An 18-year-old male patient was admitted to the Private Hospital in the South of the city of Bahía Blanca for presenting, during the return of a travel of sensing graduates from Bariloche, depression.
The only pathological antecedent was distal renal tubular acidosis diagnosed in the first year of life and treated since then with potassium bicarbonate 1 mEq/kg/day.
On physical examination she was hypotensive, sick, febrile, with depression of the sensorium and neck stiffness.
Hypokalemic metabolic acidosis (pH 7.22 pCO2 13, bicarbonate 5.3, BE -19.4, K 3.3 mEq/l) and leukocytosis with neutrophilia (GB 19,600) were detected in the admission laboratory.
The initial suspicion of suspension of potassium bicarbonate, which was usually received, was achieved through internal corrective surgery, but the patient remained acidotic, hypokalemic and with elevated anionic.
The general condition worsened, there was increasing sensory impairment and was admitted to mechanical ventilation.
With presumptive diagnosis of meningoencephalitis, lumbar puncture was performed and empirically medicated with antibiotics and corticosteroids.
Brain tomography showed diffuse edema with ventricular collapse.
Lumbar puncture was normal and cerebrospinal fluid pressure was 14 cm of water.
During the following days, the patient had temperatures above 38 °C and hypotension, with no other signs of cardiovascular instability or symptoms of disseminated intravascular coagulation.
He remained with metabolic acidosis and hypokalemia, and added hypernatremia, hypocalcemia, elevated transaminases, altered KPTT, urea and rising creatinine.
Due to persistent hypotension, physiological solution expansions were performed.
On the fourth day of hospitalization, a CPK value of 3,654 IU/l was detected, which reached a maximum value of 40,824 IU/l in the following days, with acute renal failure requiring hemodialysis.
Urine myoglobin was negative.
He recovered diuresis in 48 h.
On the 7th day, the search for drugs of abuse in urine (methadone, metacualone, cocaine, barbit assures, anomaly, metanifics), which were negative, cannabinoids was requested.
The patient remained in MRA for 9 days and later presented myoclonic movements of the lower limbs, marked hypotonia, hyporeflexia, severe generalized myalgia and total functional disability.
Upon regaining consciousness, the patient reported having consumed cocaine two days before the onset of the clinical picture, without remembering anything wrong later.
After one year of rehabilitation, the patient presented normal muscle function.
