الفهرس 
Risk Factors and Pathophysiology of Acute Pulmonary Embolism in Intensive Care UnitOnly 14 pages are availabe for public view
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Abstract
The function of the pulmonary arteries is to carry enough blood containing oxygen and nutrients to keep the lung tissue healthy and to carry carbon dioxide to the lungs for removal from the body. Pulmonary Embolism (PE) is the sudden blocking of the pulmonary artery by an embolus and the adverse outcome of acute PE depends on the size of this embolus. Accordingly PE classified into massive, sub-massive, and low risk. Massive PE may cause sudden death either by blocking so much of the pulmonary arteries leading to inadequate oxygen supply to the body to sustain life, or by placing an excessive strain on the heart explained by increased pulmonary vascular resistance (PVR) and RV afterload. Acute RV pressure overload may result in RV hypo-kinesis and dilation, tricuspid regurgitation, and RV failure. Patients also, may develop systemic arterial hypotension, cardiogenic shock, and cardiac arrest.
The most common type of embolus that travels to the lungs is a blood clot. Another type of embolus may form from fat, which can escape into the blood from the bone marrow when a bone is fractured. An embolus also may form from amniotic fluid being forced into the pelvic veins during childbirth. Air bubbles may form an embolus that causes PE after a vein has been exposed to large amounts of air, as may occur during intravenous infusion of drugs, nutrients, or fluid. Laparoscopic surgery also carries the risk of gas embolism (e.g., CO2 embolism).
Many patients with venous thromboembolism (VTE) including PE fulfill most or all of Virchow’s triad of stasis, endothelial injury, and hypercoagulability. When these abnormalities co-occur, the combination of endogenous and acquired risk factors leads to a VTE episode. For example, when reduced blood flow occurs as in the case of immobility, pooling of blood leads to activation of coagulation locally and simultaneous consumption of blood coagulation inhibitors. In other words, the pathogenesis of VTE is multi-factorial, often requiring the presence of multiple risk factors to cause a clinical event.
Many of these thrombosis risk factors precede the ICU admission, while others develop during the course of ICU stay. Advanced age, serious medical illnesses, recent surgical procedures, and trauma are common risk factors. Sepsis, heart failure, mechanical ventilation, paralysis, surgical interventions, and central venous lines are common risk factors in critically ill patients. As regard, congenital causes, deficiencies of the natural coagulation inhibitors, such as anti-thrombin, protein C, and protein S, are strong risk factors for PE but these deficiencies are rare and only account for 1% of all cases of PE. Factor V Leiden and Pro-thrombin (factor II) G 20210 are two common genetic variants that have been found to be associated with PE, but still a small proportion of PE cases.
The diagnosis of PE in the critically ill is often challenging because the presentation is non-specific. Dyspnea, tachypnea, or chest pain, are present in more than 90% of patients with PE. Isolated dyspnea of rapid onset is usually due to more central PE causing more prominent haemodynamic disturbance. Occasionally, the onset of dyspnea may be very progressive over several weeks, and the diagnosis of PE is evoked by the absence of other classic causes of progressive dyspnea.
However, in ICU, most patients require sedation and mechanical ventilation, hence the clinical manifestations usually observed in this condition (PE) cannot be exhibited by these patients and clinical presentation is usually atypical e.g., failure of weaning from mechanical ventilation. Also, PE should be suspected anytime there is hypotension accompanied by an elevated central venous pressure, which is not explained by acute myocardial infarction (AMI), tension pneumothorax, pericardial tamponade, or a new arrhythmia.
Clinical probability assessment has become a mandatory step in the investigation of patients with clinically suspected PE. It discriminates suspected PE patients into categories of high, moderate or low clinical probability. This becomes a key step in all diagnostic algorithms for PE. The most frequently used clinical prediction rule is the Canadian rule (Wells rule).
CT pulmonary angiography appears to be the most useful study for diagnosis of PE in the critically ill. For patients with renal insufficiency and contrast allergy, the ventilation perfusion scan provides an alternative. For patients too unstable to travel, echocardiography (especially TEE) is another option. A positive result on lower extremity Doppler ultrasound can aid in the decision to treat.
The recently updated European Society of Cardiology (ESC) guidelines have insisted on replacing potentially misleading terms such as “massive”, “sub massive”, and “non-massive” PE, with “high-risk”, “intermediate risk”, and “low-risk” PE using clinical probability assessment and pulmonary embolism severity score index.
Haemodynamically unstable patients with suspected high-risk PE should immediately receive a weight-adjusted bolus of unfractionated heparin while awaiting the results of further diagnostic work-up; if PE is confirmed, thrombolysis should be administered immediately. If thrombolysis is absolutely contraindicated or has failed, surgical embolectomy or catheter-based thrombus fragmentation or suction is a valuable alternative. Vasopressors are recommended for hypotensive patients with PE. Inotropes may be used in patients with PE, low cardiac output and normal blood pressure. Aggressive fluid challenge is not recommended. Oxygen should be administered in patients with hypoxaemia, while mechanical ventilation is an end step for persistent hypoxaemia.
Normotensive, intermediate-risk patients with right ventricular dysfunction, detected by echocardiography or CT, plus evidence of myocardial injury indicated by a positive troponin test, may benefit from early thrombolytic treatment.
Oral anticoagulants (vitamin K antagonists) are highly effective in preventing recurrent VTE, but they do not eliminate the risk of subsequent recurrence after their discontinuation, regardless of the duration of treatment. Vitamin K-independent, oral anticoagulants are currently under investigation for both prophylaxis and treatment of VTE. In addition, mechanical prophylaxis plays an important role in prevention of VTE especially if added to prophylactic doses of unfractionated or low molecular weight heparins.
In pregnant women with a clinical suspicion of PE, an accurate diagnosis is necessary, because a prolonged course of heparin is required. All diagnostic modalities, including CT scanning, may be used without significant risk to the fetus. Low molecular weight heparins are recommended in confirmed PE; VKAs are not recommended during the first and third trimesters and may be considered with caution in the second trimester of pregnancy. Anticoagulant treatment should be administered for at least 3 months after delivery.
In cancer patients with confirmed PE, LMWH should be considered for the first 3–6 months of treatment and anticoagulant treatment should be continued indefinitely or until definitive cure of the cancer. In right heart thrombi, thrombolysis and embolectomy are probably both effective whereas anticoagulation alone appears less effective.
With the exception of severe air and fat embolism, the haemodynamic consequences of non-thrombotic emboli are usually mild. Treatment is mostly supportive but may differ according to the type of embolic material and clinical severity.
Better outcomes in acute PE vary substantially depending on patient characteristics, early diagnosis, quick and appropriate treatment directed according to strict clinical and prognostic evaluation of the patient. Poor outcomes are elevated with presence of shock, RVD, and myocardial injury and vice versa.