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 35-year-old woman, with a history of depression, overdosed on a combination of antidepressants and alcohol, rendering her unconscious and resulting intubation and mechanical ventilation. Unfortunately, a later extubation attempt resulted in aspiration and severe respiratory failure to a degree that ECMO treatment was advocated, and the patient was started on VV ECMO. During the first week of ECMO, the patient developed progressive right ventricular heart failure (RVF), requiring conversion to VA ECMO. During the following weeks, the patient regained native lung function, but also experienced upper gastrointestinal bleeds requiring replacement of fibrinogen and platelets to prevent coagulopathy. On ED 32, the patient developed right-sided mydriasis and hypertension. A CT scan revealed a cerebellar IPH (23 mL, largest diameter 40 mm) with SAH (Fisher grade 4), IVH (Le Roux grade 4) and absent basal cisterns (). No bleeding source was found on a cerebral angiography. The heparin infusion was withdrawn, and protamine sulfate, fibrinogen, platelets and tranexamic acid was administered to reverse anticoagulation. Half an hour later an emergency cerebellar hematoma evacuation was performed. The pre-operative coagulation parameters were: platelet count 87, APTT 50, ACT 200, INR 1.0. Intra-operatively, opening of the dura resulted in uncontrollable hemorrhaging despite extensive use of local hemostatic agents and transfusions of fibrinogen, protamine sulfate, plasma, platelets, eptacog alfa (NovoSeven®, AryoSeven®) and cryoprecipitate. Due to the poor prognosis, an EVD was not placed. The post-operative CT scan showed increased IPH hematoma volume (41 ml) as well as progress of the hydrocephalus, IVH (LeRoux grade 12), SAH (Fisher grade 4) and tonsillar herniation (). Further ECMO treatment was deemed futile and, consequently, treatment was withdrawn and the patient passed away.