7 research outputs found

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

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    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

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    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

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    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

    STEC-HUS; Unusual presentation in an elderly female

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    Background: Hemolytic uremic syndrome (HUS) is a multisystem disease presenting as renal impairment, microangiopathic hemolytic anemia (MAHA) and thrombocytopenia with a peak incidence of 2.1 cases per 100,000 persons/year in general population. Case Description: 81-year-old female with history of Diabetes, presented to us with non-bloody emesis and loose stools. Labs on admission were significant for WBC 17000, Hb 12.5, PLT 241, BUN 74, Cr 8.9 and Lactate 12. She was admitted for severe metabolic acidosis and acute renal failure attributed to metformin use and undifferentiated shock. Patient developed acute worsening of respiratory status due to increasing acidosis requiring intubation. Bicarbonate infusion was started however patient had to undergo emergent dialysis for refractory acidosis. On 3rd day of admission patient developed dysentery which led to Hb drop to 7.1 and platelets to 96. Peripheral smear revealed thrombocytopenia and schistocytes. GI panel was positive for ETEC, EIEC, Shigella toxin producing E. coli (STEC) and Campylobacter. Diagnosis of STEC-HUS was made. Patient was supportively managed with fluid resuscitation, pressors, antibiotics, hemodialysis and transfusions. She demonstrated significant improvement, attained hemodynamical stability off pressors and was eventually extubated. Patient was discharged few days later at her baseline health. Conclusion: It is challenging to diagnose STEC-HUS in older patients as the prevalence is higher in children and adults present with higher hemoglobin and fibrinogen levels. However, we emphasize on considering it as a differential diagnosis especially in elderly presenting with acute renal failure and history of gastroenteritis

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

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    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

    Severe Hypokalemia Secondary to Distal Renal Tubular Acidosis in a Hispanic Man

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    Introduction: Renal tubular acidosis is a rare renal disorder that can cause severe electrolyte imbalances which can be life threatening. Case: A 21-year-old man presented to the ED on account of generalized weakness and body aches of one day duration. He reported no past medical history other than a previous episode of similar symptoms with improvement after IV hydration and electrolytes replacements about 2 months prior. He was not taking any medications and denied vomiting, diarrhea nor any significant family history. He admitted to alcohol and marijuana use. Physical examination was significant for reduced muscle power, tone, and reflexes in all extremities. He was unable to move his limbs against gravity. Admission laboratory findings revealed severe hypokalemia 1.1 mEq/L, metabolic acidosis with bicarbonate of 10.1 and EKG showed QT prolongation. Patient received a total of about 200 mEq of potassium through a central line in 24 hours with serum level of 3.7mmol/l in addition to intravenous bicarbonates with a resolution of the presenting symptoms. Discussion: The causes of hypokalemia are broad however a methodical approach can be helpful to rule out the many causes and narrow down the differential diagnosis. Distal RTA is caused by the inability of the distal renal tubule to secrete hydrogen ions due to the selective failure of activity or expression of the H+-ATPase. Conclusion: This case underscores the importance of systematic approach to the evaluation of patients with hypokalemia to uncover the cause of the underlying disease before life threatening complications occur. Our patient remains under close follow up

    Case of cryoglobulinaemia associated with chronic hepatitis B

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    We present a case of a woman in her 50s with chronic hepatitis B (CHB) who had a longstanding history of arthralgia and swollen joints associated with severe fatigue. Investigations were consistent with a diagnosis of hepatitis B virus (HBV)-related cryoglobulinaemia. Two months after treatment with tenofovir alafenamide, an antiviral therapy for HBV, there was a significant improvement of her symptoms and undetectable serum cryoglobulins. Cryoglobulinaemia is a relatively rare extrahepatic manifestation of HBV infection and only presents in about 2%-4% of the patients with CHB. Its clinical manifestations include purpura, renal dysfunction, arthralgias and neuropathy. Since the presentation of cryoglobulinaemia in CHB can be non-specific, one needs to have a high index of suspicion to avoid delay in diagnosis and treatment
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