To the Editor, Vaccine-induced thrombotic thrombocytopenia (VITT) manifesting as cerebral venous thrombosis (CVT) is rare but life-threatening complication after COVID-19 vaccination.[1] Neurogenic stunned myocardium (NSM) is a phenomenon of cardiac abnormalities occurring due to sympathetic storm after acute neurological injury.[2] This case reporting is done after obtaining written informed consent. We describe rare manifestation of VITT, CVT, and NSM after COVID-19 vaccination and its successful management. A 19-year-old lady presented with altered sensorium for 2 days. Prior to her current visit, she had low-grade fever for 2 days and holocranial headache with vomiting for one week after COVID-19 vaccination with COVAXIN® (Bharat Biotech). On examination, she was drowsy, obeying simple commands on repeated asking, aphasic, with motor power of 3/5. Her pupils were equal and reactive. Respiratory and cardiovascular system examination was normal. Brain computed tomography showed left temporo-parietal CVT with raised intracranial pressure (ICP), midline shift to right and left transverse sinus thrombosis [Figure 1]. Laboratory tests revealed thrombocytopenia (platelet count 43,000/μL), elevated D-dimer (7457 ng/mL), and prolonged prothrombin time (18.8s). VITT associated CVT was diagnosed. In view of neurological status and imaging findings, she underwent emergency temporo-parieto-occipital decompressive craniectomy. She received four units of random donor platelet transfusion and three units of fresh frozen plasma before and during surgery. She was shifted to neuro-intensive care unit for elective ventilation and further management. VITT was managed with Fondaparinux and therapeutic plasma exchange (TPE). On 2nd postoperative day (POD), she developed persistent hypotension with tachycardia resistant to fluid therapy, with abnormal arterial blood gas (PaO2 = 40.9 mmHg, PaCO2 = 25.7 mmHg, pH = 7.48, SaO2 = 80.9%). Hence, norepinephrine was started, positive end expiratory pressure (PEEP) and fraction of inspired oxygen (FiO2) increased to 8 cm water and 0.7, respectively. Following this, her heart rate was 112/min, blood pressure was 112/80 mmHg, electrocardiogram showed sinus tachycardia and oxygen saturation was 90%. The FiO2 was gradually reduced with improvement in oxygenation. Transthoracic echocardiography (TTE) showed left ventricular global hypokinesia with ejection fraction of 34%. She was diagnosed with acute left ventricular failure from NSM. Dobutamine and furosemide infusion with oral ivabradine resulted in improvement and cardiovascular medications were tapered and stopped on 9th POD and trachea was extubated on 10th POD. After 24h observation, she was shifted to ward and subsequently discharged home with improved neurological status. Follow up TTE at discharge showed normal cardiac contractility.Figure 1: Contrast computed tomography of the brain showing large temporo-parietal hematoma due to cerebral venous thrombosis with midline shift, mass effect, and significant cerebral edema with loss of gray-white differentiationVITT is characterized as vaccine-induced immune syndrome of severe thrombosis, antibodies to platelet factor 4–polyanion complexes and thrombocytopenia.[3] VITT begins 5-10 days after vaccination and is diagnosed between 5 to 30 days.[4] It is associated with CVT, splanchnic vein thrombosis, deep venous and arterial thrombosis with thrombocytopenia, and elevated D-dimer. Treatment includes non-heparin anticoagulants such as indirect Xa inhibitors (fondaparinux, danaparoid), oral anticoagulants or thrombin inhibitors (argatroban, bivalirudin), and intravenous immunoglobulin or TPE. NSM is reported after stroke, traumatic brain injury, and subarachnoid hemorrhage but not after CVT. Catecholamine excess, systemic inflammation, and neuroendocrine derangements contribute to occurrence of NSM.[5] It is likely that the NSM in our patient was due to interplay of acute increase in ICP (neurogenic) from VITT-associated malignant CVT and systemic vaccine-induced complication-associated stress on the myocardium. Treatment is supportive to improve myocardial function and prevents cardiovascular complications including sudden death.[5] Ivabradine reduces heart rate and improves cardiac failure while dobutamine improves hemodynamic instability associated with NSM.[5,6] To conclude, VITT-associated CVT leading to NSC is rare and challenging to identify and manage. Management goals include reduction of acute intracranial hypertension, restoration of platelet function, anti-coagulation, and supporting cardiac function. Patient consent form Yes. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
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Jan 2, 2024
Alben Sigamani + 26
