Age: 61.0
Sex: M
Vaccine: COVID19, COVID19
Symptoms: Ejection fraction decreased, Electrocardiogram ST segment depression, Electroencephalogram abnormal, Endotracheal intubation, Epilepsy
Clinical narrative: Deceased (10.1.21);  Hospitalized (9.17.21 - Acute massive, bilateral PE; cardiac arrest);   Fully Vaccinated (8.18 & 9.8.21)  Discharge Provider: Doctor Primary Care Physician at Discharge: Doctor  Admission Date: 9/17/2021 Date of Death: 10/1/21 Time of Death:  7:10 AM Preliminary Cause of Death: Acidosis Discharge Disposition: Deceased PRESENTING PROBLEM: Cardiac arrest Shock Acute pulmonary embolism with acute cor pulmonale, unspecified pulmonary embolism type HOSPITAL COURSE: Patient is a 61-year-old male with past medical history significant for glaucoma, hypertension, hyperlipidemia who presented to the emergency department with syncope on 9/17.  Had PEA cardiac arrest x4 secondary to bilateral massive PE with right heart strain.  Received systemic thrombolysis 9/17.  Initially in shock, likely obstcutive, and requiring pressors, though this did improve after a few days and patient came off pressors.  Also initially with metabolic/lactic acidosis, likely secondary to PEA arrest hypoperfusion.  Labs monitored with resolution.  Post arrest echo with mildly reduced EF and dilated RV.  No DVT on lower extremity Dopplers.  PE possibly provoked secondary to recent COVID-19 vaccination, though hematology felt to be unprovoked.    There was initially some concern for vaccine induced immune thrombotic thrombocytopenia secondary to patient's recent receipt of the COVID vaccine as well as thrombocytopenia.  Pf4 antibodies and serotonin release assay sent per hematology recommendation, and patient was started on argatroban for anticoagulation.  Pf4 and SRA negative with improved platelet count, so patient was transitioned to heparin infusion and remained on this throughout the course of his hospitalization.  Patient also initially with DIC, received cryoprecipitate, and labs were monitored with resolution.  He was not cooled given concerns for increased risk of bleeding secondary to DIC, thrombocytopenia, receipt of tPA.   The patient continued to require intubation and mechanical ventilation.  Initially secondary to massive PE/PEA arrest.  Continued predominantly secondary poor mental status secondary to anoxic brain injury and extremely high doses of sedating medication to control seizures.  The patient developed severely refractory seizures secondary to anoxic brain injury.  Initial EEG demonstrated status epilepticus.  He eventually required multiple antiepileptic medications as well as very deep sedation to achieve suppression. Critical Care were consulted and followed patient's course, providing recommendation.  Patient was also kept continuous EEG.  Patient was taken for MRI on 09/20 after he was sufficiently stabilized, notable for anoxic brain injury.  CT head obtained 9/27 stable, no acute abnormalities.  Ammonia level mildly elevated, not enough to explain cognitive deficit.  Per neuro recommendation, LP was not felt to be necessary given the predominantly etiology of anoxic brain injury.  Patient also developed primary lung findings of hemopneumothorax, bilateral lower lobe consolidations and pleural effusions.  Bronchoscopy performed 9/22 with removal of large amount of thick mucus, cultures negative.  Bronchoscopy again performed 9/26 with thin secretions, cultures negative.  Patient covered with Zosyn.  Chest tube placed 9/24 for hemothorax, with decrease in the amount of hemothorax confirmed on imaging.  Chest tube remained in place throughout remainder of admission. The patient was additionally found to have bilateral renal infarctions on CT as well as AKI.  Initial AKI most likely secondary to ATN in the setting of cardiac arrest.  He did not require dialysis.  Creatinine plateaued, then improved, though eventually did again worsen, unclear etiology.  Continued to make urine, though was very challenging to fully diurese, particularly given large intake from IV drips as well as hypernatremia.  Patient eventually did again develope a metabolic acidosis, likely secondary to worsened renal function.  Fluid overload caused a large amount of anasarca, particularly abdominal distension/abdominal wall edema.  Abdominal distension was initially thought to be secondary to obstruction, though imaging demonstrated no signs of obstruction and patient had bowel movements.  Patient additionally with a normocytic anemia, predominantly secondary to hemothorax.  Down trended slowly during admission.  Did require transfusion with one unit with appropriate response.  Further issues addressed during patient's hospitalization include hemoperitoneum and lower abdominal mesentery hemorrhage demonstrated on CT 9/17, improved on repeat imaging.  Chest wall fractures additionally noted on CT 9/17, though these did not require management.  The patient also had shock liver with transaminitis, though LFTs trended downward appropriately. Family was kept appraised of patient's condition and poor prognosis, particularly given severe brain injury.  Caregiving assisted, and patient's family made the decision to refrain from escalating care on 9/30.  Planned to withdraw care likely the following day once further family had had time to come and see the patient.  Patient had a worsening acidosis as well as FiO2 requirement overnight 9/30 to 10/1.  Bicarb drip was held as decision had been made for no escalation of care.  Patient expired on 10/1 at 0700.