A 20-year-old woman, with a history of IgG deficiency, presented at her local outpatient clinic with shortness of breath and was prescribed antibiotics. One week later the patient was admitted to her local hospital with signs indicative of septic shock, and shortly thereafter she went into cardiac arrest and cardiopulmonary resuscitation (CPR) was initiated. Extracorporeal cardiopulmonary resuscitation (ECPR) was commenced using VA ECMO. Shortly after cannulation the patient developed bilateral mydriasis but the cranial CT scan did not show any apparent ischemia or intracranial mass lesions. To prevent development of cerebral edema, the patient was managed with hyperosmolar therapy, hyperventilation, hypothermia and heavy sedation (Pentobarbital coma monitored with burst suppression on continuous electroencephalography (EEG)). Despite this, a CT scan performed on ECMO day (ED) 6 revealed increased cerebral edema, and the patient underwent ICP catheter (Codman®) placement. No significant bleeding events occurred during the procedure, however, post-operatively her right-sided mydriasis increased. A cranial CT scan revealed a frontal IPH (6.75 ml, largest diameter 27 mm) and a SDH with 14 mm midline shift (). The ongoing heparin infusion was withdrawn, and 30 minutes later an emergency SDH hematoma evacuation was performed. The pre-operative coagulation parameters were: platelet count 69 x109/mL, APTT 55 seconds, ACT 204 seconds and INR 1.0. Intra-operatively, no significant bleeding events occurred. However, the post-operative cranial CT scan revealed a subgaleal hemorrhage and an SDH recurrence with 14 mm midline-shift (). A new hematoma evacuation was performed without any significant intra-operative bleeding. A post-operative CT scan showed a decrease in the midline shift without any signs of hematoma recurrence (). However, the following morning her ICP increased drastically, and a new CT scan revealed a SDH and 20 mm midline shift, as well as epidural and subgaleal bleeding with impending uncal herniation (). Again, emergency hematoma evacuation was performed. Following this, the pupils regained their normal size and the CT scan showed a decreased midline shift without any signs of hematoma recurrence (). The ECMO treatment continued without heparin while prophylactic Levetirecetam was administered to prevent epileptic seizures. On ED 11 rewarming was successfully initiated, and the patient was decannulated from ECMO. At this stage, the patients had been without the heparin infusion for five days without any sign of complications. The patient was transferred to the neurosurgical ICU department, where extubation was successfully performed. After this the patient was transferred to a neurological care unit for rehabilitation. Within a year the patient had made a full recovery, with no neurological sequelae or physiological deficits, and had returned to work.
A 47-year-old woman, with a history of idiopathic nephrosis, hypertension and diabetes, was admitted to her local hospital after seven days of dyspnea, fever and myalgia. Intravenous antibiotics were administered for a suspected bacterial upper respiratory tract infection, and due to the severe dyspnea the patient was intubated. Despite this, respiratory function continued to decline, and ECMO treatment was advocated. The patient was cannulated for VV ECMO and transported to the ECMO ICU, where H1N1-influensa was diagnosed and appropriate treatment started. On ED 9 the patient developed left-sided mydriasis and level of consciousness decreased. A CT scan revealed a SAH (Fisher grade 4) with IVH (Le Roux grade 2) as well as hydrocephalus and absent basal cisterns. A cerebral angiography could not detect any bleeding source. Heparin was withdrawn, and seven hours later an EVD placement was performed. The pre-operative coagulation parameters were: platelet count 39, APTT 26, ACT 134 and INR 1.1. Intra-operatively, no significant bleeding events occurred. Post-operatively, the ECMO system continued to run without heparin. ICP was further managed through hyperosmolar therapy, hyperventilation and heavy sedation (Pentobarbital coma monitored with burst suppression on continuous electroencephalography (EEG)). In addition, Nimodipine was administered to prevent cerebral vasospasm, as well as prophylactic Levetirecetam to prevent potential epileptic seizures. On ED 10, the EVD clotted and a new EVD was placed without any complications. The following day RVF developed and the patient was converted to VA ECMO. On ED 13, her pupils were of normal size and sedation was reduced, revealing signs of consciousness and movement of the left hand. Due to clotting, a week later the ECMO circuit was replaced, and the heparin infusion was restarted. On ED 30 a CT scan showed no rebleeding, ischemia, edema or hydrocephalus and the EVD was removed. Nevertheless, the patient was still GCS 3 and respiratory function continued to decline, which resulted in increased hypercapnia. Further ECMO treatment was deemed futile and, consequently, treatment was withdrawn and the patient passed away.