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Download Diagnosis of acute pulmonary embolism
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A 46 years old man, From mahan with chief complaint of chast pain since 3dayse ago , lasting 2-3 h, with sweating and nausea Womitting: neg Dyspnea: Positive Pain radiation: neg Fever: neg Hemoptisis: neg Pleurtic chest pain: neg PMH DM: neg HTN: neg IHD: neg PULMONARY disease: neg Knee trauma since 1years ago whit car to motor accident Knee surgery:3period,last surgery 2month ago HAB HX Cig.smoker: Positive Opium addict:Positive FHX CHD: neg Respiratory disease: neg Reumatoid disease: neg Drug HX Tab.Alprazolam 1mg/daily P/E The pt is a middle age man that is contious and oriented to TPP With moderate cp Without respiratory distress Without ill and toxic BP:105/70 PR:105 RR:14 T:36/8 Osat:92% Head and Neck Jvp elevated: Positive Cianosis: neg LAP: neg Chest and Lung Lungs:bilateral clear HEART:normal heart sound without murmur Abdomen Soft Without tenderness Without organomegaly EXT Left lower exterimity edema with difference size 2cm Cianosis: neg Clubbing: neg Left knee wound with size 3*1 , 2*1cm with suppuration LAB DATA WBC:13.7 Hb:12.3 plt:218000 Urea:27 Cr:1.4 Na:136 k:4.9 Ast:26 Alt:19 TG:70 Chol:89 Troponin I:neg cpkmb:34,15,31 ESR:8 VBG: PH:7.43 BS:98 Alp:327 Billi t:0.3 d:0.2 HDL:25 LDL:60 CRP:2plus PCO2:24.2 HCO3:22.5 Coller dopler sonography Partiai vein thrombosis in left lower exterimity Echo cardio graphy 1. EF:45_ 50% Sever p.htn ( PAP: 80 ) Sever RV enlargement 2. Sever TR Sever RV enlargement McConnell’s sign” Lung perfusion scan Early assessment: ACS Early trapeutic proceeding: TNG drip,ASA,Atorvastatin,morphin,pantoprazole,alprazolam, Final assessment:Massive PTE Trapeuting proceeding in ccu: Drip heparin Warfarin Captopril N.C Digoxin Dilthiazem Acute pulmonary embolism Acute pulmonary embolism (PE) is a common and often fatal disease. Mortality can be reduced by prompt diagnosis and therapy. Unfortunately, the clinical presentation of PE is variable and nonspecific, making accurate diagnosis difficult. PE refers to obstruction of the pulmonary artery or one of its branches by material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the body. This topic review focuses on PE due to thrombus. Air emboli and fat emboli are discussed elsewhere. Massive or submassive PTE Massive PE causes hypotension, defined as a systolic blood pressure <90 mmHg or a drop in systolic blood pressure of ≥40 mmHg from baseline for a period >15 minutes. It should be suspected anytime there is hypotension accompanied by an elevated central venous pressure ,which is not otherwise explained by acute myocardial infarction, tension pneumothorax, pericardial tamponade, or a new arrhythmia .It is a catastrophic entity that frequently results in acute right ventricular failure and death. When death occurs, it is often within one to two hours of the event, although patients remain at risk for 24 to 72 hours .The PE is frequently undiscovered until autopsy. All acute PE not meeting the definition of massive PE are considered submassive PE. Certain factors can be sugesst poor prognosis Right ventricular (RV) dysfunction An elevated brain natriuretic peptide (BNP) or N-terminal pro-brain natriuretic peptide (NT-proBNP) Deep vein thrombosis RV thrombus Elevated Serum troponins Hyponatremia DDX Pneumonia, asthma, chronic obstructive pulmonary disease Congestive heart failure Pericarditis Pleurisy: "viral syndrome," costochondritis, musculoskeletal discomfort Rib fracture, pneumothorax Acute coronary syndrome Anxiety Diagnosis of acute pulmonary embolism: Laboratory: Routine laboratory findings are nonspecific. They include leukocytosis, an increased erythrocyte sedimentation rate (ESR), and an elevated serum LDH or AST (SGOT) with a normal serum bilirubin. ABG: usually reveal hypoxemia, hypocapnia, and respiratory alkalosis. Brain natriuretic peptide Troponin: Serum troponin I and troponin T are elevated in 30 to 50 percent of patients ECG: considered to be suggestive of PE (S1Q3T3 pattern, right ventricular strain, new incomplete right bundle branch block) CXR: Radiographic abnormalities are common in patients with PE V/Q scan: Patients with high clinical probability of PE and a high-probability V/Q scan had a 95 percent likelihood of having PE Patients with low clinical probability of PE and a low-probability V/Q scan had only a 4 percent likelihood of having PE A normal V/Q scan virtually excluded PE Lower extremeity ultrasound D-dimer Angiography: Pulmonary angiography is the definitive diagnostic technique or "gold standard" in the diagnosis of acute PE Spiral CT Treatment of acute pulmonary embolism Respiratory support Hemodynamic support Anticoagulant Therapy Ttrombolytic Therapy IVC filter Embolectomy Massive PTE management: For patients with massive PE and hypotension, one should administer 500 mL of normal saline. Additional fluid should be infused with extreme caution because excessive fluid administration exacerbates RV wall stress, causes more profound RV ischemia, and worsens LV compliance and filling by causing further interventricular septal shift toward the LV. Dopamine and dobutamine are first-line inotropic agents for treatment of PE-related shock. The preferred fibrinolytic regimen is 100 mg of recombinant tissue plasminogen activator (tPA) administered as a continuous peripheral intravenous infusion over 2 hours. Patients appear to respond to fibrinolysis for up to 14 days after the PE has occurred. The risk of intracranial hemorrhage with fibrinolysis has prompted a renaissance of surgical embolectomy. A possible alternative to open surgical embolectomy is catheter embolectomy. New-generation catheters are under development. Bed rest is not recommended for deep venous thrombosis unless there is substantial pain and swelling. However, the data for pulmonary embolism are not sufficient to support this recommendation. Thus, when pulmonary embolism is diagnosed, inpatient therapy with initial bed rest for 24 to 48 hours is often recommended Executive Summary Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines CHEST 2012; 141(2)(Suppl):7S–47S In patients with acute PE associated with hypotension, we suggest surgical pulmonary embolectomy over no such intervention if they have (i) contraindications to thrombolysis, (ii) failed thrombolysis or catheter-assisted embolectomy, or (iii) shock th at is likely to cause death before thrombolysis can take effect (eg, within hours), provided surgical expertise and resources are available The primary indications for placement of an inferior vena caval filter include • contraindications to anticoagulation, • major bleeding complications during anticoagulation, • and recurrent embolism while the patient is receiving adequate therapy. • Filters are sometimes placed in the case of massive pulmonary embolism, when it is believed that additional emboli might be lethal, particularly if thrombolytic therapy is contraindicated. However, this latter indication is not based on firm trial data More than 95% of patients with acute PE are (or appear to be) hemodynamically stable at presentation and are thus not considered to be at high risk a multidimensional prognostic model on the basis of 4 variables: • systolic blood pressure 90 to 100 mm Hg; • heart rate >110 beats/min; • elevated cardiac troponin; • right ventricular dysfunction on imaging Phase 3 trials investigating the new, non–vitamin K dependent oral anticoagulant agents (NOACs) apixaban , dabigatran , edoxaban , and rivaroxaban in the treatment of VTE have been completed and published. A meta-analysis showed that these agents are noninferior to the standard heparin/VKA regimen, in terms of prevention of VTE recurrence (relative risk [RR]: 0.90; 95% confidence interval [CI]: 0.77 to 1.06), and that they are probably safer in terms of major bleeding (RR: 0.61; 95% CI: 0.45 to 0.83), particularly intracranial (RR: 0.37; 95% CI: 0.21 to 0.68) and fatal (RR: 0.36; 95% CI: 0.15 to 0.84) hemorrhage . As a result, NOACs are recommended in the 2014 ESC Guidelines as an alternative to the standard heparin/VKA treatment . All 4 NOACs mentioned earlier are now licensed for treatment of VTE in the United States and the European Union (edoxaban still awaits approval in Canada);
