indicative of
pericardial tamporade (a form of obstructive shock). Pneumothorax is possible, but decreased
breath sounds would be a dominant feature. Hemorrhagic shock would not have distended neck
veins, and shock related to spinal cord injury would not have these features.
References:
American College of Surgeons. ATLS: Advanced Trauma Life Support for Doctors (Student Course
Manual). 8th ed. Chicago, IL: American College of Surgeons; 2008.Demetriades D. Cardiac
wounds. Experience with 70 patients. Ann Surg. 1986 Mar;203(3):315-317.
Agrawal A, Hasan Z, Sikachi RR, Koenig S. Beyond the Beck’s Triad: The Use of Point-of-Care
Ultrasound for Diagnosis and Treatment of Shock. Ann Am Thorac Soc. 2018 May;15(5):637-640.

Question 53

In the management of severe traumatic brain injury, when is hyperventilation therapy indicated?
Answers:
A. Only as a temporizing measure
B. Within the first 24 hours
C. In conjunction with barbiturate coma
D. When brain tissue oxygen levels are low
E. Never

Answer 53

Only as a temporizing measure

Discussion:
There is no level I evidence regarding the use of hyperventilation. According to the Guidelines for
the Management of Severe Traumatic Brain Injury, Fourth Edition, hyperventilation should only be
used as a temporizing measure such as en route to operating room or while awaiting other
interventions. It should be avoided during the first 24hrs after injury as this can lead to further
vasoconstriction and decrease of cerebral blood flow.
Carney N, Totten AM, O’Reilly C, Ullman JS, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R, Harris
OA, Kissoon N, Rubiano AM, Shutter L, Tasker RC, Vavilala MS, Wilberger J, Wright DW, Ghajar
J. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery.
2017 Jan 1;80(1):6-15. doi: 10.1227/NEU.0000000000001432. PMID: 27654000.
References:
Carney N, Totten AM, O’Reilly C, Ullman JS, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R, Harris
OA, Kissoon N, Rubiano AM, Shutter L, Tasker RC, Vavilala MS, Wilberger J, Wright DW, Ghajar
J. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery.
2017 Jan 1;80(1):6-15. doi: 10.1227/NEU.0000000000001432. PMID: 27654000.
Regional cerebrovascular and metabolic effects of hyperventilation after severe traumatic brain
injury.
Diringer MN, Videen TO, Yundt K, Zazulia AR, Aiyagari V, Dacey RG Jr, Grubb RL, Powers WJ. J
Neurosurg. 2002 Jan;96(1):103-8. doi: 10.3171/jns.2002.96.1.0103.

Question 54

Pseudohyponatremia is most likely in patients with which of the following conditions?
Answers:
A. Diabetes Insipidus
B. Hypertriglyceridemia
C. SSRI use
D. Carbamazepine use
E. Septic shock

Answer 54

Hypertriglyceridemia

Discussion:
Pseudohyponatremia consists of a state where there is a reduction in the percentage of water in
plasma relative to sodium, such as a state of hypertriglyceridemia, where there is a lower sodium
concentration as a result of high triglycerides that reduces the percentage of water, and thus
falsely lowering the concentration of sodium. SSRI and carbamazepine result in hyponatremia due
to SIADH and excessive water retention due to elevated ADH secretion. Diabetes insipidus results
in hypernatremia.
References:
Wang Y, Attar BM, Abu Omar Y, Agrawal R, Demetria MV. Pseudohyponatremia in
Hypertriglyceridemia-Induced Acute Pancreatitis: A Tool for Diagnosis Rather Than Merely a
Laboratory Error? Pancreas. 2019 Jan;48(1):126-130; Adashek ML, Clark BW, Sperati CJ, Massey
CJ. The Hyperlipidemia Effect: Pseudohyponatremia in Pancreatic Cancer. Am J Med. 2017
Dec;130(12):1372-1375.

Question 55

Which of the following parameters should be confirmed before a formal apnea test can be
performed?
Answers:
A. Patient has no autonomic responses (flushing, sweating)
B. PaO2 is normal or elevated.
C. No uptake on nuclear medicine perfusion test.
D. Non-responsive EEG.
E. Absence of deep tendon reflexes

Answer 55

PaO2 is normal or elevated

Discussion:
The apnea test is generally the last test performed to determine brain death. After confirming the
patient is in an irreversible coma and that there are no brainstem reflexes, the patient is preoxygenated, taken off the ventilator, and observed for evidence of spontaneous breathing. If the
patient remains apneic when the PaCO2 reaches ≥ 60 mm Hg (or 20 mm Hg over baseline) the
patient is declared brain dead. Prior to initiating the test it must be confirmed that the PaO2 is
normal and is typical to preoxygenate to a PaO2 > 200. After taking the patient off the ventilator,
oxygen is continuously supplied through a catheter threaded down the ET tube to ensure the
patient is not hypoxic during the test. Ancillary tests such as a nuclear medicine perfusion test or
EEG may be performed when apnea testing is indeterminate but are not required for the
determination of brain death or as a qualification for the apnea test. Autonomic functions and
DTRs are not considered brainstem mediated responses and the presence of these responses
does not exclude the diagnosis of brain death.
References:
Wahlster S, Wijdicks EFM, Patel PV, et al. Brain death declaration: Practices and perceptions
worldwide. Neurology. 2015 May 5;84(18):1870-9.
Busl, Katharina M., Ariane Lewis, and Panayiotis N. Varelas. 2020. “Apnea Testing for the
Determination of Brain Death: A Systematic Scoping Review.” Neurocritical Care, June.
https://doi.org/10.1007/s12028-020-01015-0.

Question 56

A 40-year-old woman sustained an anterior communicating artery aneurysm rupture 48 hours ago.
She now has a serum sodium level of 130 mEq/L. Assessment of which of the following
parameters is most appropriate before correction with an infusion of 100 mL/hr of sodium chloride
0.9%?
Answers:
A. Urine Osmolality
B. Fractional Excretion of Uric Acid
C. Volume status
D. Serum Osmolality
E. Urine Sodium

Answer 56

Volume status

Discussion:
The initial evaluation of hyponatremia is to distinguish true hypoosmolar hyponatremia from
translocational hyponatremia (e.g. mannitol, hyperglycemia, uremia, ethanol, etc.) or
pseudohyponatremia (e.g. hyperproteinemia, dyslipidemia) via serum osmolality. A normal or
elevated serum osmolality suggests either translocational hyponatremia or pseudohyponatremia.
Both cerebral salt wasting (CSW) and the syndrome of inappropriate antidiuretic hormone (SIADH)
are due to abnormal water or sodium excretion, and therefore do not have inappropriately high
urine osmolality. However, both SIADH and CSW have elevated urine sodium, and therefore,
cannot be distinguished based on this finding alone. SIADH and CSW are differentiated by volume
status. SIADH is associated with a euvolemic or slightly hypervolemic state, whereas CSW results
in a hypovolemic state. Fractional excretion of uric acid (FeUA) may have some clinical utility.
Initially, FeUA is elevated (> 10) in both CSW and SIADH. With normalization of sodium, FeUA
corrects in SIADH, however remains elevated in CSW. Until significant hypovolemia develops,
patients with CSW tend to have higher urine volumes and high 24 hour urinary excretion of
sodium. Alternatively in SIADH, urine volume is normal to low, and therefore sodium excretion is
also normal to low. As distinguishing mild hypovolemia from euvolemia is challenging, this feature
may have greater practical use at the bedside.
References:
Areiff AI, Gabbai R, Goldfine ID. Cerebral salt-wasting syndrome: diagnosis of urine sodium
excretion. Am J Med Sci. 2017. 354(4): 350-354.
Hoom EJ, Zietse R. Diagnosis and treatment of hyponatremia: compilation of guidelines. J Am Soc
Nephrol. 2017;28(5): 1340-1349. https://www.ncbi.nlm.nih.gov/pubmed/28174217
Imbriano LJ, Mattana J, Drakakis J, Maesaka JK. Identifying different causes of hyponatremia with
fractional excretion of uric acid. Am J Med Sci. 2016. 352(4):385-390. https://www.ncbi.nlm.nih.gov
/pubmed/27776720

Question 57

In which of the following situations are corticosteroids indicated for the treatment of sepsis?
Answers:
A. SBP >100 requiring low dose vasopressors
B. SBP>100 on multiple antibiotics
C. SBP <100 with known bacterial infection
D. SBP >100 with IV fluids
E. SBP <100 refractory to IV fluids and vasopressor administration

Answer 57

SBP <100 refractory to IV fluids and vasopressor administration

Discussion:
Corticosteroid use in septic shock is indicated as adjunctive therapy for hemodynamic support for
patients needing escalating doses of vasopressors after optimal fluid resuscitation. However, it is
not a first line treatment of hypotension in septic shock. In adults with septic shock treated with low
dose corticosteroids, short- and longer-term mortality are unaffected, adverse events increase, but
duration of shock, mechanical ventilation and ICU stay are reduced. The etiology of the septic
shock and concurrent use of antibiotics are variables that have no relevance to the concurrent use
of corticosteroids.
References:
Lyu QQ, Chen QH, Zheng RQ, Yu JQ, Gu XH. Effect of Low-Dose Hydrocortisone Therapy in Adult
Patients With Septic Shock: A Meta-Analysis With Trial Sequential Analysis of Randomized
Controlled Trials. J Intensive Care Med. 2020 Oct;35(10):971-983; Rygård SL, Butler E, Granholm
A, Møller MH, Cohen J, Finfer S, Perner A, Myburgh J, Venkatesh B, Delaney A. Low-dose
corticosteroids for adult patients with septic shock: a systematic review with meta-analysis and trial
sequential analysis. Intensive Care Med. 2018 Jul;44(7):1003-1016. Rygård SL, Butler E,
Granholm A, Møller MH, Cohen J, Finfer S, Perner A, Myburgh J, Venkatesh B, Delaney A. Lowdose corticosteroids for adult patients with septic shock: a systematic review with meta-analysis
and trial sequential analysis. Intensive Care Med. 2018 Jul;44(7):1003-1016. doi:
10.1007/s00134-018-5197-6. Epub 2018 May 14. PMID: 29761216

Question 58

Which of the following treatments is most likely to decrease the incidence of chronic subdural
hematoma recurrence?
Answers:
A. Irrigation of the subdural space
B. Bedrest with head of bed flat
C. Induced hyponatremia
D. Hyperoxygen therapy
E. Placement of subdural drain

Answer 58

Placement of subdural drain

Discussion:
In a randomized trial by Sartarius et al, the placement of a subdural drain at the time of surgery
decreased the incidence of symptomatic recurrence. All of the other methods have been utilized to
try to decrease the incidence of recurrence after surgery. None has been shown to be effective in
rigorous study. Newer techniques such as middle meningeal artery embolization are currently
being studied.
References:
Santarius T, Kirkpatrick PJ, Ganesan D, et al. Use of drains versus no drains after burr-hole
evacuation of chronic subdural haematoma: a randomised controlled trial. Lancet 2009.
374(9695):1067-73.2
Iorio-Morin C, Blanchard J, Richer M, et al. Tranexamic Acid in Chronic Subdural Hematomas
(TRACS): study protocol for a randomized controlled trial. Trials 2016. 2016;17:235

Question 59

Which of the following factors or findings would warrant a non-contrast CT scan of the head two
hours after a minor closed head injury?
Answers:
A. Any of the above
B. Vomiting, 2 or more episodes
C. Age 65 years or older
D. GCS < 15
E. Suspected open, depressed, and/or basal skull fracture

Answer 59

Any of the above

Discussion:
Significant variations exist in the utilization of CT for detection of traumatic intracranial pathology
among patients with minor head injuries. The Canadian CT Head Rule was derived from a
prospective cohort of Canadian emergency department patients with a GCS of 13-15 after head
injury. Five high-risk factors and two additional medium-risk factors were identified. The presence
of any one of them indicates need for a head CT. The high-risk factors were 100% sensitive for
predicting need for neurosurgical intervention, and would require only 32% of patients to undergo
CT. The rule is not applicable if the patient did not experience a trauma, has a Glasgow Coma
Scale score lower than 13, is younger than 16 years, is taking warfarin or has a bleeding disorder,
or has an obvious open skull fracture.
High Risk for Neurosurgical Intervention
1. Glasgow Coma Scale score lower than 15 at 2 hours after injury
2. Suspected open or depressed skull fracture
3. Any sign of basal skull fracture *
4. Two or more episodes of vomiting
5. 65 years or older
Medium Risk for Brain Injury Detection by Computed Tomographic Imaging
6. Amnesia before impact of 30 or more minutes
7. Dangerous mechanism **
* Signs of basal skull fracture include hemotympanum, racoon eyes, cerebrospinal fluid, otorrhea
or rhinorrhea, Battle’s sign.
** Dangerous mechanism is a pedestrian struck by a motor vehicle, an occupant ejected from a
motor vehicle, or a fall from an elevation of 3 or more feet or 5 stairs.
References:
Stiell IG, Wells GA, Vandemheen K, et al. Variation in ED use of computed tomography for patients
with minor head injury. Ann Emerg Med. 1997; 30:14-22.
Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor
head injury. Lancet. 2001; 357:1391-6.

Question 60

A decrease in which of the following explains the mechanism by which hyperventilation lowers
intracranial pressure?
Answers:
A. PaCO2
B. Arteriolar smooth muscle tone
C. Oxygen saturation
D. Mean arterial pressure
E. PEEP

Answer 60

PaCO2

Discussion:
Hyperventilation causes decreased PaCO2 which incites constriction of arteriolar smooth muscles
(increased tone). This results in decreased cerebral blood flow and decreased cerebral blood
volume which leads to a decrement in intracranial pressure.
References:
Rangel-Castilla L, Gasco J, Nauta HJ, et al. Cerebral pressure autoregulation in traumatic brain
injury. Neurosurg Focus. 2008 Oct;25(4):E7.
Ter Minassian A, Dubé L, Guilleux AM, et al. Changes in intracranial pressure and cerebral
autoregulation in patients with severe traumatic brain injury. Crit Care Med. 2002
Jul;30(7):1616-22.

Question 61

A 25-year-old man injured in a motor vehicle collision is admitted to the intensive care unit with a
Glasgow Coma Scale score of 6 and a CT scan demonstrating a 2-cm left temporal contusion and
scattered traumatic subarachnoid hemorrhages. Medical evidence-based clinical data support a
1-week course of prophylaxis with a drug from which of the following classes?
Answers:
A. Barbiturates
B. Antibiotics
C. Steroids
D. Anticonvulsants
E. Hyperosmolars

Answer 61

Anticonvulsants

Discussion:
Post-traumatic seizures (PTS) occur either early (within 7 days of injury) or late (after 7 days).
Clinical PTS occur in up to 12% of patients after severe TBI with electrographic seizures occurring
in up to 20-25% of cases. Anticonvulsant therapy is recommended to decrease the incidence of
early PTS but not late PTS. Results from the CRASH trial provided Level I evidence that the use of
steroids after TBI were associated with increased mortality. Therefore, the use of steroids after TBI
is currently not recommended for improving outcomes or reducing ICP. Current guidelines do not
recommend prophylactic use of antibiotics after TBI. While a study of 100 critically ill patients
(86%) with TBI showed a decreased risk of pneumonia with cefuroxime treatment after intubation,
no mortality benefit was seen and use of prophylactic antibiotics may contribute to development of
resistant organisms (Am J Respir Crit Care Med. May 1997;155(5):1729-1734. PMID: 9154884).
Prophylactic use of barbiturates after TBI is not recommended, although barbiturates may be used
to control refractory increases in ICP. Hyperosmolar therapy is a key medical therapy for treating
increased intracranial pressure, however there is no current indication for prophylactic use of
hyperosmolar therapy.
References:
1. Temkin NR, Dikmen SS, Wilensky AJ, et al. A randomized, double-blind study of phenytoin for
the prevention of post-traumatic seizures. N Engl J Med. 1990 Aug 23;323(8):497-502. 2.
Neurosurgery. 2017 Jan 1;80(1):6-15.

Question 62

The mean arterial blood pressure (MAP) at normal resting heart rate is best approximated by
which of the following formulas, where SBP is the systolic pressure and DBP the diastolic
pressure?
Answers:
A. MAP = DBP + 1/4(SBP-DBP)
B. MAP = SBP - 1/2( DBP)
C. MAP = DBP + 1/3(SBP-DBP)
D. MAP = SBP - 1/3(DBP)
E. MAP = DBP + 1/2(SBP-DBP)

Answer 62

MAP = DBP + 1/3(SBP-DBP)

Discussion:
Mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle
(systole and diastole). MAP is influenced by cardiac output and systemic vascular resistance. The
most commonly used formula to estimate MAP is: MAP = DBP + 1/3(SBP-DBP), where SBP =
systolic blood pressure and DBP = diastolic blood pressure.
References:
1. Rogers G, Oosthuyse T. A comparison of the estimate of mean arterial pressure calculated by
the conventional equation and calculated to compensate for a change in heart rate. Int J Sports
Med. 2000 Feb;21(2):90-5. 2. https://www.ncbi.nlm.nih.gov/books/NBK538226

Question 63

A 60-year-old man is admitted to the intensive care unit after sustaining an inoperative closed
head injury in a motor vehicle collision. Laboratory studies show an increased serum creatinine
level, muddy brown casts in urine sediment, and an increased fractional excretion of sodium.
Which of the following is the most likely diagnosis?
Answers:
A. Kidney laceration
B. Acute bladder obstruction
C. Dehydration
D. Cerebral salt wasting
E. Acute tubular necrosis

Answer 63

Acute tubular necrosis

Discussion:
Muddy brown epithelial casts in the urine are pathognomonic for acute tubular necrosis (ATN). The
casts form when either ischemia or toxins cause damage to the epithelial cells of the renal tubules
causing them to slough off and form casts in the renal tubule. The casts are then eventually
excreted into the urine. ATN can be caused by ischemia (usually due to shock) or toxins.
The fractional excretion of sodium is the percentage of sodium that is excreted into the urine
during renal filtration. Intrinsic kidney failure such as ATN will result in an increased FENa as
sodium recovery in the renal tubule is impaired. Extrinsic causes of renal failure such as
dehydration or acute bladder obstruction will typically have a low FENa, at least in the acute
phase. A kidney laceration would cause blood in the urine. Cerebral salt wasting can be caused by
a closed head injury and may be associated with an elevated FENa. The cause of CSW is not well
understood but has been attributed to perturbations in the sympathetic nervous system or the
release of BNP. It is not, however, a kidney injury in itself and is not associated with casts in the
urine unless there is secondary injury to the kidney due to severe hypovolemia.
References:
Green GB, Harris IS, Lin GA, Moylan KC (eds.). The Washington Manual of Medical Therapeutics.
31st ed. Philadelphia: Lippincott Williams and Wilkins, 2004; pp 252-260.
Kanbay, Mehmet, Benan Kasapoglu, and Mark A. Perazella. 2010. “Acute Tubular Necrosis and
Pre-Renal Acute Kidney Injury: Utility of Urine Microscopy in Their Evaluation- a Systematic
Review.” International Urology and Nephrology 42 (2): 425–33

Question 64

A 26-year-old man presents with severe headaches and new-onset seizures. MR image of the
brain shows a superior sagittal sinus thrombosis and a small right parietal hemorrhagic venous
infarction causing minimal mass effect. The patient is lethargic but easily arousable, and follows
complex commands on the right. Which of the following is the most appropriate initial management
strategy?
Answers:
A. Mannitol and serial imaging.
B. Craniotomy and evacuation of the hematoma.
C. Ventriculostomy.
D. Transvenous endovascular thrombectomy.
E. Intravenous anticoagulation

Answer 64

Intravenous anticoagulation

Discussion:
This patient has had a hemorrhagic venous infarction due to thrombosis of the superior sagittal
sinus. Seizures are a common presenting symptom of intracranial hemorrhage. Current AHA/ASA
guidelines suggest intravenous anticoagulation as the initial management strategy of venous sinus
thrombosis, even in the presence of intracranial hemorrhage. Mannitol is probably not indicated in
this patient has there is little mass effect and dehydration may precipitate further thrombosis. This
patient is not suffering from significant mass effect, so clot evacuation is not indicated and would
delay the administration of anticoagulation. The patient is arousable and does not have
hydrocephalus, therefore CSF drainage and invasive ICP monitoring via a ventriculostomy are not
indicated. Transvenous endovascular thrombectomy can be considered in patients who are
refractory to medical management or perhaps to patients who present in extremis, but is not
typically first line therapy.
References:
Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with
stroke and transient ischemic attack: a guideline for healthcare professionals from the American
Heart Association/American Stroke Association. Stroke. 2014 Jul;45(7):2160-236. Epub 2014 May
1.
Saposnik, Gustavo, Fernando Barinagarrementeria, Robert D. Brown Jr, Cheryl D. Bushnell, Brett
Cucchiara, Mary Cushman, Gabrielle deVeber, Jose M. Ferro, Fong Y. Tsai, and American Heart
Association Stroke Council and the Council on Epidemiology and Prevention. 2011. “Diagnosis and
Management of Cerebral Venous Thrombosis: A Statement for Healthcare Professionals from the
American Heart Association/American Stroke Association.” Stroke; a Journal of Cerebral
Circulation 42 (4): 1158–92