A previously healthy 17-year-old school girl was admitted to our hospital with acute condition characterised by comatose state and seizures. The family reported that she fainted while in the school 2 weeks earlier and was referred to the General Hospital of Hambanthota, in Southern Sri Lanka. Following unremarkable examination and baseline investigations, the patient was discharged. However, following day morning her family noticed some unusual behaviour of the patient including agitation and over talkativeness. As her agitation worsened over next few days, she underwent psychiatric consultation, in which an acute psychotic state had been diagnosed and antipsychotic was prescribed. She did not have symptoms such as fever, headache, chills or rigors at this stage of the illness. Over next 2 days she gradually became drowsy and developed several episodes of seizure. With these new symptoms she was readmitted to the same regional hospital. On admission she was reported to be drowsy with Glasgow Coma Scale (GCS) of 8/15, and had hypertonia with opisthotonus posture. She had exhibited phobic spasms including hydrophobia and aerophobia (positive fan test). Furious rabies was suspected as the most likely diagnosis on the basis of her acute encephalopathic state, phobic spasms and an unconfirmed dog bite history around a month ago. As there was no definitive treatment she was managed conservatively and the family was informed the poor prognosis. Devastated by this acute illness which has no cure; her family sought second opinion from our hospital.
On admission to our unit, she was febrile with a temperature of 39.6 °C, heart rate of 120/min, respiration of 38/min, and blood pressure of 134/82 mmHg. She was drowsy with a fluctuating level of consciousness, incoherent, and not cooperative with the examination. Pupils were equal (3 mm) and reactive to light. Fundoscopic examination revealed no abnormalities. No obvious jaundice, enlarged lymph nodes, spleen, or cranial nerve palsies, were observed. She had opisthotonus posture with hypertonia and exaggerated reflexes. She also had obvious phobic spasms including phobic spasm with air (positive fan test). Involuntary jerky movements suggestive of myoclonic jerks were observed at frequent intervals throughout the hospital stay.
Investigations showed white blood cell count of 7300 cells/μl with 74.3 % neutrophils and 18.3 % lymphocytes, haemoglobin concentration 13.2 g/dl, platelet count 156,000 μl−1, creatinine 38 μmol/l and erythrocyte sedimentation rate 32 mm/h. Urgent non contrast computed tomography showed no significant abnormality and cerebral spinal fluid examination was unremarkable with protein of 43.4 g/l and 2–4 lymphocytes/mm3. The electroencephalogram showed frequent generalized 4- to 6-Hz spikes in the back ground of slow-wave discharges. A rapid antigenic test for P. falciparum and peripheral blood smear for malarial parasite were performed as the patient was from geographical area traditionally considered as malarial endemic area. Antigen test was positive and the peripheral blood smear revealed the presence of P. falciparum ring forms (Fig. 1).
Soon after the diagnosis was made, the patient was started on intravenous quinine with intravenous dextrose. She also was treated with sodium valproate to control the seizure activities. She started to show signs of improvement on the following day and her confused mental state gradually improved over 3 days. On Day 07, she was discharged with a good mental status. The patient was reviewed monthly for 3 months and during the follow up visits she did not have any residual neurological deficit or cognitive impairment. Sodium valproate was stopped 3 months later as she did not have seizures anymore.