Haloperidol
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Various toxicities: case report An 18-year-old man developed malignant neuroleptic syndrome, leading to chronic hypernatremia, rhabdomyolysis, stupor, dehydration, electrolyte disorder, hyperosmolarity, neurological alteration, fever and acute kidney injury (AKI) during treatment with haloperidol for agitation. The man presented to emergency department for a traffic accident against a car as a bicycle rider. Physical examination of a left supraciliary blunt wound demonstrated loss of continuity of the skin and irregular edges of 5cm long with suture management and grade 2 burn due to excoriation in the left temporal zygomatic region measuring 10 × 7cm and a state of drowsiness with a total Glasgow scale score of 10/15 (ocular 3, verbal 2, motor 5). During the first 24 hours of observation, he became agitated and aggressive, requiring midazolam on two occasions, with partial control of agitation. However, due to the persistence of agitation, IV haloperidol 10mg every 8 hours for 48 hours was started, with control of the agitation. On hospital day 4, he achieved control of agitation. However, he had a neurological state similar to that upon admission, with the appearance of fever. Investigations did not show any evidence of infection. Prior to the result of determining any infection, he started receiving antibiotic treatment with piperacillin/tazobactam. On day 6, he was in a state of stupor with a Glasgow scale score of 9/15 (ocular 3, verbal 2, motor 4). Concomitant sodium chloride [saline] was administered as a diluent for the medications. Additionally, he had dry oral mucosa, with physical restriction by means of restraints of the four limbs and without companions. Due to the persistence of consciousness and a previous skull tomography, that ruled out haemorrhagic or cerebral ischaemic events, biochemical studies were performed that showed a serum sodium of 181 mEq/L and an increase in the blood urea nitrogen/serum creatinine ratio. It was considered that the fever and the neurological alteration were attributed to chronic hypernatraemia. In the context of head trauma, central diabetes insipidus was initially suspected. Replacement of free-water with glucose [dextrose] in distilled water was started, considering a deficit of water of 7.8L. Also, urine studies were indicated in order to calculate urinary osmolarity. He developed hyperosmolarity and AKI. Piperacillin/tazobactam was stopped due to the negative procalcitonin report. Urine tests ruled out diabetes insipidus. In order to find out aetiology of chronic hypernatraemia (with preserved renal function concentration) investigation was carried out, which revealed normal serum glucose, normal lipid profile and highly elevated creatinine phosphokinase (CPK). The man developed severe dehydration. On day 8, an improvement was observed in the sodium concentrations and serum and urinary osmolarities. However, the CPK had a marked increase, which ruled out the possibility that rhabdomyolysis was secondary to the trauma. The medical history was reviewed consideri
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