J Emerg Med
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Alcoholic ketoacidosis (AKA) is a complex syndrome that results from disrupted metabolism in the setting of excessive alcohol use and poor oral intake. Dehydration, glycogen depletion, high redox state, and release of stress hormones are the primary factors producing the characteristic anion gap metabolic acidosis with an elevated β-hydroxybutyrate (β-OH) and lactate. ⋯ We present the case of a 47-year-old man who presented to the emergency department with metabolic acidosis and profoundly elevated lactate levels who had AKA. He recovered completely with intravenous fluids and parenteral glucose administration. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Emergency physicians should always consider the immediately life-threatening causes of a severe anion gap metabolic acidosis and treat aggressively based on the situation. This case highlights the fact that AKA can present with an impressively elevated lactate levels. Emergency physicians should keep AKA in the differential diagnosis of patients who present with a similar clinical picture.
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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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Approximately 1% of emergency department (ED) visits are due to anaphylaxis. Symptoms can include skin rash, facial and laryngeal edema, dyspnea, vomiting, hypotension, and shock. A transient loss of consciousness can also be a manifestation of anaphylaxis. A variety of electrocardiographic changes due to anaphylaxis have been described for Kounis syndrome, also known as allergic angina. ⋯ Here we describe the case of a male patient presenting at an ED with syncope, anaphylactic shock, and ST-segment elevation on electrocardiogram (ECG). The diagnostic workup led to the diagnosis of ruptured hepatic echinococcal cyst complicated by anaphylactic shock and syncope. ECG alterations were a manifestation of anaphylaxis, as defined by the type I Kounis syndrome. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Kounis syndrome represents an underestimated disease. Its prompt diagnosis in an ED has important clinical and therapeutic implications, such as modifications in the anaphylaxis treatment protocol, that is, adrenaline should be avoided because it could worsen vasospasm and myocardial ischemia.
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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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It has been speculated that freestanding emergency departments (FEDs) draw more affluent, better-insured patients away from urban hospital EDs. It is believed that this leaves urban hospital-based EDs less financially secure. ⋯ There were less privately insured patients and more self-pay, Medicaid, and Medicare patients at the main ED compared to the FEDs. Privately insured patients decreased at both the FEDs and main ED during the study. Insurance distribution was significantly different between the main ED, and three FEDs, and between individual FEDs.