Accumulation Of Pericardial Fluid Research Articles

Constrictive pericarditis with massive pericardial effusion.

A 27-year-old man was admitted to our hospital for the investigation of pericardial effusion (PE) and ascites. Despite the accumulation of excessive pericardial fluid, vital signs of cardiac tamponade were not observed. He had no prior medical history except for a blunt chest trauma 10 years earlier. Echocardiography showed a tiny heart in extraordinarily retained massive PE (panel A, Supplementary data online, Video S1). Computed tomography (CT) revealed a distended overfilling pericardial cavity that remarkably compressed his heart and lung (panels B and C). Magnetic resonance imaging showed a thickened pericardium and a respiratory septal bounce phenomenon (see Supplementary data online, Video S2). Heart catheterization followed by a pericardial drainage of gigantic 6500 mL amount of exudative fluid suggested constrictive property of diastolic square root sign in left and right ventricular simultaneous pressure tracings (panel D). He was diagnosed with effusive–constrictive pericarditis. Despite the removal of pericardial fluid and the treatment with anti-inflammatory medications, the underlying pericardial constricted property continued to cause symptoms. He underwent a surgical removal of the thickened pericardium uneventfully (panel E). Further analysis of the volume of the thoracic cavity utilizing a comprehensive 3D-rendered CT revealed a significantly greater pre-operative volume of 9569 mL compared with the post-operative volume of 5903 mL (panel F, Supplementary data online, Video S3). This is the first report to suggest that the compensative and elastic ability of both the thoracic and pericardial cavities plays a role in protecting hemodynamics in effusive–constrictive pericarditis.

Saved by point of care echo.

A 40-year-old black male with a past medical history of sickle cell disease, cardiomyopathy, and pulmonary hypertension presents as a transfer from an outside facility to a tertiary care hospital for evaluation after a formal echocardiogram reported “biatrial enlargement and small cystic structure adjacent to the right atrium.” The patient arrived at the receiving hospital in acute severe distress with altered mental status, tachycardia, tachypnea, hypoxia, and hypotension with near agonal respirations on bilevel positive airway pressure. He was also noted to have bilateral jugular venous distention to the angle of mandibles and bilateral lower extremity edema. Given the acuity of the patient's condition, a bedside point-of-care (POC) ultrasound was done using the Rapid Ultrasound for Shock and Hypotension (RUSH) protocol. Bilateral lung slide was present with a bilateral A-line profile. Inferior vena cava (IVC) interrogation showed a markedly dilated non-distensible IVC. In the apical 4-chamber cardiac view, with color Doppler, it became obvious that there was a very large extracardiac cystic mass nearly completely compressing the right atrium (Video 1). Mitral valve inflow velocity was assessed via pulse wave Doppler and was found to demonstrate echocardiographic pulsus paradoxus (Figure 1). The emergency physician made the diagnosis of an extracardiac cystic mass compressing the right atrium causing pericardial tamponade rapidly at the bedside. A multidisciplinary team was mobilized by the emergency physician and the epicardial cyst was drained under ultrasound guidance in the emergency department resulting in 1300 cc of serous fluid with the restoration of the right atrium volume, normalization of the patient's vital signs, and return to his normal mental status. Pericardial tamponade occurs when there is an impairment of ventricular filling due to atrial compression by pericardial fluid or blood.1 Far more rarely, cardiac tamponade can be caused by extrinsic compression.2 Traumatic pericardial effusions typically occur rapidly and present as acute hemodynamic compromise in the setting of trauma. Medical causes of tamponade can be much more insidious given the usually slower accumulation of pericardial fluid. Pericardial tamponade presents typically as either cardiogenic or obstructive shock. Although physical exam findings such as Beck's triad, are often cited, echocardiography provides an invaluable tool in the detection of tamponade.3 In one case series, the sensitivity of the presence of all 3 components of Becks Triad was 0%, whereas any single element had a sensitivity 50%.4 Emergency physicians can rapidly diagnose pericardial tamponade with POC ultrasound and thus render lifesaving treatment, as in this case.

Transdiaphragmatic pericardial washout post penetrating cardiac injury found incidentally at diagnostic laparoscopy

A 22-year-old male presented following a precordial stab. He was haemodynamically and metabolically normal. Initial investigations did not reveal pericardial fluid or haemothorax. At diagnostic laparoscopy, we encountered haemoperitoneum and a diaphragmatic injury through which the heart was visible. After pericardial washout, laparoscopic repair was effected. This case highlights a potential problem with extended focused assessment with sonography in trauma (eFAST) in that it will only be positive if there is an accumulation of pericardial fluid. It also confirms the utility of diagnostic laparoscopy for penetrating left thoracoabdominal injuries and shows that principles of open surgery can be safely applied laparoscopically in select patients.

BE CAREFUL, THAT CARDIAC TAMPONADE MAYBE MALIGNANT

TOPIC: Lung Cancer TYPE: Medical Student/Resident Case Reports INTRODUCTION: Cardiac tamponade results from the accumulation of pericardial fluid under pressure which causes impaired cardiac filling and hemodynamic compromise. The causes of cardiac tamponade include infection, inflammation, autoimmune diseases, malignancy, drugs, and radiation. Malignancies including lungs, breast, gastrointestinal and hematological may lead to pericardial effusion with or without tamponade. Cardiac tamponade as an initial presentation of malignancy is rare. CASE PRESENTATION: A 63-year-old male presented with altered mental status for 2 weeks, intermittent cough for 6 months, and unintentional weight loss of about 20 lbs. His vitals were blood pressure 125/86, MAP 94, HR 100, and RR 18. He has a medical history of Type 2 diabetes mellitus, hypertension, dyslipidemia, depression, anxiety, tuberculosis (treated in 1970), exposure to radiation during military service, and a family history of multiple malignancies. CT head showed no acute intracranial abnormality. Chest X-ray showed right perihilar pneumonia and the patient was started on antibiotics. CT chest showed multilobar pneumonia, underlying nodularities within the right lung, diffuse sclerotic lesions throughout the skeleton suggestive of metastatic disease, right small pleural effusion, large pericardial effusion. TTE showed moderate to large pericardial effusion with tamponade physiology. He underwent an urgent pericardial window to relieve cardiac tamponade. On analysis, pericardial fluid was malignant. It showed metastatic adenocarcinoma, consistent with lung primary. Immunohistochemical stains show that tumor cells are positive for Ber-EP4, CD15, CK7, and TTF-1. DISCUSSION: There are three routes through which the malignancies involve pericardium – local extension, hematogenous and lymphatic. Pericardial effusion is common in malignancy and when present associated with poor prognosis and can be fatal. Cardiac tamponade is however a rare initial presentation of malignancy. EKG findings in tamponade include low voltage QRS, PR segment depression, electrical alternans, and sinus tachycardia. Diagnosis can be made by echocardiography. CONCLUSIONS: Pericardial effusion with cardiac tamponade may be malignant. Pericardiocentesis in cardiac tamponade has therapeutic efficacy including high diagnostic yield. Pericardial fluid cytology should be examined even if the malignancy is not suspected, especially if the chest x-ray is abnormal. REFERENCE #1: Pericardial diseases in patients with cancer: contemporary prevalence, management, and outcomes. BMJ Volume 106 Issue 8 https://doi.org/10.1136/heartjnl-2019-315852 REFERENCE #2: Cardiac tamponade as the initial presentation of malignancy: is it as rare as previously supposed? BMJ Volume 70 Issue 828 https://doi.org/10.1136/pgmj.70.828.703 REFERENCE #3: Relation of Acute Pericardial Disease to Malignancy. American Journal of Cardiology https://doi.org/10.1016/j.amjcard.2005.01.094 DISCLOSURES: No relevant relationships by Nimesh Adhikari, source=Web Response No relevant relationships by Nouran Eshak, source=Web Response No relevant relationships by Kenneth Iwuji, source=Web Response No relevant relationships by Kenneth Nugent, source=Web Response No relevant relationships by Upama Sharma, source=Web Response No relevant relationships by Anupama Sharma, source=Web Response

THE DEADLY PACE

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Myocardial perforation remains as a rare but important complication of pacemaker insertion. Perforation can occur acutely within 24 h after implantation, sub-acutely between 24 h to one month after implantation and chronically occurring more than one month after implantation. (Sidhu). Acute perforations are well described at medical literature, but chronic perforations are much less common and can be difficult to diagnose (Ahmed). This is the case of atypical presentation of a chronic right ventricular perforation caused by RV ICD lead presenting with tamponade and left sided compression atelectasis. CASE PRESENTATION: A 73-year-old Male with PMHx of A-Fib, CHF class II, A-HTN, NIDDM, RA, PUD, TAA, S/P ICD placement 3 months before presentation, that comes to the ED with pleuritic chest pain, dizziness, SOB and fatigue of 3 months of evolution. Patient states that the symptoms slowly worsened over the last 3 days. At physical examination was found with BP 90/40, HR 105 bpm, RR 21rpm Sat 95% in acute distress, using accessory muscles with muffled heart sounds and + JVD. COVID-19 Ag was negative. EKG shows sinus tachycardia and low voltage on precordial leads. A bedside echocardiogram shows large pericardial effusion with tamponade physiology, ventricular perforation and emergent pericardiocentesis was performed. A total of 515 ml of bloody pericardial fluid was removed and patient vital signs improves. Chest CT scan later confirmed the presence of pericardial fluid accumulation and left sided compression atelectasis. The ICD lead was removed and relocated at the ventricular septum to avoid ventricular perforation in the future. DISCUSSION: In rare circumstances when a large effusion develops over time, it may cause compression atelectasis of the surrounding bronchi and lung (Amin). Compression atelectasis caused by ventricular perforation are better described in cases of acute or subacute ventricular perforation at the medical literature. The most common presentation of chronic perforation is SOB and hypoxemia. This patient presentation after 3 months of ICD placement, with sudden onset cardiac tamponade and no hypoxemia is an atypical presentation of chronic ventricular perforation. The rapid fluid accumulation over time in the pericardium, is what causes that this space stretches to accommodate the excess fluid, that later cause a compression atelectasis of the surrounding bronchi and lung (Amin). CONCLUSIONS: This patient atypical presentation of ventricular perforation wasn't described before in the literature. Is very important not to assume that any perforation may the sequelae of a recent intervention and can present acutely like in this life-threatening clinical scenario. As clinicians we need to keep in mind that ventricular perforation may present with large effusion causing compression atelectasis, with or without tamponade physiology. REFERENCE #1: Sidhu B, Rajani R, Rinaldi C. Chronic Ventricular lead perforation: Expect the Unexpected. Clin Case Rep. 2019, 7: 455-468 REFERENCE #2: Ahmed A, Shokr M, Lieberman R. Subacute right ventricular perforation by pacemaker lead causing left sided hemothorax and epicardial hematoma. Case Reports in Cardiology. 2017: 1-5 REFERENCE #3: Amin H, Gyawali B, Chaudhuri D. A large pericardial effusion culminating in left lung collapse. Cureus. 2019, 11: e5287 DISCLOSURES: No relevant relationships by Jesse Aleman, source=Web Response No relevant relationships by Francisco Caraballo, source=Web Response No relevant relationships by Greisha Gonzalez Santiago, source=Web Response

Pericardiocentesis in children: 20-year experience at a tertiary children's hospital.

Pericardiocentesis is the invasive percutaneous procedure for acute and chronic excessive accumulation of pericardial fluid. There is a paucity of data on the effectiveness and safety of pericardiocentesis in children. To evaluate the effectiveness and safety of pericardiocentesis and factors associated with acute procedural failure and adverse events. This was a single-centered retrospective study to describe all the children aged ≤20 years who underwent pericardiocentesis. Data on demographics, etiologies of pericardial effusion, and repeat intervention at follow-up were collected. A total of 127 patients underwent 153 pericardiocentesis. The median age was 6.5 years (1 day-20 years) with weight of 17 kg (0.5-125). Most common etiology was post-pericardiotomy syndrome (n = 56, 44%), followed by infectious (12%), malignant (10%), and iatrogenic (9%). Pericardiocentesis was performed more commonly in the catheterisation laboratory (n = 86, 59%). Concurrent pericardial drain placement was performed in 67 patients (53%). Acute procedural success was 92% (141/153). Repeat intervention was performed in 33 patients (22%). The incidence of adverse events was 4.6% (7/153): hemopericardium requiring emergent surgery (n = 2); hemopericardium with hypotension (n = 2); seizure with anesthesia induction (n = 1); and right ventricle puncture with needle (n = 2). Pericardiocentesis at the bedside had a higher rate of acute procedural failure than that in the catheterisation lab (17 versus 1%, p < 0.01). No identifiable risk factors were associated with adverse events. Pericardiocentesis was life-saving in children with its high effectiveness and safety even in urgent situations. Although initial pericardiocentesis was effective, one of five patients required re-intervention for recurrent pericardial effusion.

Diagnostic pitfalls: intramyocardial lymphoma metastasis mimics acute coronary syndrome in a diffuse large B cell lymphoma patient\u2014case report

BackgroundCardiac tumors are very uncommon compared to other cardiac diseases. Their clinical symptoms can vary from absent to non-specific. The most common symptoms are arrhythmias, blood flow obstruction due to valvular dysfunction, shortness of breath, systemic embolization, and accumulation of pericardial fluid. Hereby, we describe a very rare case of a diffuse large B cell lymphoma patient who presented with the symptoms and signs of acute coronary syndrome (ACS) but the patient’s complaints were caused by his intramyocardial lymphoma metastasis.Case presentationForty-eight-year-old diffuse large B cell lymphoma patient was admitted to our emergency department with chest pain, effort dyspnea, and fever. The patient had normal blood pressure, blood oxygen saturation, sinus tachycardia, fever, crackles over the left lower lobe, novum incomplete right bundle branch block with Q waves and minor ST alterations, elevated C-reactive protein, high-sensitivity troponin-T, and d-dimer levels. Chest X-ray revealed consolidation on the left side and enlarged heart. Bed side transthoracic echocardiography showed inferior akinesis with pericardial fluid. Coronary angiography showed no occlusion or significant stenosis. Chest computed tomography demonstrated the progression of his lymphoma in the myocardium. He was admitted to the Department of Hematology for immediate chemotherapy and he reached complete metabolic remission, followed by allogeneic hematopoietic stem cell transplantation. Unfortunately, about 9 months later, he developed bone marrow deficiency consequently severe sepsis, septic shock, and multiple organ failure what he did not survive.ConclusionsOur case demonstrates a very rare manifestation of a heart metastasis. ACS is an unusual symptom of cardiac tumors. But our patient’s intramyocardial lymphoma in the right atrium and ventricle externally compressed the right coronary artery and damaged the heart tissue, causing the patient’s symptoms which imitated ACS. Fortunately, the quick diagnostics and immediate aggressive chemotherapy provided the patient’s remission and suitability to further treatment.

Complement C9 expression is associated with damaged myocardial cells in pediatric sudden death cases of fulminant myocarditis

BackgroundBecause disease progression is so fast in sudden death of acute fulminant myocarditis, damage of myocardial cells is not evident in routine hematoxylin and eosin staining. To understand damage to myocardial cells and the mechanism of sudden death, immunohistochemical staining was performed for two forensic autopsy cases.Case presentationThe patients were a healthy 5-year-old girl and 8-year-old boy. They suddenly died within 2 days of appearance of flu-like symptoms. An autopsy showed accumulation of yellowish-clear pericardial fluid containing fibrin deposits, fluid blood in the heart, and congestion of visceral organs. Histologically, minor necrosis or degeneration of myocardial cells with mainly lymphocytic infiltration was observed sometimes in tissue sections. Immunohistochemically, positive complement C9 staining and negative sirtuin 1 staining were found. These findings suggested wide damage of myocardial cells, even in regions with no marked changes in myocardial cells with hematoxylin and eosin staining. These areas corresponded to those with strong accumulation of lymphocytes.ConclusionsImmunohistochemistry for complement C9 and sirtuin 1 might become a new tool for evaluating damage of myocardial cells of fulminant acute myocarditis.

CARDIAC TAMPONADE FROM RAPID UREMIC PERICARDITIS IN PATIENT WITH WARFARIN OVER-ANTICOAGULATION

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Cardiac tamponade constitutes a medical emergency, which requires prompt recognition, diagnosis and treatment that is geared towards preventing cardiovascular collapse and cardiac arrest. CASE PRESENTATION: 81-year-old male patient with end stage renal disease on hemodialysis, paroxysmal atrial fibrillation on warfarin anticoagulation, diabetes mellitus type II, and morbid obesity, who was evaluated for history of 24-hour progression of general malaise, orthopnea, dyspnea on exertion, and dizziness after missing two sessions of hemodialysis. Physical exam was remarkable for borderline low blood pressure, +3 leg edema, distended jugular veins, bibasilar crackles, distant heart sounds, absence of cardiac murmurs or heart sounds. ECG showed pulsus alternans and low voltage criteria. Limited bedside echocardiogram was remarkable for a moderate pericardial effusion with minimal ventricular and atrial compression abnormalities. Patient was provided hemodialysis for volume overload without hemodynamic decompensation and was monitored with telemetry and bedside hemodynamics. Shortly after hemodialysis, patient developed worsening shortness of breath and became hypotensive. Patient was started on norepinephrine vasopressor therapy. A bedside limited echocardiogram showed diastolic right ventricular and right atrial collapse, non-collapsibility of the inferior vena cava and severe pericardial effusion that duplicated in size. Bedside emergent subxiphoid echocardiography-guided pericardiocentesis with instillation of agitated saline was performed with removal of about 400cc of serosanguineous fluid with resolution of hypotension and electric alternans. Labs reflected marked uremia, elevated ESR and C-reactive protein and warfarin overanticoagulation with INR of 4.5. Pericardial fluid resulted with a culture-negative exudative effusion composed of bloody material and inflammatory cells. Chest non-contrast computed tomography showed nonspecific mild mediastinal adenopathy. Positron emission tomography–computed tomography showed no significant F-18 Fluorodeoxyglucose avid lesions that were identified. Patient was provided ultrafiltration for 5 days, and started on colchicine and indomethacin with weekly follow-up of inflammatory markers and echocardiography, with marked improvement of pericardial effusion size and return of normal hemodynamics. DISCUSSION: Uremic pericarditis was identified in setting of acute pericarditis in a patient with over-anticoagulation. The hemorrhagic component resulted in rapid fluid accumulation and tamponade. The instillation of agitated saline can help assess for inadvertent chamber puncture during procedure. CONCLUSIONS: Uremic pericarditis is now an uncommon cause of pericarditis, but it can be exacerbated in the setting of inflammatory pericarditis and over-anticoagulation, leading to rapid accumulation of bloody pericardial fluid and cardiac tamponade. Reference #1: Maggiolini S, Gentile G, Farina A, et al. Safety, efficacy, and complications of pericardiocentesis by real-time echo-monitored procedure. Am J Cardiol 2016;117:1369-74. Reference #2: Sadjadi SA, Mashahdian A. Uremic pericarditis: a report of 30 cases and review of the literature. Am J Case Rep. 2015;16:169-173. Reference #3: Osuch JR, Khandekar JD, Fry WA. Emergency subxiphoid pericardial decompression for malignant pericardial effusion. Am Surg. 1985;51(6):298-300. DISCLOSURES: No relevant relationships by VICTOR MOLINA-LOPEZ, source=Web Response No relevant relationships by Hector Santiago, source=Web Response No relevant relationships by Francisco Tirado-Polo, source=Web Response

Mechanical Cardiac Tamponade as an Initial Presentation of Malignant Lymphoma: Case Report

Cardiac tamponade results from an accumulation of pericardial fluid under pressure, leading to impaired cardiac filling and haemodynamic compromise. In malignant lymphoma, cardiac and pericardial involvement, even though relatively uncommon, can be one early manifestations of this neoplastic disease. We describe a case of a 21 year old female with no medical history, whose first presentation for mediastinal lymphoma was a mechanical cardiac tamponade.

Echo-Guided Pericardiocentesis: When and How Should It Be Performed?

Abnormal accumulation of pericardial fluid is a common cardiac condition with different etiologies. Draining of the pericardial fluid (pericardiocentesis) is often indicated for diagnostic and therapeutic purposes and is performed in an elective or emergent setting. Echocardiography is the primary imaging method for diagnosing, localizing, and quantifying pericardial effusion as well as evaluating its hemodynamic effects, including the presence of cardiac tamponade. In this manuscript, we review the indications for pericardiocentesis and provide practical step-by-step guidance for echo-guided pericardiocentesis. Echo-guidance is an effective method to improve the safety and efficacy of pericardiocentesis. In experienced hands and with a stepwise approach, procedural outcomes are excellent, and complication rates are very low. Asymptomatic small idiopathic effusions have a benign course and can be left untreated. Prolonged drainage with an indwelling pericardial catheter is key for preventing fluid re-accumulation, and the use of colchicine to prevent fluid recurrence is encouraged whenever possible. Understanding how to evaluate the significance of a pericardial effusion as well as the procedural steps in the performance of a pericardiocentesis are essential for optimal outcomes in treating patients with pericardial effusions and tamponade.

CARDIAC TAMPONADE: A RARE MANIFESTATION OF MYXEDEMA COMA

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: Myedema coma is a medical emergency requiring prompt recognition and appropriate treatment. This condition often results from uncontrolled long-standing hypothyroidism or triggered by an acute event such as a myocardial infarction, infection, or a variety of systemic illnesses. Symptomology can affect a broad range of systems, including but not limited to hypotension, hypothermia, hypoglycemia, altered mental status, and hyponatremia. In this case report we discuss a case of an unstable patient with myxedema coma presenting with paranoid delusions and cardiac tamponade. CASE PRESENTATION: 66 year old Ethiopian female with hypothyroidism and chronic lymphedema, noncompliant with levothyroxine, presented to the hospital via EMS, due to altered mental status, paranoid outbursts, and a subacute history of visual and auditory hallucinations. Review of symptoms were unable to be obtained due to paranoid delusions and nonsensical speech. Physical exam revealed a temperature of 90.5 degrees Fahrenheit, blood pressure of 64/43mmhg, heart rate of 56 bpm, and she was on three liters nasal canula oxygen. A thyroid goiter, distal heart sounds and pretibial myxedema were present on exam. TSH was 20.26 and free T4 was undetectable. WBC count was 2.5, sodium 135mmol/L, blood glucose 80, with normal renal function. Urine drug screen was negative. Chest x-ray showed an enlarged cardiac silhouette, and an echocardiogram revealed cardiac tamponade. She underwent an emergent pericardiocentesis with removal of more than 1300mL of transudative fluid. She was diagnosed with myxedema coma and treated with IV levothyroxine, liothyronine and hydrocortisone. TSH normalized and the patient was transitioned into oral levothyroxine. Mental status, hemodynamics, and metabolic derangements resolved, and the patient was subsequently discharged with close outpatient follow up. DISCUSSION: The thyroid gland is intimately involved in the regulation of metabolic and physiologic demands of the living organism. An imbalance could potentially lead to catastrophic multisystem collapse. Myxedema coma is a rare manifestation of hypothyroidism with only 0.1% prevalence (1). Patients present with neuropsychiatric manifestations, hypothermia, cardiovascular collapse and multiorgan failure (1,2). The severity of hypothermia is proportionally related to the risk of mortality. CONCLUSIONS: Cardiac tamponade is a rare cardiac manifestation of hypothyroidism, however prompt recognition, urgent pericardiocentesis, and thyroid hormone replacement therapy are critical in preventing pericardial fluid accumulation and reduction in mortality (2-4). Reference #1: Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, Mukhopadhyay S, Chowdhury S. Myxedema coma: a new look into an old crisis. J Thyroid Res. 2011;2011:493462. Reference #2: Kabadi UM, Kumar SP. Pericardial effusion in primary hypothyroidism. Am Heart J. 1990;120(6 Pt 1):1393–1395 Reference #3: Patil VC, Patil HV, Agrawal V, Patil S. Cardiac tamponade in a patient with primary hypothyroidism. Indian J Endocrinol Metab. 2011;15(Suppl 2):S144–S146. DISCLOSURES: No relevant relationships by Shoheb Ali, source=Web Response No relevant relationships by Rupesh Dave, source=Web Response No relevant relationships by Joshua Lovelock, source=Web Response No relevant relationships by Arish Maknojia, source=Web Response No relevant relationships by mustaf shariff, source=Web Response

An Unusual Presentation of Tuberculosis

The normal pericardium is a fibroelastic sac containing a thin layer of fluid that surrounds the heart. Cardiac tamponade, which may be acute or subacute, is characterized by the accumulation of pericardial fluid under pressure. Tuberculous pericarditis is a complication of tuberculosis which is often diagnose late due to the difficulty in establishing this diagnosis. We present a case of pericardial tuberculosis diagnosed in a 20-year-old young retroviral disease patient who presented with signs of cardiac tamponade. His clinical condition improved post-pericardial tapping and he was discharged with antituberculosis medications. This case highlight the importance of having a high level of suspicion as this condition is easily curable.

Clinical characteristics and prognosis of cardiac tamponade patients: 5‑year experience at atertiary center.

Cardiac tamponade (CT) is characterized by compression of the cardiac chambers due to pericardial fluid accumulation. The etiology and prognosis may vary in different regions, and thus patient series from various regions can be useful for exploring the etiological and prognostic disparities. The aim of this study was to determine the clinical characteristics of patients with imminent CT, to evaluate the diagnostic performance of biochemical, microbiologic, and pathologic laboratory analysis, and to ascertain the prognosis of CT patients. We enrolled all patients with imminent CT who underwent percutaneous pericardiocentesis between July 2012 and December 2017 in this retrospective study. The patients were classified into three etiology groups: (a)malignancy (MRCT); (b) iatrogenic/mechanical complication of myocardial infarction (IMCT); and (c) other causes (OCT). Clinical information, laboratory findings, and survival data were recorded. In total, 186 pericardiocentesis procedures were performed on 153 consecutive patients with CT. The median follow-up was 137days (range: 1-1937). The MRCT group had the highest mortality rate (79%) in 12months, while the OCT group had the lowest rate (27%). We determined that increased age, higher serum urea levels, and malignancy-related CT were independent predictors of mortality. The mortality rates of the MRCT and IMCT groups were similar, with both of them being significantly higher than the rate of the OCT group. In all, 15 patients were diagnosed with anew malignancy via pericardial fluid cytology. Patients in the MRCT and IMCT groups had apoor prognosis. The presence of malignancy was found to be the most powerful predictor of mortality in CT patients.

Ten questions about cardiac tamponade

Cardiac tamponade is a pericardial syndrome characterized by diastolic impairment due to the accumulation of pericardial fluid under pressure. It may be an acute life-threatening condition if not recognized and treated (e.g. cardiac tamponade by hemopericardium), or may present as a subacute condition allowing in some cases a delayed treatment.The causes of cardiac tamponade are the same as for pericardial effusion, primarily cancer in one third of cases (being lung cancer the most common type of cancer), bacterial infections (25% of cases), iatrogenic factors (15% of cases), and acute aortic disease with aortic dissection. Cardiac tamponade is reported in <1% of cases of myocardial infarction and is mainly due to heart rupture, or more rarely to hemorrhagic evolution of post-myocardial infarction pericarditis.Cardiac tamponade is a clinical diagnosis that is confirmed by echocardiography. The risk of recurrent cardiac tamponade is around 10% at 10-year follow-up and is mainly determined by the underlying etiology, with cancer patients showing the highest mortality.In this focused review, we will try to provide answers to the most common questions on the causes, presentation, diagnosis, treatment, and outcomes of cardiac tamponade.

Thoracentesis-Reverting Cardiac Tamponade Physiology in a Patient with Myxedema Coma and Large Pleural Effusion

A large pleural effusion causing cardiac tamponade physiology and severe hemodynamic compromise is an uncommon event. We report a case of a 53-year-old woman with severe hypothyroidism presenting with myxedema coma and refractory shock. Her hemodynamic status failed to respond to fluid resuscitation and vasopressors. A transthoracic echocardiogram and chest radiograph demonstrated a pericardial fluid accumulation associated with a large left-sided pleural effusion. Thoracostomy tube insertion resulted in prompt improvement of the patient's hemodynamic status. Our finding demonstrates that a large pleural effusion may play an important role in cardiac tamponade physiology.

Expression of pericardial fluid T-cells and related inflammatory cytokines in patients with chronic heart failure.

Pericardial fluid, as a biochemical indicator of heart status, directly indicates pathological alteration to the heart. The accumulation of pericardial fluid can be attributed to an underlying systemic or local inflammatory process. However, the pericardial fluid expression of cellular surface markers, as well as several cytokines in chronic heart failure (CHF), remain unclear. In order to evaluate these issues further the pericardial fluid expression of several cytokines and the surface expression of activity markers between CHF patients and non-heart failure (NHF) patients were analyzed. The pericardial fluid expression of cytokines was measured by immunofluorescence and biomarker of plasma N-terminal propeptide of B-type natriuretic peptide (NT-proBNP), while pericardial fluid levels of soluble glycoprotein 130 (sgp130) were analyzed by ELISA in 50 CHF and 24 NHF patients. In addition, the surface expression of activation markers for T-cells was measured by immunohistochemistry. Patients with CHF demonstrated increased levels of plasma NT-proBNP and pericardial fluid sgp130. Surface expression of cellular activation markers CD25 and Foxp3 in the pericardial fluid was increased in patients with CHF. Moreover, the pro- and anti-inflammatory cytokines interferon (IFN)-γ, interleukin (IL)-6 and IL-10 in patients with CHF also demonstrated an increased expression within its pericardial fluid. In addition, there was infiltration of inflammatory cells and enhanced expression of inflammatory cytokines in the pericardial fluid of patients with CHF, which may reflect T cell activation, suggesting that systemic inflammation is important in the progression of CHF. This evidence could indicate a possible novel target for future therapeutics and prevention of CHF.

The influence of oral copper-methionine on matrix metalloproteinase-2 gene expression and activation in right-sided heart failure induced by cold temperature: A broiler chicken perspective

This study was designed to investigate the expression, activation and activity of matrix metalloproteinase-2 (MMP-2) in the heart of broiler chickens reared in cold conditions and fed with copper-methionine supplement at different levels. The chickens (n=480) were randomly allotted to six treatments and four replicates. Treatments included two rearing temperatures (i.e. normal and cold temperatures) each combined with three levels of supplemental copper-methionine (i.e. 0, 100 and 200mg/kg). On d 38 and 45 of age, four broilers from each treatment were sacrificed and their hearts were stored at −80°C. Right-sided heart failure, as evident from abdominal and pericardial fluid accumulation, was observed in broilers under cold stress and not receiving supplemental copper. This clinical observation was confirmed at molecular level through increased MMP-2 expression, activation and activity in this group. Birds reared under normal temperature, however, were not involved in right-sided heart failure nor benefitted from copper-methionine supplementation. In contrast, gelatin zymography and real-time PCR demonstrated that dietary supplementation with copper-methionine decreased pro-MMP-2 and MMP-2 in the heart of chickens reared in cold conditions. However, gelatin reverse zymography did not show any difference between treatments in tissue inhibitor of metalloproteinase-2. Level of supplementation showed similar effects on parameters determined. It is concluded that dietary supplementation with copper-methionine reduced right-sided heart failure at clinical and molecular levels in cold-stressed chickens.

Effects of Dietary Copper-Methionine on Matrix Metalloproteinase-2 in the Lungs of Cold-Stressed Broilers as an Animal Model for Pulmonary Hypertension.

The objective of the present study was to investigate the effects of different levels of copper (as supplemental copper-methionine) on ascites incidence and matrix metalloproteinase-2 (MMP-2) changes in the lungs of cold-stressed broilers. For this purpose, 480 1-day-old Ross 308 broiler chickens were randomly assigned to six treatments. Treatments consisted of two ambient temperatures (thermoneutral and cold stress) each combined with 0, 100, and 200mgsupplementalcopper/kg as copper-methionine in a 2×3 factorial arrangement in a completely randomized design with four replicates. Ascites was diagnosed based on abdominal and pericardial fluid accumulation at 45days of age. Fourty-eight broilers were killed at 38 and 45days of age, and their lungs were collected for biological analysis. Results showed that MMP-2 increased in the lungs of ascitic broilers and that copper-methionine supplementation significantly reduced MMP-2 in cold-stressed broiler chickens. Treatments did not affect tissue inhibitor of metalloproteinase-2 (TIMP-2) at 38 and 45days of age, and no difference was observed between 100 and 200mg/kg copper-methionine treatments. In conclusion, copper-methionine at higher than conventional levels of supplementation decreased ascites incidence in low temperature through reduced MMP-2 concentration. Further research is warranted to investigate the effect of copper on MMP-2 concentrations in other tissues with high oxygen demand.

Tuberculous Pericarditis is Multibacillary and Bacterial Burden Drives High Mortality

BackgroundTuberculous pericarditis is considered to be a paucibacillary process; the large pericardial fluid accumulation is attributed to an inflammatory response to tuberculoproteins. Mortality rates are high. We investigated the role of clinical and microbial factors predictive of tuberculous pericarditis mortality using the artificial intelligence algorithm termed classification and regression tree (CART) analysis. MethodsPatients were prospectively enrolled and followed in the Investigation of the Management of Pericarditis (IMPI) registry. Clinical and laboratory data of 70 patients with confirmed tuberculous pericarditis, including time-to-positive (TTP) cultures from pericardial fluid, were extracted and analyzed for mortality outcomes using CART. TTP was translated to log10 colony forming units (CFUs) per mL, and compared to that obtained from sputum in some of our patients. FindingsSeventy patients with proven tuberculous pericarditis were enrolled. The median patient age was 35 (range: 20–71) years. The median, follow up was for 11.97 (range: 0·03–74.73) months. The median TTP for pericardial fluid cultures was 22 (range: 4–58) days or 3.91(range: 0·5–8·96) log10CFU/mL, which overlapped with the range of 3.24–7.42 log10CFU/mL encountered in sputum, a multi-bacillary disease. The overall mortality rate was 1.43 per 100 person-months. CART identified follow-up duration of 5·23months on directly observed therapy, a CD4+ count of ≤199.5/mL, and TTP≤14days (bacillary load≥5.53 log10 CFU/mL) as predictive of mortality. TTP interacted with follow-up duration in a non-linear fashion. InterpretationPatients with culture confirmed tuberculous pericarditis have a high bacillary burden, and this bacterial burden drives mortality. Thus proven tuberculosis pericarditis is not a paucibacillary disease. Moreover, the severe immunosuppression suggests limited inflammation. There is a need for the design of a highly bactericidal regimen for this condition.