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He was treated with fluid resuscitation. His BP continued to fall further, and hence noradrenaline infusion at a rate of 8 ��g/min was started. BP was monitored every 15 min and noradrenaline was then increased every 15 min upto a maximum dose of 12 ��g/min. Dopamine infusion was then instituted beginning at a rate of 4 ��g/kg/min and titrated for every 15 min upto dosage of 15 ��g/kg/min. Laboratory parameters on day 3 were as follows: Urea-124.1 mg%, creatinine-9.84 mg%, sodium-147 mEq/l, potassium-4.62 mEq/l, and chloride-106.3 mmol/l. Patient could not survive inspite of various modalities of intensive and aggressive care due to multiorgan dysfunction syndrome. DISCUSSION Pheniramine maleate is a first generation H1 antagonist and is the principal antihistamine used in the treatment of allergic conditions. H1 antagonists inhibit most of the effects of histamine on smooth muscles, especially respiratory smooth muscle PR 171 constriction. They may produce central nervous system (CNS) depression or stimulation. CNS stimulation; in the form of restlessness, nervousness, and inability to sleep; is occasionally encountered in patients receiving conventional doses. Excitation of CNS commonly results in convulsions, particularly in infants. All the available H1 receptor antagonists are reversible competitive Protein Tyrosine Kinase inhibitor inhibitors of the interaction of histamine with H1 receptors.[1] Alkylamine derivatives are among the most potent antihistamines producing more CNS stimulation and less drowsiness. They also have potent competitive inhibition of muscarinic receptors causing anticholinergic side effects. The maximum therapeutic dose of the pheniramine maleate should not exceed 3 mg/kg/day.[2] Our patient had consumed the potentially lethal dose of approximately 4.077 g. Pheniramine is associated with a relatively YES1 high incidence of seizures (30%).[2] On chronic usage, it is known to cause autoinduction of hepatic enzymes to develop tolerance to the psychomotor performance and sedative effects.[2] Rhabdomyolysis is the rapid breakdown of skeletal muscle and leakage of myocyte contents into extracellular compartment due to traumatic or nontraumatic cause. The causes include polymyositis, heat stroke, prolonged convulsions, marathon running, hypokalemia, and viral illness (Epstein�CBarr, influenza, and coxsackie viruses).[1] Of late, drugs, including alcohol, have assumed greater importance and in published series have been implicated in up to 81% of cases. Rhabdomyolysis causes myoglobinuria which can lead to AKI, the mechanism of which includes impairment of renal vascular flow due to sympathetic overactivity, activation of the renin�Cangiotensin system, altered prostaglandin synthesis, high circulating levels of antidiuretic hormone, the deposition of microthrombi, obstruction of tubular lumina by myoglobin casts, direct nephrotoxicity due to ferrihemate (breakdown product of myoglobin at pH
