Evidence Of Right Ventricular Strain Research Articles

Clinical outcomes and factors associated with pulmonary infarction following acute pulmonary embolism: a retrospective observational study at a US academic centre

ObjectivePulmonary infarction is a common clinical and radiographic finding in acute pulmonary embolism (PE), yet the clinical relevance and prognostic significance of pulmonary infarction remain unclear. The study aims to...

THIRD TIME'S A CHARM: TREATING PULMONARY EMBOLISM WITH MECHANICAL THROMBECTOMY AFTER TWO FAILED ATTEMPTS WITH THROMBOLYTIC THERAPY

TOPIC: Procedures TYPE: Medical Student/Resident Case Reports INTRODUCTION: Pulmonary embolism (PE) can be a life-threatening condition. Massive PE, characterized by hemodynamic instability with signs of shock, comprises 4.5%-10% of all PE cases and has over 50% mortality rate. When medical therapy fails, aspiration thrombectomy is a treatment option for acute massive or submassive PE in patients with hemodynamic compromise or right ventricular (RV) dysfunction (Dopazo et al, 2018). CASE PRESENTATION: A 61-year-old male presented after an episode of syncope, chest pain, and dyspnea. Due to profound hypoxia, he was intubated. ECG as seen in figure 1 was changed from prior. Troponin was 0.80. In the ED, he was placed on norepinephrine and epinephrine due to hypotension. Bedside echocardiogram (ECHO) showed enlarged RV with severely reduced RV systolic function, hypokinetic RV free wall, and apex. The patient subsequently developed pulseless electrical activity (PEA) arrest. Two cycles of CPR were performed to achieve the return of spontaneous circulation. Due to the possibility of PE, weight-based tPA was administered. He had PEA arrest a second time and CPR was done for 9 minutes. A second dose of weight-based tPA was given after which his hemodynamics transiently improved. Epinephrine drip was discontinued, but norepinephrine drip was continued. He was transferred to ICU for monitoring and was placed on a heparin drip. Over the next 12 hours, despite multiple tPA doses, he progressively decompensated with systolic blood pressure to 40mmHg while on norepinephrine. Vasopressin drip was initiated. Lactic acidosis increased from 3.8 to 6.6 mmol/L, creatinine worsened from 1.6 to 4.0 mg/dL, and Hb 12.2 to 8.5 g/dL. CTA for PE confirmed saddle pulmonary embolism with evidence of RV strain with RV/LV ratio 1.1. He was taken emergently for cardiac catheterization on multiple vasopressors. A bilateral pulmonary artery thrombectomy with a T24 Inari catheter was done successfully, with subsequent improvement in hemodynamics. ECHO after the procedure showed improved RV function and RV size reduction. Within 24 hours of the thrombectomy, vasopressors were titrated off and the patient remained hemodynamically stable. DISCUSSION: Though systemic thrombolytic therapy is typically indicated for hemodynamically unstable patients with suspected pulmonary emboli, it was not effective in our patient, despite multiple doses. Catheter-directed therapies for PE can remove obstructive emboli directly, allowing for rapid patient improvement as seen in our case. Furthermore, though it is an invasive strategy, catheter-directed thrombectomy has the potential to offer both short- and long-term benefits over systemic thrombolysis including early recovery, reduced risk of bleeding, pulmonary hypertension, and reversal of RV failure. CONCLUSIONS: Catheter-directed techniques should be considered on a case-by-case basis, especially in patients who do not improve with thrombolysis. REFERENCE #1: 1.Ciampi-Dopazo, Juan José et al. "Aspiration Thrombectomy for Treatment of Acute Massive and Submassive Pulmonary Embolism: Initial Single-Center Prospective Experience.” Journal of vascular and interventional radiology : JVIR vol. 29,1 (2018): 101-106. doi:10.1016/j.jvir.2017.08.010 REFERENCE #2: 2.Tu, Thomas et al. "A Prospective, Single-Arm, Multicenter Trial of Catheter-Directed Mechanical Thrombectomy for Intermediate-Risk Acute Pulmonary Embolism: The FLARE Study.” JACC. Cardiovascular interventions vol. 12,9 (2019): 859-869. doi:10.1016/j.jcin.2018.12.022 DISCLOSURES: No relevant relationships by Mukul Bhattarai, source=Web Response No relevant relationships by radhika deshpande, source=Web Response no disclosure on file for Abdul Hafiz; No relevant relationships by Cameron Koester, source=Web Response No relevant relationships by Abhishek Kalidas Kulkarni, source=Web Response no disclosure on file for Mohsin Salih; No relevant relationships by Omar Siddiqui, source=Web Response

High Prevalence of Persistent Breathlessness Following Sub-Massive Pulmonary Embolism in Patients Presenting to a Large Regional Hospital in South Wales.

There is a broad literature exploring the investigation, treatment, management and outcomes of patients suffering from pulmonary embolism (PE). Chronic thromboembolic pulmonary hypertension (CTEPH) has been studied but less is known about outcomes for the large majority of individuals surviving PE who do not have persistent thrombus or CTEPH. Radiology, hospital and primary care records were reviewed in patients with central pulmonary emboli presenting to a large hospital in South Wales between 2013-16. 2501 CTPA were reviewed. 380 (15.2%) showed PE and of these 127 (33.4%) involved the main pulmonary arteries or the pulmonary trunk. 4 patients received systemic and 1 catheter directed thrombolysis. 16 (12.6%) patients died of PE during the admission. Excluding patients dying within 3 months, 49 patients (48.5%) were more SOB than before the pulmonary embolus (73.7 % if there was evidence of right heart strain during admission). Of these 6 patients (12.2%) had evidence of persisting PE and/or pulmonary hypertension. In patients with no evidence of persisting clot or pulmonary hypertension where full lung function was performed there was an isolated reduction in gas transfer measurement (mean TLCO 57%). Many patients remain breathless following large volume PE particularly if there is evidence of Right ventricular strain at presentation. The pathophysiology is unclear but lung function testing is consistent with persisting damage to the pulmonary vascular bed. These findings may allow clinicians to better advise patients of expected outcomes following major pulmonary embolus and may avoid unnecessary further investigation.

To Thrombolyse or Not to Thrombolyse: Two Years Experience of Thrombolysis of Sub-Massive Pulmonary Embolism in a District General Hospital.

AimsCurrent British Thoracic Society (BTS) guidelines only recommend thrombolysis of pulmonary embolism (PE) in patients who are haemodynamically compromised. Newer evidence suggests a mortality benefit for the thrombolysis of sub-massive PE with right ventricular strain. We wanted to assess the outcome and safety of thrombolysis in patients with sub-massive PE in a DGH.MethodsThe notes for patients with sub-massive PE and thrombolysis from a two-year period were reviewed. Evidence of right ventricular strain and myocardial necrosis based on bedside echocardiography, computed tomography (CT) scan and troponin T were indications for thrombolysis.ResultsA total of 22 patients had thrombolysis of PE in the study period (56±14 years). Fourteen patients were classified as sub-massive PE (55±15 years). Out of eight patients who had thrombolysis of massive PE (58±14 years), three were initially classified as sub-massive PE but deteriorated within the next 48 hours and became haemodynamically unstable. In all patients, the diagnosis was confirmed with a CT pulmonary angiography (CTPA).Mean troponin was 82 in the sub-massive PE group and 102 in the massive PE group. The clinical condition and haemodynamic of patients improved rapidly within a few hours after thrombolysis.Post-thrombolysis echocardiography was performed, 17 patients had normal right ventricles with normal pulmonary arterial pressures.ConclusionThrombolysis of sub-massive pulmonary embolism is feasible in a district general hospital and seems to be a safe procedure, particularly in younger patients. It results in rapid improvement in the clinical condition of patients with a small incidence of bleeding complications.

A systematic review for the role of systemic thrombolysis in intermediate-risk (submassive) pulmonary embolism

Background: Pulmonary emboli (PE) represents an extended spectrum of diseases. 10% of submassive PE progress to massive PE, and while overall mortality is around 5%, it can reach 30%,1 highlighting the potential severity of submassive PE. Treatment of low and high-risk PE is rather straightforward. However, treating intermediate risk PE is challenging due to the potential risks associated with aggressive therapy. We assessed the effect of adding thrombolytic therapy to standard treatment with heparin on short-term mortality, clinical deterioration, and bleeding in intermediate-risk PE cases. Intermediate-risk PE in this systematic review is objectively confirmed PE either by computer tomography (CT) or ventilation/perfusion (V/Q) scan in normotensive patients (systolic blood pressure ≥ 90 mmHg) with evidence of right ventricular strain by echocardiography or CT with or without evidence of myocardial injury by raised cardiac biomarkers.2 Methods: A literature search was conducted using PubMed, OvidSP Platform, Google Scholar, BestBETs, The Cochrane Library - Databases, American College of Chest Physicians (ACCP), American Heart Association (AHA), European Society of Cardiology (ESC), American College of Emergency Physicians (ACEP), and NICE guidelines from 1946 to the 21st March 2018. References of retrieved articles were reviewed for other possibly related citations. The randomized controlled trials (RCTs) were studied and appraised using the Cochrane risk-of-bias tool (Table 1). Results: From 66 potentially relevant studies, six RCTs were published between 2002 and 2017 and included in this systematic review (Table 2). A total of 1568 patients were enrolled: 747 received thrombolytic therapy with alteplase (two trials, 155 patients) or tenecteplase (four trials, 592 patients), and 821 were treated with heparin only. None of these RCTs proved that adding thrombolytic therapy to standard anticoagulant treatment statistically decreased early mortality. The five studies looking at clinical deterioration proved that thrombolysis was beneficial. Five out of six RCTs resulted in a non-significant difference in major bleeding prevalence. Only the PEITHO3 trial proved the opposite. The incidence of minor bleeding was significantly higher in the four studies in which it was measured (Table 3). Conclusions: Currently, there is inadequate evidence to support the use of systematic thrombolysis for patients with acute intermediate-risk PE. Although it may prevent clinical deterioration which necessitates escalation of treatment in the short term, it comes with increased risk of bleeding. Individual risk-benefit patient assessment and shared decision making may be wise until better evidence to proceed otherwise is demonstrated. Larger clinical trials concerning reduced thrombolytic doses and prolonged infusion rate is essential.

Consideration for thrombolysis for significant pulmonary embolism in haemodynamically stable patients—is it time for a rethink?

Pulmonary embolism (PE) is a common diagnosis made in the emergency department with 60–70 cases per 100,000. The clinician needs to have up to-date knowledge and potential treatment strategies for management of this common condition. Thrombolysis for PE is one of the options that can be considered in the Emergency Department. The British Thoracic Society (BTS) has formed a set of recommendations for consideration of thrombolysis. We will discuss two clinical cases of differing severity and discuss the rationale behind the treatment strategies. Firstly, we present a lady in her late 40s with acute shortness of breath with pleuritic chest pain. She was brought in by ambulance and the resuscitation suite was pre-alerted that she was due to arrive. She had been recently treated for a lower limb deep venous thrombosis (DVT) and had presented to a local hospital 2/7 previously with some associated pleuritic chest pain. She was noted to be profoundly compromised from a cardiovascular perspective. She was treated with a systemic thrombolytic agent and she was subsequently discharged soon afterwards. The second case we present is that of a 50-year-old previously fit and well gentleman who presented with acute shortness of breath on minimal exertion for the previous 3 days. There was no background history of airway diseases with no smoking. He was noted to be marked hypoxic requiring 5 litres of oxygen to maintain an oxygen saturation of 95%. His blood pressure was noted to be stable throughout his time in the department. There was imaging and electrocardiographic evidence of right ventricular strain. It was also noted to be a marked rise in cardiac enzymes indicating cardiac involvement, based on the findings he subsequently underwent treatment with a systemic thrombolytic agent and made subsequently satisfactory recovery. The presence of raised troponin in the presence of an acute PE classifies as a massive PE. Systemic thrombolysis is the first line treatment for massive PE and should be started on clinical grounds alone if cardiac arrest in imminent with alteplase being the drug of choice. The decision to perform systemic thrombolysis in the haemodynamically stable patient is multifactorial and should be assessed in a case by case manner as highlighted by this article.

AN UNUSUAL CASE OF NON SMALL CELL LUNG CANCER PRESENTING AS NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION

SESSION TITLE: Monday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Non-ST-elevation myocardial infarction (NSTEMI) is a mismatch in the myocardial oxygen demand and consumption. Common causes include poor coronary flow, unmet increased oxygen demand, and cardiac inflammation. We present a case of NSTEMI as a result of a cause not yet reported in the literature. CASE PRESENTATION: An 84-year-old man with a history of coronary artery disease (CAD), coronary artery bypass grafting, hypertension, 10 pack-year smoking history presented with a 1-week history of typical chest pain. Review of systems was otherwise non-contributory. He reported medication adherence and denied illicit drug use. Initial vitals were stable. Electrocardiogram (EKG) was unchanged from prior with no dynamic ST changes. Cardiac enzymes showed a troponin of 0.720 ng/ml, CKMB of 72.50 ng/ml and CK of 585 IU/L. Heparin drip was started for presumed NSTEMI. Troponins subsequently rose to 22.530 ng/ml and peaked at 49.160 ng/ml after which they trended downwards. Serial EKGs were unchanged. His chest pain resolved with the initiation of heparin drip. Given the downtrend in troponins and lack of EKG changes, cardiac catheterization was not performed. The echocardiogram revealed a right ventricular mass obstructing the right ventricular outflow tract (RVOT) without evidence of right ventricular strain. As the position of the mass was unclear a CT chest and cardiac MRI were done which showed an anterior mediastinal mass 5.0 cm x 5.5 cm x 6.5 cm effacing the right ventricle and pulmonary artery and also encasing the left main coronary artery, the left internal mammary artery and left anterior descending artery graft with invasion of the superficial epicardial margin of the left ventricle basal anterior segment. The heparin drip was discontinued at this point given the risk of hemorrhagic conversion of the mass. Biopsy of the mass revealed a non-small cell lung cancer (NSCLC). Further imaging revealed no metastatic lesions. Due to the size of the mass and cardiac invasion, he was not a candidate for cardiothoracic surgery. Given that he was stable from a cardiac standpoint, he was discharged with followup with hematology-oncology. DISCUSSION: Cardiac metastasis has been reported in 9% of NSCLC cases. It typically presents as dyspnea and pleuritic chest pain. While myocardial metastasis has been reported to be associated with acute STEMI [2], its presentation as NSTEMI has not been previously reported [1]. We hypothesize that this unusual presentation may have resulted from the encasement of the coronary vessels by the tumor, which led to disruption and stasis of blood flow promoting a prothrombotic state. This may have resulted in a thrombus causing ischemia which responded to heparin as treatment. CONCLUSIONS: Cardiac metastasis should be considered as a differential diagnosis for NSTEMI in patients with CAD presenting with typical chest pain given the potential to alter treatment Reference #1: Chiles, C., Woodard, P., Gutierrez, F., Link, K. (2001). Metastatic involvement of the heart and pericardium: CT and MR imaging. Radiographics, 21(2), 439-449. Reference #2: Suga, T., Akuzawa, N., Hatori, T., Imai, K., Kitahara, Y., & Kurabayashi, M. (2015). ST segment elevation in secondary cardiac cancer: a case report and review of the literature. International journal of clinical and experimental medicine, 8(5), 7719-27. DISCLOSURES: No relevant relationships by Hassaan Arshad, source=Web Response No relevant relationships by Aishwarya Bhardwaj, source=Web Response No relevant relationships by Dayna Panchal, source=Web Response no disclosure on file for Kumar Satya; No relevant relationships by Umar Jamshed Sharif Khawaja, source=Web Response No relevant relationships by Rehan Umar, source=Web Response No relevant relationships by Jun Chih Wang, source=Web Response

SUBMASSIVE PULMONARY EMBOLISM: ARE WE FALSELY REASSURED BY NORMOTENSION?

Acute pulmonary embolism (PE) is associated with significant morbidity and mortality. Current risk stratification tools utilize clinical parameters such as blood pressure (BP), cardiac biomarkers, and evidence of right ventricular strain to prognosticate patients with acute PE. We sought to

Implementation of a Modified Pulmonary Embolism Response Team (PERT) in a Community Hospital: Targeting Intermediate-Risk Pulmonary Embolism

SESSION TITLE: Diagnosis and Evaluation of Venous Thromboembolism SESSION TYPE: Original Investigation Slide PRESENTED ON: Wednesday, November 1, 2017 at 08:45 AM - 10:00 AM PURPOSE: Catheter directed thrombolysis (CDT) has recently been established as the preferred treatment in intermediate-risk pulmonary embolisms (PE). Despite acquiring the technology for CDT in July 2015, the under diagnosis of intermediate risk PE has led to under utilization of this modality in our facility. We implemented a modified pulmonary embolism response team (PERT) based on Massachusetts General Hospital’s existing PERT model with aims to streamline referral process and to increase rates of referral for CDT among eligible patients. METHODS: A retrospective chart review was performed on all patients admitted with a diagnosis of PE from July 2015 to February 2017. Pre-intervention phase was from July 2015 to September 2016 and post-intervention phase was from October 2016 to February 2017. The intervention consisted of educational sessions with hospitalists and internal medicine and family medicine residents. A referral algorithm which both risk-stratified patients and directed them to appropriate therapy was created. Data was collected to risk stratify patients into “high risk”, “intermediate risk” or “low risk” based on hemodynamic stability and evidence of right ventricular strain. The patients that fulfilled the criteria for intermediate risk PE were assessed for CDT eligibility and the treatment modality offered was studied. RESULTS: In the pre-intervention phase, 141 patients were admitted with a diagnosis of PE. Of those, 24 were identified as intermediate-risk PE (17%). Of those 24, 3 (12.5%) received CDT and 21 (87.5%) did not. Of those patients that did not receive CDT but were potentially eligible, 1 had an absolute contraindication and 5 had relative contraindications. Thus, 15 patients (62.5%) were eligible but were not offered CDT. In the post-intervention phase from October 2016 to February 2017, 48 patients were admitted with a diagnosis of PE. Of those, 7 were identified as intermediate-risk PE (14.5%). Of those 7, 3 (42.9%) received CDT and 4 (57.1%) did not. Of those patients that did not receive CDT but were potentially eligible, 1 had an absolute contraindication and 1 had a relative contraindication. Thus, 2 patients (28.6%) were eligible but were not offered CDT. CONCLUSIONS: Despite meeting criteria for intermediate risk PE and not having contraindications to therapy, a large number of patients were not referred for CDT. This could be due to incorrect stratification of patients and inadequate knowledge on the topic. Often hemodynamically stable, these patients are frequently stratified as “low-risk.” Classic risk stratification tools such as PESI and sPESI do not take into account right ventricular dysfunction, myocardial damage, or clot burden, and therefore cannot readily identify this subset of patients. Post-intervention, we saw an increase by 33.9% for the appropriate referral of CDT. Physician education and early risk stratification is the cornerstone of appropriate management of patients with PEs. CLINICAL IMPLICATIONS: Our education based modified PERT model is easily replicable in smaller, community-based hospitals and has been shown to be effective in the identification and appropriate management of patients with intermediate risk PEs. DISCLOSURE: The following authors have nothing to disclose: Amirahwaty Abdullah, Lydia Winnicka, Zabu Aung, Manidhar Lekkala, Crystal Duran, Shilpa Pedapati, Kim Norville, Sudhakar Sattur No Product/Research Disclosure Information

EVALUATION OF RIGHT VENTRICULAR STRAIN BY ECHOCARDIOGRAPHY, COMPUTED TOMOGRAPHY, AND ELECTROCARDIOGRAPHY IN PATIENTS WITH ACUTE PULMONARY EMBOLISM

Introduction: Evidence of right ventricular strain (RVS) on either transthoracic echocardiography (TTE), computed tomography (CT), or electrocardiography (ECG) has been shown to increase the risk of adverse outcomes in patients with acute pulmonary embolism (APE). We evaluated the combined

Current Controversies in Thrombolytic Use in Acute Pulmonary Embolism

BackgroundAcute pulmonary embolism (PE) has an annual incidence of 100,000 cases in the United States and is divided into three categories: nonmassive, submassive, and massive. Several studies have evaluated the use of thrombolytics in submassive and massive PE. ObjectiveOur aim was to provide emergency physicians with an updated review of the controversy about the use of thrombolytics in submassive and massive PE. DiscussionNonmassive PE is defined as PE in the setting of no signs of right ventricular strain (echocardiogram or biomarker) and hemodynamic stability. Submassive PE is defined as evidence of right ventricular strain with lack of hemodynamic instability. Massive PE occurs with occlusive thromboembolism that causes hemodynamic instability. Thrombolysis is warranted in patients with massive PE. Thrombolytic use in submassive PE with signs of right ventricular strain or damage presents a quandary for physicians. Several recent studies have evaluated the use of thrombolytics in patients with submassive PE. These studies have inconsistent definitions of submassive PE, evaluate differing primary outcomes, and use different treatment protocols with thrombolytics and anticoagulation agents. Although significant study heterogeneity exists, thrombolytics can improve long-term outcomes, with decreased bleeding risk with half-dose thrombolytics and catheter-directed treatments. Major bleeding significantly increases in patients over age 65 years. The risks and benefits of thrombolytic treatment—primarily improved long-term outcomes—should be considered on a case-by-case basis. Shared decision-making with the patient discussing the risks and benefits of treatment is advised. ConclusionsThrombolytic use in massive PE is warranted, but patients with submassive PE require case-by-case analysis with shared decision making. The risks, including major hemorrhage, and benefits, primarily improved long-term outcomes, should be considered. Half-dose thrombolytics and catheter-directed treatment demonstrate advantages with decreased risk of bleeding and improved long-term functional outcomes. Further studies that assess risk stratification, functional outcomes, and treatment protocols are needed.

Modification of Simplified Pulmonary Embolism Severity Index and its Prognostic Value in Patients with Acute Pulmonary Embolism

Various risk stratification systems have been used to predict the clinical outcome of patients with pulmonary embolism (PE). In this study we present a modification of the simplified Pulmonary Embolism Severity Index (S-PESI) score and evaluate its accuracy in predicting the outcome of these patients. Patients older than 18 years with documented PE were enrolled in this study. S-PESI was calculated in all patients. We added electrocardiographic evidence of right ventricular strain as a new criteria and replaced the O2 saturation of <90% in S-PESI score with PaO2 /PaCO2 ratio obtained from the arterial blood gas analysis as two newly modified criteria to define a modified form of S-PESI system (modified s-PESI). Patients were followed for about one year in outpatient clinics. Any deaths attributable to PE or for unknown reasons were considered as PE related. We defined Major Adverse Cardio-Pulmonary Events (MACPE) as sum of one-year mortality, need for thrombolysis and mechanical ventilation during index hospitalisation. Among 300 enrolled patients, in-hospital mortality occurred in 38 (12.7%) and one-year mortality in 73 (24.3%) patients. Considering a cut-off point of 3, modified s-PESI score had a lower sensitivity (49.3% vs. 89%) and higher specificity (79.4% vs. 37.7%) than S-PESI to predict one-year mortality. Area Under Curve (AUC) to predict MACPE was significantly higher for modified s-PESI (0.692 vs 0.730, P=0.012). The modified s-PESI is superior to S-PESI in predicting one-year outcome in patients with PE and can be used for more accurate risk stratification of these patients.

Outcome of pulmonary embolism and clinico-radiological predictors of mortality: Experience from a university hospital in Saudi Arabia.

OBJECTIVES:The objective of this study is to determine the outcome of pulmonary embolism (PE) and the clinico-radiological predictors of mortality in a university hospital setting.METHODS:A Prospective observational study conducted at King Khalid University Hospital, Riyadh Saudi Arabia between January 2009 and 2012. A total of 105 consecutive patients (49.9 ± 18.7 years) with PE diagnosed by computed tomography pulmonary angiography were followed until death or hospital discharge.RESULTS:Overall in hospital mortality rate was 8.6%, which is lower than other international reports. Two-thirds of patients developed PE during the hospitalization. The most common risk factors were surgery (35.2%), obesity (34.3%) and immobility (30.5%). The localization of the embolus was central in 32.4%, lobar in 19% and distal in 48.6%. A total of 26 patients (25%) had evidence of right ventricular strain and 14 (13.3%) were hypotensive. Multivariate analysis revealed that heart failure (Beta = −0.53, P < 0.001), palpitation (Beta = −0.24, P = 0.014) and high respiratory rate (Beta = −0.211, P < 0.036) were significant predictors of mortality.There was no significant difference in the localization of the embolus or obstruction score between survivors and non-survivors.CONCLUSION:The outcome of PE is improving; however, it remains an important risk factor for mortality in hospitalized patients. Congestive heart failure, tachypnea and tachycardia at presentation were associated with higher mortality. These factors need to be considered for risk stratification and management decisions of PE patients. Radiological quantification of clot burden was not a predictor of death.

Hampton’s Hump and Palla’s Sign in Pulmonary Embolism

A 33-year-old female smoker came to our emergency department complaining of dyspnea, pleuritic left chest pain, and an episode of mild hemoptysis. One week previously, she had experienced left calf pain. There was no history of recent trauma or immobilization. Her only medication was an oral contraceptive. On admission, her heart rate was 110 beats per minute in sinus rhythm, with a normal physical examination and arterial blood gases and without evidence of right ventricular strain on ECG (Figure 1). A chest …

Illicit narcotic injection masquerading as acute pulmonary embolism

A 23-year-old male presented from a nursing home with hypotension, tachycardia, diaphoresis and electrocardiographic evidence of right ventricular strain that was confirmed by echocardiography. His differential diagnosis included sepsis and pulmonary embolism. A high-resolution computed tomography scan demonstrated no pulmonary emboli but did demonstrate multiple bilateral pulmonary nodules. Upon questioning he admitted to injecting a long-acting narcotic that had been manually macerated, dissolved in saline, and injected through an indwelling intravenous line. Lung biopsy findings were consistent with cellulose-induced perivascular granulomatosis. Cellulose granulomatosis can be seen in patients who inject medications designed for oral use and should be considered in patients who present with acute pulmonary hypertension.

Fat embolism syndrome : A diagnostic dilemma

Fat embolism syndrome (FES) is a constellation of clinical manifestations following fracture of long bones. In retrospective review, incidence of FES was less than 1% [1]. Fat embolism syndrome is a clinical diagnosis. This condition is often misdiagnosed and fatal if the treatment is delayed. We present two cases of fat embolism syndrome to highlight problems of missed diagnosis. Case 1 A 19 year old male sustained bilateral closed tibial and fibular fracture. Plaster of Paris (POP) slab was applied over both lower limbs and surgery planned. While awaiting fixation of fractures patient developed high grade fever from second day. Surgery was deferred to investigate fever. No specific cause for fever could be found and empirical treatment for malaria administered. Four days after the injury, patient suddenly developed tachypnea (breath rate 55/minute), tachycardia (pulse 145/minute), and altered sensorium. Oxygen saturation on pulse oximetry (SpO2) was 60% with high flow oxygen by facemask. He was intubated and mechanically ventilated with 100 % oxygen using anaesthesia circuit and later placed on ventilator in control mode with positive end expiratory pressure (PEEP). As oxygen saturation did not improve, PEEP was gradually increased to 20 cm of H2O. The high level PEEP resulted in pneumothorax for which an intercostal chest drain was inserted and patient was shifted to a tertiary care hospital. On arrival to the intensive care unit quick clinical evaluation revealed marked pallor, pulse 140/minute, blood pressure of 130/70 mm Hg, SpO2 90%, breath rate and neurological status could not be ascertained as patient was under effect of muscle relaxants. Patient was placed on Seimens Servo i ventilator in synchronized intermittent mandatory ventilation (SIMV) mode with PEEP. Initial ventilator settings were tidal volume 350 ml, mandatory breath rate 16/minute, fraction of inspired oxygen (FiO2) 0.7 and PEEP 10 cm H2O. With these settings peak inspiratory pressure of 23 cm H2O, plateau pressure of 20 cm H2O, mean airway pressure of 12 cm H2O and dynamic compliance of 30 ml/cm H2O was recorded. There were no petechial or subconjuctival haemorrhages. Chest auscultation revealed bilateral extensive crepitations and bronchial breath sounds. Fundoscopy revealed multiple haemorrhages along the vessel in entire field of both eyes. Doppler study of lower limb showed no evidence of venous thrombosis. Investigations revealed haemoglobin (Hb) 6.8 gm %, chest radiograph showed bilateral non homogenous opacities with predominant basal distribution (Fig. 1). Arterial blood gas (ABG) showed pH of 7.25, partial pressure of oxygen in arterial blood (PaO2) 55 mm Hg, partial pressure of carbon dioxide in arterial blood (PaCO2) 35 mmHg, bicarbonate (HCO3) 18 mmol/L and PaO2/FiO2 ratio of 78. Other investigations were within normal limits. Right internal jugular vein was cannulated and central venous pressure (CVP) of 12 cm of saline was recorded. Frank blood was noted on endotracheal suction. Fig. 1 Chest radiograph (antero-posterior view) shows bilateral non homogenous opacities in a predominantly basal distribution On the basis of clinical background, chest radiograph and arterial blood gas analysis report, the case was diagnosed as fat embolism syndrome with acute respiratory distress syndrome (ARDS). Patient was kept sedated, muscle relaxants discontinued and mechanical ventilation continued. Tachycardia and tachypnea settled down after eight hours of ventilation and patient started responding to simple verbal commands. The case was discussed with orthopaedic surgeon for fixation of fractures on fifth day. A consensus decision was taken to wait for some time. Next day while on ventilator, patient suddenly desaturated (SpO2 70%), became restless and developed tachypnea (breath rate 60/minute) and tachycardia (heart rate 150/minute). There were no specific changes on electrocardiogram and transthoracic echocardiography did not show any evidence of right ventricular strain. Patient improved within one hour with readjustment of ventilator settings. This episode was thought to be fresh episode of fat embolism. In view of recurring fat embolism, it was decided to fix fractures early. On sixth day bilateral open reduction and dynamic compression plating of both fractures was done under general anesthesia. Intraoperative course was uneventful. Postoperatively, ventilation, adequate analgesia, and antibiotics were continued. On seventh day patient improved and he was placed on oxygen mask. After eight hours of extubation patient again developed tachycardia, tachypnea, diaphoresis, and mild desaturation (SpO2 90%). This time noninvasive ventilation was used to tide over the crisis. After six hours of mask ventilation SpO2 improved to 97%. Thereafter he made an uneventful recovery.

Modern treatment of pulmonary embolism.

Modern treatment of acute pulmonary embolism requires rapid and accurate diagnosis followed by risk stratification to devise an optimal management strategy. Patients at low risk have good outcomes simply with intensive anticoagulation treatment. Higher-risk patients may require more aggressive intervention with thrombolysis or embolectomy. Clinical risk factors for an adverse outcome include increasing age, cancer, congestive heart failure, systemic arterial hypotension, chronic obstructive pulmonary disease and right ventricular dysfunction. A promising approach is the Geneva Prognostic Score, which is based upon a rapid clinical assessment. On physical examination, signs of right ventricular failure, including distended jugular veins and a right-sided S3 gallop, should be looked for. The electrocardiogram may show evidence of right ventricular strain with a new right bundle branch block or T wave inversion in leads V1-V4. The troponin level may be elevated as a marker of cardiac injury and right ventricular microinfarction, even in the absence of coronary artery disease. The most useful imaging marker of high risk is the presence of moderate or severe right ventricular dilatation and hypokinesis on the echocardiogram, especially with progressively worsening right ventricular function despite intensive anticoagulation treatment. Patients at high risk should be considered for thrombolytic therapy or embolectomy rather than management with anticoagulation therapy alone. Special care must be taken to avoid thrombolytic therapy among patients who might be susceptible to intracranial haemorrhage. Intracranial haemorrhage reached a surprisingly high rate of 3.0% in the International Cooperative Pulmonary Embolism Registry of 2,454 prospectively evaluated acute pulmonary embolism patients at 52 hospitals in seven countries. An alternative approach to patients at high risk is a catheter-based or open surgical embolectomy. It is crucial to refer these patients as quickly as possible, rather than delaying intervention until cardiogenic shock has ensued. Fortunately the current tools for risk stratification provide an "early window" for prognostication and can help the coordination of a definitive treatment plan with optimal results.

The Results of Mitral Commissurotomy One to Three Years After Surgery

CONCLUSION The large majority of carefully selected cases of mitral stenosis with functional impairment submitted to commissurotomy benefit from the procedure and in many cases this benefit persists for at least one to three years. A greater degree of benefit can be anticipated in otherwise satisfactory cases when the right ventricular pressure is markedly elevated. Such elevation can usually be predicted when evidence of right ventricular strain is present on the electrocardiogram. In addition to evidence of improvement in respect to functional capacity, hemoptysis, and paroxysmal dyspnea, a large proportion of cases had objectively demonstrable improvement. This is evident in reduction of right ventricular pressure and decrease of right ventricular force on the electrocardiogram. Decrease in heart size by x-ray is an exceptional finding. Mitral commissurotomy with auricular appendectomy is an effective method for controlling peripheral emboli in patients with mitral stenosis. The presence of a calcified valve may not necessarily prevent lasting or significant benefit from the procedure.

The heart in bronchial asthma

A study was made of the heart in 84 cases of bronchial asthma. There were nine deaths in this group, and six cases came to autopsy. From a pathologic standpoint the heart was not greatly involved in uncomplicated cases of bronchial asthma. In one patient dying of acute asphyxia there was found dilatation of the right heart. Two cases complicated by various degrees of emphysema, bronchiectasis and lung abscess showed hypertrophy, dilatation, and congestive heart failure. Pathologic findings of these six autopsied cases are reported. No clinical evidence of heart disease was found in the majority of cases. Definite evidence of right ventricular strain with a tendency to myocardial involvement was noted in the electrocardiographic study. It must be concluded, therefore, that the heart does not remain singularly free from injury in bronchial asthma, and that right ventricular strain with a tendency to myocardial involvement and heart muscle damage does occur as the disease progresses and emphysema ensues.