Sex: M
Vaccine: COVID19
Symptoms: PCO2, Physical examination, Platelet count, Protein C, Protein S
Clinical narrative: COVID-19 infection (fully vaccinated with Pfizer); COVID-19 infection (fully vaccinated with Pfizer); This is a literature report.  A 57-year-old male patient received BNT162b2 (BNT162B2), as dose 1, single (Batch/Lot number: unknown) and as dose 2, single (Batch/Lot number: unknown) for covid-19 immunisation. The patient's relevant medical history included: "hypertension" (unspecified if ongoing); "hyperlipidemia" (unspecified if ongoing); "tobacco use" (ongoing). The patient's concomitant medications were not reported. The following information was reported: DRUG INEFFECTIVE (hospitalization, medically significant), COVID-19 (hospitalization, medically significant), outcome "unknown" and all described as "COVID-19 infection (fully vaccinated with Pfizer)". The event "covid-19 infection (fully vaccinated with pfizer)" required emergency room visit. The patient underwent the following laboratory tests and procedures: Activated partial thromboplastin time (24.6-34.7): 34.2 seconds; Alanine aminotransferase (1-45): 36, notes: Units: U/L; Amphetamines (normal high range 1000): Negative; Angiogram: revealed small filling defects, notes: revealed small filling defects in both the ascending and descending thoracic aorta in correlation to the aortic thrombus; Anion gap: normalized; Anion gap (7-16): 23 mmol/L; Antibody test (0-25): less than 9, notes: Unit: GPI IgA; Aspartate aminotransferase (1-35): 26, notes: Units: U/L; Bilirubin conjugated (0-0.8): 0.2 mg/dl; Blood alkaline phosphatase (38-126): 114, notes: Units: U/L; Blood bicarbonate (21-28): 19.7 mEq/l; Blood bilirubin (0.1-1.2): 0.8 mg/dl; Blood chloride (96-108): 100 mmol/L; Blood creatinine (0.5-1.1): 1.24 mg/dl; Blood fibrinogen (212-516): 769 mg/dl; Blood homocysteine (normal high range 11): 7 umol/l; Blood lactic acid (0.5-2): 2.75 mmol/L; Blood magnesium (1.5-2.5): 1.9 mg/dl; Blood phosphorus (2.4-4.7): 4.7 mg/dl; Blood potassium (3.5-5.2): 4 mmol/L; Blood pressure measurement: 167/97 mmHg; Blood sodium (134-145): 134 mmol/L; Blood urea (6-23): 22 mg/dl; Brain natriuretic peptide (0-100): 72.4 pg/mL; Bronchoscopy: significant mucous plugging, notes: Later found to have significant mucous plugging on bronchoscopy, which was successfully removed; Cardiovascular examination: significant for tachycardia, notes: significant for tachycardia otherwise unremarkable. Stroke code was called; Chest X-ray: ventilator associated pneumonia, notes: with new opacities worrisome for ventilator associated pneumonia; Computerised tomogram: which revealed no signs of intracranial hemorrhage, notes: which revealed no signs of intracranial hemorrhage of the head; with no evidence of bleeding again; infarcts, notes: it revealed subacute right frontal, right parietal and right cerebellar infarcts consistent with right posterior inferior cerebellar artery infarct, with mass effect evident with mild compression of brainstem, fourth ventricle compression with signs of early hydrocephalus; Echocardiogram: 1x1 cm mobile thrombus, notes: which revealed a 1x1 cm mobile thrombus in the distal descending aorta; Electrocardiogram: revealed a new right bundle branch block; Glucose urine (normal high range 500): Negative; Haemoglobin (12-15): 14.8 g/dl; Haemoglobin (13.9-16.3): 14.8 g/dl; Heart rate: 106, notes: Units: beats/minute; International normalised ratio (0.9-1.1): 1.1; Anticardiolipin antibody (0-14): less than 9, notes: Unit: GPL U/mL; Antithrombin activity (81-113): 110 %; Barbiturate Screen (normal high range 200): Negative; Negative; Beta-Hydroxybutyrate (normal high range 0.3): 1.79 mmol/L; Cannabinoid (THC) Screen (normal high range 50): Negative; Cocaine Screen (normal high range 300): Negative; D-Dimer (normal high range 0.5): 3.96 ug/ml, notes: FEU; Lupus anticoagulant panel [Dilute Russell's viper venom time (dRVVT)] (27-41): 37.4 seconds; Negative; Negative; Phencyclidine Screen (normal high range 25): Negative; WBC NO./AREA URNS HPF (0-5): 2, notes: Unit: HPF; Laboratory workup: Notable for diabetic ketoacidosis; Negative, notes: negative for factor 5 Leiden and factor 2 gene mutation; Magnetic resonance imaging: right-sided infarcts, notes: revealed (MRI) right-sided infarcts with posterior fossa mass effect, signs of early hydrocephalus, and hemorrhagic conversion (Brain magnetic resonance imaging (MRI) performed with axial plane utilizing gradient echo sequence which revealed right sided hyperintense lesion in the cerebellum with minimal midline shift); Nitrite urine: Negative; Oxygen saturation: 96 %, notes: on room air; PCO2 (35-45): 33.2 mmHg; pH body fluid (7.35-7.45): 7.39; physical exam: slurred speech and left-sided facial droop, notes: the patient was lying comfortably in bed speaking in complete sentences with slurred speech and left-sided facial droop, cranial nerves II-XII were intact. Left-sided upper arm strength was 4/5, the right arm was 5/5, and no pronator drift was noted. Lower extremities strength was 5/5 with intact sensation in both upper and lower extremities; Platelet count (150-400): 285 x10 3/mm3; Protein C (75-133): 148 %; Protein S (52-151): 80 %; Protein urine: 30 mg/dl; Prothrombin time (12-14.2): 13.8 seconds; Red blood cells urine positive (0-3): 5, notes: Unit: HPF; SARS-CoV-2 test: Negative, notes: Negative on presentation; Positive, notes: On 5th day of admission; Specific gravity urine (1.004-1.036): 1.016; Troponin (normal low range 0.031): 0.01 mg/dl; Ultrasound Doppler: Negative; Urine analysis: Negative; Urine ketone body: Negative, notes: Trace; Urine leukocyte esterase: Negative; White blood cell count (5-11): 14.4 x10 3/mm3. Therapeutic measures were taken as a result of drug ineffective, covid-19. Clinical course: Patient presented to the emergency room with complaints of slurred speech, left-sided facial droop, and left-sided arm weakness. In the emergency room, his vital signs revealed blood pressure of 167/97 mmHg, heart rate of 106 beats/minute, and oxygen saturation (SPO2) of 96% on room air. On physical exam, the patient was lying comfortably in bed speaking in complete sentences with slurred speech and left-sided facial droop, cranial nerves II-XII were intact. Left-sided upper arm strength was 4/5, the right arm was 5/5, and no pronator drift was noted. Lower extremities strength was 5/5 with intact sensation in both upper and lower extremities. Cardiovascular exam was significant for tachycardia, otherwise unremarkable. Stroke code was called, and the patient was immediately taken for non-contrast computed tomography (CT) of the head, which revealed no signs of intracranial hemorrhage. The patient was given intravenous (IV) tenecteplase which caused a mild improvement of the neurological deficits. However, the patient became acutely diaphoretic and had multiple episodes of nonbilious and non-bloody emesis. Suddenly he became less responsive, somnolent, with right gaze preference, worsening left hemiparesis and left facial droop. The patient was taken to repeat head CT with no evidence of bleeding again. An electrocardiogram (EKG) revealed a new right bundle branch block (RBBB). He was admitted to the intensive care unit (ICU). Laboratory workup was also notable for diabetic ketoacidosis, and the patient was started on an insulin drip in the ICU, which was later bridged to long-acting insulin after the anion gap normalized. The CT head was repeated, and it revealed subacute right frontal, right parietal, and right cerebellar infarcts consistent with right posterior inferior cerebellar artery infarct, with mass effect evident with mild compression of brainstem, fourth ventricle compression with signs of early hydrocephalus. Bilateral lower extremity doppler was negative. Magnetic resonance imaging revealed (MRI) right-sided infarcts with posterior fossa mass effect, signs of early hydrocephalus, and hemorrhagic conversion. The patient was continuously lethargic in the ICU with worsening orientation (awake, alert, and oriented to person and place [AAOx2]), still complaining of nausea and inability to tolerate anything orally. The neurosurgery team was consulted, given concerns of worsening mental status changes, and a new hydrocephalus. Patient underwent sub-occipital craniectomy with external ventricular drain (EVD) placement under general anesthesia. The hospital course was complicated by new onset of fevers and chest x-ray with new opacities worrisome for ventilator-associated pneumonia; the patient was started on vancomycin and cefepime and was later found to be COVID-19 positive on the fifth day of admission. He underwent a transesophageal echocardiogram (TEE) which revealed a 1x1 cm mobile thrombus in the distal descending aorta. Hypercoagulation workup was ordered. Also, laboratory workup was negative for factor 5 Leiden and factor 2 gene mutation. The CVA was attributed to remote infection from COVID-19 after ruling out the other secondary causes of hypercoagulability. The patient's hospital course was further complicated by pulseless electrical activity (PEA) cardiac arrest with return of spontaneous circulation (ROSC) after six minutes. Later found to have significant mucous plugging on bronchoscopy, which was successfully removed. A repeat computed tomography angiogram (CTA) of the chest revealed small filling defects in both the ascending and descending thoracic aorta in correlation to the aortic thrombus. Cardiothoracic surgery (CTS) was consulted and deemed the patient unstable for surgical intervention. Given the significant risk of hemorrhagic conversion with recent CVA, multiple specialties were consulted to decide whether to start the patient on anticoagulation. After a risk vs. benefit discussion, it was decided to start the patient on a heparin drip which was later switched to apixaban 5mg two times daily. His condition continued to improve; the patient completed his antibiotic treatment after observation on the medicine floors; he was deemed stable and was discharged home on apixaban 5mg two times daily. In his follow-up visits, the patient was seen to be healthy and doing well.