8. a) Universal precautions b) Methods of perioperative acute pain management. c) Preoperative risk factors for postoperative deep vein thrombosis and its prophylactic management

jun 2018

universal precautions

 8. a) Universal precautions  











  b) Methods of perioperative acute pain management.








 c) Preoperative risk factors for postoperative deep vein thrombosis and its prophylactic management. 

Pulmonary Embolism and Venous Thromboembolism                                         sabiston

Causes

VTE comprises DVT and pulmonary embolism (PE). PE is a serious postoperative complication that represents a source of preventable morbidity and mortality in the United States and is responsible for 5% to 10% of all in-hospital deaths. Undiagnosed PE has a hospital mortality rate of 30%, which decreases to 8% if diagnosed and treated appropriately. VTE is caused by a perturbation of the homeostatic coagulation system induced by intimal injury, stasis of blood flow, and a hypercoagulable state.

Risk factors for the development of VTE are listed in Table 12-7. 18 Thrombophilia describes hereditary and acquired biochemical states that predispose to VTE. One in four fatal PE cases occurs in surgical patients. Survivors of VTE are at increased risk for recurrence. The highest risk of VTE occurs in patients hospitalized for surgery. The prevalence of PE in patients with malignancy is 11%. The relative risk of DVT and PE in patients with inflammatory bowel disease is approximately 5% and 3%, respectively. In victims of major trauma, the incidence of DVT exceeds 50%, with fatal emboli occurring in 0.4% to 2% of cases. Critically ill patients and patients in the intensive care unit (ICU) have multiple risk factors and are also at higher risk for VTE. Central venous catheter–related thromboses are more common with femoral placement. Thrombosis ranges from 4% to 28% after subclavian vein cannulation and 4% to 33% after internal jugular catheterization. Among patients with subclavian or axillary vein thrombosis, PE is reported in 9.4%.

Most pulmonary emboli originate from an existing DVT in the legs, and the iliofemoral venous system represents the site from which most clinically significant pulmonary emboli arise. Approximately 50% of patients with proximal DVT develop PE. Rare causes of PE include a fat embolus associated with fractures of long bones and air embolism, often related to operative procedures and the presence of central lines.

Presentation and Diagnosis

The physiologic response to PE depends on the size of the thrombus, coexisting cardiopulmonary disease, and various neurohormonal effects. More than 50% of DVTs are silent, and PE may be the first manifestation of the disease. Most symptoms and signs associated with symptomatic PE are nonspecific and may be encountered with other disease states, such as MI, pneumothorax, and pneumonia (Box 12-5). Chest radiograph has limited value in the diagnosis of PE and is mainly used to rule out other causes of a patient’s symptoms. Approximately 5% to 10% of patients develop a massive PE that results in hemodynamic instability (hypotension, with or without shock) and death. The probability of an individual having PE (pretest probability) is assessed by the sum of points given to VTE risk factors: the patient’s symptoms, signs, and laboratory results (e.g., electrocardiogram [ECG], chest radiograph, and arterial blood gas) most likely to be associated with PE. Using various scoring systems, patients are stratified into low-probability, moderate-probability, and high-probability categories.

Establishing the diagnosis of PE requires confirmatory tests (helical CT scan or pulmonary angiogram) and ancillary tests (venous duplex ultrasound [VUS] and D dimer assay). Helical CT, also known as spiral CT or CT pulmonary angiography, has high specificity (92%) and sensitivity (86%), especially for central PE (main pulmonary artery or subsegmental branches) and has replaced the ? V/Q scan as the initial test of choice. In addition to the findings listed in Box 12-5, spiral CT also allows diagnosis of other pulmonary causes of a patient’s symptoms. However, the test requires an IV contrast agent; may be unavailable after normal working hours; requires a cooperative patient to avoid artifacts; may miss emboli in subsegmental arteries, which account for 20% of all pulmonary emboli; and may be inconclusive in approximately 10% of cases. Pulmonary angiogram is the gold standard test because it visualizes the arterial tree directly and detects intravascular filling defects. However, it is used less commonly because it is invasive, it requires expertise, and after-hours availability is limited. Echocardiography is a rapid, noninvasive, available bedside test that provides quick results in a critically ill or hemodynamically unstable patient. Transthoracic echocardiography shows the hemodynamic consequences of acute ventricular pressure overload—right ventricular dysfunction (hypokinesia and dilation), interventricular septal flattening and paradoxical motion, elevated tricuspid gradient, pulmonary hypertension, and patent foramen ovale. 19 Dysfunction of the right ventricle occurs in 30% to 50% of patients with PE who undergo echocardiography.

Transesophageal echocardiography also shows secondary changes in cardiac chamber size and functions caused by hemodynamic effects of PE and may reveal a proximal intrapulmonary or free floating intracardiac clot. Echocardiography also rules out other causes of shock, such as a pericardial tamponade. Transesophageal echocardiography is not always available and requires specialty training.

VUS of the extremities is used as an indirect test for diagnosing PE. Approximately one third of patients with PE demonstrate lower extremity findings consistent with DVT, and 80% of patients with PE have a DVT on the venogram. D dimer is a degradation product of a cross-linked fibrin blood clot. Levels are typically elevated in patients with acute thromboembolism. Of the many D dimer tests, enzyme-linked immunosorbent assay (ELISA) is the most sensitive, with quick results. A negative test excludes the diagnosis, but a positive test does not rule in the diagnosis. Based on the pretest clinical probability, a patient suspected to have PE requires a chest radiograph, ECG, arterial blood gas analysis, and D dimer assay. If leg symptoms are present, VUS is performed. If VUS is positive, the patient is considered to have PE and receives anticoagulant medication because treatment is similar to that for PE. If leg symptoms are absent, the spiral CT approach may be used. If the findings on spiral CT are suboptimal or negative and there is a high clinical probability of PE, an angiogram is obtained. This approach is inappropriate for patients with iodinated dye allergy.

In critically ill patients in whom there is a high suspicion for PE and patients with suspected massive PE, the workup depends on their hemodynamic stability. In stable patients, anticoagulation is started if there are no contraindications, VUS is performed, and a spiral CT scan is obtained urgently. In unstable patients, anticoagulation is started, and VUS and echocardiography are performed. If the echocardiographic results are positive, thrombolytic therapy is started; if results are negative, a pulmonary angiogram is obtained.

Treatment

Medications used in the treatment of VTE include heparins, fondaparinux, VKAs, and thrombolytic agents. Heparin prevents the thrombin-mediated conversion of fibrinogen to fibrin and stops propagation of the thrombus. UFH is inexpensive and highly effective, enhances antithrombotic activity of antithrombin III and factor Xa, and has a short plasma half-life. LMWH primarily inactivates factor Xa and has a longer half-life and more predictable anticoagulant property. VKAs (e.g., warfarin) have a delayed onset of action and the potential to interact with other medications. Fondaparinux is a synthetic pentasaccharide that selectively inhibits factor Xa. Thrombolytic agents (e.g., streptokinase, urokinase, recombinant tissue plasminogen activator) are used in the treatment of massive PE. Treatment of PE starts with prevention. Because most pulmonary emboli originate from existing clots in the deep venous system of the legs in at-risk patients, identifying patients at risk for DVT and applying preventive measures is the only way to decrease VTE-related morbidity and mortality. The intensity of prophylaxis must match the risk for VTE and potential complications of the medication (e.g., bleeding, heparin-induced thrombocytopenia). According to the American College of Chest Physicians, assessment of patients into low-risk, moderate-risk, and high-risk categories for VTE is based on the type of surgery performed, patient mobility, risk of bleeding, and VTE risk based on the presence of additional risk factors.  Age is a significant risk factor, with the risk doubling with each decade beyond age 40 years. Most hospitalized patients have at least one risk factor for VTE, and approximately 50% have more than three risk factors. Pharmacologic prophylaxis is an accepted and effective strategy.  In critically ill patients, heparin is first-line prophylaxis. Prophylaxis is achieved with the administration of low-dose UFH given subcutaneously every 8 hours or LMWH given as a daily dose. Studies have suggested that LMWH is more effective prophylaxis than low-dose UFH in critically ill patients and is associated with a reduced risk of major hemorrhage. Overt bleeding and thrombocytopenia are contraindications to chemical prophylaxis. In patients undergoing surgery, low-dose UFH is administered (5000 U, 3 to 4 hours preoperatively and then every 8 hours). Fondaparinux has emerged as an alternative prophylactic after major orthopedic surgery. Nonpharmacologic prophylaxis can be achieved with elastic stockings, graduated compression stockings, intermittent pneumatic compression devices, or venous foot pumps. Compression devices are not associated with bleeding. They produce a satisfactory reduction in risk for DVT in high-risk surgical patients. However, little is known about their efficacy as sole prophylaxis in critically ill patients, and they may be most beneficial in combination with pharmacologic prophylaxis in the subset of high-risk patients or solely in patients for whom the risk of bleeding is high. The presence of leg ulcers and peripheral vascular disease precludes the use of mechanical devices. Anticoagulation is the standard of care treatment for VTE. It prevents clot propagation and allows endogenous fibrinolytic activity to dissolve existing thrombi, a process that occurs over weeks and months. Incomplete resolution is common and predisposes to recurrent VTE. The initial treatment is with LMWH, UFH, or fondaparinux, followed by VKA, which is administered on the same day as LMWH or UFH, with overlap for 5 days or longer until the target INR is achieved. In patients with VTE and active cancer, anticoagulation is continued indefinitely. Surgical patients within 24 hours of surgery may be considered for a retrievable inferior vena cava filter until anticoagulation is initiated. In patients with a contraindication to anticoagulation, placement of an inferior vena cava filter protects against PE.

UFH is given intravenously (a weight-adjusted bolus of 70 U/kg is followed by 1000 U/hr) to achieve a partial thromboplastin time 1.5 to 2 times the control value. Activated partial thromboplastin time is determined 6 hours after the loading dose and then on a daily basis, and the dose of heparin is adjusted accordingly. UFH is easily reversible and the agent of choice. LMWH is given subcutaneously once or twice daily (enoxaparin, 1.5 mg/kg/day, or dalteparin, 10,000 to 18,000 U/day, depending on weight).

Monitoring of LMWH is unnecessary. UFH and LMWH may be associated with heparin-induced thrombocytopenia, and the platelet count is monitored between days 3 and 5. Warfarin is given orally, and this therapy is allowed to overlap with heparin therapy until the INR is therapeutic for 2 consecutive days before heparin is discontinued. Therapy is continued for more than 3 months, with the goal to reach an INR of 2.5.

In massive PE, the goal of therapy is to maintain hemodynamic stability, enhance coronary flow, and minimize right ventricular ischemia. When massive PE is suspected, resuscitation is initiated, oxygen is administered, and IV UFH therapy is started. In hemodynamically unstable patients, IV vasoactive medications are required. Thrombolytic therapy, if not contraindicated, has the advantage of dissolving the clot quickly, with rapid improvement in pulmonary perfusion, hemodynamic alterations, gas exchange, and right ventricular function. The role of surgical embolectomy is controversial. The transcatheter technique (with or without low-dose thrombolytic therapy) is another therapeutic approach. Placement of an inferior vena cava filter reduces the risk for recurrence of PE. Novel anticoagulants under investigation include factor Xa inhibitors (direct inhibitor [hypermethylated derivative of fondaparinux with a long half-life given intravenously or subcutaneously] or indirect inhibitor mediated by antithrombin [given orally or parenterally]) and direct thrombin inhibitors.