PULMONARY EMBOLISM PREPARED BY: DR. IBRAHIM AYOUB DR. SUHAIL KHOJAH

INTRODUCTION Acute pulmonary embolism (PE) is a common and often fatal disease. Mortality can be reduced from 30% to up to 2-8% by prompt diagnosis and therapy. Acute pulmonary embolism (PE) is a common and often fatal disease. Mortality can be reduced from 30% to up to 2-8% by prompt diagnosis and therapy. Unfortunately, the clinical presentation of PE is variable and nonspecific, making accurate diagnosis difficult. Unfortunately, the clinical presentation of PE is variable and nonspecific, making accurate diagnosis difficult.

CLASSIFICATION PE can be classified as acute or chronic PE can be classified as acute or chronic -Patients with acute PE typically develop symptoms and signs immediately after obstruction of pulmonary vessels. -In contrast, patients with chronic PE tend to develop slowly progressive dyspnea over a period of years due to pulmonary hypertension.

Acute PE can be further classified as massive or submassive: -Massive PE causes hypotension, defined as: -Massive PE causes hypotension, defined as: a systolic blood pressure <90 mmHg a systolic blood pressure <90 mmHgor a drop in systolic blood pressure of ≥40 mmHg from baseline for a period >15 minutes. 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 (or neck vein distension), which is not otherwise explained by acute myocardial infarction, tension pneumothorax, pericardial tamponade, or a new arrhythmia. It should be suspected anytime there is hypotension accompanied by an elevated central venous pressure (or neck vein distension), which is not otherwise explained by acute myocardial infarction, tension pneumothorax, pericardial tamponade, or a new arrhythmia. -All acute PE not meeting the definition of massive PE are considered submassive PE. -All acute PE not meeting the definition of massive PE are considered submassive PE.

RISK FACTORS PE is a common complication of deep vein thrombosis (DVT), occurring in more than 50% of cases confirmed to have DVT. So, factors that promote the development of DVT also increase the risk for PE. These include: -immobilization -surgery within the last three months -stroke, paresis, paralysis -history of venous thromboembolism -malignancy -central venous instrumentation within the last three months -chronic heart disease. -Additional risk factors identified in women include obesity (BMI ≥29 kg/m2) obesity (BMI ≥29 kg/m2) heavy cigarette smoking (>25 cigarettes per day) heavy cigarette smoking (>25 cigarettes per day) hypertension. hypertension.

SYMPTOMS The most common symptoms are: -dyspnea at rest or with exertion (73%) -pleuritic pain (44%) -cough (34%) ->2-pillow orthopnea (28%) -calf or thigh pain (44%) -calf or thigh swelling (41%) -wheezing (21%). *The onset of dyspnea was usually within seconds (46%) or minutes.

SIGNS The most common signs are: -tachypnea (54%) -tachycardia (24%) -rales (18%) -decreased breath sounds (17%) -loud P2 (15%) -jugular venous distension (14%)

DIFFERENTIAL DIAGNOSES Acute coronary syndrome Tention pneumothorax Cardiac tamponade Aortic dissection Esophageal disorder

INVESTIGATIONS Routine laboratory findings (non-specific): -leukocytosis -leukocytosis -increased erythrocyte sedimentation rate (ESR) -increased erythrocyte sedimentation rate (ESR) -elevated serum LDH or AST (SGOT) -elevated serum LDH or AST (SGOT) -normal serum bilirubin -normal serum bilirubin ABG: usually reveal hypoxemia, hypocapnia, and respiratory alkalosis. The typical ABG findings are not always seen. As an example, massive PE with hypotension and respiratory collapse can cause hypercapnia and a combined respiratory and metabolic acidosis (the latter due to lactic acidosis). In addition, hypoxemia can be minimal or absent. The typical ABG findings are not always seen. As an example, massive PE with hypotension and respiratory collapse can cause hypercapnia and a combined respiratory and metabolic acidosis (the latter due to lactic acidosis). In addition, hypoxemia can be minimal or absent.

TROPONIN: Serum troponin I and troponin T are elevated in % of patients who have a moderate to large pulmonary embolism. presumed mechanism is acute right heart overload. ECG: ECG abnormalities are also common in patients without PE, limiting the diagnostic usefulness of the ECG. ECG abnormalities historically considered to be suggestive of PE ECG abnormalities historically considered to be suggestive of PE -S1Q3T3 pattern -S1Q3T3 pattern -right ventricular strain -right ventricular strain -new incomplete right bundle branch block -new incomplete right bundle branch block ECG changes are infrequent during acute PE. However, they are common among patients with massive acute PE and cor pulmonale. ECG changes are infrequent during acute PE. However, they are common among patients with massive acute PE and cor pulmonale.CXR: -Atelectasis (69%) -Atelectasis (69%) -Pleural effusion (47%) -Pleural effusion (47%) -Normal (12%) -Normal (12%)

V/Q SCAN: Diagnostic accuracy is greatest when the V/Q scan is combined with clinical probability. Ultrasound: used to diagnose DVT which is the most common cause of PE. D-dimer: have good sensitivity and negative predictive value, but poor specificity and positive predictive value. Angiography: Pulmonary angiography is the definitive diagnostic technique or "gold standard" in the diagnosis of acute PE. Spiral CT: spiral (helical) CT scanning with intravenous contrast (ie, CT pulmonary angiography or CT-PA) is being used increasingly as a diagnostic modality for patients with suspected PE. Initial reports suggested that 98% of patients with PE were detected by CT-PA. Initial reports suggested that 98% of patients with PE were detected by CT-PA.

RECOMMENDED DIAGNOSTIC APPROACH When PE is suspected (eg, in a patient with sudden onset of dyspnea, deterioration of existing dyspnea, or onset of pleuritic chest pain without another apparent cause), the clinician should determine which diagnostic modalities are available and how much the hospital is experienced in performing and interpreting spiral CT (CT-PA)

When PE is suspected, the modified Wells criteria should be applied to determine if PE is unlikely (score 4). The modified Wells Criteria include the following: 3.0 Clinical symptoms of DVT (leg swelling, pain with palpation) 3.0 Other diagnosis less likely than pulmonary embolism 1.5 Heart rate > Immobilization (3 days) or surgery in the previous four weeks 1.5 Previous DVT/PE 1.0Hemoptysis 1.0Malignancy ScoreProbability Traditional clinical probability assessment >6.0High 2.0 to 6.0 Moderate <2.0Low Simplified clinical probability assessment >4.0 PE likely < or = 4.0 PE unlikely

Patients classified as PE unlikely should undergo quantitative D-dimer testing. If the D-dimer level is <500 ng/mL, the diagnosis of PE can be excluded. Patients classified as PE likely and patients classified as PE unlikely who have a D-dimer level >500 ng/mL should undergo CT-PA. A positive CT-PA confirms the diagnosis of PE. Alternatively, a negative CT-PA excludes the diagnosis of PE.

Modified wells criteria PE unlikely PE likely PE unlikely PE likely Quantitative D-dimer test 500 ng/ml 500 ng/ml Exclude PE CT-PA

In case you are working in CT inexperienced hospital or the patieng can’t undergo CP-PA (e.g. renal insufficiency or morbid obecity), a ventilation-perfusion (V/Q) scan is then performed, with the following combinations of outcomes possible: -Normal V/Q scan plus any clinical probability excludes PE. -Low probability V/Q scan plus low clinical probability excludes PE. -High probability V/Q scan plus high clinical probability confirms PE. Any other combination of V/Q scan result plus clinical probability should prompt either a pulmonary angiogram or serial lower extremity venous ultrasound exams. A reasonable alternative approach for patients with a low or intermediate clinical probability of PE is to obtain a D- dimer. A negative D-Dimer by the SimpliRed assay excludes PE.

MANAGEMENT RESUSCITATION: Respiratory support: -oxygen supplement -severe hypoxemia or respiratory failure Intubation Hemodynamic support (If the patient presents with systemic hypotension): -IVF -if not resolved: -norepinephrine -dopamine -dopamine -combined norepinephrine and dobutamine -combined norepinephrine and dobutamine

ANTICOAGULANT THERAPY: Anticoagulant therapy reduces mortality and is considered primary therapy for PE. The goal of anticoagulation is to decrease mortality by preventing recurrent PE. For patients in whom there is a high clinical suspicion of PE and no excess risk of bleeding, empiric anticoagulation should be initiated immediately and continued during the diagnostic evaluation. Heparin: Dose :loading: 80U/Kg IV Dose :loading: 80U/Kg IV :maintenance :18U/Kg/h :maintenance :18U/Kg/h T ½ : 90m T ½ : 90m Route of administration: IV/SC Route of administration: IV/SC Duration :7-10 d Duration :7-10 d Reversal :stop heparin Reversal :stop heparin protamine sulphate :1U neutralize 100 IU heparin protamine sulphate :1U neutralize 100 IU heparin No FFP No FFP

LMWH:LMWH: -Dose :brand dependent -Mechanism of action :anti-X > anti-II -Route of administration :IV or S/C -Monitoring : not indicated -Indication for monitoring : pregnancy,morbid obesity, sever renal or liver derangement -Duration : 7-10 d -Reversal :stop heparin protamine sulphate :un-predictable response protamine sulphate :un-predictable responseWarfarin: -Route of administration: P.O -Monitoring :INR -Desired target INR:2.5

Further management: -Thrombolysis. -IVC filter. -Embolectomy