A 48-year-old woman was recently admitted for pyelonephritis and discharged home on trimethoprim-sulfamethoxazole based on urinary culture results. She returns to the ER 5 days later with fever, nausea, and vomiting. Right-sided hydronephrosis was seen on renal ultrasound and the patient was admitted to ICU for presumed urosepsis and postureteric stent placement. On examination, widespread morbilliform itchy rash was noted all over the body. On physical examination, the patient is found to be febrile. Her mucous membranes are normal. She has 3 cm lymph nodes in the anterior cervical and axillary regions and a liver edge palpable 4 cm below the costal margin.
Some facial swelling is also noted, but there was no difficulty in breathing. Medical history is otherwise unremarkable, and she was taking no other medications at home.
Which of the following is the most appropriate next step in diagnosis of this patient?
Correct Answer: D
She has a widespread morbilliform eruption with fever, facial edema, and lymphadenopathy that started 5 days after taking trimethoprimsulfamethoxazole. This is typical of a systemic drug hypersensitivity syndrome known as drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome. Diagnosis can be challenging in the presence of concurrent sepsis. DRESS is a rare life-threatening druginduced hypersensitivity reaction. Clinical features typically includes skin eruption, hematologic abnormalities (atypical lymphocytosis and eosinophilia), lymphadenopathy, and internal organ involvement (including liver, kidneys, and lungs) that occurs 5 to 10 days after starting the offending medication. Lymph node biopsy and skin biopsy are not helpful in its diagnosis. Since it can be associated with multiorgan system involvement, additional laboratory testing including complete metabolic panel is indicated.
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A 24-year-old man with no past medical history was scheduled for elective inguinal hernia repair under general anesthesia. Intraoperatively he becomes increasingly tachycardic and hyperthermic, and blood gas demonstrates severe metabolic acidosis. He is treated for malignant hyperthermia (MH) in the OR with good response and post procedure, is transferred to the ICU for close monitoring.
Which of the following anesthetic agents used is most likely to trigger MH?
MH is a rare, genetic, life-threatening condition that is a result of unregulated release of calcium from the sarcoplasmic reticulum. The incidence of MH episodes during anesthesia is between 1:10,000 and 1:250,000 anesthetics. It can be triggered by all volatile anesthetics and by succinylcholine. Halothane is most potent trigger for MH compared to the other volatile anesthetics. Classic signs of MH include hyperthermia, tachycardia, tachypnea, increased carbon dioxide production, increased oxygen consumption, acidosis, hyperkalemia, muscle rigidity, and rhabdomyolysis, all related to a hypermetabolic response. The syndrome is likely to be fatal if untreated. An increase in end-tidal carbon dioxide despite increased minute ventilation provides an early diagnostic clue. Dantrolene sodium is a specific antagonist and should be available wherever general anesthesia is administered. Increased understanding of the clinical manifestation and pathophysiology of MH has led to a decrease in mortality from 80% thirty years ago to less than 5% in 2006.
References:
A 78-year-old woman with past medical history of hypertension, coronary artery disease, and stage III chronic kidney disease is admitted to ICU with symptoms of lethargy, altered mental status, hypotension, and bradycardia. On further history obtained from patient’s daughter, she has been experiencing constipation and was taking over-the-counter laxatives. Over the past week, she had increased the magnesium-based laxative uptake to several times a day. On physical examination her:
Her chemistries reveal a creatinine that has worsen from baseline, and her serum magnesium is 8.4 mg/dL.
What is the next best step in immediate management of this patient?
Correct Answer: C
Massive oral ingestion of magnesium can occasionally exceed renal excretory capacity, particularly if there is underlying renal insufficiency. Severe hypermagnesemia with life-threatening symptoms has been described with accidental poisoning with Epsom salts (almost 100% magnesium sulfate) in children, in laxative abusers, and during the treatment of a variety of drug overdoses using magnesium as a cathartic. In most such cases, initial treatment consists of cessation of magnesiumcontaining medications and administration of intravenous isotonic fluids (eg, normal saline) and a loop diuretic (eg, furosemide). Higher diuretic doses may be required in these patients since they have reduced glomerular filtration rate (GFR). Dialysis may be required in patients with severe or symptomatic hypermagnesemia who have end-stage renal disease (GFR less than 15 mL/min/1.73 m2 ) or who have moderate to severe acute kidney injury. Since preparation for hemodialysis often takes 1 hour or longer, patients with symptomatic hypermagnesemia should be immediately treated with intravenous calcium to reverse the neuromuscular and cardiac effects of hypermagnesemia. The usual dose is 100 to 200 mg of elemental calcium over 5 to 10 minutes.
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