A young boy with malignant hypertension and intracranial bleed

Abstract

A 12-year-old male child presented to pediatric emergency with complaints of abnormal movements involving the right side of body, which rapidly progressed to alteration of sensorium along with repeated bouts of vomiting since last one day. He developed all problems acutely and was apparently well before this. In a local hospital he was noted to have weakness of right side of the body and was referred to PGI. There was no history of fever, loose stools, head trauma or excessive bleeding prior to this. The past history was totally unremarkable. The child was born to a gravida 2 mother by full-term normal vaginal delivery and there were no adverse prenatal events. His developmental milestones were normal. He was appropriately immunized. He was born of a non-consanguineous marriage. His elder sibling had died at the age of 1.5 years due to some unknown illness. There was no history of contact with tuberculosis. On examination, he weighed 25 kg, had no pallor, icterus, clubbing, edema or skin bleed. His heart rate was 140 beats/minute, respiratory rate 36 per minute, capillary filling time 2 seconds, blood pressure (BP) 220/160 mm Hg and oxygen saturation was 100% on room air. All the peripheral pulses were palpable. The BP in the upper limbs was 180/130 mm Hg and in the lower limbs was 170/120 mm Hg. Ophthalmoscopic examination showed bilateral disk blurring with hemorrhages. On systemic examination, he had a Glasgow coma score of E2, M4, V2, both the pupils were 2 mm and reacted to light, and there was no cranial nerve palsy. There was hypotonia of all four limbs, more on the right side. The deep tendon reflexes were normally elicitable on the left side; but absent on the right side. Plantars were upgoing in both the legs. Neck rigidity and Kernig’s sign were positive. Cardiovascular, abdominal and respiratory examinations were normal. Investigations are shows in Tables ​Tables11 and ​and22. Table 1 Investigations Table 2 Investigations (Contd.) Blood culture (26/08/06): sterile; Urine RE (28/08/06): protein, nil; sugar, nil; no RBC. Pus cells: 2–3/hpf. Oxalate crystals ++; Urine sugar (30/08/06): ++++; Urine electrolytes (28/08/06): Na, 75 meq/L; K, 28.3 mEq/L; creatinine: 50.4 mg/dL. The child was started on sodium nitroprusside infusion and oral amlodepine. The intracranial pressure (ICP) was 70–80 mm Hg. Measures for raised ICP were instituted. A neurosurgery consultation was obtained and the hematoma was evacuated. Thereafter, he was shifted to intensive care unit. Post-evacuation, the ICP dropped to 30–35 mm Hg, BP came down and nitroprusside drip was discontinued. Later, the BP continued to drop to <5th centile requiring fluid boluses, dopamine and adrenaline infusions were started. Twelve hours postevacuation, ICP began to rise again and reached up to 180 mm Hg. A mannitol bolus was given and a repeat computerized tomography (CT) was done. Anti-edema measures (dexamethasone, lasix, mannitol and hyperventilation) were continued but raised ICP persisted. He had fever in the postoperative period. Ceftriaxone + sulbactum and cloxacillin were started empirically. He also developed hyperglycemia with polyuria, which was treated with insulin infusion and vasopressin. Despite all the measures, the cerebral perfusion pressure continued to remain low. The neurological status and shock progressively deteriorated and he expired on 31.08.06.