A 23-year-old man with no morbid history presented with ictal headache and progressive quantitative consciousness compromise.
She was initially diagnosed with a 42 ml right parietal intraparenchymal hematoma associated with acute hydrocephalia by computed tomography (CT) of the brain in another hospital.
An external ventricular drainage (EVD) was installed urgently in the operating room.
An initial intracraneal pressure (ICP) of 45 cm of H2O was recorded.
She was connected to mechanical ventilation (MV) and deep sedation was indicated.
Initially, intracranial hypertension was treated with cerebrospinal fluid drainage and intravenous hypertonic sodium bolus, as needed.
He stayed in our service three days later.
He was intubated and connected to MV, sedated with propofol 0.71 mg/kg/h, and hemodynamically supported with noradrenaline at 0.06 μg/kg/min, ICP and cerebral perfusion pressure of 6 cm H2O.
Neurological examination revealed coma, right-sided fixed mydriasis, abolished corneal reflexes, blurred oculocephalic reflexes, decreased tone and bilateral indifferent plantar reflexes.
General admission tests: Na+ 146 mEq/L, K+ 3.5 mEq/L, hematocrit 31%, lactate 1.4 mmol/L, leukocytes 9,600 per mm3 and C-reactive protein 11.4 mg/dl.
Six-vessel cerebral angiography showed a right parietal mesial arteriovenous (AVM) with signs of recent rupture, associated with three paranidal aneurysms.
Embolization with N-butyl-cyanoacrylate (Histoacryl®, Braun, Germany) was performed, reducing the nest of the AVM and excluding its aneurysms.
After the procedure, the CT of the encephalon showed the Histoacryl® correctly located.
However, there was an increase in hematoma with marked mass effect and presence of diffuse cerebral edema with obliteration of the convexity grooves, in addition to subfalcine and uncal herniations with midline deviation of the gland.
The hematoma was evacuated and an extensive fronto-occipital craniectomy was performed 5, 2 x 9.3 cm. The control encephalon CT showed a significant reduction of the hematoma line at 11 ml.
1.
Despite craniectomy with ICP greater than 20 cm H2O (23 ± 5 cm H2O; mean ± SD).
ECH was staged medically with deep sedation (fentanyl 2.86 μg/kg/h, midazolam 0.11 mg/kg/h and propofol 1.43 mg/kg/h), frequent bolus administration of PICO
Nonconvulsive epileptic activity was ruled out by electroencephalogram and CT scan of the brain 48 h after craniectomy showed no significant changes.
Due to the persistence of ICP levels > 20 cm H2O, it was decided to initiate therapeutic hypothermia.
Moderate hypothermia, with target temperature of 33°C, was performed using the intravascular technique (Alsius, Zoll, Chelmsford, allergic rhinitis, USA).
Central temperature was measured with an intravesical catheter.
Once hypothermia was achieved (~12 h from the diagnosis of refractory ECH), rapid ICP control was achieved with values between 9 and 12 cm H2O (~3 from the beginning of the procedure).
Neuromuscular blockade was maintained by continuous infusion during the first two days of hypothermia to avoid chills.
After 48 h in hypothermia, programmed rewarming attempts were made at a rate of 0.5°C/h.
However, all of them were interposed due to ICP rebound.
After the 20th day of evolution of the clinical picture and showing a decrease in cerebral edema in neuroimaging, the definitive control of ICP was achieved.
The patient stayed 13 days in moderate hypothermia without arrhythmias, coagulation disorders or electrolyte disturbances.
She presented with mechanical ventilation associated bronchitis, which resolved satisfactorily with antibiotic therapy.
Sedation was progressively suspended, the patient acquired wakefulness and a mild hemiparesis with hemineglect and left hemianopsia was observed.
After extubation, appropriate language was found.
Neurorehabilitation was started and, after 40 days of hospitalization, the patient was discharged.
Two years later, Rankin 2 showed mild spastic left hemiparesis and completed his university studies.
