J Emerg Med
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Case Reports
Acute Aortic Dissection Presenting as Bilateral Lower Extremity Paralysis: A Case Report.
First described by Morgagni in 1761, aortic dissection (AD) is an acute life-threatening and time-sensitive disease process with an increasing mortality approaching 1% for every 1-hour delay in diagnosis within the first 48 hours. Despite continued surgical advancement, overall in-hospital mortality remains significant (27.4%). ⋯ A 56-year-old woman presented to an outlying emergency department with a complaint of isolated lumbar pain associated with right lower extremity paresthesia and paralysis that progressed to the left. Her medical history and a review of symptoms were significant for chronic obstructive pulmonary disease and tobacco abuse. The initial evaluation in the emergency department included laboratory values and a computed tomography scan of the lumbar spine that revealed minimal disease. After transfer to our tertiary care center for an emergent magnetic resonance imaging scan of the lumbar spine, her vital signs were as follows: blood pressure, 176/84 mm Hg; heart rate, 76 beats/min; respiratory rate, 24 breaths/min; afebrile; and oxygen saturation 98% on room air. A repeat examination revealed cold extremities with mottling, bilateral symmetric lower extremity flaccid paralysis, and a loss of pulses and reflexes. She was insensate below the T10 dermatome. Her upper extremities and cranial nerves were normal. She underwent computed tomography angiography, revealing an extensive Stanford type A AD with interim thrombus formation. After successful endograft stenting, she died 24 hours later. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Comprising <2% of all ADs, the pathophysiology of paraplegia as the initial presentation of AD is caused by compression of the anterior spinal artery, resulting in ischemia of the spinal cord. Acute AD is a life-threatening medical emergency that requires a high clinical level of suspicion because of its often variable presentation and high incidence of mortality.
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There are multiple clinical manifestations of hypercalcemia and several causes of hypercalcemia. Hypercalcemia caused by milk-alkali syndrome is increasing in frequency. ⋯ A 26-year-old woman presented after having undergone caesarian section. She complained of severe myalgias, arthralgias, an inability to ambulate, nausea, vomiting, abdominal pain, and marked depression. Each of these symptoms has a broad differential diagnosis, but when considered together the theme "stones, bones, moans, and groans," seen in patients with hypercalcemia, is evident. This patient was found to have hypercalcemia caused by milk-alkali syndrome related to the ingestion of calcium carbonate. Her symptoms and hypercalcemia resolved with treatment. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Emergency physicians should be aware of the many different symptoms of hypercalcemia. This case emphasizes the need for a careful medication history for any patient presenting with hypercalcemia, including over the counter medications. Physicians should have a high level of suspicion for milk-alkali syndrome in patients with hypercalcemia because milk-alkali syndrome is no longer a rare etiology but rather one of the most common causes of hypercalcemia.
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Case Reports
Bilateral Quadriceps Femoris Tendon Rupture in a Patient With Chronic Renal Insufficiency: A Case Report.
Simultaneous bilateral quadriceps femoris tendon rupture is a relatively rare occurrence. As such, patients frequently experience a delay in receiving an accurate diagnosis. It is often associated with significant morbidity and loss of function. We report a case of simultaneous bilateral quadriceps tendon ruptures in a patient with chronic renal insufficiency. ⋯ A 46-year-old white man presented to the Emergency Department (ED) via ambulance, reporting sudden onset of bilateral lower limb weakness. He had a medical history of renal insufficiency due to immunoglobulin-A-induced glomerulopathy, with secondary hyperparathyroidism and gout. Examination of his lower limbs revealed significant swelling in his distal thighs anteriorly and suprapatellar defects at the insertion of the quadriceps tendon. No other palpable deficits were identified. The patella was in a normal position and there was minimal tenderness on palpation. He had complete loss of active knee extension. Bilateral patella reflexes were absent. Lower-limb sensation was intact bilaterally and no other neurovascular deficits were elicited. Thompson test was negative and the rest of the clinical examination was unremarkable. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The inability to walk is a common ED presentation. The differential diagnosis is vast and includes but is not limited to: spinal cord injury, Guillain-Barré syndrome, myopathies, and even malingering. This case report details an uncommon cause for a common ED presentation. Furthermore, this case illustrates the importance of a detailed clinical history and physical examination, which narrowed the differential diagnosis and ultimately led to the clinical diagnosis. Knowledge of the patient's past medical history combined with simple imaging modalities permitted a prompt clinical diagnosis of an uncommon condition, which facilitated early operative management.
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In 1998, emergency medicine-pediatrics (EM-PEDS) graduates were no longer eligible for the pediatric emergency medicine (PEM) sub-board certification examination. There is a paucity of guidance regarding the various training options for medical students who are interested in PEM. ⋯ EM-PEDS graduates found combined training to be an asset in their career. They felt that it provided flexibility in job searches, and that it was ideal training for the skill set required for the practice of PEM. EM-PEDS graduates' practices varied, including mixed settings, free-standing children's hospitals, and community emergency departments.
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Acute encephalopathy in a patient with alcoholic liver disease (ALD) is a commonly encountered emergency situation occurring most frequently due to liver failure precipitated by varying etiologies. Acute reversible cerebellar ataxia with confusion secondary to prolonged metronidazole use has been reported rarely as a cause of encephalopathy in patients with ALD. ⋯ We describe a decompensated ALD patient with recurrent pyogenic cholangitis associated with hepatolithiasis who presented to the emergency department with sudden-onset cerebellar ataxia with dysarthria and mental confusion after prolonged use of metronidazole. Magnetic resonance imaging (MRI) of the brain was suggestive of bilateral dentate nuclei hyper intensities on T2 and fluid-attenuated inversion recovery sections seen classically in metronidazole-induced encephalopathy (MIE). Decompensated liver cirrhosis resulted in decreased hepatic clearance and increased cerebrospinal fluid concentration of metronidazole leading to toxicity at a relatively low total cumulative dose of 22 g. Both the clinical symptoms and MRI brain changes were reversed at 7 days and 6 weeks, respectively, after discontinuation of metronidazole. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: A patient with ALD presenting with encephalopathy creates a diagnostic dilemma for the emergency physician regarding whether to continue metronidazole and treat for hepatic encephalopathy or to suspect for MIE and withhold the drug. Failure to timely discontinue metronidazole may worsen the associated hepatic encephalopathy in these patients. Liver cirrhosis patients have higher mean concentration of metronidazole and its metabolite in the blood, making it necessary to keep the cumulative dose of metronidazole to < 20 g in them.