Surgery · 2010
Late association of hyperparathyroidism in septic patients with multiple organ failure.
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Lucas Charles E, Ledgerwood Anna M, Jeffries Christopher C, Vernier Patricia
Аннотация
BACKGROUND: Hypocalcemia after severe shock or sepsis stimulates release of parathyroid hormone (PTH), which abates with recovery. Sustained sepsis with multiple organ failure (MOF), however, may cause a resurgent release of PTH and life-threatening hypercalcemia.
METHODS: Thirty critically ill patients with prolonged sepsis developed combined hypercalcemia with elevated serum PTH levels. The primary insult was trauma in 12 patients, peritonitis in 14, and pancreatitis in 4. MOF involved the lungs in 30 patients, kidney in 16, gut in 30, brain in 13, and a coagulopathy in 10. There were 12 deaths; hospital stay averaged 81 days.
RESULTS: Hypercalcemia with increased serum levels of PTH occurred usually 3-4 weeks after the septic insult. Bradycardia, thought to be caused by the hypercalcemia, occurred in 19 patients, was attributed to a vasovagal reaction, and was treated with atropine. When asystole resulted, epinephrine and cardiopulmonary resuscitation were administered. Five patients required placement of an intravenous pacemaker. Bradycardia was acutely lethal in 4 patients; in a 5th patient, the decision was made for comfort care alone, and he died 9 days later. Bisphosphonate was given to 7 patients with this hypercalcemic-induced bradycardia and, prophylactically, to prevent bradycardia in 9 others. Hypercalcemia corrected in all patients; bradycardia abated in 7 patients.
CONCLUSION: Hyperparathyroidism may occur with MOF secondary to sepsis. The mechanism is unclear, but the resultant bradycardia can be life threatening. Treatment with bisphosphonate corrects the hypercalcemia and bradycardia. Both the hypercalcemia and the bradycardia normalize when the MOF resolves.
METHODS: Thirty critically ill patients with prolonged sepsis developed combined hypercalcemia with elevated serum PTH levels. The primary insult was trauma in 12 patients, peritonitis in 14, and pancreatitis in 4. MOF involved the lungs in 30 patients, kidney in 16, gut in 30, brain in 13, and a coagulopathy in 10. There were 12 deaths; hospital stay averaged 81 days.
RESULTS: Hypercalcemia with increased serum levels of PTH occurred usually 3-4 weeks after the septic insult. Bradycardia, thought to be caused by the hypercalcemia, occurred in 19 patients, was attributed to a vasovagal reaction, and was treated with atropine. When asystole resulted, epinephrine and cardiopulmonary resuscitation were administered. Five patients required placement of an intravenous pacemaker. Bradycardia was acutely lethal in 4 patients; in a 5th patient, the decision was made for comfort care alone, and he died 9 days later. Bisphosphonate was given to 7 patients with this hypercalcemic-induced bradycardia and, prophylactically, to prevent bradycardia in 9 others. Hypercalcemia corrected in all patients; bradycardia abated in 7 patients.
CONCLUSION: Hyperparathyroidism may occur with MOF secondary to sepsis. The mechanism is unclear, but the resultant bradycardia can be life threatening. Treatment with bisphosphonate corrects the hypercalcemia and bradycardia. Both the hypercalcemia and the bradycardia normalize when the MOF resolves.