Abstract
Introduction: Twenty-one-month old female with past medical history of egg allergy, presented to our hospital emergency room with perioral rash, emesis, cough, and generalized itching. One hour prior to admission she had meat loaf (containing milk, eggs). Child was given an antihistaminic medication and brought to emergency room. In the emergency room, patient received three doses of epinephrine 0.01mg/kg (1:1000 concentration; one dose IM and two doses IV) and racemic epinephrine nebulization over a period of twenty minutes for respiratory distress. Work of breathing continued to get worse and she became hypotensive. Three normal saline boluses of 20ml/kg each were given for hypotension and she was started on epinephrine drip at 1 mcg/kg/min in the emergency room before transferring the child to PICU. In PICU, the child had increased work of breathing, tachycardia (180-200 bpm) and poor peripheral perfusion. Child was intubated in the PICU and was placed on mechanical ventilator. She started developing pink frothy secretions. X-ray chest was consistent with pulmonary edema. EKG showed sinus tachycardia with nonspecific ST T wave changes and an echocardiogram revealed depressed left ventricular systolic function with an ejection fraction of 44%. Initial troponin (3.2 ng per ml), CPK-MB (11.5 ng per ml) and beta type natriuretic peptide (5000 pg per ml) levels were elevated. She was started on milrinone and lasix drips and epinephrine drip was weaned off. Over the next ten days, serial echocardiograms showed improvement in cardiac function with a final ejection fraction of 69% and normalization of cardiac enzymes. Child was discharged home fourteen days after admission. Discussion: Children with severe anaphylaxis may present with non-cardiogenic pulmonary edema and vasodilatory shock. However, in our patient clinical status worsened after starting epinephrine therapy and her cardiac enzymes were elevated along with cardiac dysfunction suggesting myocardial injury. As the child improved once the epinephrine was stopped catecholamine induced cardiomyopathy is a distinct possibility. Epinephrine is the cornerstone of anaphylaxis treatment. However, it has a narrow therapeutic index and can results in serious side effects. It is known that high dose of epinephrine administration can cause myocardial stunning and global myocardial hypokinesis. Diffuse myocardial injury was observed in experimental studies with excessive catecholamines. Such changes are also seen in patients with catecholamine excess states like, pheochromocytoma, stress induced cardiomyopathy (Tako-tsubo cardiomyopathy), and neurogenic myocardial stunning. This child was managed with ventilatory support, milrinone infusion and discontinuation of epinephrine. In refractory cases ECMO may be needed as a temporary support. Catecholamine induced cardiomyopathy is reversible within days to weeks. Caution should be exercised giving multiple doses of epinephrine for the management of anaphylaxis. Catecholamine induced cardiomyopathy should be considered in a child with poor cardiac function and high dose of epinephrine.
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