We report the case of a 20-year-old female patient who was found unconscious in the bathtub.
The patient was evaluated locally by the emergency department (SAMU) in Glasgow 5 with hypothermia (34.5°), tachycardic (119/min), without electrocardiographic abnormalities and normal blood pressure.
His oxygen saturation was 98%, but he was polypneic.
The patient was admitted to the Hospital del Salvador with myiasis and reactive light pupils, with extensor hypertonia of the extremities (in generalized debinski sign, brief hyperreflexia crisis).
Examinations: leukocytosis of 36,400/mm3, CRP 0.4 mg/dl, pH 7.01, bicarbonate of 15.9 mmol/l, BE -15.7 mmol/l.
Anion gap increased to 16 mmEq/l, carbon monoxide (HbCO) 1.6%, INR 1.32, prothrombin 67%.
Urine toxicology was negative.
Colourless cerebrospinal fluid (CSF), glucose 0.50 g/l, albumin 34.4 mg/dl, 3 cells/mm3, Gram negative, herpes zoster PCR negative (HSV 1 and 2)
Computed tomography (CT) of the brain on admission showed changes in hippocampal density, these changes were detected in the TAC of the following day, which defined a significant hippocampal hypodensity.
1.
On the fourth day she began to show sporadic ocular opening with reactive isochory, preserved oculocephalic and corneal reflexes.
The stimulus showed reactivity in the right limbs, maintaining generalized hyperreflexia and Babinski.
Electroencephalogram showed generalized slow activity at 3 cps, and high voltage at 30 mmV.
On the seventh day a follow-up glance appeared and, although she did not emit language, she fulfilled orders.
MRI showed hyperintensity and swelling of both hippocampus in all its extension with diffusion restrictions, without pathological impregnations after contrast administration.
Also, hyperintense T2 and FLAIR images of the white substantia of the semioval center and subcortical areas in both temporo-occipital regions showed no diffusion restrictions.
Symmetrical hyperintensity of the cerebellar cortex.
1.
From the 14th day she presented longer periods of wakefulness and moved the right limbs in a persistent iterative fashion, without apparent purpose, the left limbs only occasionally moved them on the Babinski side.
On the sixteenth day she underwent protective tracheostomy.
After the twenty-first day, the rhythm wakefulness and wakefulness became evident during the day, although passive without being able to communicate.
The control MRI showed greater hypersignal in the hippocampus and decreased swelling of these structures; the hyperintensity of the subcortical white substantia and oval center persisted.
In the weeks that followed there was a significant recovery, achieving to stand and punish.
Hypophonic language was decannulated within a few days.
On the thirty-eighth day he had recovered expressive language and marched, but still passive, incapable of spontaneous communication.
Thirty-nine days after surgery, a formal neuropsychological assessment was performed, which found orientation and easy distractability with attentional failures, memory impairment evoked (great memory assessment and antegrade memory assessment).
It also showed alterations in executive functions with defects in fixation and programming functions, as well as loss of inhibitory control.
She was discharged on day forty and controlled one month later, normal gait and conserved language were verified, even maintaining hyperreflexia in lower limbs.
Plantar reflexes were flexor, with minimal left brachial paresis associated with dysesthesia of the index fingers and thumbs of that hand.
Control MRI showed areas in the oval center in those sectors of previously affected white substantia, with both hippocampus and cystic bulb or filament.
He maintained cognitive deficit.
