MED MISCCertified-in-NeuroCritical-Care-ABEM-(NCC)

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) ...

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 resuscitatedùa 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 ôautotransfusion,ö 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 patientí»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 35íÒC (95íÒF) is associated with sinus tachycardia. As the core body temperature drops further (<90íÒF or 32íÒC), 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 86íÒF or 30íÒC. 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 patientÆs 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 C5ûC6 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. Millerû Fisher syndrome is a demyelinating cranial and peripheral neuropathy, which is a variant of GuillainûBarrÚ 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 patientÆs condition? A. MillerûFisher 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. Millerû Fisher syndrome is a demyelinating cranial and peripheral neuropathy, which is a variant of GuillainûBarrÚ 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.