Hemorrhagic Pericardial Effusion Research Articles

Thoracic and abdominal aortic dissection in a hypertensive hyperthyroid cat

Aortic dissection is an uncommon finding in both dogs and cats. The precise pathophysiological mechanisms responsible for the development of aortic dissection remain unclear. In humans, aortic dissection is usually secondary to another systemic disease, such as systemic arterial hypertension, an abnormality of connective tissues or a parietal trauma. This is a case of an aortic dissection in a hypertensive hyperthyroid cat, presenting with haemorrhagic pericardial effusion. The dissection affected both thoracic and abdominal aorta, with histopathological confirmation. This case is an example of the utility of both thoracic and abdominal ultrasound for the diagnosis of aortic dissection in cats and it highlights the importance of rigorous clinical examination. Aortic dissection should be considered in the differential diagnosis of pericardial effusion in cats. Further investigations are fundamental to understand how dissections develop and extend to achieve good clinical results.
 REFERENCES
 
 Braverman et al. (2012) Diseases of the aorta. In: Braunwald’s Heart Disease. A textbook of cardiovascular medicine. 9th Eds Bonow R, Mann D, Zipes D, Libby P. Elsevier Saunders, Philadelphia, pp 1319-1331.
 Chetboul et al. (2006) Quantitative assessment of velocities of the annulus of the left atrioventricular valve and left ventricular free wall in healthy cats by use of two-dimensional colour tissue Doppler imaging. Am. J. Vet. Res. 2006, 67: 250-258.
 Cojocaru et al. (2013) Evaluation of oxidative stress in patients with acute ischemic stroke. Romanian Journal of Internal Medicine. 51(2):97-106.
 D’Ancona et al. (2014) Computational analysis to predict false-lumen perfusion and outcome of type B aortic dissection. The Journal of Thoracic and Cardiovascular Surgery. 148 (4):1756-1758.
 Gouni et al. (2018) Aortic dissecting aneurysm associated with systemic arterial hypertension in a cat. Schweiz Arch Tierheilkd. 160(5):320-324.
 Liao et al. (2008) A proteomic study of the aortic media in human thoracic aortic dissection: implication for oxidative stress. Journal of Thoracic and Cardiovascular Surgery. 136(1):65-72.
 Liu et al. (2016) Ursodeoxycholic acid attenuates acute aortic dissection formation in angiotensin II-infused apolipoprotein E-deficient mice associated with reduced ROS and increased Nrf2 levels. Cellular Physiology and Biochemistry. 38(4): 1391-1405.
 Phillippi et al. (2009) Basal and oxidative stress-induced expression of metallothionein is decreased in ascending aortic aneurysms of bicuspid aortic valve patients. Circulation. 119(18):2498-2506.
 Qin et al. (2016) Dynamic monitoring of platelet activation and its role in post-dissection inflammation in a canine model of acute type A aortic dissection. Journal of Cardiothoracic Surgery. 11(1):86.
 Qing et al. (2012) Ex-vivo haemodynamic models for the study of Stanford type B aortic dissection in isolated porcine aorta. European Journal of Vascular and Endovascular Surgery. 44(4):399-405.
 Waldrop et al. (2003) Aortic dissection associated with aortic aneurysms and posterior paresis in a dog. Journal of Veterinary Internal Medicine. 17(2):223-229.
 Wang et al. (2013) An experimental model of Stanford type B aortic dissection with intravenous epinephrine injection. Kaohsiung Journal of Medical Sciences. 29(4):194-199.
 Wey AC, Atkins CE (2000). Aortic dissection and congestive heart failure associated with systemic hypertension in a cat. Journal of Veterinary Internal Medicine. 14(2):208-213.

Idiopathic Pericarditis Leading to Hemorrhagic Pericardial Effusion- A Case Report and Review

Pericardial effusion presentation is a large spectrum that can vary from asymptomatic to cardiac tamponade. It is a relatively common syndrome and has a diverse set of etiologies including infections, malignancy, radiation/iatrogenic, pericardial injury, metabolic disturbances, endocrine disease, connective tissue disease, autoimmune disorders, trauma, or idiopathic. Pericardial drainage is recommended in most large pericardial effusions or those causing cardiac tamponade. Pericardial fluid can be either purulent, serous, serosanguinous, or hemorrhagic. In the case of hemorrhagic effusion, the common etiologies include malignancy, iatrogenic, and tuberculosis (in endemic regions). Large hemorrhagic pericardial effusions resulting from idiopathic (presumed viral) pericarditis are rare but possible. We present an interesting case of a woman with a large hemorrhagic pericardial effusion presenting as subacute cardiac tamponade caused by idiopathic pericarditis in the setting of known malignancy. This report aims to increase awareness about pericarditis as a potential cause of significant hemorrhagic pericardial effusions, rather than solely attributing them to malignancy. J MEDICINE 2024; 25: 87-89

Abstract 14933: A Rare Case of Cardiac Angiosarcoma Presenting as Hemorrhagic Pericardial Effusion

Cardiac sarcomas are exceptionally rare, with an incidence of only 0.02% and comprising less than 1% of all primary cardiac tumors. Consequently, diagnosis of the disease can be challenging due to non-specific presenting symptoms and diverse clinical manifestations. We present a unique case of cardiac sarcoma that highlights these challenges. A 70-year-old man with a history of hypertension, hyperlipidemia, and latent tuberculosis presented with palpitations, chest pain, and dyspnea, was found to have hemorrhagic pericardial effusion with tamponade. Pericardial fluid studies were negative for malignancy, and echo not suggestive of cardiac mass or pericardial abnormalities. He presented several months later with hemoptysis and was found to have innumerable pulmonary nodules on CT chest and a mediastinal mass adjacent to the right atrium. Bronchoscopy was negative for infection or malignancy. Ultimately the patient underwent CT-guided lung biopsy, which showed a malignant spindle cell neoplasm with a positive stain for vimentin and vascular markers suggestive of angiosarcoma of unknown primary. Given unclear relation of his mediastinal mass, cardiac MRI was done which showed a rapidly enhancing bulky neoplasm with abnormal contrast enhancement arising from the lateral right atrium (Figure 1) consistent with metastatic cardiac angiosarcoma. Patient was started on systemic anthracycline-based chemotherapy; however the overall prognosis remains poor. Given the rarity of cardiac sarcomas, prognosis is generally poor due to the advanced stage at the time of diagnosis. These tumors exhibit aggressive behavior and have a high propensity for metastasis. Due to their infrequency, knowledge and research is limited regarding effective treatments. This case highlights the significance of considering cardiac angiosarcoma in cases of hemorrhagic pericardial effusion even in the absence of obvious cardiac mass or pericardial nodularity on initial presentation.

Abstract 13611: Right Ventricular Perforation and Subsequent Tamponade Due to Fractured Inferior Vena Cava Filter Strut

Description of Case: A 39-year-old woman with a remote history of unprovoked pulmonary embolism (PE) treated with a retrievable inferior vena cava (IVC) filter presented with chest pain and syncope. Initial vital signs and examination were unremarkable. ECG showed diffuse ST elevations with PR depression consistent with acute pericarditis (Figure 1A). Given her history, CT angiogram (CTA) was performed and revealed complex pericardial effusion without PE. Echocardiogram confirmed large pericardial effusion with evidence of right ventricular diastolic collapse, raising concern for impending cardiac tamponade (Figure 1B). Urgent pericardiocentesis yielded 500 mL of sanguineous fluid, with resolution of effusion. A pericardial drain was left in place. Overnight she became hypotensive, tachycardic, diaphoretic, with muffled heart sounds on exam. Rapid re-accumulation of blood was noted from the drain, confirmed by repeat echo showing enlargement of the pericardial effusion. She was diagnosed with recurrent hemorrhagic pericardial effusion (HPE) of unclear etiology and was emergently taken for mediastinal exploration, where a metal shard measuring 2.2 cm was seen protruding though the RV (Figure 1C), confirmed on intraoperative TEE (Figure 1D). It was determined that a fractured IVC filter strut had migrated into the RV causing perforation and recurrent HPE. The strut was removed and RV defect patched. The patient did well post-operatively without effusion recurrence. Follow up CTA confirmed fractured IVC filter strut, with another filter strut also seen extending through the IVC wall (Figure E). Discussion: Rapid reaccumulation of a hemorrhagic, hemodynamically significant pericardial effusion without clear etiology, as in this case, should prompt consideration of surgical exploration to assess for bleeding source. As strut fractures are a known complication of retrievable IVC filters, these filters should be removed when no longer indicated.

Abstract 17356: Recurrent Hemorrhagic Pericardial Effusion Requiring a Multimodality Imaging Approach: A Case Report

Background: A 24-year-old female with no medical history presented to the ED with chest pain and dyspnea. Vitals were notable for tachycardia to 120s. Physical examination was unremarkable. Clinical Course: Initial evaluation was notable for thrombocytopenia, NT-proBNP of 151 and high sensitivity troponin T of 18. Transthoracic echocardiogram (TTE) revealed a small pericardial effusion with tamponade physiology prompting urgent pericardiocentesis. Bloody pericardial fluid was drained and fluid studies were consistent with hemorrhagic effusion with no evidence of infection or malignancy on cytology. Surveillance TTEs showed rapid reaccumulation of pericardial fluid within 72 hours of the initial intervention. Urgent pericardial window with drain placement was performed and intraoperative transesophageal echocardiogram (TEE) revealed a right atrial (RA) mass not detected on prior TTE. Cardiac MRI confirmed the presence of a large (50 mm x 31 mm) immobile and heterogeneous mass in the superior aspect of the RA suggestive of a malignant etiology with invasion to the adjacent pericardium. Positron Emission Tomography (PET) scan demonstrated hypermetabolic activity concerning for malignancy with no evidence of mediastinal, hilar adenopathy, or distant disease. She underwent mini-sternotomy and biopsy with pathology suggestive of primary cardiac angiosarcoma. Due to the high-risk nature and location of the tumor, she was unable to undergo primary surgical resection. Neoadjuvant chemotherapy was initiated with plan for subsequent surgical reassessment. Conclusion: Workup of recurrent hemorrhagic pericardial effusions require a multimodal imaging approach.

FRI244 Autoimmune Polyglandular Syndrome Type 2 And Peripartum Cardiomyopathy: A Case Report

Abstract Disclosure: A.G. Jimenez: None. J.D. Christensen: None. P. Surampudi: None. S. Phatak: None. J. Yoon: None. Background: Peripartum cardiomyopathy (PPCM) is a diagnosis of exclusion with evolving understanding of pathophysiology. There is limited consideration of the autoimmune processes contributing to PPCM. Case Presentation: A 20-year-old female had a recent delivery complicated by placenta previa, hemorrhage requiring transfusion, and pelvic infection. She presented 2 weeks postpartum with altered mental status and abdominal pain, found to be in septic shock, acute respiratory failure, acute liver injury initially thought to be secondary to retained products of conception. Subsequently, she was diagnosed with moderate-to-severe PPCM as she developed signs of heart failure, low ejection fraction <35%, mild ventricular dilatation, cardiogenic shock, hemorrhagic pericardial effusion with tamponade. She had no other prior cardiovascular history. She was briefly started on bromocriptine for treatment of suspected prolactin-mediated PPCM, in addition to digoxin, as her blood pressure was unable to sustain other treatments for PPCM. However, she hemodynamically decompensated and required persistent pressor support, leading to evaluation for other causes. Due to her prior history of hypothyroidism, an adrenal evaluation with a cosyntropin stimulation test was done. It demonstrated an undetectable cortisol at 0, 30, 60 minutes, with an elevated ACTH (1256, n=7-63 ng/dL), consistent with primary adrenal insufficiency (PAI). Workup for PAI did not reveal any infectious, infiltrative, vascular, pharmacological, or neoplastic etiology. Lab workup for concomitant hypophysitis was significant for low IGF-1 (Z-score -5.8, n= -2.0 to +2.0), but otherwise had expected elevated prolactin (121 ng/mL, n=5.2-26.5 ng/mL), suppressed LH (0.3 mIU/mL) and FSH (2.4 mIU/mL), and normal TSH (3.87 mIU/mL, n=0.27-4.20 mIU/mL) on levothyroxine 100 mcg. She had normal parathyroid hormone and hemoglobin A1c levels with no history of chronic candidiasis. Further workup showed positive antibodies to adrenal 21-hydroxylase enzyme, thyroid peroxidase, and glutamic acid decarboxylase 65, suggestive of autoimmune polyglandular syndrome (APS) type 2. She was started on glucocorticoids and mineralocorticoids for adrenal insufficiency resulting in a significant clinical improvement. She was subsequently discharged in stable condition. Conclusion: Due to increased rates of mortality in PPCM (4-11%), thought should be given to nontraditional etiologies of cardiac failure. Although rare, adrenal insufficiency must be considered in those with moderate-to-severe PPCM who continue to decompensate despite treatments. Untreated adrenal insufficiency can result in fatal consequences if not immediately treated. APS type 2 should be considered even in those without any confirmed family history of autoimmune disease. Those with autoimmune tendencies may be at higher risk of PPCM. Presentation: Friday, June 16, 2023

Haemorrhagic Pericardial Effusion as the Presenting Symptom of Scurvy.

Vitamin C deficiency (or scurvy) usually takes weeks to become apparent as cutaneous signs and impaired wound healing. Haemorrhagic pericarditis remains a rare complication of scurvy, which has never been reported as an isolated condition. We report the case of a haemorrhagic pericarditis revealing a vitamin C deficiency in a 56-year-old patient. A 56-year-old woman presented with a 2-week history of worsening chest pain and dyspnoea, with no significant medical history. Upon admission, the patient exhibited tachycardia, tachypnoea, low blood pressure, elevated jugular venous pressure, muffled heart sounds and multiple petechiae on her lower limbs. An ultrasound revealed a large pericardial effusion, and an emergency pericardiocentesis was performed, which yielded haemorrhagic fluid without atypical cells. An initial workup including haemoculture, PT and PTT, tuberculosis workup, autoantibodies, tumour markers and infectious disease was negative. A whole-body CT scan showed no evidence of tuberculosis or lymphoma. Additional testing showed that her vitamin C level was <3 umol/L. Following stabilisation, high-dose vitamin C therapy was initiated. Subsequently, she showed continued clinical improvement and remained asymptomatic upon her discharge. While uncommon, it is crucial to investigate vitamin C deficiency when confronted with an unexplained haemorrhagic pericardial effusion, particularly in patients with risk factors. Our case highlights the significance of early detection of this condition in promptly addressing the diverse complications of scurvy, thereby enhancing the prognosis of a potentially fatal condition. Haemorrhagic pericarditis could be an initial indication of scurvy.Vitamin C deficiency must be included in the differential diagnostic of haemorrhagic tamponade, even in the absence of a typical signs and symptoms of scurvy.

Rare Adenosquamous Lung Cancer Inducing Large Hemorrhagic Pericardial Effusion in An Undiagnosed Patient

While lung cancer is the leading cause of cancer mortality, only 2% of non-small cell lung cancer (NSCLC) cases are classified as the adenosquamous subtype. Here we present a case of a middle-aged man who presented with atypical symptoms of massive malignant hemorrhagic pericardial effusion without cardiac tamponade, induced by adenosquamous non-small cell lung carcinoma. Malignant hemorrhagic pericardial effusions are rare, and large volume ones are even rarer. The patient’s advanced malignancy was undiagnosed at presentation and was only discovered through investigations carried out for his pericardial disease. Malignant pericardial effusion may be the initial symptom of malignancy in some patients. Furthermore, adenosquamous carcinoma is a rare type of NSCLC whose response to chemotherapy is limited. Further studies of this rare subtype are warranted to improve patient prognosis.

An Unusual Case of Hemorrhagic Filarial Pericardial Effusion Presenting as Cardiac Tamponade

Filariasis presenting as pericardial effusion with cardiac tamponade is rare. We report a case of 34-year-old male who presented with a short history of fever, bilateral pedal edema and left sided chest discomfort of 10 days duration. On evaluation he was found to have pericardial effusion. Extensive work up to evaluate routine causes of pericardial effusion was unremarkable. His pericardial fluid showed microfilaria, however there was no microfilariae in peripheral blood smear. He was managed with pericardiocentesis and 04 weeks of Albendazole, diethylcarbamazine to which he responded. In the tropics filarial pericardial effusion should always be considered in cases of pericardial effusion of unknown etiology.

Sustained Apnea for Epicardial Access With Right Ventriculography: The SAFER Epicardial Approach

BackgroundEpicardial access (EA) has emerged as an increasingly important approach for the treatment of ventricular arrhythmias and to perform other interventional cardiology procedures. EA is frequently underutilized because the current approach is challenging and carries a high risk of life-threatening complications. ObjectiveThe purpose of this study was to determine the efficacy and safety of the SAFER (Sustained Apnea for Epicardial Access With Right Ventriculography) epicardial approach. MethodsConsecutive patients who underwent EA with the SAFER technique were included in this multicenter study. The primary efficacy outcome was the successful achievement of EA. The primary safety outcomes included right ventricular (RV) perforation, major hemorrhagic pericardial effusion (HPE), and bleeding requiring surgical intervention. Secondary outcomes included procedural characteristics and any complications. Our results were compared with those from previous studies describing other EA techniques to assess differences in outcomes. ResultsA total of 105 patients undergoing EA with the SAFER approach from June 2021 to February 2023 were included. EA was used for ventricular tachycardia ablation in 98 patients (93.4%), left atrial appendage closure in 6 patients (5.7%), and phrenic nerve displacement in 1 patient (0.9%). EA was successful in all subjects (100%). The median time to EA was 7 minutes (IQR: 5-14 minutes). No cases of RV perforation, HPE, or need of surgical intervention were observed in this cohort. Comparing our results with previous studies about EA, the SAFER epicardial approach resulted in a significant reduction in major pericardial bleeding. ConclusionsThe SAFER epicardial approach is a simple, efficient, effective, and low-cost technique easily reproducible across multiple centers. It is associated with lower complication rates than previously reported techniques for EA.

P416 A RARE CASE OF CHEST PAIN

Abstract 81–year–old woman, affected by arterial hypertension, paroxysmal atrial fibrillation treated with DOACs. She came to our emergency service for oppressive chest pain emerging after two weeks from the implantation of a dual–chamber pacemaker. The EKG showed 1 mm ST segment elevation in leads DII and aVL. Global and segmental function were normal, mild pericardial effusion along right chambers was reported on the echocardiogram. This case was managed as a STE–ACS and then the patient was given dual antiplatelet therapy and unfractioned heparin and taken to the cath lab. The coronary angiography didn’t show any significant stenosis. She was admitted to CCU, where pericardial effusion was noticed to be significantly increased. A CT scan revealed the ventricular pacemaker lead projecting into the pericardial sac with a 13 mm hemorrhagic pericardial effusion. Antithrombotic therapy was stopped and colchicine was started. The patient refused to undergo a trans–venous lead extraction. She was asymptomatic and hemodinamically stable at the time of discharge and was given a follow up program. This case shows a subacute complication of pacemaker implantation, in which antithrombotic agents administration made the real diagnosis to be shown after the increase of pericardial effusion. Ventricular lead perforation is a rare condition (0.1–0.8%). Some risk factors can be old age, female sex, anticoagulants, DMARDs and NSAIDs, the ventricular lead being positioned along the right ventricular free wall. Symptoms and signs depend on lead position. Diagnosis can be made by echocardiography, chest X–ray, CT scan. The best treatment for this patients is debated. In hemodinamically unstable patients an emergency treatment is recommended, while it is unclear which therapeutic option should be offered in the other cases. Lead perforation can be managed with transvenous or surgical lead extraction or a conservative treatment with a watchful waiting strategy can be performed. Acute, subacute and symptomatic perforations could better benefit from invasive strategies, otherwise chronic and asymptomatic cases could be followed up during time without invasive treatment.

Aortic Intramural Hematoma Mimicking Acute Coronary Syndrome

Type A Aortic intramural haematoma (IMH), a variant form of classic aortic dissection, has been accepted as an increasingly recognised and potentially fatal entity of acute aortic syndrome.It is a very dangerous, fatal, and emergency condition. It is very important to recognize the symptoms of acute aortic syndrome related to appropriate management Case Illustration A 52 year old man patient suffered from chest pain with moderate intensity while he was working at home. It was sharp , tear-like sensation, in the middle of the chest radiated to the back, accompanied with cold sweating, and did not relieve by rest. Because of this condition he brought to hospital. From examination at Emergency room, he had cardiomegaly, aortic dilatation. From the Electrocardiography an st elevation at V1-V2 and T inverted V4-V6 precordial lead,I aVL extremities lead and slightly elevated cardiac enzymes with risk factors for active smoking and uncontrolled hypertension. Initially he was suspected of having acute coronary syndrome with differential diagnose acute aortic syndrome. To exclude the diagnose he had underwent cardiac catheterization, the cardiologist in charge suspicious this patient with aortic dissection because of trapping contrast durante procedure and coronary minor disease. For a better diagnosis, transtransthoracic echocardiography and Aortic Computed Tomography angiography was performed on the patient which confirmed the evidence of dissection. After being diagnosed, we treat the patient as an acute aortic syndrome and we stabilize the patient's condition. The patient was planned for cardiac surgery Discussion Acute aortic syndrome, which includes Acute Aortic Dissection, Intramural Hematoma and penetrating aortic ulcer, is difficult to diagnosed. Aortic intramural hematoma, which is one of the acute aortic syndromes, is characterized by the presence of a hematoma in the medial layer of the aortic wall without the appearance of an intimal tear. The incidence of intramural hematoma differs slightly from that of aortic dissection syndrome. Patients with intramural hematomas often occur in older patients, more often with aortic aneurysms The patient receive treatment aggressively to control blood pressure by administering a non-dihydropyridine calcium channel blocker intravenously and then beta blocker, angiotensin II receptor blockers, was also needed. Acute aortic syndrome, where an intramural aortic hematoma can present with varying symptoms of varying severity, which can lead to misdiagnosis and delay in cases of life-threatening disease. In the case of our patient, who had strong cardiac risk factors, His initial presentation described an acute myocardial infarction; the diagnosis was made after CT scan was performed and the patient remained stable Conclussion Complaints of chest pain due to symptoms of acute aortic syndrome are very important to be recognized immediately because they need proper management. Complaints in this syndrome have similarities with complaints in acute coronary syndrome, pulmonary embolism and others. Patients with aortic intramural hematoma are at high risk for developing periaortic hematoma and hemorrhagic pericardial effusion. In patients with an intramural aortic hematoma, Stanford A, the most appropriate management is surgical technique. Initial management of blood pressure control, heart rate and anti-pain can be given. In this case, the choice of a combination of surgery with endovascular may be a logical choice of therapy

1256: DIFFERENTIATING OBSTRUCTIVE SHOCK: A CASE OF SIMULTANEOUS CARDIAC TAMPONADE AND PULMONARY EMBOLISM

Introduction: Obstructive shock is an obstruction of blood flow in the central vessels of the systemic or pulmonary circulation causing hemodynamic compromise. Here, we describe the unique challenge of managing a patient in shock with simultaneous hemorrhagic pericardial effusion and bilateral mainstem pulmonary emboli (PE) in setting of disseminated intravascular coagulation (DIC). Description: A 63-year-old female former smoker with recent deep venous thrombosis presented with 4 days of weakness, shortness of breath, and inability to tolerate oral intake, including apixaban. She was tachycardic, tachypneic and hypotensive. She was fluid resuscitated and BP improved from 83/43mmHg to 104/56mmHg. She later became hypoxic, requiring 6L oxygen by nasal cannula. Labs showed platelets 20k/mm3, D-dimer >35.2mg/L, Troponin T 0.56ng/mL and NT-proBNP 1864pg/mL. Bedside echocardiogram showed a large pericardial effusion. Chest CT angiography showed an acute PE involving the bilateral main pulmonary arteries and a new 4.0 cm spiculated right lung mass. A heparin drip was started and her oxygenation improved, however she became more hypotensive, requiring further fluid resuscitation. Repeat labs showed lactate 4.8mmol/L, platelets 4k/mm3, INR 3.6, aPTT 47s, haptoglobin < 10mg/dL and fibrinogen 50mg/dL, demonstrating DIC. Follow up echocardiogram showed tamponade physiology. The patient was transfused with fresh frozen plasma and platelets, eventually requiring vasopressor support. She was taken for CT-guided pericardiostomy with resolution of her shock. The pericardial fluid was grossly bloody, and the pathology showed adenocarcinoma. Discussion: This patient presented a diagnostic dilemma in ascertaining the primary cause of her obstructive shock. Echocardiographic features of obstructive shock due to RV failure secondary to central pulmonary embolism may not be evident in the setting of concurrent pericardial effusion. The clinical findings of a small right ventricle, worsening hypotension after heparinization as well as improvement in hemodynamics after pericardiostomy confirms that cardiac tamponade was the primary etiology for her obstructive shock. Findings of RV dilatation and hypokinesis after near complete drainage of pericardial effusion suggests that the PE was causing hemodynamic compromise as well.

Large Hemorrhagic Pericardial Effusion and Cardiac Tamponade Following BNT162b2 (BioNTech/Pfizer) Vaccine

The introduction of mRNA-based COVID-19 vaccinations has been useful in decreasing risks of severe illness with COVID-19 infection. Cardiac tamponade is a rare cardiovascular emergency that has been observed following both mRNA-based COVID-19 vaccinations and COVID-19 infections. We report the first case of a hemorrhagic pericardial effusion with cardiac tamponade in a 52-year-old woman occurring one week following the second dose of the BNT162b2 (BioNTech/Pfizer) SARS-CoV-2 vaccination. The time sequence in this case report correlates with reports submitted to the Vaccine Adverse Event Reporting System (VAERS), which indicates that cases of pericarditis following mRNA vaccination most commonly occur within 1-2 weeks following the second dose of vaccination.

SARS-COV-2-INDUCED COAGULOPATHY DEMONSTRATING HEMORRHAGIC CARDIAC TAMPONADE: A TIGHT SQUEEZE

SARS-COV-2-INDUCED COAGULOPATHY DEMONSTRATING HEMORRHAGIC CARDIAC TAMPONADE: A TIGHT SQUEEZE

MIMICKER OF MYOCARDIAL INFARCTION (MI): PHENYLEPHRINE-ASSOCIATED CORONARY VASOSPASM

MIMICKER OF MYOCARDIAL INFARCTION (MI): PHENYLEPHRINE-ASSOCIATED CORONARY VASOSPASM

Hemophagocytic Lymphohistiocytosis in the Setting of Therapy-Induced Acute Myeloid Leukemia: An Autopsy Report

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyper-inflammatory disorder that occurs due to immunologic dysregulation. HLH can be primary (hereditary) or secondary to infections, autoimmune diseases, immune deficiencies, metabolic diseases, drugs, or malignancies. Lymphoid neoplasms mostly accompany malignancy-associated HLH. We present a case of a 12-year-old boy with a history of precursor B lymphoblastic leukemia (B-ALL), who subsequently developed chemotherapy-induced acute myeloid leukemia (t-AML). The patient was admitted for febrile neutropenia and initial laboratory tests revealed hemophagocytic lymphohistiocytosis (HLH). The hospital course was complicated by multiple infections and septic shock. The patient received several broad-spectrum antimicrobials, dexamethasone, as well as a pericardial drain to drain the hemorrhagic pericardial effusion. Despite intervention, the patient expired, and an autopsy was performed. We provide a synopsis of the main autopsy findings.

Painless Aortic Dissection Revealed After its Rupture to the Pericardium: About a Case and Review of the Literature

Stanford type A aortic dissection is a rapidly evolving pathological process often with poor prognosis if no urgent surgical management. However, it may be asymptomatic in the acute phase with late symptomatic presentation or incidental diagnosis on chest imaging. We report the case of a 52-year-old man in whom a painless aortic dissection was discovered incidentally following a pericardial effusion assessment. The patient's condition was successfully managed with uneventful open heart surgery. This case demonstrates an extremely rare presentation of accidental hemorrhagic pericardial effusion caused by painless aortic dissection.

COVID-19 mRNA Vaccine Induced Pericarditis With Large Pericardial Effusion Followed by New-Onset Arrhythmia

Several cases of myocarditis and pericarditis have been reported after mRNA COVID-19 vaccination. Interestingly, most cases were seen in male adolescents and young adults, commonly after 3-4 days of the second dose of mRNA vaccine. The vaccine contains the viral spike glycoprotein in the nucleoside-modified mRNA of the coronavirus that activates the proinflammatory cascades and immunological pathways, which can cause myocarditis and pericarditis. Here we report a case of a middle-aged Caucasian male who presented with progressive dyspnea, fever, and chills seven days after the second dose of the COVID-19 vaccine. He was found to have pericarditis with massive hemorrhagic pericardial effusion, large bilateral pleural effusions, circulatory shock, and cardiac arrhythmia. The patient required pericardiocentesis and thoracentesis and was discharged home on antiarrhythmic and anti-inflammatory therapy. Our case report describes a correlation between mRNA COVID-19 vaccine and pericarditis, suggesting the importance of pharmacovigilance and reporting of adverse outcomes and encourages a high index of clinical suspicion in physicians to facilitate early diagnosis and interventions.

Hemorrhagic pericardial effusion resulting in constriction in hereditary hemorrhagic telangiectasia

BackgroundWe report the first ante-mortem diagnosis of hemorrhagic pericardial effusion in hereditary hemorrhagic telangiectasia resulting in constriction; the case also demonstrates the unusual but well-described complication of right-sided heart failure requiring extracorporeal membrane oxygenation (ECMO) support after pericardiectomy.Case presentationA previously healthy 48 year old man with a strong family history of Osler–Weber–Rendu disease presented to our institution with signs and symptoms of advance heart failure. His workup demonstrated a thickened pericardium and constrictive physiology. He was brought to the operating room where old clot and inflamed tissue were appreciated in the pericardial space and he underwent complete pericardiectomy under cardiopulmonary bypass. Separation from bypass, hampered by the development of right ventricular dysfunction and profound vasoplegia, required significant pressor and inotropic support. The right heart dysfunction and vasoplegia worsened in the early postoperative period requiring a week of ECMO after which his right ventricle recovered and he was successfully de-cannulated.ConclusionGiven the poor outcome of severe postoperative right ventricular failure after pericardiectomy, with high central venous pressure, a low gradient between central venous and pulmonary artery pressures and high vasopressor requirements, ECMO should be instituted promptly.