Evidence Of Pericardial Effusion Research Articles

Abstract 4144743: From Tummy Trouble to Heart Hassle: A Case of Traveler's Diarrhea Triggering Myopericarditis

Case description: >A 38-year-old male with a history of paroxysmal atrial fibrillation status post-RFA ablation, presented to the emergency department (ED) with a 3-week history of non-bloody diarrhea, abdominal cramping, nausea, fever, and headache after a trip to Guatemala. In the ED, his vital signs were temperature (99.3 °F), and heart rate (116 bpm). Notable physical exam findings were diffuse erythematous macular rash and conjunctival injection. Initial labs demonstrated elevated white count (15,100 K/mcL) and lactate (3.2 mmol/L). He was treated with ceftriaxone and metronidazole, with clinical improvement. Stool cultures were positive for salmonella and cyclospora cayetanensis. On hospital day 3, he developed severe substernal chest pain, minimal ST elevation in the anterolateral leads on ECG and elevated HS- troponin levels of 7000 ng/ml, peak of 12000 ng/ml. Transthoracic echocardiogram showed normal LV systolic function, with no evidence of pericardial effusion and regional wall motion abnormalities. Subsequent cardiac MRI demonstrated evidence of myopericarditis(anterior and lateral pericardial enhancement, along with focal epicardial late gadolinium enhancement in the mid inferolateral wall of the left ventricle with associated myocardial edema, and a small pericardial effusion). He was discharged home on Trimethoprim-Sulfamethoxazole and started on colchicine, with no recurrent chest pain. Discussion: Myopericarditis is a complication of acute pericarditis due to pericardial inflammation extension to the myocardium. It is usually caused by a virus and rarely due to bacteria as demonstrated by this case, presenting as elevated troponin levels and ST-segment elevation on ECG. To our knowledge, there are no known reports of cyclospora cayetanensis causing myopericarditis. The adherence of the salmonella bacteria to the cardiac endothelium can result in myocyte necrosis and release of self-antigens leading to the development of antibodies and autoimmune myocarditis. Long-term management of bacterial myopericarditis is dependent on the severity of the clinical presentation and includes antibiotics, anti-inflammatory medications, and colchicine. Most patients recover within one month, but persistent cardiac dysfunction and progression to end-stage dilated cardiomyopathy can occur, thus follow-up echocardiography is recommended.

Efficacy and determinants of response to inhaled treprostinil in pulmonary hypertension - interstitial lung disease

Inhaled treprostinil has shown to improve exercise capacity in patients with pulmonary hypertension-interstitial lung disease (PH-ILD). We evaluated the efficacy and determinants of favorable response to inhaled treprostinil at six months. MethodsOf the 106 patients screened, 42 were eligible for this retrospective single-center study. Assessments included rate of patients who achieved ≥30m improvement on 6-min walk test (6MWT), and death or transplantation rates at 6 months of treatment initiation. ResultsPatients were predominantly female (n = 26, 62 %) with autoimmune PH-ILD (n = 23, 55 %), and a median age of 68 (61, 75) years. Ten (38.5 %) patients achieved a distance increase ≥30 m in 6MWT. No statistically significant determinants of walking ≥30 m were noted on univariate analysis; however, responders had a lower right ventricular (RV) tissue Doppler S' velocity (9.2 [7.0, 11.0] vs. 11.9 [10.0, 14.4], p = 0.018) cm/s and evidence of pericardial effusion on baseline echocardiogram (82 % vs. 26 %, p = 0.003). PH-ILD patients who died or underwent transplantation were more likely to have progressive pulmonary fibrosis (PPF) (95 % vs 50 %, p < 0.001) ConclusionsIn real-world setting, treatment with inhaled treprostinil for six months increased the 6MWT by ≥ 30 m in about a third of PH-ILD patients. Lower RV tissue Doppler S' velocity and presence of pericardial effusion at baseline were associated with favorable response to inhaled treprostinil. PPF portends a poor survival in PH-ILD.

Gone without a Trace: A Rare Case of Pericardial Effusion Resolving after Cardiopulmonary Resuscitation

Abstract Pericardial effusion is collection of fluid in pericardial space. It is commonly seen as a part of multisystem infections, malignancy, and renal failure. It can progress to life-threatening pericardial tamponade, leading to cardiac arrest. Cardiopulmonary resuscitation (CPR) is well-established protocol for all types of cardiac arrests. CPR serves as a therapeutic intervention, reversing cardiac arrest and providing time to address the underlying cause. However, CPR can involve multiple complications, including thoracic skeleton and organ injuries. In this case report, we present a case of massive pericardial effusion in a male patient who was admitted to our hospital with abdominal pain and a medical history of diabetes, hypertension, ischemic heart disease, acute kidney injury, and coagulopathy. Massive pericardial effusion was identified using point-of-care ultrasonography (POCUS) of the heart. While his coagulation abnormalities were being corrected, he had a cardiac arrest in intensive care unit before any invasive intervention could be performed for pericardial effusion. Return of spontaneous circulation was achieved, and surprisingly, post-CPR POCUS of the heart did not reveal much evidence of pericardial effusion. The resolution of pericardial effusion was also confirmed with computed tomography of the chest once the patient was stabilized. We observe that the pleural effusion, initially minimal, increased following CPR. Thus, we report this interesting case to highlight the unintended therapeutic effect of CPR on pericardial effusion. In addition, we emphasize the importance of POCUS during critical care situations as it assisted us in avoiding blind pericardiocentesis and the potential traumatic complications associated with such a procedure.

P421 INTRA–CARDIAC AND ALL LAYERS CARDIAC INVOLVEMENT BY SQUAMOUS NON–SMALL CELL LUNG CANCER

Abstract A 73 year–old man was referred by his general practitioner to our ambulatory for worsening dyspnea. He also reported substantial weight loss (almost 20 kg during the last three months), new onset dysphonia and dry cough. The patient’s medical history also included a former tobacco addiction, arterial hypertension and dyslipidemia. There was not history of cardiomiopathy. Electrocardiogram, showed: sinus rhythm, 60/min with inferior and anterior–lateral abnormality of repolarization. No laboratory exams were available at the first visit. An echocardiogram was performed, showing: marked septal hypertrophy (IVSd= 23 mm), septal hypokinesia, with an ejection fraction at lower limits of normality (EF= 54%), neither systolic anterior motion of the mitral valve. Minimal pericardial effusion was seen. We required a CT scan of the chest, that showed a large (5x8x11cm) mass in the left upper lobe with ipsilateral mediastinal lymphadenopathy. The mass directly extended into the mediastinum with infiltration of pericardial leaflet, left atrium and the left wall of the aortic arch. A hypodense formation of approximately 4 cm in the interventricular septum in the apical portion was reported. PET–CT with FDG was performed, which documented hypercaptation of the radioactive tracer at the level of the above–mentioned lesions. The patient underwent fine–needle aspiration biopsy of the lung mass and the histological examination led to the diagnosis of squamous cell carcinoma of the lung. Systemic treatment with carboplatin plus placlitaxel and pembrolizumab was subsequently started. A cardiac CMR was performed, which documented an area of 30x17x31 mm located at the septal (mid–apical portion), apex and parapical portion of the free wall of the right ventricle with transmural extension. At this area, extensive late gadolinium enanchement (LGE) at marginal level with a central non–capillary core and hyperintense in T2 sequences (compatible with central necrotic lesion). The pericardium also showed LGE and a mild pericardial effusion (maximum 8 mm); left atrium involvement, seen on CT, was not documented . After he completed the third cycle of CHT, at 5 months from the diagnosis, the echocardiogram showed a substantial disappearance of the mass infiltrating the interventricular septum without evidence of pericardial effusion. The ecg was substantially unchanged. The patient stopped carboplatin and paclitaxel after 3 cycles and kept maintenance pembrolizumab still ongoing.

Too Much Too Soon? The Catch-22 of Catching COVID-19

IntroductionMyocarditis has become a well-recognised cardiac complication of SARS-CoV-2 infection. Now, there are growing reports of rare incidences of myocarditis following receipt of mRNA COVID-19 vaccines.Case ReportA previously healthy 35-year-old male tested positive for COVID-19 on 8/12/21. He never required hospitalisation and was thought to have cleared the infection by 9/5/21. Three weeks later he received the first dose of Pfizer-BioNTech BNTT162b2/Comirnaty mRNA COVID-19 vaccine. Five days later he presented to emergency with chest pain alongside myalgia, headache and cough. His troponin-T was below reference range (RR), electrocardiogram showed sinus rhythm with mild, diffuse T-wave flattening, and no evidence of pericardial effusion was seen on bedside transthoracic echocardiogram (TTE) so was discharged. Two days later he represented to hospital with fevers, vomiting, diarrhea and a maculopapular rash. His subsequent admission was complicated by rapid deterioration and his management reflected a diagnostic dilemma with wide differentials. On day 2 of admission he became haemodynamically unstable requiring vasopressor therapy with a high sensitivity (hs) troponin-I of 103ng/L (RR <26ng/L). On day 4 he developed atrial fibrillation, worsening respiratory distress, peak hs troponin-I of 1474ng/L and required intubation, direct-current cardioversion and venoarterial extracorporeal membrane oxygenation (ECMO) for intractable heart failure. TTE here showed severe global systolic impairment with a left ventricular ejection fraction of 15% and small pericardial effusion. His subsequent treatment targeted possible multiorgan sepsis with antibiotics, vaccine-induced myocarditis with immunosuppressive therapy including anakinra and parental corticosteroids, or delayed COVID-19 myocarditis with supportive care. He was later extubated and successfully decannulated from 5 days on ECMO on day 11. Cardiac magnetic resonance imaging on day 12 showed elevated T1 and T2 values consistent with ongoing myocardial edema, but normal ventricular volume, thickness and function.SummaryThis is a case of fulminant myocarditis whereby the aetiology is unclear considering recent COVID-19 infection and mRNA vaccination. This raises questions as to the ideal timing of vaccine, type of vaccine and requirement for cardiac screening prior to vaccination in patients who have recovered from COVID-19.

Cardiovascular Manifestations of Systemic Lupus Erythematosus: An Overview

Systemic Lupus Erythematosus(SLE) is a multisystem autoimmune disease with variable presentations. A proposed mechanism for the etiology of SLE involves the development of autoantibodies that result from a defect in apoptosis. The specific defect involves the “find-me” (adenosine triphosphate [ATP]/uridine triphosphate [UTP]) or “eat-me” (phosphatidylserine) signals activated upon release of red cell nuclei. In the absence of apoptosis, the nuclei break down, causing inflammation and contributing to the development of autoimmunity. Many signs and symptoms of SLE are caused by either circulating immune complexes or direct effects of antibodies on cells. A genetic predisposition for SLE exists, and the concordance rate in monozygotic twins is between 25% and 70%. If a mother has SLE, her daughter’s risk of developing the disease is 1:40, and her son’s risk is 1:250. The course of SLE consists of intermittent remissions punctuated by disease flares, and organ damage often progresses over time. Pericarditis is the most frequent cardiac manifestation; it can be documented by ECG, auscultation of a friction rub, or evidence of pericardial effusion. It usually responds to anti-inflammatory therapy and infrequently leads to tamponade. More serious cardiac manifestations are myocarditis and fibrinous endocarditis of Libman-Sacks. The endocardial involvement can lead to valvular insufficiencies, most commonly of the mitral or aortic valves, or embolic events. It has not been proven that glucocorticoid or other immunosuppressive therapies improve lupus myocarditis or endocarditis. Still, it is usual practice to administer a trial of high-dose steroids and appropriate supportive treatment for heart failure, arrhythmia, or embolic events. As discussed above, patients with SLE are at increased risk for myocardial infarction, usually due to accelerated atherosclerosis, which probably results from immune attack, chronic inflammation, and chronic oxidative damage to arteries.

Neoplasia-Associated Pericarditis—Predictor of Cancer Progression?

Pericarditis may signal the presence of cancer, even in the absence of other clinical or paraclinical signs. Corollary, the following question arises: Could the discovery of a newly developed pericarditis be used in patients with known neoplasia as a marker of cancer progression? In an attempt to find an answer to this question, this two-centre study included 341 consecutive patients with a confirmed diagnosis of cancer and evidence of pericardial effusion at echocardiography and/or CT/MRI scan. The patients’ data were collected retrospectively if they further fulfilled the following inclusion criteria: available medical data from confirmation of pericarditis until evidence of cancer progression or until at least 12 months without progression. The average age of the patients was 62.16 years (22–86 years), and the study comprised 44.28% males and 55.71% females. All types of the most common neoplasms were represented. The results showed that 85.33% of patients had cancer progression temporally linked to pericarditis. Of these, 41.64% had cancer progression within 18 months after the diagnosis of pericarditis with a median time to progression of 5.03 months, ranging from 0 to 17 months; 43.69% had progression within a maximum of 2 months before the diagnosis of pericarditis. Only 14.66% had no cancer progression during the observation period. We concluded that pericarditis could be a sensitive marker of cancer evolution that could be widely used as a follow-up investigation for cancer patients as a marker of progression or recidive.

Abstract 16918: COVID-19 Associated Acute Myocardial Injury With Prolonged Troponin Elevation

Introduction: Acute myocardial injury in the setting of COVID-19 has been well described and is associated with higher mortality. Hypothesis: Myocarditis has been reported as a rare cause of myocardial injury in at least seven recent case reports. Methods: A 70-year-old man with coronary artery disease status post bypass surgery with recent hospitalization for left shoulder septic arthritis with MSSA bacteremia was readmitted 10 days later with a positive PCR test for SARS-CoV-2 at a local nursing facility. His symptoms were dyspnea, chest pain, fever, nausea, and diarrhea. Previous hospitalization he underwent evaluation for chest pain with cardiac catheterization revealing ejection fraction (EF) of 45% and patency of all three grafts. Results: Laboratory investigation showed elevated markers of myocardial injury with high sensitivity troponin I (hs-TnI) of 17,643 ng/L and B-type natriuretic peptide of 2,627 pg/mL, elevated C-Reactive Protein, D-dimer, and sedimentation rate. Chest X-ray showed hazy opacity in the infrahilar right lung. ECG notable for a first degree AV block with no ST-segment elevation. Transthoracic echocardiogram (TTE) showed an EF of 20% with global left ventricular dysfunction with hypokinesis of the right ventricle. No evidence of pericardial effusion. Blood cultures were negative. Management of heart failure led to clinical improvement. Over the next three months, Hs-TnI level stayed elevated at 11,339 ng/L for four weeks and trended down to 6,791 ng/L. The patient was seropositive for COVID-19 IgG eight weeks after the diagnosis of COVID-19 was made. Conclusions: We report the first case of COVID-19 related myocardial injury with prolonged and extreme troponin elevation. Recent favorable cardiac catheterization further supports immune mediated myocarditis over ischemic cardiomyopathy. Unfortunately, no endomyocardial biopsy has been performed.

Vein of Galen Malformation.

* Abbreviations: CPAP: : continuous positive airway pressure Fio2: : fraction of inspired oxygen MFCC: : Maternal Fetal Care Clinic MRA: : magnetic resonance angiography MRI: : magnetic resonance imaging MRV: : magnetic resonance venography PGE1: : prostaglandin E1 VOGM: : vein of Galen malformation A 37-year-old gravida 3, para 1 pregnant woman was referred to the Maternal Fetal Care Center (MFCC) at Boston Children’s Hospital at 36 weeks’ gestation for the finding of vein of Galen malformation (VOGM). The patient’s pregnancy was complicated by gestational diabetes. Her surgical history was notable for adenoidectomy, a previous cesarean section, and dilation and curettage following a spontaneous abortion. Maternal medications included prenatal vitamins and glyburide. Family history was noncontributory. This pregnancy was planned and naturally conceived. The woman received appropriate prenatal care. Noninvasive prenatal screening showed her to be at low risk and cell-free fetal DNA screening was negative. She had a normal anatomy scan at 20 weeks’ gestation. Fetal ultrasonography performed at 36 weeks' gestation for evaluation of fetal growth demonstrated a prominent rounded vascular structure in the quadrigeminal cistern with turbulent flow consistent with a VOGM. Fetal echocardiography at that time revealed dilation of the right atrium and right ventricle with normal biventricular function. There was no evidence of hydrops. Imaging at 37 weeks’ gestation in the Boston Children’s Hospital MFCC included repeat comprehensive fetal echocardiography, fetal ultrasonography, and fetal brain magnetic resonance imaging (MRI). Echocardiography revealed a markedly enlarged right atrium and right ventricle with mild right ventricular dysfunction. Moderate tricuspid regurgitation was noted, the innominate vein was markedly dilated, and the superior vena cava had increased flow. The interventricular septum was dyskinetic, suggesting increased pressure within the right ventricle. There was a patent foramen ovale and a patent ductus arteriosus with right-to-left shunting throughout the cardiac cycle. No evidence of pericardial effusion or hydrops fetalis was seen. Fetal ultrasonography showed a singleton male fetus with biometry measurements, including head circumference, corresponding to estimated gestational age. Amniotic fluid volume was normal. The fetal survey demonstrated a large midline intracranial vascular structure in the expected …

P1707 Strain imaging - resolving the diagnostic conundrum of cardiac amyloidosis

Abstract Introduction Cardiac amyloidosis is a common cardiac condition and is still significantly underdiagnosed. Autopsy studies revealed that myocardial tranthyretin amyloid deposition is found in up to 30% of patients with HFpEF (heart failure with preserved ejection fraction). A study in 2015 reported that 13% of patients hospitalised due to HFpEF (older than 60 years old and with left ventricular hypertrophy - LVH) had moderate to severe uptake on the Technetium DPD scintigraphy. Strain imaging through Echocardiography can be a useful diagnostic tool and can provide valuable clues towards the aetiology of LVH. Relative "apical sparing" pattern of longitudinal strain has been reported to have good sensitivity and specificity in differentiating patients with cardiac amyloidosis from controls. Case A 66 year old man presented with progressive breathlessness and peripheral oedema. His past medical history included peripheral neuropathy, bilateral decompression procedures for carpal tunnel syndrome and IgM Monoclonal Gammopathy of Undetermined Significance (MGUS). His B-type natriuretic peptide levels were elevated and his ECG showed normal sinus rhythm, RsR" pattern on the anterior leads and no evidence of LVH. The transthoracic echocardiogram showed moderate concentric LVH, normal left ventricular systolic function and mildly impaired left ventricular diastolic function. No evidence of pericardial effusion. Urine protein:creatinine ratio findings were consistent with nephrotic range proteinuria. He had a cardiac MRI that confirmed normal biventricular wall motion and systolic function and a moderate increase in the wall thickness of both ventricles, but showed no evidence of late gadolinium enhancement. At this point, we repeated his transthoracic echocardiogram with the use of strain imaging and it revealed a pattern of apical sparing suggestive of cardiac amyloidosis. After collaboration with the Haematology team, a bone marrow biopsy was performed that showed that the MGUS had progressed to IgM multiple myeloma. There was however no evidence of amyloid deposits. He was subsequently referred to the national amyloidosis centre (as per family request), where a SAP (serum amyloid P) scan showed renal and splenic amyloid deposits confirming Light-chain Amyloidosis. To exclude the possibility of TTR Amyloidosis, he also had a 99mTc-DPD scintigraphy which did not detect any amyloid deposits. He was treated under the care of the Haematology team with Velcade/Cyclophosphamide/Dexamethasone chemotherapy. Conclusion In patients with a clinical suspicion of cardiac amyloidosis, Echocardiography with strain imaging can be very useful and should be performed routinely. Furthermore, in patients with high clinical suspicion of cardiac amyloidosis, diagnostic investigations should persist even if the initial workup does not yield specific findings. Abstract P1707 Figure. Strain imaging findings

Bilateral pulmonary agenesis diagnosed in the 13 th week of gestation - a case report and literature review

Bilateral pulmonary agenesis (BPA) is a rare congenital lung malformation incompatible with extra-uterine life, diagnosed by various prenatal imaging modalities in the second and third trimesters. Essentials for diagnosis are complete absence of lungs and bronchi and no pulmonary vascular supply. In the present case, both convex and vaginal ultrasound scan performed at 13th GW revealed an anechoic content in the entire fetal thorax with no evidence of pericardial effusion, fetal heart diseases, or any other accompanying congenital malformations. On three-vessel view (3VV), bifurcation of pulmonary artery could not be identified, which confirmed the diagnosis of BPA. In conclusion, clinical importance of combining the up-to-date technological tools and clinical expertise in establishing the diagnosis as early as in the first trimester allows the clinicians to terminate the pregnancy with the lowest incidence rate of eventual complications related to the procedure. According to the literature data, this is the first and therefore unique case of BPA diagnosed in the 13th week of gestation.

Cardiac A-lines in fast scan as a sign of pneumopericardium

BackgroundTraumatic pneumopericardium is rare and usually results from blunt injury. Diagnosis through clinical and chest X-ray is often difficult. Ultrasound findings of A-line artifacts in the cardiac window may suggest pneumopericardium.Case presentationA young man involved in a car accident and sustained blunt thoracic injuries, among others. As part of primary survey, FAST scan was performed. Subxiphoid view to look for evidence of pericardial effusion showed part of the cardiac image obscured by A-lines. Other cardiac windows showed only A-lines, as well. A suspicion of pneumopericardium was raised and CT scan confirmed the diagnosis.ConclusionsAlthough FAST scan was originally used to look for presence of free fluid, with the knowledge of lung ultrasound for pneumothorax, our findings suggest that FAST scan can also be used to detect pneumopericardium.

Symptomatic pericardial effusion in Hodgkin's lymphoma: a rare occurrence. Case report and review of the literature.

Pericardial effusion is observed in approximately 5% of patients with Hodgkin's lymphoma but is rarely symptomatic. We report a case in which a 21-year-old woman with newly diagnosed Hodgkin's lymphoma was found to have symptoms and radiographic evidence of pericardial effusion. Symptomatic pericardial effusion in patients with Hodgkin's lymphoma is extremely rare, with few reports in the literature. The mechanism for the heart and pericardial involvement is reviewed along with a description of the presenting symptoms and differential diagnosis.

In this issue – April 2016

In this issue – April 2016

Diagnostics and therapy of pericarditis and pericardial effusion

This article describes the diagnostics, differential diagnostics, multimodal imaging, medicinal and invasive diagnostic therapy of acute and chronic pericarditis, constrictive pericarditis, pericardial effusion and cardiac tamponade under etiological aspects and on the basis of the guidelines of the European Society of Cardiology (ESC). The starting point of the decision tree is the symptomatic patient with echocardiographic evidence of pericardial effusion. The principle feature of the diagnostics is the etiopathogenetic allocation of the pericardial disease which influences the clinical picture, course therapy and prognosis. Infectious pericarditis (e.g. viral, bacterial and tuberculous) is differentiated from sterile autoreactive pericarditis and from neoplastic pericardial effusion by the cytology of the effusion and immunohistological and molecular investigations of the pericardial and epicardial biopsies. Pericardioscopy plays an important role in the recognition of suspicious areas. In many cases intrapericardial administration of cisplatin for neoplastic pericardial effusion and instillation of triamcinolone for autoreactive pericarditis prevent recurrence just as a treatment of several months with colchicine.

Pneumopericardium: an uncommon complication of atrial lead perforation following pacemaker implantation

Cardiac perforation is an infrequent but potentially life-threatening complication of pacemaker implantation. We report a case of right atrial lead perforation complicated by pneumopericardium shortly after pacemaker lead insertion. Transthoracic echocardiography revealed no evidence of pericardial effusion and pacemaker lead displacement, but a thoracic computed tomography scan illustrated the lead course and confirmed the diagnosis. This case suggests that computed tomography is a sensitive modality to confirm the diagnosis at the early stage of this complication.

Intramyocardial Dissecting Hematoma Following Myocardial Infarction

An 80-year-old woman with hypertension and a double aortocoronary bypass 20 years previously was hospitalized with a diagnosis of subacute infarction. At 24 hours after hospitalization, she experienced an onset of heart failure symptoms. Transthoracic color Doppler echocardiography in apical four-chamber view showed features of a neocavity in the laterobasal region (delimited by arrows), with end-diastolic flow in the interior, a communication with the cardiac chamber, and no evidence of pericardial effusion (Figure 1. LA, left atrium; LV, left ventricle; MV, mitral valve). Multidetecter chest computed tomography with electrocardiogram gating was performed, with contrast enhancement in the arterial phase. The study showed a collection communicating with the ventricular chamber, with extravasated contrast in the interior and an ascending course lateral to the left atrium, consistent with myocardial rupture in the laterobasal region (Figures 2 and 3). A decision was made to perform percutaneous closure of the ventricular wall defect by placement of an Amplatzer device, which failed. The procedure was converted to open surgery, which revealed pericardial adhesions and an intramyocardial cavity that did not communicate with the pericardium. Plication of the left ventricular border and tip was performed. Unfortunately, the patient experienced multiorgan failure in the postoperative period and died 72 hours later. Intramyocardial dissection is an uncommon condition that usually occurs in inferoposterior infarctions. Echocardiography and computed tomography are the imaging modalities used for the diagnosis. It is difficult to evaluate the prognosis of these cases or the appropriate management, which should be individualized according to the clinical situation and the experience of the surgical or interventional teams. LV 10 10

Application of rapid ultrasound in shock protocol in the ICU for management of shock.

Sir, One of the most challenging tasks in the Intensive Care Unit (ICU) is to rapidly determine the cause of shock in a critically ill patient and decide the most appropriate treatment in a short time. We describe a case of 34-year-old male with shock and impending respiratory failure presenting to ICU and its management based on information provided by rapid ultrasound in shock (RUSH) protocol. A 34-year-old male patient presented to the ICU with the complaints of recent onset severe dyspnea and dry cough. There was no history of chest pain, fever, and chest trauma. His physical examination revealed tachycardia (pulse rate: 112/min), tachypnea (respiratory rate: 48/min) and hypotension (blood pressure: 80/50 mmHg). Electrocardiogram showed sinus tachycardia, right axis deviation with S1Q3T3 pattern. Patient was intubated and mechanically ventilated in view of impending respiratory failure and shock. Along with initial resuscitation for the shock, she underwent ultrasound according to RUSH Protocol to evaluate the cause of shock. Pump: Grossly enlarged right atrium and right ventricle with D shaped left ventricle. McConnell's sign was present. Pulmonary artery was dilated with pulmonary artery systolic pressure 80 mm of Hg. Left ventricular contractility was adequate. There was no evidence of pericardial effusion or valvular dysfunction. Tank: Inferior vena cava was full and noncollapsing with respiration. Pipes: Deep venous thrombosis screening was done (femoral vein in the femoral canal, popliteal vein in popliteal fossa) which was normal. Screening of the aorta was also normal [Figure 1]. With this information, diagnosis of pulmonary thromboembolism (PTE) causing obstructive shock was considered. Computerized tomography based pulmonary angiography (CTPA) could not be as the patient was on the ventilator and hemodynamically unstable. We thrombolysed the patient with recombinant tissue-type plasminogen activator 100 mg intravenous infused over 90 min. SpO2 with subsequent improvement in hemodynamic parameters. Patient was gradually weaned off the ventilator by 5th day. Subsequently, CTPA showed embolism in the main and segmental branches of both pulmonary arteries. Figure 1 (a) ECG showing S1Q3T3 pattern (b) Chest x-ray showing Palla's sign (prominent right descending pulmonary artery) (c) Dilated right atria and ventricle (d) “D” shaped left ventricle (e and f) Non collapsible IVC seen on m mode (g) Femoral ... Rapid ultrasound in shock protocol is recently proposed systemic algorithm for evaluation of shock.[1] This protocol involves a three-step bedside sonographic assessment simplified as step 1: Evaluation of pump, step 2: Evaluation of tank, step 3: Evaluation of pipes [Table 1]. By focusing on both the anatomy and the physiology, points of care ultrasound by intensivists may help in differentiating between various etiologies of hypotension in the unstable patient. Characteristic ultrasonography finding facilitates the early diagnosis as well as provides prognostic information in PTE.[2,3] These findings needs to be interpreted in the context of the clinical picture as similar finding can be seen in chronic obstructive pulmonary disease, obstructive sleep apnea, pulmonary hypertension and right sided myocardial infarction. The relatively poor sensitivity of ultrasound findings necessitates other investigations to rule out the diagnosis of PTE in critically ill patients. Table 1 Rapid ultrasound in shock protocol: Ultrasonographic findings seen with classic shock states**

Acute Aortic Syndrome

An 83-year-old woman presented with mild, nonradiating, central chest pain. The results of her physical examination were unremarkable, and her pulses were symmetrical and bilaterally palpable. Her ECG revealed normal sinus rhythm with no acute ST/T-wave changes. Her transthoracic echocardiogram showed good left ventricular systolic function, with mild dilatation of the ascending aorta (4.5 cm) (Figure 1A), without evidence of pericardial effusion. Figure 1. A , Transthoracic echocardiogram (parasternal long-axis view) showing mildly dilated proximal aorta at 4.5 cm. B , Transthoracic echocardiogram (parasternal short-axis view at aortic valve level) showing large pericardial effusion with the collapse of the right atrium in diastole (thick arrow) suggesting cardiac tamponade. C , Transthoracic echocardiogram (subcostal view) showing a large pericardial effusion (thick arrow). D , Axial contrast-enhanced CT scan shows penetrating atheromatous ulcer of the aorta (thick arrow) filling with contrast material. Ao indicates the proximal aorta; AoV, aortic valve; CT, computed tomography; LA, left atrium; LV, left ventricle; PEff, pericardial effusion; RA, right atrium; and RV, right ventricle. Two hours later, she developed severe chest pain and collapsed. She was cold, clammy, and her blood pressure dropped to 60/30 mm Hg. Her jugular venous pressure was elevated. An urgent bedside transthoracic echocardiogram revealed cardiac tamponade (Figure 1B and 1C). Urgent computed tomography (CT) demonstrated a penetrating atheromatous ulcer (Figure 1D) with a large intramural hematoma. Acute aortic syndrome (AAS) refers to the acute presentation of closely related life-threatening entities having similar clinical features and challenges, including the aortic dissection, intramural hematoma, and penetrating atheromatous ulcer1 (Figure 2). Figure 2. Classification of acute aortic syndrome. A , Aortic dissection. B , Intramural hematoma. C , Penetrating atheromatous ulcer. Reprinted from Berger et al1 with permission from the publisher. Copyright © 2006, Radiological Society of the Netherlands. It has been suggested that aortic dissection, …

Pocket-size imaging device: effectiveness for ward-based transthoracic studies

Pocket-size imaging devices (PSID) are now available; their potential role in a hospital environment has been investigated but still remains undefined. We evaluated the effectiveness of PSID in 92 patients referred for bedside transthoracic echocardiogram (TTE). Patients were included where there was a focused clinical question: quantification of left ventricular function (LVF); presence of regional wall motion abnormalities (RWMA); evidence of pericardial effusion, exclusion of significant valve pathology. Each patient underwent an echocardiography evaluation using PSID and TTE. In 83 patients [k = 90%, 95% CI (82.2-95.4)], it was possible to answer the clinical question by PSID examination alone. There was agreement between the findings of PSID and TTE in 86 cases [79%; k = 47%, 95% CI (12.8-82.0)], in three cases, the clinical question was not answered by both modalities. When the clinical question was focused on LVF, the agreement was excellent [k = 96%, 95% CI (95.3-97.9)], as was the agreement in the detection of RWMA [k = 94.57%, 95% CI (82.4-95.1)]. There was also good concordance in the detection of valve pathology and pericardial effusion. Using PSID, the reduction in the scanning and reporting time was 66%. The cost-effectiveness analysis produced very favourable results: with PSE, we obtained an overall cost saving per scan of 76%, compared with TTE. This study demonstrates that PSID can provide a valuable alternative to TTE in the presence of focused clinical questions and can provide an efficient way of delivering a ward-based transthoracic echo service.