Sudden Onset Shortness Of Breath Research Articles

Needle Aspiration in Tuberculosis-Associated Secondary Spontaneous Pneumothorax

Introduction: The management of tuberculosis-associated secondary spontaneous pneumothorax mostly requires chest tube insertion for complete drainage and resolution. We reported a case of tuberculosis-associated secondary spontaneous pneumothorax that improved with needle aspiration. Case: A 29-year-old female with pulmonary tuberculosis presented with sudden onset shortness of breath. Chest examination revealed asymmetry, decreased vocal fremitus, hypersonor, and decreased vesicular sound in the right lung field. Chest radiograph showed right pneumothorax with a 2 cm intrapleural distance. Needle aspiration was performed because the patient refused chest tube insertion. The first needle aspiration evacuated approximately 615 cc of air. The second needle aspiration was repeated 24 hours later due to clinical deterioration, and 610 cc of air was evacuated. Chest radiograph evaluation on the 6th day of treatment showed no pneumothorax. During hospitalization, the patient received oxygen therapy, anti-tuberculosis drugs, chest physiotherapy, and other symptomatic therapies such as mucolytics. The patient's condition improved, and she was discharged on the 9th day of hospitalization. Tuberculosis-associated secondary pneumothorax occurs in 1-3% of cases. Conclusion: Needle aspiration is a therapeutic modality for tuberculosis-associated secondary spontaneous pneumothorax. This modality has several advantages, including shorter length of stay, less cost and pain, and fewer complications. Needle aspiration combined with oxygen therapy, anti-tuberculosis drugs, and chest physiotherapy should be the modality of treatment for tuberculosis-associated secondary pneumothorax.

Case Report: Disseminated hydatid cyst: Unusual presentation and therapeutic challenges

Introduction: Cystic echinococcosis (CE), caused by Echinococcus granulosus sensu lato, is a parasitic disease prevalent in endemic regions. CE frequently leads to the formation of hydatid cysts in various organs, with the liver being the most commonly affected site. Involvement of the spleen has been rarely reported in the literature. Managing disseminated hydatid cyst disease presents significant diagnostic and therapeutic challenges. Case presentation: A 40-year-old female with a past medical history of hypothyroidism presented with sudden onset shortness of breath, dry cough, and chest pain for 3 days. She had a recent travel history to Egypt. Physical examination revealed mild right upper quadrant tenderness. Laboratory findings showed elevated white blood cell count with eosinophilia and increased inflammatory markers. Chest X-ray and pan-computed tomography (Pan-CT) scans identified multiple cystic lesions in the lung, liver and spleen. Serological tests confirmed the presence of anti-Echinococcus antibodies, leading to a diagnosis of disseminated hydatid cyst disease. The patient was managed medically and surgically by a multidisciplinary team. Conclusion: Disseminated hydatid cyst disease, though rare, presents complex diagnostic and management challenges. Timely recognition, supported by clinical, radiological, and serological assessments, is essential. Surgical intervention should be considered in a patient when multiple extrahepatic cysts are present, and rupture is evident, as this approach can significantly reduce patient morbidity and mitigate life-threatening complications.

An Unusual Cause of Aortic Regurgitation in a Patient With Bicuspid Aortic Valve

Aortic fibrous strands are considered residual tissue from aortic valve development. Rupture of these strands is an important albeit uncommon cause of aortic regurgitation (AR). The authors describe a 67-year-old man who was admitted to the authors' hospital with sudden onset shortness of breath and diagnosed with severe AR. The patient was scheduled for Bentall surgery. The transesophageal echocardiogram (TEE) found multiple fibrous strands that were present in multiple locations of the aortic valve, some of which were ruptured. Ruptured fibrous strands are in the differential diagnosis in patients presenting with acute AR without a more conventional explanation, and TEE is instrumental in securing the diagnosis.

A RARE CASE OF DISSEMINATED MYCOBACTERIUM AS THE CAUSE OF RECURRENT PNEUMOTHORAX

A RARE CASE OF DISSEMINATED MYCOBACTERIUM AS THE CAUSE OF RECURRENT PNEUMOTHORAX

WITHDRAWN

SESSION TITLE: Drug-Induced Lung Injury Pathology Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Nitrofurantoin is a common antibiotic prescribed for urinary tract infections. Acute pulmonary toxicity from nitrofurantoin can present in many ways that can be confused with a COPD exacerbation. This case gives us insight into a unique diagnosis of acute nitrofurantoin pulmonary toxicity on a patient who became immediately symptomatic after taking the medication. CASE PRESENTATION: An 80 y/o patient with COPD and DM presented to the hospital due to sudden onset shortness of breath. His symptoms began immediately after starting nitrofurantoin for an UTI. His symptoms were chest tightness, cough with sputum production, and body shakes. On admission, the patient was hemodynamically stable, but hypoxic requiring 10L NC to maintain an oxygen saturation of 90%. Laboratory evaluation demonstrated an elevated white count (12K/uL), eosinophils (5.6%), AST/ALT (209/380 U/L), and a lactic acid of 3.1 mmol/L. His sputum culture, coccidioidomycosis, viral panel, and blood cultures were negative. A CTA of his lungs showed emphysematous changes with bilateral ground glass opacities and no pulmonary embolism. Physical exam was relevant for end expiratory wheezing. The patient was started on bronchodilators and steroids for a COPD exacerbation on admission but failed to respond to treatment. Pulmonology was consulted for the persistent hypoxia. We found after chart review that the patient had prior admissions for COPD exacerbations that correlated with him starting nitrofurantoin as an outpatient. We decided to stop treating him for a COPD exacerbation, resume his home inhalers, and stop the nitrofurantoin. The patient was titrated off his oxygen within 24 hours and all his laboratory values were normalized. A follow up CT Chest showed resolution of the ground glass opacities. DISCUSSION: Nitrofurantoin toxicity is described in literature as hepatoxicity, pulmonary fibrosis, and rarer instances of acute pulmonary toxicity such as the case reported here (1). Our case highlights how nitrofurantoin toxicity can mimic a COPD exacerbation and if this diagnosis is not considered, patients have prolonged hospitalization or improper treatment. Most cases of pulmonary toxicity from nitrofurantoin usually respond well to stopping the antibiotic, like our patient (2). While nitrofurantoin has an excellent safety profile, it is important to be aware that there have been fatalities from pulmonary toxicity from nitrofurantoin (3). CONCLUSIONS: Pulmonary toxicity from nitrofurantoin can easily mimic a COPD exacerbation or a pneumonia. The symptoms from an acute toxicity usually occur within several hours to days of taking the antibiotic. When patients are admitted for acute hypoxia and infectious workup is negative, there needs to be a thorough review of medications and if nitrofurantoin is listed, it should be discontinued and listed to not be used again. Reference #1: Huttner A, Verhaegh EM, Harbarth S, Muller AE, Theuretzbacher U, Mouton JW. Nitrofurantoin revisited: a systematic review and meta-analysis of controlled trials. J Antimicrob Chemother. 2015 Sep;70(9):2456-64. doi: 10.1093/jac/dkv147. Epub 2015 Jun 11. PMID: 26066581. Reference #2: Khan TMA, Ansari Y, Siddiqui AH, Matthew H, Siddiqui F. Nitrofurantoin-associated Acute Pulmonary Toxicity Mimicking Severe Sepsis with Significantly Elevated Procalcitonin. Cureus. 2019;11(8):e5516. Published 2019 Aug 29. doi:10.7759/cureus.5516 Reference #3: Livanios K, Karampi ES, Sotiriou A, Tavernaraki K, Styliara P, Kainis E. Nitrofurantoin-induced acute pulmonary toxicity. Respirol Case Rep. 2016;4(1):25-27. Published 2016 Jan 14. doi:10.1002/rcr2.131 DISCLOSURES: No relevant relationships by Adnan Abbasi No relevant relationships by Bhargav Patel

Management of Psychiatric Disorders in Patients with Respiratory Diseases.

Management of Psychiatric Disorders in Patients with Respiratory Diseases.

NON-CARDIOGENIC PULMONARY EDEMA FOLLOWING CARDIAC ABLATION: WILL THE REAL CULPRIT PLEASE STAND UP?

TOPIC: Diffuse Lung Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Non-cardiogenic pulmonary edema (NCPE) is an entity with a variety of etiologies and pathology that include alveolar damage due to direct toxicity or catecholamine surge. We present a case of non-cardiogenic pulmonary edema 48 hours following ablation for atrial fibrillation. CASE PRESENTATION: A 72-year-old woman with a history of atrial fibrillation, coronary artery disease with bypass grafting, and heart failure with preserved ejection fraction presented with sudden onset shortness of breath for a few hours. She had undergone cardiac ablation with pulmonary vein isolation and cavotricuspid isthmus line 2 days prior, with no periprocedural complications. She was tachypneic and hypoxic (oxygen saturation 51% on room air), with reduced breath sounds on auscultation but no peripheral edema or jugular venous distension. Laboratory workup was notable for leukocytosis, elevated N-terminal proBNP (9,853 pg/mL), elevated C-reactive protein (257 mg/L), with normal procalcitonin and negative viral panel, including SARS-CoV-2. Electrocardiography showed no acute abnormalities. Computed tomography (CT) of the chest did not show pulmonary embolism but demonstrated bilateral ground glass opacities. Oxygen was administered via high-flow nasal cannula, and diuresis was initiated in the inpatient setting. Echocardiography revealed mild left ventricular diastolic dysfunction, with left atrial enlargement and mild pulmonary hypertension (39 mm of Hg). Right heart catheterization demonstrated normal filling and pulmonary artery pressures (pulmonary capillary wedge pressure (PCWP) of 6 mm Hg and mean pulmonary artery pressure or 16 mm Hg). Systemic corticosteroids were empirically initiated for suspicion of an inflammatory etiology. The combination of steroids and diuresis produced symptomatic and radiographic improvement, and she was discharged with supplemental oxygen. Her oxygen was unable to be completely weaned off as of follow-up 6 weeks later. DISCUSSION: Catheter ablation for atrial fibrillation is a widely adopted rhythm control strategy with a favorable safety profile. NCPE appears to be an exceedingly rare complication of ablation, with only a few cases being reported in our literature review. The diagnosis of NCPE can be challenging to make, as it must be distinguished for cardiogenic edema. The lack of peripheral edema or jugular venous distension in our patient suggested the absence of cardiac etiology, but a right heart catheterization demonstrating normal PCWP definitively excluded it. Hypotheses for mechanisms for this reaction include a systemic inflammatory response syndrome, autoimmune reaction to ablation, and vagus nerve injury with consequent dysregulation of immunomodulation. Treatment is primarily supportive, including adequate ventilation, with consideration for diuresis and corticosteroids. CONCLUSIONS: NCPE is a rare adverse effect of ablation, and treatment is primarily supportive. REFERENCE #1: Weber R, Minners J, Restle C, et al. Pulmonary edema after extensive radiofrequency ablation for atrial fibrillation. J Cardiovasc Electrophysiol. 2008 Jul;19(7):748-52. DISCLOSURES: No relevant relationships by Dan Kazmierski, source=Web Response No relevant relationships by jacob miller, source=Web Response No relevant relationships by Pius Ochieng, source=Web Response No relevant relationships by NISHANT SHARMA, source=Web Response

TRANSFUSION-RELATED ACUTE LUNG INJURY ASSOCIATED WITH BANLAMIVIMAB INFUSION

TOPIC: Lung Pathology TYPE: Medical Student/Resident Case Reports INTRODUCTION: Transfusion-related acute lung injury (TRALI) is a well-known risk of intravenous infusions, but the true incidence is poorly defined. With the arrival of COVID-19, a new intravenous medication, Banlamivimab, may be associated with TRALI. We present a unique case of Banlamivimab TRALI from COVID-19 treatment. CASE PRESENTATION: A 69-year-old female presented to the Emergency Department with complaints of fevers, generalized weakness, nausea, vomiting, and dyspnea on exertion. She was febrile to 101.2 Fahrenheit and maintaining a normal oxygen saturation level on ambient air. Laboratory tests were positive for SARS-COV-2, elevated CRP, and troponin up to 1.37 ng/mL. Complete blood count and chemistry were both normal. Chest x-ray was unremarkable. Initially, she was set to be discharged home. Infectious Disease was consulted regarding her COVID infection and recommended Banlamivimab infusion prior to discharge. Approximately 45 minutes after starting the infusion, the patient experienced sudden onset shortness of breath and rigors. She was hypoxic to 85% on ambient air, tachypneic, febrile to 102.9 Fahrenheit, hypertensive and in acute respiratory distress. She had no evidence of an allergic reaction nor anaphylaxis. The infusion was stopped immediately and she was given Solumedrol and Benadryl. Her troponin increased to 3.23 ng/mL, white blood cell count rose to 19,300/mL and her lactic acid was 6.8. Chest x-ray showed new pulmonary edema. Echocardiogram showed normal systolic and diastolic function. She was diagnosed with transfusion related lung injury and fully recovered with supportive treatment. DISCUSSION: Banlamivimab is an investigational medicine used in patients who are considered high risk for being hospitalized or progressing to severe COVID-19 infection. Although TRALI is a well-defined risk factor of blood transfusions, there is insufficient data related to transfusion related lung injuries caused by Banlamivimab infusion or other human monoclonal antibodies. When treating COVID-19 patients with Banlamivimab, TRALI must be a side effect taken into consideration due to the possibility of causing a second hit to COVID-19 damaged lungs. As highlighted by the acuity of our patient's illness, it is feasible that such an event could increase patient mortality. CONCLUSIONS: This case uniquely demonstrates the possibility of TRALI with Banlamivimab infusions and highlights the importance of early recognition and management. Furthermore, clinicians should maintain a high index of suspicion for TRALI in patients receiving not only blood transfusions, but also any human monoclonal antibody infusions. REFERENCE #1: (2021, March 18). FACT SHEET FOR HEALTH CARE PROVIDERS EMERGENCY USE AUTHORIZATION (EUA) OF BAMLANIVIMAB AND ETESEVIMAB. Eli Lilly and Company. Retrieved April 30, 2021, from https://www.covid19.lilly.com/bam-ete/getting-started REFERENCE #2: Petraszko, T. (2019, February 26). Transfusion-related acute lung Injury (trali). Retrieved April 30, 2021, from https://professionaleducation.blood.ca/en/transfusion/publications/transfusion-related-acute-lung-injury-trali REFERENCE #3: Kleinman, S., MD. (n.d.). Transfusion-related acute lung injury (TRALI). Retrieved April 30, 2021, from https://www.uptodate.com/contents/transfusion-related-acute-lung-injury-trali#H1588910 DISCLOSURES: No relevant relationships by Pankaj Aggarwal, source=Web Response No relevant relationships by Jenna Dumovich, source=Web Response No relevant relationships by Justin Haloot, source=Web Response No relevant relationships by Jane O'Rorke, source=Web Response

Self-assessment questions

A 42-year-old patient in her 4th pregnancy presents to the labour ward triage with sudden onset shortness of breath. As her observations are recorded, she collapses. What is the most likely cause of the collapse?A.ThromboembolismB.Amniotic fluid embolismC.Aortic dissectionD.CardiomyopathyE.Sudden arrhythmia

THE EVANESCENT LUNG

SESSION TITLE: Medical Student/Resident Obstructive Lung Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Vanishing lung syndrome (VLS), also known as giant bullous emphysema, is a chronic progressive condition predominantly seen in upper lobes of lungs, occupying at least one-third of the hemithorax and can compress normal lung parenchyma. It is commonly seen in young males with a history of chronic smoking. Other risk factors include α-1-antitrypsin deficiency and marijuana (1). Complications include tension pneumothorax. Bullectomy is usually the treatment of choice. Herein, we describe a rare case where an elderly male with symptoms of pneumonia was found to have an incidental finding of VLS on computed tomography pulmonary angiogram (CTPA). CASE PRESENTATION: A 76-year-old African American male with a medical history of prostate cancer status post-radiotherapy and hypertension came in with a 2-day history of sudden onset shortness of breath, cough with yellowish-brownish sputum and subjective fevers. He had a 60 pack-year smoking history. Vitals were remarkable for a body mass index of 15, heart rate of 125/min, respiratory rate of 22/min, and fever of 100.8 but there was no hypoxia. On comprehensive physical examination, he had stage 3 nail clubbing. Pulmonary examination revealed hyper resonant percussion in the right upper zone and decreased air entry. Laboratory investigation was unremarkable except for leukocytosis of 15.8 X 103 /mm3. A chest radiograph demonstrated acute infiltrates in the right lung inferior to the right hilum. There was a large bleb within the right hemithorax occupying most of the right hemithorax. Left hemithorax exhibited chronic emphysematous changes with peripheral blebs. Since the patient had a history of malignancy and was tachycardic on admission. CTPA was done which revealed very large right pulmonary bleb and air space opacities suggestive of acute bronchopneumonia or bronchitis. Ceftriaxone and azithromycin were started after which the patient clinically improved in one day. Investigating the imaging findings, α-1 antitrypsin levels were normal. HIV testing was negative. Cardiothoracic surgery was consulted and a decision was taken to do bullectomy but the patient refused the procedure as he was asymptomatic. DISCUSSION: VLS is a rare condition usually seen in young males with chronic smoking history or marijuana abuse. A common presentation is tension pneumothorax as a result of the rupture of the bulla. What makes this case unique is that our patient was an asymptomatic elderly male without any prior diagnosis of the same. He presented with clinical features of pneumonia and was incidentally found to have VLS at this age(2). CONCLUSIONS: VLS becomes evident as it progresses and can lead to tension pneumothorax. Patients should be referred for pulmonary function tests for diagnosis of chronic obstructive pulmonary disease and cardiothoracic surgery for bullectomy which is the treatment of choice and improves the function of the lung significantly (3). Reference #1: 1. Barry Ladizinski, M.D., and Christopher Sankey, M.D.; Vanishing Lung Syndrome N Engl J Med 2014; 370:e14, DOI: 10.1056/NEJMicm1305898 Reference #2: 2. Amarjit Singh Vij, Robert James, Akashdeep Singh, Amrinder Singh Dhaliwal, Ajay Chhabra, Kamaljeet Kaur Vij; A Rare Case of Vanishing Lung Syndrome; J Assoc Physicians India. 2014 Dec;62(12):51-3. PMID: 26259424 Reference #3: 3. Nidhi Sood, Nikhil Sood; A Rare Case of Vanishing Lung Syndrome; Case Rep Pulmonol. 2011; 2011: 957463. doi: 10.1155/2011/957463. PMID: 22937434 DISCLOSURES: No relevant relationships by Ankit Agrawal, source=Web Response No relevant relationships by Sanya Chandna, source=Web Response No relevant relationships by Monarch Shah, source=Web Response

SUN-515 Use of Plasmapheresis for Treatment of Thyroid Storm Resistant to Antithyroidals

Management strategies of thyroid storm include measures to reduce thyroid hormone synthesis, hormone release, conversion from T4 to T3, and inhibition of the peripheral effects of excessive thyroid hormone. Plasmapheresis has been described as a treatment option when traditional therapy is not successful or not feasible.We present a case of an adult patient who presented in thyroid storm in whom plasmapheresis was used successfully as a bridge to thyroidectomy.51-year-old female with history of hypertension presented with sudden onset shortness of breath, and palpitations. She had an irregular heart rate of 140BPM, respiratory rate of 40, mean arterial blood pressure 65mmHg. Electrocardiogram confirmed atrial fibrillation with rapid ventricular response and the patient was admitted to the intensive care unit. She was started on diltiazem drip and subsequently received amiodarone and electrical cardioversion due to persistent rapid heart rate. She developed respiratory distress and required endotracheal intubation.Initial thyroid profile revealed low TSH and normal FreeT4, but her FT4 increased above normal on day 2, treatment for thyroid storm was initiated with potassium iodine, hydrocortisone and propylthiouracil. She was kept on propranolol 80 mg q/4h, intravenous esmolol 50 mcg/kg/min, diltiazem drip 5 mg/hr, and was started on Digoxin 0.25 mg q/4h. TSI and TPO were undetectable, and thyroid ultrasound revealed a right nodule measuring 5 x 2.2 x 3.7cm. Thyroid storm was attributed to a toxic nodule exacerbated by exposure to excess iodine (contrast for imaging and amiodarone). Propylthiouracil, hydrocortisone and beta blocker were maximized, and cholestyramine was added, but their heart rate remained elevated, blood pressure worsened requiring synchronized cardioversion.Because of persistent hyperthyroid state, refractory to medical treatment, patient was started on plasmapheresis on day 10 of hospitalization, she underwent 5 sessions with significant reduction in Free T3 and Free T4 (Figure 1), and remarkable improvement in her hemodynamic status and resolution of tachycardia. Patient underwent total thyroidectomy on day 16, without complications.Plasmapheresis has been described as a treatment option for refractory thyroid storm, as a bridge therapy prior thyroidectomy. During plasmapheresis, thyroid-binding globulin, thyroid hormones, cytokines and putative antibodies are removed with the plasma; then the colloid replacement provides new binding sites for circulating free thyroid hormone (2). Although albumin binds thyroid hormone less avidly than TBG, it provides a much larger capacity for low-affinity binding that may contribute to lower free thyroid hormone levels, providing a window for thyroidectomy.1.Muller C et al, Role of Plasma Exchange in the Thyroid Storm, Therapeutic Apheresis and Dialysis15 (6): 522–531

TISSUE PLASMINOGEN ACTIVATOR IN CARDIAC ARREST SECONDARY TO MASSIVE PULMONARY EMBOLUS

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Cardiac arrest secondary to massive pulmonary embolism carries a poor prognosis. In most cases, the diagnosis is made post-mortem. CASE PRESENTATION: 64-year-old lady with past medical history of DVT and pulmonary embolus (PE) not on anticoagulation, type 2 diabetes, hypertension, coronary artery disease presented with sudden onset shortness of breath and mild chest pain of less than 1 day duration. Upon presentation, she was hypotensive, tachycardic, and tachypneic. Initial EKG showed ST-elevation in leads 3 and V1 with deep S wave in lead 1. CTA chest showed extensive bilateral pulmonary emboli and RV to LV ratio greater than 2. Shortly after returning from CT, she became hypoxia and bradycardia followed by asystole. CPR was started and she attained ROSC after 1 cycle of CPR. She was given 50 mg IV tPA bolus followed by continuous infusion of 50 mg over 1 hour. Blood pressure improved after administration of tPA and she was intubated thereafter for airway protection. She had cardiac arrest again after intubation and attained ROSC after 1 cycle of CPR. She was transferred to the ICU and started on heparin drip and vasopressors. Her condition continued to improve and she was extubated the next day. She was ultimately discharged in stable condition on direct-acting oral anticoagulant. DISCUSSION: The diagnosis of PE during an in-hospital cardiac arrest can be difficult. In most cases, thrombolytic therapy is given based on high clinical suspicion, often due to the presence of echocardiogram changes on point-of-care ultrasound. “McConnell sign,” which is a specific pattern of RV dysfunction is observed in massive PE and is characterized by akinesis of the mid free wall and normal contractility of the apical wall. It is approximately 77% sensitive and 94% specific [3]. However in clinical practice, McConnell sign can be difficult to recognize. tPA may also be underutilized due to concern for major bleeding. However, there is literature to suggest that administration of tPA during cardiac arrest is not associated with increased risk of bleeding and often leads to decreased time to return of spontaneous circulation [1]. The optimal timing of tPA administration has yet to be determined. In retrospective studies, tPA is either given as a single 50 mg bolus, 50 mg bolus followed by a second 50 mg bolus, or as 50 mg bolus followed by 85 mg over 90 minutes [2]. However, there are no trials that compare the utility and efficacy of these protocols against each other. CONCLUSIONS: There is general consensus that tPA should be administered during cardiac arrest in patients with high suspicion of PE, however the optimal dose and timing of tPA administration is yet to be determined. In our patient, a dose of 50mg IV bolus followed by 50mg infusion over 1 hour had resulted in a favorable outcome. Reference #1: Yousuf T, Brinton T, Ahmed K, et al. Tissue Plasminogen Activator Use in Cardiac Arrest Secondary to Fulminant Pulmonary Embolism. J Clin Med Res. 2016;8(3):190-5. Reference #2: Kürkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160(10):1529-1535. Reference #3: Borloz, Matthew P., William J. Frohna, Carolyn A. Phillips, and Michael S. Antonis. "Emergency Department Focused Bedside Echocardiography In Massive Pulmonary Embolism.” The Journal of Emergency Medicine 41, no. 6 (2011): 658-60. https://doi.org/10.1016/j.jemermed.2011.05.044. DISCLOSURES: No relevant relationships by basma al-bast, source=Web Response No relevant relationships by Mirza Ali, source=Web Response No relevant relationships by Abdisamad Ibrahim, source=Web Response No relevant relationships by Thamer Sartawi, source=Web Response No relevant relationships by Tareq Zaza, source=Web Response

TO CLOT OR NOT TO CLOT

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Autoimmune disorders predispose to venous thromboembolism (VTE), which can be difficult to manage. We present a unique case of difficult to control acute on chronic VTEs in a patient with multiple, overlapping, autoimmune disorders. CASE PRESENTATION: A 48-year-old nulligravida African-American female with a history of recurrent VTEs requiring inferior vena cava filter presented with sudden onset shortness of breath. On presentation, the patient was tachycardic but otherwise stable. Physical exam revealed an obese female in distress with an exquisitely tender left calf. Heparin drip was started for presumed new VTE. EKG showed sinus tachycardia without S1Q3T3 or ST segment or T wave abnormalities. CT PE confirmed bilateral segmental mismatched defects concerning for pulmonary emboli in the bilateral lung bases. Echocardiogram revealed flattening of the interventricular septum consistent with right ventricular strain. Lower extremity ultrasound revealed occlusive DVTs in both common femoral veins. The patient was admitted to the intensive care unit for possible thrombolysis vs thrombectomy, however, she had an acute 3 point drop in Hb (to 6.1) secondary to severe menorrhagia. She was deemed ineligible due to her refusal of blood transfusions and was started on medroxyprogesterone. Given a history of acute on chronic VTEs, autoimmune work up was pursued, which revealed positive lupus anticoagulant and ANA, elevated SSA, anti-Smith, and anti-RNP, and decreased antithrombin-III. Given her highly prothrombotic status, chronic anticoagulation therapy was discussed. The patient specifically requested an easily manageable non-Warfarin regimen. She was started on rivaroxaban and discharged to home with close follow up. The patient re-presented 9 days later with similar symptoms. Her Hb was 3.5. She was transfused 6 units of pRBCs with her consent. An intrauterine device was emergently placed with plans for future hysterectomy. Heparin drip was started post-procedure, however, the patient developed worsening tachycardia and left calf pain. Repeat ultrasound revealed propagation of her known DVT to the left greater saphenous vein. However, vascular surgery noted that the patient would need definitive treatment of uterine bleeding prior to any intervention. Per hematology, the patient was bridged to warfarin given her underlying coagulopathy. The patient’s clinical status remained stable for the next few days, and she was discharged to home on warfarin, medroxyprogesterone, and follow ups within one week. DISCUSSION: Autoimmune diseases are more common in females of reproductive age and can predispose to recurrent VTEs. Anticoagulation with warfarin is preferred, especially in patients with antiphospholipid syndrome. CONCLUSIONS: Patient comorbidities, and preferences, must be taken into account for proper management of the potentially deadly pulmonary manifestations of systemic autoimmune disorders. Reference #1: Cohen H, Hunt BJ, Efthymiou M et al. Rivaroxaban versus warfarin to treat patients with thrombotic antiphospholipid syndrome, with or without systemic lupus erythematosus (RAPS): a randomised, controlled, open-label, phase 2/3, non-inferiority trial. Lancet Haematol. 2016 Sep;3(9):e426-36. https://doi.org/10.1016/S2352-3026(16)30079-5. DISCLOSURES: No relevant relationships by Temidayo Abe, source=Web Response No relevant relationships by Iheoma Alinnor, source=Web Response No relevant relationships by Eric Chang, source=Web Response No relevant relationships by Anyanwoke Chisom, source=Admin input No relevant relationships by Melvin Crawford, source=Web Response No relevant relationships by Chima Odinkemere, source=Web Response No relevant relationships by Parris Tanksley, source=Web Response No relevant relationships by Benjamin Wibonele, source=Web Response

Electrocardiographic changes mimicking acute coronary syndrome in a large intracranial tumour: A diagnostic dilemma

BackgroundST elevation Myocardial infarction is a medical emergency. A variety of noncardiac conditions had been known to mimic the ECG changes that are seen in acute coronary syndrome. Although the common ECG changes that are documented with raised intracranial pressure are T inversions, prolongation of QT interval and sinus bradycardia, ST elevation or depression, arrhythmias and prominent U waves have also been recognized. However, ST elevations in association with primary intracranial tumours are rarely reported.Case presentationA 68-year-old female patient with a large left sided frontoparietal sphenoidal ridge meningioma with mass effect developed sudden onset shortness of breath while awaiting surgery. Her ECG showed ST segment elevations in the inferior leads along with reciprocal T inversions in anterior leads. The patient was treated with dual antiplatelet therapy and unfractionated heparin. The ST elevations in the ECG remained static and the cardiac Troponin assay was repeatedly negative. 2D ECHO, coronary angiogram and CT pulmonary angiography were normal. The repeat noncontract CT scan of the brain revealed two small areas of haemorrhage in the tumour.ConclusionThe two mechanisms for ECG changes described in subarachnoid haemorrhage are the neurogenic stunned myocardium due to the catecholamine surge on the myocytes and stress cardiomyopathy. The same mechanisms could be the reasons for the ECG changes seen in intracranial tumours. These ECG changes could be easily misdiagnosed as acute coronary syndrome. This case emphasizes the importance of the cardiac biomarkers, 2D ECHO and coronary angiogram when confronted with such a diagnostic dilemma. Thus a more holistic analysis should be practiced in diagnosing acute coronary events in patients with intracranial pathologies to obviate a myriad of unnecessary investigations, interventions, costly treatment strategies which may well be detrimental to the patient.

P-85 Thrombolysis for pulmonary embolism in palliative care: a case report

Background Thrombolysis for pulmonary embolism (PE) in a patient with advanced cancer has never been reported in the literature. Whilst not an absolute contraindication, most clinicians would be wary of thrombolysing a patient with a limited life expectancy. A case is presented of a patient with advanced mesothelioma who received thrombolysis treatment with a resultant significant improvement in pleuritic chest pain and dyspnoea. History The patient was a 69 year old man who was diagnosed with epithelioid mesothelioma and received radiotherapy to his right chest followed by palliative chemotherapy. Subsequent CT scanning showed disease progression and the patient declined further chemotherapy. Thrombolysis The patient was admitted to hospital with sudden-onset shortness of breath and right sided chest discomfort which was felt to be due to disease progression. Three days later the patient developed new, severe left sided pleuritic chest pain and acute breathlessness. The patient was thrombolysed with alteplase (50 mg IV over 1 hour) on clinical suspicion of a PE. The pleuritic chest pain resolved completely and the acute severe dyspnoea improved significantly within two hours of treatment and a CTPA later confirmed acute-on-chronic pulmonary thromboembolism as well as progressive mesothelioma. The patient was transferred to the hospice four days later for ongoing management and end-of-life care. Effect of Thrombolysis on Symptom Control On admission to the hospice, the patient contined to complain of mild to moderate dyspnoea but had no pain. He was commenced on regular immediate-release morphine (10 mg QDS) for breathlessness but only required one breakthrough dose of analgesia before his condition deteriorated. The patient died comfortably nine days after thrombolysis treatment. Conclusion Thrombolysis was very effective in controlling pleuritic chest pain and acute severe dyspnoea in this patient with PE and advanced cancer with a limited life expectancy.

Spontaneous Pneumothorax in a Patient with Marfanoid Habitus

A 39-year-old smoker with Marfanoid habitus presented with sudden onset shortness of breath. The diagnosis of right-sided primary spontaneous pneumothorax was made. It was successfully managed by drainage with inter costal tube. Presence of Marfanoid phenotype and smoking will increase the risk of spontaneous pneumothorax.

Endobronchial Cartilage Rupture: A Rare Cause of Lobar Collapse

Endobronchial cartilage rupture is a rare clinical condition, which can present in patients with severe emphysema with sudden onset shortness of breath. We present a case of a 62-year-old male who presented to our emergency department with sudden onset shortness of breath. Chest X-ray showed lung hyperinflation and a right lung field vague small density. Chest Computed Tomography confirmed the presence of right middle lobe collapse. Bronchoscopy revealed partial right middle lobe atelectasis and an endobronchial cartilage rupture. Endobronchial cartilage rupture is a rare condition that can present as sudden onset shortness of breath due to lobar collapse in patients with emphysema and can be triggered by cough. Bronchoscopic findings include finding a collapsed lung lobe and a visible ruptured endobronchial cartilage. A high index of suspicion, chest imaging, and early bronchoscopy can aid in the diagnosis and help prevent complications.

Medicolegal aspects of Maternal Deaths due to Pulmonary Thromboembolism

A state of hypercoagulability protects pregnant women from bleeding tendency which leads to pulmonary thromboembolism and results in medicolegal issues. Case 01 32 year old pregnant female who developed weakness of legs, and was suspected to have Spinal Tuberculosis. Lower Segment Caesarian Section was performed and Heparin was started as she was immobile. Vertebral surgery was performed and anticoagulants were stopped. She died due to sudden onset difficulty of breathing. Allegations of medical negligence were raised by the relatives at the autopsy. The autopsy revealed bilateral Deep Vein Thrombosis (DVT) and pulmonary embolism. Case 02 A mother who presented with a first trimester abortion and pain in right leg died following sudden onset shortness of breath. She also had a history of a previous first trimester abortion. Autopsy revealed an embolus in the pulmonary artery with swollen and congested right leg without DVT. CONCLUSIONS Case 01 Regarding the allegations of medical negligence, the legal authorities will consider whether the discontinuation of prophylactic anticoagulants before the 2nd surgery was a necessity and whether it was for the best interest of the patient. Case 02 Immunological syndromes and inherited thrombophilia could be considered as underlying causes for multiple first trimester abortions and Deep Vein Thrombosis. The Importance of performing the risk assessment of DVT when indicated is highlighted. Sri Lanka Journal of Forensic Medicine, Science & Law-December 2014-Vol.5 No.2; 20-22

Left Ventricular Noncompaction: A Rare Cause of Heart Failure in a HIV Patient

Background: Heart failure in patients with human immunodeficiency virus (HIV) is often from dilated cardiomyopathy as a result of HIV itself, drug myotoxicity, secondary infections, or druginduced atherosclerosis. Left ventricular noncompaction (LVNC) is a rare cardiac congenital abnormality which occurs due to early arrest of endomyocardial morphogenesis. Case: A 47- year-old female patient with HIV presented with sudden onset shortness of breath and symptoms of congestive heart failure. Echocardiography showed noncompacted endocardium with reduced left ventricular function. She was subsequently diagnosed with LVNC. Discussion: Multiple etiologies have been implicated in cardiomyopathy among HIV patients. LVNC is a rare cause of left ventricular failure, particularly in this population. Echocardiography plays a pivotal role in the diagnosis. Conclusion: It is often challenging to identify the underlying cause of cardiomyopathy in a patient with HIV. While LVNC is a rare cause of left ventricular failure, typical findings on echocardiography can obviate the need for a more complex evaluative strategy.

Chilaiditi's Sign in a Patient on Peritoneal Dialysis

A 87-year-old gentleman with end stage renal failure on peritoneal dialysis presented to the emergency department for sudden onset shortness of breath. A chest x-ray was obtained, revealing apart from a left sided pneumothorax, there was alarmingly a gas density under the right hemidiaphragm. It is diagnosed as Chilaiditi's sign in a peritoneal dialysis patient.