COVID-19 as a second hit for Anti-phospholipid syndrome

Background: Anti-phospholipid syndrome (APS) is an autoimmune disorder characterized by venous and arterial thrombosis, usually in setting of underlying autoimmune disorders. Here, we present a case of anti-phospholipid syndrome post covid infection. Case Presentation: 41-year-old lady presented to the ER with complaints of left sided facial droop for 3-day duration. On further evaluation, she was found to have subacute ischemic stroke and was managed with anticoagulation and supportive treatment. Past medical history is significant for a recent diagnosis of Covid infection and for subsequent development of lower extremity deep vein thrombosis (DVT). She was started on anticoagulation with rivaroxaban for the DVT. However, anticoagulation had to be held due to hemorrhagic transformation of the ischemic stroke. Further work up for young stroke revealed having elevated PTT, elevated titers for anticardiolipin Ab IgG and IgM, positive lupus anticoagulant by screen and confirmatory tests leading to diagnosis of APS. She was readmitted a few days later for acute DVT of left lower extremity and underwent thrombectomy. Warfarin was initiated to bridge from heparin in setting of acquired anti-phospholipid syndrome. The goal INR 2.5-3.5 was reached uneventfully, and she was discharged home. Conclusions: In Anti-phospholipid syndrome, patients typically have a history of multiple pregnancy loss and underlying autoimmune disorders. Our patient has no typical risk factors for anti-phospholipid syndrome and is likely triggered by covid infection. Acquired APS in setting of recent covid infection needs to be considered in the setting of recurrent thrombotic events

Mallory-Weiss Syndrome in the Setting of Multiple Seizures

Background: Mallory-Weiss syndrome is a longitudinal mucosal laceration in the distal esophagus and proximal stomach, usually associated with forceful retching or vomiting. Here, we present a case of Mallory Weiss syndrome in the setting of multiple seizures without any retching or vomiting. Case Presentation: A 64-year-old man with history of epilepsy on anticonvulsant medications presented to the emergency department with complaints of multiple seizures. During the initial evaluation, he was alert, in no acute distress and was answering questions appropriately. He denied any trauma, loss of consciousness, nausea, vomiting, retching, tongue biting or incontinence. On examination, blood pressure was 92/53 mmHg and heart rate 98. His labs were significant for normocytic anemia with a hemoglobin of 9.7. In the ED, he had another seizure with no reported nausea, vomiting or retching. He was stabilized with anticonvulsants and IV hydration. Despite adequate fluid resuscitation, the patient remained hypotensive and was started on norepinephrine for undifferentiated shock. A few hours later, he had large volume hematemesis and developed hemorrhagic shock. On examination, he was lethargic but arousable. Repeat labs showed a drop in hemoglobin from 9.7 to 4.7. Patient received IV fluids, blood transfusions and required an additional pressor. He was also started on pantoprazole infusion, metoclopramide, and octreotide. After the patient was stabilized, EGD was performed and revealed a Mallory Weiss tear at gastroesophageal junction which was treated with an epinephrine injection. Patient was subsequently weaned off the pressors and discharged home with adjustments to anticonvulsants and a follow up appointment. Conclusion: It is essential to recognize gastrointestinal bleeding as a cause of cardiovascular collapse in the setting of seizures, despite absence of typical symptoms such as nausea, vomiting or retching. High suspicion may lead to early surveillance and prevention of Mallory-Weiss tear in epileptic patients

Bactrim Induced BRASH Syndrome In Elderly Female: A Case Report

Background: BRASH syndrome is a clinical entity comprising of bradycardia, renal failure, AV blockade, shock, and hyperkalemia. It is a vicious cycle in which AV nodal blockers and hyperkalemia act synergistically to precipitate bradycardia in patients with renal dysfunction resulting in cardiovascular collapse. Case Presentation: 89-year-old lady with history of Stage 4 CKD, hypertension, and diabetes mellitus presented with worsening generalized body weakness. On medication review, she was recently started on bactrim for treatment of a foot ulcer. Other home medications included diltiazem, lisinopril and dulaglutide. Initial vitals were significant for pulse 34, BP 90/35 mmHg and RR 19. Patient appeared somnolent but arousable. EKG was significant for third-degree heart block. Pertinent labs included potassium 6.7 and creatinine 5.8. She was treated with IV fluids and pressors for shock. She received calcium gluconate, insulin, dextrose and sodium polystyrene in the interim, until she was started on emergent dialysis. Following two sessions of dialysis, EKG reverted to sinus rhythm with resolution of complete heart block. She was eventually titrated off pressors. She was discharged on scheduled dialysis and follow up in a nephrology clinic. Conclusion: BRASH syndrome comprises of series of events that perpetuates itself. Caution should be exercised when prescribing bactrim as it might potentiate hyperkalemia, especially in patients with chronic kidney disease who are also on AV nodal blockers. Trimethoprim in Bactrim increases this risk by inhibiting potassium excretion from the kidneys. This could lead to a cycle of clinical events resulting in BRASH syndrome

A Rare Case of Takotsubo Cardiomyopathy In An Elderly Lady During Hospital Stay

Introduction: Takotsubo Cardiomyopathy (TTC) is an acute, reversible form of left ventricular systolic dysfunction, most often triggered by a sudden physical, or less commonly emotional event. Here, we describe a patient who developed Takotsubo Cardiomyopathy during her hospital stay. Case Description: 74-year-old Hispanic lady, a nursing home resident presented to the ED with altered mental status. She was admitted for septic shock due to UTI. Echocardiogram demonstrated normal systolic function, with 60-65% LV ejection fraction. After initiation of antibiotic therapy, she showed clinical improvement with resolution of shock. On day 8 of hospitalization, patient became emotionally upset and her clinical status deteriorated. Troponin peaked at 7.2, CK-MB 29.9, and EKG demonstrated borderline ST-elevation in lateral leads. Repeat echocardiogram demonstrated a significant reduction in the LVEF to 15%, moderately dilated left ventricle with akinesis of the apex and middle third of LV with hyperkinetic base, consistent with Takotsubo Cardiomyopathy. Unfortunately, her condition continued to deteriorate, leading to cardiac arrest and the patient expired. Discussion/Conclusion: There is a paucity in the literature describing the in-hospital occurrence of TTC. A high index of suspicion should be exercised in patients with recent physical or emotional stress with new-onset or refractory shock as the clinical picture of TTS overlaps with ACS