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Certified in NeuroCritical Care (ABEM) Exam Dumps

NCC Exam Format | Course Contents | Course Outline | Exam Syllabus | Exam Objectives

The following are specific diseases, conditions, and clinical syndromes commonly managed by a neurointensivist:

A. Cerebrovascular Diseases

1. Infarction and ischemia

• Massive hemispheric infarction

• Basilar artery occlusion and stenosis

• Carotid artery occlusion and stenosis

• Crescendo TIAs

• Occlusive vasculopathies (Moya-Moya, sickle cell)

• Spinal cord infarction

2. Intracerebral hemorrhage

• Supratentorial

• Cerebellar

• Brainstem

• Intraventricular

3. Subarachnoid hemorrhage - aneurysmal and other Vascular malformations

• Arteriovenous malformations

• AV fistulas

• Cavernous malformations

• Developmental venous anomalies

4. Dural sinus thrombosis

5. Carotid-cavernous fistulae

6. Cervical and cerebral arterial dissections

B.Neurotrauma

1. Traumatic brain injury

• "Diffuse axonal injury"

• Epidural hematoma

• Subdural hematoma

• Skull fracture

• Contusions and lacerations

• Penetrating craniocerebral injuries

• Traumatic subarachnoid hemorrhage

2. Spinal cord injury

• Traumatic injury (transection, contusion, concussion)

• Vertebral fracture and ligamentous instability

C. Disorders, Diseases, Seizures, and Epilepsy

1 . Seizures and epilepsy

• Status epilepticus (SE) Convulsive

Non-convulsive (partial-complex and "subtle" secondarily generalized SE) Myoclonic

2. Neuromuscular diseases

• Myasthenia gravis

• Guillain-Barre syndrome

• ALS

• Rhabdomyolysis and toxic myopathies

• Critical illness myopathy and neuropathy

3. Infections

• Encephalitis (viral, bacterial, parasitic)

• Meningitis (viral, bacterial, parasitic)

• Brain and spinal epidural abscess

4. Toxic-metabolic disorders

• Neuroleptic malignant syndrome/malignant hyperthermia

• Serotonin syndrome

• Drug overdose and withdrawal (e.g., barbiturates, narcotics, alcohol, cocaine, acetaminophen).

• Temperature related injuries (hyperthermia, hypothermia)

5. Inflammatory and demyelinating diseases

• Multiple sclerosis (Marburg variant, transverse myelitis)

• Neurosarcoidosis

• Acute disseminated encephalomyelitis (ADEM)

• CNS vasculitis

• Chemical or sterile meningitis (i.e. posterior fossa syndrome, NSAID induced)

• Central pontine myelinolysis

• Others

6. Neuroendocrine disorders

• Pituitary apoplexy

• Diabetes insipidus (including triple phase response)

• Panhypopituitarism

• Thyroid storm and coma

• Myxedema coma

• Addisonian crisis

D. Neuro-oncology

1 . Brain tumors and metastases

2. Spinal cord tumors and metastases

3. Carcinomatous meningitis

4. Paraneoplastic syndromes

E.Encephalopathies

1. Eclampsia, including HELLP Syndrome

2. Hypertensive encephalopathy

3. Hepatic encephalopathy

4. Uremic encephalopathy

5. Hypoxic-ischemic and anoxic encephalopathy

6. MELAS

F.Clinical syndromes

1.Coma

2. Herniation syndromes with monitoring & ICP

3. Elevated intracranial pressure and Intracranial hypotension/hypovolemia

4. Hydrocephalus detection & treatment

5. Cord compression

6. Death by neurologic criteria, end of life issues, and organ donation

7. Vegetative state

8. Dysautonomia (cardiovascular instability, central fever, hyperventilation)

9. Reversible posterior leukoencephalopathy

10. Psychiatric emergencies (psychosis)

G. Perioperative Neurosurgical Care

H.Pharmacotherapeutics

II. General Critical Care: Pathology, Pathophysiology, and Therapy

A. Cardiovascular Physiology, Pathology, Pathophysiology, and Therapy

1. Shock (hypotension) and its complications (vasodilatory and cardiogenic)

2. Myocardial infarction and unstable coronary syndromes

3. Neurogenic cardiac disturbances (ECG changes, stunned myocardium)

4. Cardiac rhythm and conduction disturbances; use of antiarrhythmic medications; indications for and types of
pacemakers

5. Pulmonary embolism

6. Pulmonary edema: cardiogenic versus noncardiogenic (including neurogenic)

7. Acute aortic and peripheral vascular disorders (dissection, pseudoaneurysm)

8. Recognition, evaluation and management of hypertensive emergencies and urgencies

9. Calculation of derived cardiovascular parameters, including systemic and pulmonary vascular resistance,
alveolararterial gradients, oxygen transport and consumption

B.Respiratory Physiology, Pathology, Pathophysiology and Therapy

1.Acute respiratory failure

• Hypoxemic respiratory failure (including ARDS)

• Hypercapnic respiratory failure

• Neuromuscular respiratory failure

2. Aspiration

3. Bronchopulmonary infections

4. Upper airway obstruction

5. COPD and status asthmaticus, including bronchodilator therapy

6. Neurogenic breathing patterns (central hyperventilation, Cheyne-Stokes respirations)

7. Mechanical ventilation

• Positive pressure ventilation (BIPAP)

• PEEP, CPAP, inverse ratio ventilation, pressure support ventilation, pressure control, and non- invasive ventilation

• Negative pressure ventilation

• Barotrauma, airway pressures (including permissive hypercapnia)

• Criteria for weaning and weaning techniques

8. Pleural Diseases

• Empyema

• Massive effusion

• Pneumothorax

9. Pulmonary hemorrhage and massive hemoptysis

10. Chest X-ray interpretation

11. End tidal C02 monitoring

12. Sleep apnea

13. Control of breathing

C. Renal Physiology,Pathology, Pathophysiology and Therapy

1.Renal regulation of fluid and water balance and electrolytes

2.Renal failure: Prerenal, renal, and postrenal

3.Derangements secondary to alterations in osmolality and electrolytes

4. Acid-base disorders and their management

5.Principles of renal replacement therapy

6. Evaluation of oliguria and polyuria

7.Drug dosing in renal failure

8. Management of rhabdomyolysis

9. Neurogenic disorders of sodium and water regulation (cerebral salt wasting and SIADH).

D. Metabolic and Endocrine Effects of Critical Illness

1. Enteral and parenteral nutrition

2. Endocrinology

• Disorders of thyroid function (thyroid storm, myxedema coma, sick euthyroid syndrome)

• Adrenal crisis

• Diabetes mellitus

Ketotic and hyperglycemic hyperosmolar coma Hypoglycemia

3. Disorders of calcium and magnesium balance

4. Systemic Inflammatory Response Syndrome (SIRS)

5. Fever, thermoregulation, and cooling techniques

E.Infectious Disease Physiology, Pathology, Pathophysiology and Therapy

1. Antibiotics

• Antibacterial agents

• Antifungal agents

• Antituberculosis agents

• Antiviral agents

• Antiparasitic agents

2. Infection control for special care units

• Development of antibiotic resistance

• Universal precautions

• Isolation and reverse isolation

3. Tetanus and botulism

4. Hospital acquired and opportunistic infections in the critically ill

5. Acquired Immune Deficiency Syndrome (AIDS)

6. Evaluation of fever in the ICU patient

7. Central fever

8. Interpretation of antibiotic concentrations, sensitivities

F.Physiology, Pathology, Pathophysiology and therapy of Acute Hematologic Disorders

1 . Acute defects in hemostasis

• Thrombocytopenia, thrombocytopathy

• Disseminated intravascular coagulation

• Acute hemorrhage (GI hemorrhage, retroperitoneal hematoma)

• Iatrogenic coagulopathies (warfarin and heparin induced)

2. Anticoagulation and fibrinolytic therapy

3. Principles of blood component therapy (blood, platelets, FFP)

4. Hemostatic therapy (vitamin K, aminocaproic acid, protamine, factor VIla)

5. Prophylaxis against thromboembolic disease

6. Prothrombotic states

G. Physiology, Pathology, Pathophysiology and Therapy of Acute Gastrointestinal (GI) and Genitourinary (GU)

Disorders

1. Upper and lower gastrointestinal bleeding

2. Acute and fulminant hepatic failure (including drug dosing)

3. Ileus and toxic megacolon

4. Acute perforations of the gastrointestinal tract

5. Acute vascular disorders of the intestine, including mesenteric infarction

6. Acute intestinal obstruction, volvulus

7. Pancreatitis

8. Obstructive uropathy, acute urinary retention

9. Urinary tract bleeding

H. Immunology and Transplantation

1. Principles of transplantation (brain death, organ donation, procurement, maintenance of organ donors, implantation)

2. Immunosuppression, especially the neurotoxicity of these agents

I. General Trauma and Burns

1. Initial approach to the management of multisystem trauma

2. Skeletal trauma including the spine and pelvis

3. Chest and abdominal trauma - blunt and penetrating

4. Burns and electrical injury

J. Monitoring

1. Neuromonitoring

2. Prognostic, disease severity and therapeutic intervention scores

3. Principles of electrocardiographic monitoring

4. Invasive hemodynamic monitoring

5. Noninvasive hemodynamic monitoring

6. Respiratory monitoring (airway pressure, intrathoracic pressure, tidal volume, pulse oximetry, dead space,
compliance, resistance, capnography)

7. Metabolic monitoring (oxygen consumption, carbon dioxide production, respiratory quotient)

8. Use of computers in critical care units for multimodality monitoring

K. Administrative and Management Principles and Techniques

1. Organization and staffing of critical care units

2. Collaborative practice principles, including multidisciplinary rounds and management

3. Emergency medical systems in prehospital care

4. Performance improvement, principles and practices

5. Principles of triage and resource allocation, bed management

6. Medical economics: health care reimbursement, budget development

L. Ethical and Legal Aspects of Critical Care Medicine

1. Death and dying

2. Forgoing life-sustaining treatment and orders not to resuscitate

3. Rights of patients, the right to refuse treatment

4. Living wills, advance directives; durable power of attorney

5. Terminal extubation and palliative care

6. Rationing and cost containment

7. Emotional management of patients, families and caregivers

8. Futility of care and the family in denial

M. Principles of Research in Critical Care

1. Study design

2. Biostatistics

3. Grant funding and protocol writing

4. Manuscript preparation

5. Presentation preparation and skills

6. Institutional Review Boards and HIPAA

Ill. Procedural Skills

A. General Neuro-Critical Care

1 . Central venous catheter placement; dialysis catheter placement

2. Pulmonary artery catheterization

3. Management of mechanical ventilation, including CPAP/BiPAP ventilation

4. Administration of vasoactive medications (hemodynamic augmentation and hypertension lysis)

5. Maintenance airway and ventilation in nonintubated, unconscious patients

6. Interpretation and performance of bedside pulmonary function tests

7. Direct laryngoscopy

8. Endotracheal intubation

9. Shunt and ventricular drain tap for CSF sampling

10. Performance and interpretation of transcranial Doppler

11. Administration of analgosedative medications, including conscious sedation and barbiturate anesthesia

12. Interpretation of continuous EEG monitoring

13. Interpretation and management of ICP and CPP data

14. Jugular venous bulb catheterization

15. Interpretation of Sjv02 and Pbt02 data

16. Management of external ventricular drains

I 7. Management of plasmapheresis and IVIG

18. Administration of intravenous and intraventricular thrombolysis

19. Interpretation of CT and MR standard neuroimaging and perfusion studies and biplane contrast neuraxial
angiography

20. Perioperative and postoperative clinical evaluation of neurosurgical and interventional neuroradiology patients

21. Performance of lumbar puncture and interpretation of cerebrospinal fluid results

22. Induction and maintenance of therapeutic coma and hypothermia

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Certified in NeuroCritical Care (ABEM)
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Question: 710
A 55-year-old man, admitted with a Hunt and Hess grade 4aneurysmal subarachnoid hemorrhage (SAH), is now
post bleed day5 with increasing Transcranial Doppler (TCD) velocities. Meanarterial pressure (MAP) is 76 mmHg
on norepinephrine 12mcg/min, up from 5 mcg/min 24 hours earlier, intracranial pressure(ICP) is 12 mmHg, and
heart rate (HR) is 110/min with sinusvolume control mechanical ventilation receiving 7 mL/kg tidalvolume (TV)
with positive end-expiratory pressure (PEEP) of 10White blood cell (WBC) count is 11,000 with a new infiltrate
onchest x-ray (CXR); and serum creatinine has increased to 1.5mg/dL. Fluid balance over the past 24 hours is 2 L
positive withgood urine output. In addition to sending blood cultures, lactate, andstarting antibiotics, how can
volume status be assessed to determinewhether additional fluid is needed for adequate resuscitation?
A. Bolus 2 L normal saline (NS) over 2 hours and assess change in
B. Perform a straight leg raise and assess for change in cardiac
C. Place a Swan-Ganz catheter given the presence of shock and
D. Measure inferior vena cava size change during inspiration and
E. Insert arterial line and measure pulse pressure or stroke volume
G. mmHArterial blood gas (ABG) reveals a PaO2/FiO2 ratio of 250.
Answer: B
Explanation:
Our patient is in septic shock, which requires timely acquisition of cultures, lactic acid, initiating antibiotics, and
fluid resuscitation. This question is focused on how to best determine whether a patient in shock has been
adequately resuscitated�a critical question, since too little fluid leads to inadequate preload, reduced cardiac output
(CO) and oxygen delivery, and consequently tissue hypoperfusion. Conversely, excessive volume loading, without
further increase in CO, would lead to hemodilution and tissue edema. Fluid overload has been associated with
worse outcomes in critically ill patients, and current guidelines recommend frequent assessment for ongoing need
for resuscitation prior to fluid administration. Fluid responsiveness can be assessed by several methods. Traditional
static measures of cardiac preload, such as central venous pressure (CVP) and pulmonary capillary wedge pressure
(PCWP) are unreliable for predicting fluid responsiveness. Dynamic measures of cardiac preload, such as stroke
volume variation (SVV) and pulse pressure variability (PPV) require an arterial line, and are excellent measures of
volume responsiveness in shock patients - with some notable exceptions: spontaneous respiration; tidal volume
(TV) <8 mL/kg; PEEP >5; low lung compliance (i.e., ARDS); and when arrhythmias are present. Our patient was
spontaneously breathing, limiting the diagnostic accuracy of SVV/PPV. Variation in inferior vena caval size during
mechanical ventilation, as measured by echocardiography, is another means of assessing fluid responsiveness, but
seems to be less sensitive and specific than SVV/PPV, with similar limitations. A third technique involves an
�autotransfusion,� by passively raising the legs to 40 degrees in a supine patient, which has been shown to be a
sensitive and specific assessment for volume responsiveness, potentially even in spontaneously breathing patients,
during low-tidal ventilation, and with cardiac arrhythmia.
Question: 711
An 18-year-old man admitted to the hospital with a gunshot woundto the head and intractable intracranial
hypertension is being deescalatedfrom hyperosmolar therapy with hypertonic saline andpotassium is 2.0 mEq/L,
despite having received approximately 120mEq of potassium chloride in replacement that day, and the urineoutput
has been consistently greater than 200 mL/hour. Additionalpertinent labs include Na 153 mEq/L, Mg 1.5 mEq/L,
and HCO3 20mEq/L. You notice a change on the telemetry monitor and order aabnormality?
A. Acute myocardial infarction (MI)
B. Acute pulmonary embolism
C. Hypokalemia
D. Acidosis
E. Hypothermia
G. stat ECWhat is the likely cause of this
Answer: C
Explanation:
These ECG changes are typically seen with severe refractory hypokalemia. The earliest ECG changes associated
with hypokalemia are a decrease in T-wave amplitude followed by a ST segment depression and T-wave
inversions. Subsequently, the PR interval may be prolonged with an increase in amplitude of the P wave. U waves
(a positive deflection after the T wave) may be seen and in severe hypokalemia may fuse with the T wave to form
giant U waves as seen in the ECG. A pseudo-prolonged QT interval may be seen, which is actually a QU interval
in the absence of a T wave. The most common cause of hypokalemia is renal losses after diuretic use (more
commonly thiazide than loop or osmotic diuretics), especially if two diuretics acting on different parts of the
tubular system are used. Patients who develop secondary hypoaldosteronism from liver disease, congestive heart
failure (CHF), or nephrotic syndrome are also at risk. Antibiotics such as penicillins and aminoglycosides can
promote potassium loss. In the neurocritical care setting, patients receiving mannitol or hypertonic saline infusions
have been noted to develop hypokalemia because of the diuretic effect and as a consequence of the high-sodium
load reaching the collecting ducts. For this reason some centers use potassium-sparing diuretics in conjunction with
mannitol to avoid symptomatic hypokalemia in the setting of intracranial pressure (ICP) management. Hypokalemia
can be refractory if concomitant hypomagnesaemia is not corrected. The exact etiology of this is not known, but it
may be multifactorial. Low intracellular magnesium levels may increase potassium wasting from the collecting
tubules, especially in the setting of additional factors such as an increase in distal sodium delivery. ECG changes in
hypomagnesemia include an increased PR and QT interval, widened QRS complex, and flattened T wave. The
findings can be identical to those seen in hypokalemia; however, in this case, the patient��s potassium level is
much lower than his magnesium level and, given the refractory nature of his disease, hypokalemia is the more
likely cause. Hypothermia at 35��C (95��F) is associated with sinus tachycardia. As the core body temperature
drops further (<90��F or 32��C), sinus bradycardia with prolongation of PR interval, QRS widening, and QT
interval are seen. Osborn waves (an upward deflection after the QRS complex) are seen below 86��F or 30��C.
Question: 712
A 44-year-old morbidly obese woman with hypertension anddiabetes is found slumped over in a bathroom stall. At
the scene, herblood pressure (BP) is documented at 180/90 with a pulse of 78; herblood sugar is 180 mmol/L. CT
scan of the head is shown. What isthe likely cause of this patient�s findings?
A. Hypertensive intracerebral hemorrhage (ICH)
B. Embolic stroke with hemorrhagic conversion
C. Venous sinus thrombosis
D. Aneurysmal subarachnoid hemorrhage (SAH)
E. Hemorrhagic encephalitis
Answer: D
Explanation:
This axial CT scan of the head shows an intraparenchymal hemorrhage (IPH) with a sylvian SAH and a small
subdural hematoma (SDH), with the outline of an aneurysm visible lateral to the IPH. Approximately 20% of
patients with aneurysmal rupture have associated IPH, occurring more commonly in patients with anterior
communicating artery (AComm), distal anterior cerebral artery, and distal middle cerebral artery (MCA)
aneurysms. These patients present with callosal, interhemispheric, and sylvian/temporal hematomas. In addition,
patients may have concurrent intraventricular hemorrhage (IVH) and SDH. Rarely, patients may present with IPH,
IVH, or SDH without any evidence of SAH. In these cases, a history of thunderclap headache, absence of risk
factors for IPH or IVH, and absence of a history of trauma should raise the suspicion of a saccular aneurysm.
Likely causes of the absence of SAH are the location of the dome of the aneurysm close to the ventricular system
or brain parenchyma and delayed presentation after the hemorrhage, with radiographic resolution of subarachnoid
blood. Another theory is that the IPH/IVH may represent a rebleed after the subarachnoid space has been scarred
down by a sentinel hemorrhage.
Question: 713
A 29-year-old C5�C6 quadriplegic patient is being prepared fortransfer to a rehabilitation facility when you are
paged for with thecondition?
A. Permanent pacemaker
B. PRN intravenous (IV) atropine
C. PO albuterol
D. PO theophylline
E. All of the above
G. following findinWhat is an appropriate long-term therapy for this
Answer: E
Explanation:
Patients with acute spinal cord injury suffer a myriad of complications of which pulmonary and cardiac are the
most common. Among the cardiac complications, shock and hypotension occur early and are usually the reason for
ICU admission in the first week after injury. Sinus bradycardia, dysrhythmia, and cardiac arrest can occur
subsequently, usually within the first 14 days after injury. Acute spinal cord injury above T6 can disrupt the
descending sympathetic pathways to the intermediolateral cell column in the T1-L2 spinal cord. This results in loss
of supraspinal sympathetic control and unopposed parasympathetic activity in the respiratory and cardiac systems
in quadriplegic patients, making them prone to prolonged episodes of bradycardia, pauses, and intermittent heart
blocks, especially when suctioned or turned. Atropine should be readily available for patients with bradycardia, and
0.5 to 1 mg should be administered when symptomatic or prophylactically before suctioning. Oral albuterol and
theophylline can be used to increase resting heart rate, although there are no randomized trials to support this. Some
patients with significant heart block or recurrent cardiac arrests may require a permanent pacemaker.
Question: 714
Answer: C
Explanation:
The history of ovarian cancer and the diffuse leptomeningeal enhancement are suggestive of meningeal
carcinomatosis. Meningeal carcinomatosis is seen in 1% to 5% of patients with solid tumors (commonly breast,
nonsmall-cell lung cancer, and melanoma), 5% to 15% of patients with leukemia/lymphoma
(leukemic/lymphomatous meningitis), and 1% to 2% of patients with primary brain tumors. Neurologic symptoms
usually localize to several regions of the neuraxis, with those involving the spinal cord and cauda equina being
most common, followed by cranial neuropathies and hemispheric dysfunction. Patients often present with signs of
hydrocephalus and elevated intracranial pressures (ICP). Diagnosis is made by having a high index of suspicion,
meningeal enhancement (often most prominent in the basal meninges, dorsal spinal column, and cauda equina),
cerebrospinal fluid (CSF) monocytosis, and isolating tumor cells in CSF on cytology. Although the latter is the
gold standard, tumor cells are isolated in only 50% of samples on the first LP, with the yield increasing to 80% on
the second puncture. There is no added benefit of subsequent LPs. Treatment is mostly palliative, with median
survival of 2 to 3 months. Whole brain radiation therapy and intrathecal chemotherapy are the mainstays of
treatment and may prevent further neurologic deterioration and improvement in quality of life. Supportive
treatments such as antiepileptic medications, pain medications, and occasionally corticosteroids in patients with
concomitant parenchymal disease should be prescribed. Miller� Fisher syndrome is a demyelinating cranial and
peripheral neuropathy, which is a variant of Guillain�Barr� syndrome (GBS) and is defined by a triad of areflexia,
ophthalmoplegia, and ataxia. Patients classically do not have signs of encephalitis or encephalopathy. Anti-GQ1b
antibodies are present in 90% of patients. Bickerstaff brainstem encephalitis presents with ataxia, ophthalmoplegia,
hyperreflexia, and alteration of consciousness. Hyperintense lesions are seen in the midbrain, pons, and medulla on
MRI. A significant number of patients have evidence of concurrent axonal GBS, suggesting that this may be
another variant of the disease. The progression of symptoms and MRI findings preclude pontine infarction, and the
EEG does not support a diagnosis of NCSE.
Question: 715
A 67-year-old woman was transferred from an outside facility withoutside hospital with complaints of nausea,
vomiting, ataxia, andprogressive lethargy. The patient had a history of ovarian cancer inremission for 3 years and
was otherwise healthy. CT scan and MRIblood cell (WBC) count of 15 (40% N, 20% L, and 40% M), redblood
cell (RBC) count 250, glucose 40, and protein 100. Allbacterial and viral cultures and polymerase chain reactions
(PCRs)were negative, and she was empirically treated with acyclovir. Uponyour evaluation, the patient was
comatose with sluggish pupillaryresponse, dysconjugate gaze, absent oculocephalic reflexes,extensor posturing
bilaterally, and brisk reflexes. She was breathingrepeated and showed WBC 18 (100% M), RBC 50, glucose 28,
andprotein 150. Serum glucose was 150 mg/dL. EEG revealedgeneralized delta and theta activity without
rhythmicity. Brain MRIwith contrast is shown on the right. What is the most likely cause ofthe patient�s
condition?
A. Miller�Fisher syndrome
B. Bickerstaff brainstem encephalitis
C. Meningeal carcinomatosis
D. Pontine infarction
E. Nonconvulsive status epilepticus (NCSE)
Answer: C
Explanation:
The history of ovarian cancer and the diffuse leptomeningeal enhancement are suggestive of meningeal
carcinomatosis. Meningeal carcinomatosis is seen in 1% to 5% of patients with solid tumors (commonly breast,
nonsmall-cell lung cancer, and melanoma), 5% to 15% of patients with leukemia/lymphoma
(leukemic/lymphomatous meningitis), and 1% to 2% of patients with primary brain tumors. Neurologic symptoms
usually localize to several regions of the neuraxis, with those involving the spinal cord and cauda equina being
most common, followed by cranial neuropathies and hemispheric dysfunction. Patients often present with signs of
hydrocephalus and elevated intracranial pressures (ICP). Diagnosis is made by having a high index of suspicion,
meningeal enhancement (often most prominent in the basal meninges, dorsal spinal column, and cauda equina),
cerebrospinal fluid (CSF) monocytosis, and isolating tumor cells in CSF on cytology. Although the latter is the
gold standard, tumor cells are isolated in only 50% of samples on the first LP, with the yield increasing to 80% on
the second puncture. There is no added benefit of subsequent LPs. Treatment is mostly palliative, with median
survival of 2 to 3 months. Whole brain radiation therapy and intrathecal chemotherapy are the mainstays of
treatment and may prevent further neurologic deterioration and improvement in quality of life. Supportive
treatments such as antiepileptic medications, pain medications, and occasionally corticosteroids in patients with
concomitant parenchymal disease should be prescribed. Miller� Fisher syndrome is a demyelinating cranial and
peripheral neuropathy, which is a variant of Guillain�Barr� syndrome (GBS) and is defined by a triad of areflexia,
ophthalmoplegia, and ataxia. Patients classically do not have signs of encephalitis or encephalopathy. Anti-GQ1b
antibodies are present in 90% of patients. Bickerstaff brainstem encephalitis presents with ataxia, ophthalmoplegia,
hyperreflexia, and alteration of consciousness. Hyperintense lesions are seen in the midbrain, pons, and medulla on
MRI. A significant number of patients have evidence of concurrent axonal GBS, suggesting that this may be
another variant of the disease. The progression of symptoms and MRI findings preclude pontine infarction, and the
EEG does not support a diagnosis of NCSE.
Question: 716
A 60-year-old patient with diabetes and hypertension is transferredto your ICU from another facility, where he was
being treated forurosepsis. The patient has been on stable, low-dose vasopressors for4 days, is on antibiotics, and
appears adequately volumenot received nutrition since his admission to the hospital 5 days agobecause he was on
vasopressors. You would:
A. Insert a feeding tube and advance to full dose tube feeds despite
B. Order total parenteral nutrition (TPN)
C. Order peripheral parenteral nutrition (PPN)
D. Start a dextrose solution�it should provide enough calories!
E. Start trophic feeds through the gut at 10 to 20 mL/hour while he
Answer: A
Explanation:
Initiation of enteral nutrition (EN) in critically ill patients is not always clear cut. It is preferable to use EN in
critically ill patients as it reduces infectious complications, promotes enterocyte health while maintaining a strong
mucosal barrier, and has a lesser stress response than parenteral nutrition (PN). However, there is concern that
initiating EN in a patient with hemodynamic compromise and possible splanchnic vasoconstriction may promote
nonocclusive mucosal ischemia (NOMI) due to increased oxygen demand. Turza et al. recommend a four-stage
approach to initiating EN in patients requiring vasopressors: a. Evaluate the patient�s medical and nutritional
history. Patients with multiple vascular risk factors may be predisposed to NOMI, while those with poor nutritional
response or high metabolic demand will benefit from early nutrition. b. Evaluate the current physiologic state.
Low-dose, nonescalating vasopressors in patients who are volume resuscitated and able to maintain a mean arterial
pressure (MAP) greater than 60 should not deter the initiation of EN. Alternately, patients with dropping urine
output, worsening lactate levels, and base deficit and those requiring frequent transfusions may not be able to
tolerate EN. c. Establish gastrointestinal (GI) access and pick appropriate tube feeds. The use of formulas with
lower osmolarity (<700 mOsm) and fiber content and simpler sugars will reduce metabolic demands, improve
transit time, and reduce dysmotility, thereby alleviating factors which may result in the bacterial overgrowth that
worsens NOMI. d. Postinitiation monitoring includes serial abdominal examinations and gastric residual checks.
Laboratory monitoring of lactate, white blood cell counts, and hemoglobin levels or radiologic testing may be
performed if there is concern for ileus. At times, a combination of trophic EN and supplemental PN is adopted as
an intuitive compromise. This has been shown to increase the risk of nosocomial infections in a retrospective
review of trauma patients.
Question: 717
A 40-year-old woman is admitted to the hospital after witnessedcardiac arrest for 20 minutes. Bystanders
performed CPR untilwas initiated after admission to the hospital, and the patient wasnoted to have frequent
myoclonic jerks during rewarming.Brainstem reflexes were intact and the patient had flexor posturingto painful
stimulation. MRI brain revealed scattered diffusionweightedimaging changes in the cortex but no damage to the
deepstructures. EEG was performed and is shown in the following
A. Have a family discussion regarding irreversible brain damage
B. Load with an antiepileptic agent until myoclonic jerks stop since
C. Continue EEG monitoring and titrate antiepileptic agents until
D. Load with antiepileptic drugs until clinical myoclonus stops and
E. Recool the patient and rewarm more slowly next time
Answer: C
Explanation:
The EEG is consistent with postanoxic status epilepticus (PSE). Although this diagnosis usually portends a poor
prognosis, the administration of therapeutic hypothermia (TH) to postcardiac arrest patients has made the prediction
of outcomes based on American Academy of Neurology (AAN) criteria more difficult. In a prospective study by
Rossetti et al., three clinical variables were demonstrated to have higher false-positive rates compared to the AAN
guidelines: incomplete brainstem reflexes, myoclonus, and absent motor responses to pain. Early lack of reactivity
on continuous EEG, prolonged periods of discontinuity, epileptiform discharges or seizures, and absent cortical
responses on somatosensory evoked potentials (SSEP) were strongly associated with mortality. PSE is
independently associated with a poor outcome after anoxic injury. However, in the presence of brainstem reflexes,
SSEP responses, and EEG reactivity can have a favorable outcome if the condition is treated as status epilepticus
(SE).
Question: 718
A 60-year-old woman with a history of hypertension presented witha cerebellar intraparenchymal hemorrhage
(IPH), fourth ventricleintraventricular hemorrhage (IVH), hydrocephalus with partialbrainstem dysfunction, and
somnolence on examination. She wasemergently taken for surgical decompression and did well. Aconventional
angiogram was subsequently performed and is shownin the following images. Your next steps in management
include allof the following, except:
A. Wean external ventricular drain (EVD) and tightly control blood
B. Use intrathecal tissue plasminogen activator (tPA) to allow quick
C. Take a detailed family history
D. Send genetic testing
E. Continue outpatient, staged management of this condition
Answer: B
Explanation:
The patient has multiple arteriovenous malformations (AVMs) warranting a detailed family history and genetic
workup. Intrathecal tPA is contraindicated in this setting. Intracranial vascular malformations include
developmental venous anomalies (DVA), capillary telangiectasias, AVM, and cavernous malformations, each of
which have different natural histories and treatment options. � Capillary telangiectasias are usually
angiographically occult lesions, detected incidentally on contrast-enhanced MRI or CT scans, and are rarely
symptomatic. They are benign, thin-walled capillaries surrounded by normal brain parenchyma, do not need
treatment or follow-up, and account for 4% to 12% of all vascular malformations. De novo development has been
reported. � DVA also known as venous angiomas are congenitally enlarged, thickened, hyalinized venous vessels
draining normal brain tissue. They are the most common intracranial vascular malformation, with a prevalence of
2.5%, discovered mostly incidentally and often associated with cavernous malformations. A causative link between
the two has been suggested, with DVAs being a precursor to cavernous malformations. DVAs can be detected on
MRI, CT scan, and angiogram as a single dilated vein or caput medusa. They usually have a benign clinical course
with low morbidity and mortality and do not warrant treatment. � AVMs are a collection of abnormal blood
vessels, comprising arteries, veins, and an intervening collection of abnormal vessels called the nidus. They are
congenital lesions with an incidence of 1 per 100,000, often presenting as an intracerebral hemorrhage (ICH) in the
third to fourth decade. The bleeding risk varies according to size, location, draining pattern, and so on. Magnetic
resonance angiography (MRA) and CT angiography (CTA) can both visualize AVMs; however, conventional
angiography remains the gold standard for diagnoses, formulation, and implementation of a treatment plan which
may include a combination of surgery, embolization, and radiation therapy. � Cavernous malformations are
acquired or congenital lesions formed by endothelium-lined vascular spaces without intervening brain parenchyma.
They can be seen on CT and MRI as �popcorn�-shaped dystrophic calcifications or hemosiderin deposits from
prior hemorrhages. They are angiographically occult and most commonly present with seizures. Treatment is not
always warranted, but surgical resection is often necessary if associated with recurrent hemorrhages or intractable
epilepsy. � Dural arteriovenous fistulas are malformations located in the meninges fed by dural arteries and drained
by dural or leptomeningeal venous channels. The most common location is the transverse sinus. They can develop
after trauma, venous thrombosis, or spontaneously, and account for 10% to 15% of all cranial malformations.
Clinical presentation includes headache, neurologic deficits, bruits, and hemorrhage, with a cortical drainage
pattern consistent with more aggressive behavior. Sixvessel cerebral angiogram remains the gold standard in
diagnosing a fistula. Treatment includes endovascular or surgical interventions, with surgery being the more
definitive approach.
Question: 719
A 35-year-old, 2 days postpartum woman had sudden onset of thethe ED was 180/90, and she was somnolent but
had a nonfocalneurologic examination. Opening pressure was normal on lumbarpuncture (LP), and cerebrospinal
fluid (CSF) was clear with normalchemistries and cell count. Imaging studies are shown in thefollowing images.
What is the most likely diagnosis?
A. Eclampsia/preeclampsia
B. Posterior reversible encephalopathy syndrome (PRES)
C. Venous sinus thrombosis
D. Reversible cerebral vasoconstriction syndrome (RCVS)
E. Sheehan�s syndrome
Answer: D
Explanation:
RCVS unifies a group of disorders with similar clinical and radiographic characteristics, such as Call�Fleming
syndrome, benign angiopathy of the central nervous system (CNS), migrainous angiitis, drug-induced cerebral
angiopathy (selective serotonin reuptake inhibitors [SSRIs], marijuana), and postpartum angiopathy (hormonal
changes, serotonergic surge). Typically, patients present with a thunderclap headache with or without focal
neurologic signs, normal CSF analysis without evidence of CNS inflammation, exclusion of other causes of sudden
severe headache (aneurysm or vascular abnormalities), and presence of segmental cerebral arterial vasoconstriction
on catheter, CT, or magnetic resonance angiography (MRA), which resolves within 12 weeks. Cortical
(nonaneurysmal) subarachnoid hemorrhage (SAH) is the most common radiographic finding. The gold standard for
diagnosis is detecting the presence and subsequent resolution of segmental vasoconstriction on conventional
angiography. In most cases the vascular changes resolve without treatment. Calcium channel blockers (nimodipine,
verapamil), glucocorticoids, and intravenous (IV) magnesium have been tried with limited success. Although the
course is usually benign, severe vasospasm has been reported resulting in transient ischemic attacks (TIAs),
seizures, and ischemic and hemorrhagic infarctions. Intraarterial milrinone and verapamil as well as angioplasty
have been attempted with some success in severe or refractory cases. Preeclampsia is defined as pregnancy-induced
hypertension with proteinuria, but there is no information about urine studies in this case and the condition is not
associated with the imaging findings of cerebral vasoconstriction. Eclampsia, a life-threatening condition occurring
in pregnancy or early puerperium, is the occurrence of a tonic�clonic seizure in the setting of preeclampsia.
Treatment includes IV magnesium to a goal of 4 to 7 mEq/L (4�6 g IV loading dose, then 1�2 g/hour), BP control
with IV hydralazine or labetalol, and emergent termination of pregnancy. If the patient continues to have seizures,
the dose of magnesium may be increased (with close observation for respiratory failure or heart block). IV
anticonvulsants and mechanical ventilation can be initiated in refractory cases. PRES is characterized by headache,
confusion, seizures, and visual loss with acute subcortical and cortical edema on MRI. Although classically seen in
the parietooccipital lobes, brainstem, and cerebellum, the edema can extend as far anteriorly as the temporal and
frontal lobes. PRES can be seen in the setting of malignant hypertension, eclampsia, hypercalcemia, and due to
drugs such as tacrolimus and cyclosporine. Sheehan�s syndrome, or postpartum pituitary necrosis, is a
complication of postpartum hypovolemic shock resulting in panhypopituitarism. The most common presenting
symptom is agalactorrhea.
Question: 720
An 18-year-old G1P0 woman presented with a severe headachebehind her right ear, followed by a left-sided
tingling sensation andmonitoring and treatment while she continues to have frequentcomplex partial seizures. On
examination, she is awake, butsomnolent with left-sided hemiparesis. Imaging studies are shown
A. Eclampsia/preeclampsia
B. Posterior reversible encephalopathy syndrome (PRES)
C. Cerebral venous sinus thrombosis (CVST)
D. Reversible cerebral vasoconstriction syndrome (RCVS)
E. Sheehan�s syndrome
Answer: C
Explanation:
CVST is a rare disorder affecting 3 to 4 adults per million annually. With the increasing use of oral contraceptives
(OCP) in the past few decades, the disease has become more prevalent in adult women of child-bearing age with an
almost sixfold increase in the risk of CVST among OCP users. This is followed by patients with inherited
thrombophilia, hypercoagulability associated with pregnancy and puerperium, and head and neck infections.
Presentation is varied and dependent on the location and extent of venous involvement. Headache is a ubiquitous
presenting complaint, accompanied by seizures in 47% and paresis in 43% of patients. The majority of patients
have an indolent course with symptoms developing over days to months. Rarely, they may resemble an arterial
infarction but with a waxing and waning course. Focal edema and infarctions are often seen when cortical veins are
involved. Larger infarctions and hemorrhages are associated with worsening mental status and coma. Abnormal
signal change in the venous sinus on MRI with concomitant loss of flow on magnetic resonance venography
(MRV) is diagnostic. Treatment includes systemic anticoagulation with weight-based low molecular weight heparin
or unfractionated heparin with transition to vitamin K antagonists to a goal International Normalized Ratio (INR) of
2 to 3 for 3 to 6 months. Patients with a history of deep vein thrombosis (DVT) or recurrent CVST will need
indefinite treatment. Intraparenchymal hemorrhage (IPH) is not a contraindication to anticoagulation in this
population. Local administration of endovascular thrombolysis has been reported, but there is insufficient efficacy
or safety data available to justify its utility in patients who are not refractory to systemic anticoagulation.
Decompressive hemicraniectomy can be performed in the setting of malignant cerebral edema with reasonable
outcomes. Over 80% of the patients have favorable recovery. Mortality of 7% to 13% is seen within the first
month, usually due to cerebral edema in the acute phase or due to underlying cause on subsequent follow-up.
Question: 721
A 65-year-old alcoholic with traumatic brain injury (TBI), bifrontalcontusions, and right-sided epidural hematoma
with midline shiftand uncal herniation is admitted to your ICU. After initialdecompression, intracranial pressure
(ICP) remained within normallimits. Four days postoperatively, the patient is now off all sedationwithdraws on the
right, and flexes on the left. What is the cause of hispoor mental status?
A. Bifrontal injury
B. Diffuse axonal injury
C. Persistent effects of midline shift after initial injury
D. Nonconvulsive status epilepticus (NCSE)
E. All of the above
Answer: E
Explanation:
The patient has suffered a severe head injury with multiple contusions, cerebral edema, and herniation.
Individually, each of these conditions can result in a persistent comatose state. In addition, the patient is having
nonconvulsive focal seizures, which may be contributing to the encephalopathy. The growing recognition of
nonconvulsive seizures (NCS) in the critically ill population and the need for treatment has been a topic of debate
in recent years. Are these seizures a cause of the encephalopathy or simply a manifestation of the dying brain?
Similarly, should they be aggressively treated with the hope of resolution of coma or are they a hallmark of
irreversible brain injury and a poor prognostic sign? Although case reports supporting both arguments exist, these
questions are yet to be answered in a randomized controlled trial. Additionally, many reports of NCSE lump
together patients who are delirious with patients who are deeply comatose in the setting of NCS, making it all the
more difficult to establish prognosis. Until the availability of further evidence, the best way to approach these
situations is to look at the entire clinical picture. Aggressive treatment, with its risks, may be warranted if the
clinical picture looks worse than can be explained by the level of injury. Similarly, in the setting of a devastating
injury, administration of further sedatives to treat focal NCSE may not be worthwhile.
Question: 722
A 46-year-old man is admitted to your ICU after facial assault witha penetrating object through his orbit. You are
called to the bedsideon postop day 1 after removal of the object because the patient is insevere pain. Upon your
examination, the eye is swollen, injected,movements are difficult to assess because of pain. He has lightperception
on visual acuity, which is unchanged from the time ofpresentation. What is the most likely diagnosis?
A. Orbital cellulitis
B. Orbital hematoma
C. Cavernous sinus thrombosis
D. Carotid-cavernous fistula (CCF)
E. Orbital compartment syndrome
G. and pulsatinThe pupil is minimally reactive and extraocular
Answer: D
Explanation:
The patient has a CCF, which is an abnormal communication between the arterial and venous blood within the
cavernous sinus and is characterized by pain, chemosis, pulsatile proptosis, ocular bruit, and progressive vision
loss. The most common form of CCF is a direct communication between the internal carotid artery (ICA) and
cavernous sinus (type A) usually as a result of trauma (young males) or aneurysm rupture (older women).
Traumatic CCFs are the most common type, accounting for 75% of all CCFs, and occur in 0.2% of all head trauma
and 4% of basilar skull fractures. Conventional angiogram is the gold standard for diagnosis. Endovascular
transvenous embolization of the fistula while maintaining patency of the ICA is the mainstay of treatment, with
greater than 80% cure rates at 1 year. Symptoms of chemosis and proptosis usually resolve within hours to days of
intervention, while cranial nerve (CN) palsies may persist for a few weeks. Visual loss may or may not be reversed
depending on the degree of blindness at presentation and the underlying cause. Cavernous sinus thrombosis is a
close differential diagnosis and usually presents with ptosis, chemosis, proptosis, CN palsies, vision loss, and a
dilated, sluggishly reactive pupil. The most common etiology is infectious with direct spread from the nose,
sinuses, or teeth. Diagnosis is made by clinical findings, MRI, and magnetic resonance venography (MRV), and
treatment includes intravenous (IV) antibiotics and close monitoring for complications such as meningitis, vision
loss, sepsis, or septic emboli. Orbital cellulitis is a bacterial infection of the tissues surrounding the eye, including
eyelids, eyebrows, and cheeks, resulting in swelling of the eyelids, pain with eye movements, fever, and decreased
vision if not treated promptly. Orbital hematomas can be preseptal or postseptal. Preseptal hemorrhages are usually
posttraumatic and benign, resulting in extensive ecchymoses of the eyelids. Postseptal hemorrhages may occur due
to trauma, surgical intervention, arteriovenous malformations, or bleeding diathesis, among other causes, and can
lead to orbital compartment syndrome with increase in intraocular pressures and vision loss from orbital nerve
compression.
Question: 723
A 78-year-old man with a history of hypertension, hyperlipidemia,and mild hearing loss is brought to the hospital
by ambulance after amotor vehicle accident. He is intubated in the ED for airwayprotection and undergoes massive
blood transfusion forhemorrhagic shock. He is admitted to the ICU. Which of thefollowing reduces the risk of
delirium in the ICU?
A. Benzodiazepine-induced coma
B. Mechanical ventilation
C. Polytrauma
D. Metabolic acidosis
E. Sedation with dexmedetomidine
Answer: E
Explanation:
A systematic review identified eleven risk factors for developing delirium in the ICU. These included age,
dementia, hypertension, poly-trauma, emergency surgery prior to ICU admission, sedative-induced coma, delirium
on the day prior, use of mechanical ventilation, metabolic acidosis, multi-organ failure and APACHE II score.
Factors that were clearly associated with reduction in delirium were dexmedetomidine. It is unclear if this was a
physiological effect of the drugs itself or because dexmedetomidine use was associated with less benzodiazepine
use.
Question: 724
A 65-year-old man with a history of hypertension andhyperlipidemia is found down at home by his son at 6 p.m.
after hedoes not show up at his granddaughter�s birthday. He was last seenvital signs are blood pressure (BP)
178/92 mmHg, heart rate (HR)examination, the HR is irregularly irregular. He is awake butaphasic with right lower
facial droop and flaccid right arm. Hisinitial National Institutes of Health Stroke Scale (NIHSS) score is18. A
noncontrast CT scan of the brain shows loss of grey-whitematter differentiation in the left frontal lobe and
hypoattenuation ofCT angiogram of the head shows an occlusion of the first segmentof the middle cerebral artery
(MCA); and perfusion CT estimates aninfarct size of 28 mL. At baseline, the patient is independent withnext step
in management?
A. Start aspirin 325 mg. Patient is not eligible for either intravenous
B. Initiate IV thrombolysis with alteplase based on neuroimaging
C. Proceed with endovascular thrombectomy based on mismatch
D. Initiate IV thrombolysis with alteplase followed by endovascular
E. Need to calculate the ratio of the volume of ischemic tissues on
Answer: C
Explanation:
The patient is out of 4.5-hour time window for IV thrombolysis. However, he is a candidate for endovascular
thrombectomy based on the recent DWI or CTP Assessment with Clinical Mismatch in the Triage of Wake-Up and
Late Presenting Strokes Undergoing Neurointervention with Trevo (DAWN) trial. In this trial, patients with
occlusion of the intracranial internal carotid artery (ICA) or proximal middle cerebral artery (MCA) who had last
been known to be well 6 to 24 hours earlier and showed evidence of salvageable brain tissue were randomly
assigned to thrombectomy plus standard care (the thrombectomy group) or to standard care alone (the control
group). Enrolled patients had good premorbid baseline defined as modified Rankin scale (mRS), 0 to 1. Infarct
volume was assessed on diffusion-weighted imaging (DWI) sequence of brain MRI or perfusion CT scan using the
automated RAPID software. Presence of salvageable brain tissue was based on a mismatch between severity of
their neurological deficits and the volume of infarcted brain, and not the ratio of the volume of ischemic tissue at
risk to infarct volume: DAWN trial measured �utility-weighted mRS� at 90 days as the primary outcome. In
contrast to mRS, a lower score in �utilityweighted mRS� indicates a better outcome (ranges from 0 = death to 10 =
no deficits). At 90 days, the �utility-weighted mRS� was 5.5 for the thrombectomy group compared to 3.4 in the
control group, and 49% of patients in the thrombectomy group achieved functional independence versus only 13%
in the control group. These translate to number-to-treat (NTT) of 2 and 2.8 for less disability and functional
independence at 90 days, respectively. Rate of procedurerelated complications was very low. Serious adverse events
including mortality and stroke-related death at 90 days as well as and symptomatic intracerebral hemorrhage (ICH)
were similar between the two groups.
Question: 725
A 72-year-old woman with a past medical history of diabetes,hypertension, hyperlipidemia, and atrial fibrillation
on warfarinpresents to the ED with a new severe dysarthria, left-sidedweakness, and neglect (National Institutes of
Health Stroke Scale[NIHSS] score 17). Her vital signs are blood pressure (BP) 169/83mmHg, heart rate (HR)
87/min, respiratory rate (RR) 18/min, and1.3. She was last seen 12 hours prior to presentation. MRI of thebrain
shows an acute stroke in the territory of the right middlecerebral artery (MCA) without evidence of intracranial
hemorrhage.Infarct volume on diffusion-weighted imaging (DWI) is measured48 mL; and volume of ischemic
tissue on MRI perfusion scan iscalculated as 110 mL. Magnetic resonance angiography (MRA)treatment for her
stroke?
A. Start intravenous (IV) alteplase infusion based on clear evidence
B. Start heparin drip with a goal partial thromboplastin time (PTT)
C. Start warfarin for secondary stroke prevention
D. Immediate endovascular thrombectomy
E. Start aspirin 325 mg
Answer: D
Explanation:
The patient is not a candidate for IV alteplase as she presents out of 4.5-hour treatment time window. However, she
is a candidate for endovascular thrombectomy. In DEFUSE 3 trial, patients 6 to 16 hours after they were last
known to be well who had a proximal MCA or internal carotid artery (ICA) occlusion, an initial infarct size of less
than 70 mL, and a ratio of the volume of ischemic tissue on perfusion imaging to infarct volume of 1.8 or more
were randomly assigned to thrombectomy plus standard medical therapy (thrombectomy group) or standard
medical therapy alone (control group). Thrombectomy was associated with better functional outcomes (odds ratio,
2.77) and lower mortality (14% vs. 26% in the control group) without a difference in symptomatic intracranial
hemorrhage or serious adverse events.
Question: 726
A 70-year-old man is admitted to the neurointensive care unit foraneurysmal subarachnoid hemorrhage (SAH). He
is intubated onmechanical ventilation. On day 3 of admission, he develops septicshock. He is fluid resuscitated and
broad-spectrum antibiotics withearly and aggressive treatment, 12 hours later, he remainshemodynamically
unstable necessitating escalating doses ofnorepinephrine (>1 mg per hour) to maintain a systolic blooddecrease
vasopressor requirement and mortality in septic shock?
A. Switch antibiotics to linezolid plus meropenem
B. Add vasopressin infusion
C. Add intravenous (IV) infusion of hydrocortisone 200 mg per day
D. Add oral fludrocortisone 50 mcg daily
E. Add IV hydrocortisone 50 mg 4 times a day plus fludrocortisone
G. pressure (SBP) >90 mmHWhich intervention has been shown to
Answer: E
Explanation:
Two recent trials (ADRENAL and APROCCHSS) studied the effects of adjunctive glucocorticoid therapy and
glucocorticoid + mineralocorticoid therapy in patients with septic shock. In the former study, 3,800 patients with
septic shock who were undergoing mechanical ventilation were randomized to receive hydrocortisone (at a dose of
200 mg per day) or placebo for 7 days (or until death or discharge from the ICU). Although patients in the
hydrocortisone group had faster resolution of shock (3 days vs. 4 days in the control group), no significant
between-group difference was found in mortality. In APROCCHSS, the effect of hydrocortisone plus
fludrocortisone in patients with septic shock was compared to the placebo. Mortality was significantly lower in the
hydrocortisone-plus-fludrocortisone group than in the placebo group at ICU and hospital discharge, and at 90 and
180 days. In addition, hydrocortisone plus fludrocortisone therapy increased the number of vasopressorfree and
organ-failure-free days without increasing the rate of serious adverse events except for hyperglycemia.
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