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 67-year old man, with a history of alcohol addiction and rheumatoid arthritis, was admitted to his local hospital with a respiratory tract infection. Despite treatment with antibiotics, the patient developed septic shock with refractory respiratory failure. ECMO was indicated and cannulation for VV ECMO initiated. However, during cannulation the patient suffered multiple transient cardiac arrests and VA ECMO was commenced instead. On ED 3 a routine cranial CT scan showed no abnormalities. By ED 6, the patient’s native lung function had improved to a degree that the sedation was reduced, with the patient subsequently decannulated and withdrawn from ECMO. However, the patient did not wake up and a CT scan showed a cerebellar IPH (10 mL, largest diameter 25 mm), several minimal parietal IPHs as well as hydrocephalus and imminent cerebral herniation. Two hours later the patient underwent emergency EVD placement and evacuation of the cerebellar hematoma. Because enough time had passed since decannulation (24 hours), pre-operative hemostatic intervention was deemed unnecessary. The pre-operative coagulation parameters were: platelet count 77, APTT 30, ACT N/A, INR 1.2. Intra-operatively no significant bleeding occurred. Post-operatively, the patient was taken back to the ICU where ICP was further managed through hyperosmolar therapy and hyperventilation. After three days the EVD was removed. However, while the cranial CT scan showed resorption of IPHs, his GCS was still 3. An EEG showed slow wave activity indicative of an unspecific cerebral pathology, but a magnetic resonance imaging scan and lumbar puncture revealed no signs of encephalopathy. After transfer to the neurological ward the patient began to show signs of minor neurological improvement, but a few weeks later the patient suffered a massive pulmonary embolism. Showing no signs of further neurological improvement, life-sustaining treatment was withdrawn and the patient passed away.\nsummarizes the clinical course of these five patients.