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Category: Critical Care Medicine-Neurologic Disorders--->Neuromuscular Disorders
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Question 1# Print Question

A 51-year-old woman with antibody-positive myasthenia gravis, on immunosuppressive therapy with azathioprine, is admitted to the intensive care unit for increased work of breathing. Two weeks prior she had an upper respiratory tract infection, and when it did not improve, she was prescribed a course of levofloxacin, which she started 3 days ago. Since that time she has had a progressive dyspnea and was unable to walk up a flight of stairs. Her initial vital signs in the emergency department (ED) were normal and her oxygen saturation was 98% on room air with a respiratory rate of 24. She appeared comfortable, and although tachypneic she did not have accessory muscle use. She underwent bedside spirometry testing and was found to have a negative inspiratory force of −40 mm Hg and forced vital capacity of 0.75 L (weight 79.6 kg). An arterial blood gas was obtained in the intensive care unit and was:

  • pH 7.32
  • pCO2 32
  • pO2 171

Should this patient be intubated?

A. Yes, given her tachypnea, low-forced vital capacity, and respiratory alkalosis, she should be intubated. Intubation should be completed using a depolarizing neuromuscular blocker
B. Yes, given her tachypnea, low-forced vital capacity, and respiratory alkalosis, she should be intubated. Intubation should be completed using a nondepolarizing neuromuscular blocker
C. No, given her comfortable appearance, appropriate negative inspiratory force, and respiratory alkalosis, she should not be intubated and continue with close neurologic and respiratory monitoring
D. No, given her comfortable appearance, appropriate negative inspiratory force, and respiratory alkalosis, she should not be intubated, however, bilevel positive airway pressure support (BiPAP) should be initiated


Question 2# Print Question

A 14-year-old woman with medically intractable epilepsy presents to ED in status epilepticus. Three weeks prior, she had a “virallike illness” and had never fully returned to normal. She was having increased seizure frequency during that time. While in the ED, she was intubated for airway protection. Her workup reveals pyelonephritis, and she is treated with an appropriate course of antibiotics with improvement in her vitals and laboratory results. She had limited improvement in her mental status initially, and long-term electroencephalogram (EEG) monitoring revealed subclinical status epilepticus. Following 24 hours of burst suppression with propofol and midazolam, she had improvement in her EEG. Over the course of the next 72 hours, she had improvement in her mental status but was unable to be weaned from the ventilator because of poor tidal volumes during spontaneous breathing trials. On examination, she has marked proximal weakness in all four extremities. Electodiagnostic testing is completed, which demonstrates prolonged compound muscle action potential (CMAP) on nerve conduction studies and positive sharp waves and decreased recruitment on electromyography.

What is the MOST likely cause of her weakness?

A. Critical illness neuropathy
B. Critical illness myopathy
C. Acute demyelinating encephalomyelitis (ADEM)
D. Guillain-Barré syndrome (GBS)
E. Inflammatory myopathy (eg polymyositis)


Question 3# Print Question

A 56-year-old man with essential thrombocytosis (baseline approximately 800 000) and prior renal cell carcinoma status post left nephrectomy 5 years before presentation presents with progressive bilateral lower extremity weakness and ascending paresthesia over the course of 7 days. He has mild proximal weakness in his bilateral legs, but is able to ambulate, and decreased sensation in his bilateral legs to mid-shin. No reflexes noted on examination. Additional testing including a lumbar puncture, demonstrating elevated protein with no white blood cells, and nerve conduction study, demonstrating dispersion of motor and sensory nerve responses with conduction block, confirms the diagnosis of GBS.

What is the most appropriate treatment?

A. Intravenous immunoglobulin (IVIg) at 2 g/kg in divided doses of 0.4 g/kg/d for 5 days
B. Plasmapheresis (PLEX) exchange volume 250 mL/kg for five sessions on alternating days
C. Intravenous methylprednisolone at 1 g/day for 5 days
D. PLEX exchange volume 250 mL/kg for five sessions on alternating days followed by IVIg at 2 g/kg in divided doses of 0.4 g/kg/d for 5 days


Question 4# Print Question

A previously healthy 36-year-old male was admitted to the medical intensive care unit following a cardiac arrest. On the day of admission to the hospital, he was getting ready for work, but felt quite fatigued and short of breath. He was talking with his wife, and she noted that he looked “blue” and then fell to the floor. He did not have a pulse, and she started emergency medical services (CPR) and contacted emergency medical services (EMS). On arrival, he did not have a pulse and received one dose of epinephrine and was intubated in the field with return of spontaneous circulation. On arrival to the ED, he was hemodynamically stable with normal vital signs, localizing with his arms and opening his eyes to noxious stimulation. He remained intubated and his mental status recovered, but he was unsuccessfully extubated because of hypercarbic respiratory failure over the course of several hours. A full cardiac and pulmonary workup was completed without underlying etiology for his respiratory failure. The neurology serviced was consulted for evaluation of failure to wean. Further history noted progressive dyspnea and fatigue over the last 6 months, but he attributed this to his stress at work. Also, he noted more difficulty with lifting his young children. His neurologic examination was pertinent for mild symmetric deltoid weakness and moderate symmetric hip flexion weakness. The remainder of the neurologic examination was normal. Electrodiagnostic tests were completed with normal nerve conduction studies, but abnormal electromyography with positive sharp waves and fibrillation potentials demonstrated in the deltoid, supraspinatus, iliopsoas, and thoracic paraspinal musculature. The paraspinal musculature also demonstrated complex repetitive discharges and myotonic discharges.

What is the MOST likely underlying cause of the patient’s presentation?

A. Acid maltase deficiency
B. C9orf72 genetic mutation
C. Glucose-6-phosphatase deficiency
D. Laminin A/C gene mutation
E. Zinc finger 9 genetic mutation




Category: Critical Care Medicine-Neurologic Disorders--->Neuromuscular Disorders
Page: 1 of 1