A 41-year-old male of Indian ethnicity with no comorbidities presented with an 8 day history of fever and dyspnoea. His COVID-19 RT PCR test was positive. He did not have any significant past medical or surgical history. He had no known drug allergies. He was not on any medication at the time of presentation. His family history was not significant for any inheritable conditions. There was no history of alcohol consumption or smoking. He initially received treatment at a local hospital where his oxygen requirement at admission was 15 lit O2/min via a non-rebreathing mask. HRCT chest scan done on day 8 of illness showed CT severity score of 14/25. A repeat HRCT chest scan done on day 15 of illness showed a CT severity score of 20/25. Due to worsening hypoxia and tachycardia, CT pulmonary angiogram was done on day 20 of illness which was negative for pulmonary thromboembolism. His oxygen support was extended to intermittent non-invasive ventilation (NIV). On day 26 of illness, he developed severe respiratory distress and was placed on mechanical ventilator support.\nAt this stage, he was shifted to our hospital for extra corporeal life support. At the time of referral, he was on ventilator support with 90% FiO2 and a PEEP of 10. P/F ratio was 60 and driving pressures were 30 cms H2O. Acute Physiology and Chronic Health Evaluation (APACHE II) score was 14. He was maintained on prone ventilation for 16 hours. After the first cycle of proning, he continued to have persistent hypoxemia and carbon dioxide retention despite lung-protective ventilation. His Respiratory Extracorporeal Membrane Oxygenation Survival Prediction Score (RESP) was 3, with a predicted survival chance of 76%. A decision was made to initiate V–V ECMO (Maquet Rotaflow) on day 3 of mechanical ventilation. Cannulation was done with a double-lumen single 27F jugular venous cannula (paraglide) under transesophageal echocardiography guidance. Heparin infusion was started for anticoagulation. Monitoring of anticoagulation was done using activated clotting time (ACT) and activated partial thromboplastin time (aPTT) levels with a target range of 180–220 seconds for ACT and 60–80 seconds for aPTT. Mechanical ventilation settings were changed to ultra lung-protective ventilation. Driving pressures were adjusted to 15 cm H2O.\nOn day 3 of ECMO, his GCS was E1VTM1, and anisocoria was noted. A non-contrast CT brain scan revealed a large intraparenchymal hemorrhage (). The ECMO run continued hereafter without heparin and prophylactic levetiracetam was added to prevent seizures. ACT levels were noted to be in the range of 140–170 sec. A decision to proceed with decompressive craniectomy was taken by the neurosurgery team. After taking consent surgery was performed by the chief of neurosurgery under general anaesthesia at our hospital, which is a multi-specialty tertiary care center. Pre-operatively coagulation parameters included a platelet count of 1.5 lakh cells/mm3, ACT of 150 seconds, aPTT of 30 seconds, an INR of 1.2. Within 3 hours of diagnosis of the ICH, right frontotemporoparietal decompressive craniectomy was done with lax duroplasty.\nOn postoperative day 4 (day 8 of V–V ECMO), the patient showed spontaneous eye-opening and non-purposeful movements of the right upper limb (with a power of 3/5) and lower limb (with a power of 1/5). However, on day 9 of V–V ECMO, the patient developed septic shock. Blood cultures were positive for E.coli and multi-drug resistant Klebsiella pneumoniae. Antibiotic therapy was escalated as per culture and sensitivity reports and inotrope support was initiated. Despite aggressive invasive organ-supportive care the patient progressively deteriorated and eventually succumbed due to refractory septic shock with multi-organ dysfunction syndrome on day 12 of V–V ECMO.
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.