Massive Pulmonary Embolism
2007; American Association of Critical-Care Nurses; Volume: 27; Issue: 1 Linguagem: Inglês
10.4037/ccn2007.27.1.39
ISSN1940-8250
Autores Tópico(s)Blood Coagulation and Thrombosis Mechanisms
ResumoMassive pulmonary embolism in the setting of syncope and cardiac arrest is often fatal if not rapidly diagnosed. The author presents a case study of a patient with pulmonary embolism, and discusses risk factors, signs and symptoms, diagnostic findings, treatment goals, and patient education.Whenever a “Code Blue Maternity” is announced over the hospital’s loudspeaker, a collective sigh and silent prayer go up among the staff. Such an event is especially traumatic to hospital personnel during the holiday season. Our surgical intensive care and maternity units are worlds apart, but these worlds collided one December afternoon when a 35-year-old patient, whom we will refer to as Shelby, had a cardiac arrest shortly after an uneventful cesarean-section delivery at 35 weeks’ gestation. The delivery had produced a healthy, beautiful baby girl. Reports of the patient becoming acutely dyspneic, hypotensive, syncopal, and suffering cardiac arrest quickly filtered through the hallways.Only moments after the code blue maternity was called, a group of emergency personnel responded to the scene. In conjunction with the medical professionals already present, they acted without hesitation to save this patient.Pulseless electrical activity was quickly identified at the beginning of the code, and cardiopulmonary resuscitation was initiated. The patient was immediately intubated and ventilated with 100% oxygen. Boluses of intravenous epinephrine and atropine were then given, followed by an infusion of isotonic sodium chloride solution. The patient responded to treatment, as evidenced by reestablishment of a pulse and adequate blood pressure.The patient’s hemodynamic stability provided the multidisciplinary team with an opportunity to perform diagnostic tests to look for a possible cause for the cardiac arrest. A 2-dimensional echocardiogram showed dilatation of the right ventricle and moderate tricuspid regurgitation with pulmonary artery systolic pressures of 60 to 65 mm Hg, all abnormal findings in a healthy heart. This result, coupled with the postpartum arrest, led to a tentative diagnosis of pulmonary embolism. A ventilation/perfusion scan indicated a high probability of pulmonary embolism, and a computed tomography scan of the thorax showed a saddle embolism, which confirmed the diagnosis.The definitive diagnosis of pulmonary embolism proved a great threat to the patient’s survival, and an urgent interdisciplinary team meeting ensued. Physician representatives from obstetrics, cardiology, pulmonary medicine, and cardio-thoracic surgery, as well as a variety of nursing representatives who directly provided care for the patient, played a crucial part in the decision-making process. The critical care nurses reported decerebrate posturing of the patient after the cardiac arrest, which may be indicative of poor neurological functioning. Because time was of the essence, a plan was quickly formulated and put into action. Surgical embolectomy was proposed because thrombolytic therapy was contraindicated in this patient’s immediate postoperative state. Measures were quickly taken by the nurses to ready the patient for surgery. They also provided support to the patient’s shocked, desperate husband and family, who were agreeable to any treatment that would offer Shelby a chance for survival.As the cardiothoracic surgical nurses worked quickly to prepare Shelby for surgery, they were acutely aware that small fragments of thrombus could dislodge and travel farther into the pulmonary arterial tree, causing pulmonary infarction and irreversible hypoxia. An intraoperative transesophageal echocardiogram obtained on the patient’s arrival in the operating room confirmed a massive pulmonary embolism. The procedure was started by placing the patient on cardiopulmonary bypass (heart-lung machine) via femoral cannulation to shunt blood away from the main pulmonary artery and provide a bloodless operating field. The pulmonary artery was incised, and the incision was extended into the left and right pulmonary arteries. A 10-cm-long thrombus was then manually removed with forceps.Transesophageal esophagography after the procedure showed resolution of the tricuspid regurgitation, good left ventricular function, and unobstructed blood flow in the pulmonary arteries. The patient was successfully weaned from cardiopulmonary bypass and transported to the cardiac surgery intensive care unit in stable condition. A Gunther Tulip (Cook, Bloomington, Ind) filter was placed in the inferior vena cava to decrease the likelihood of further embolization. Surgery had eliminated the primary problem, but the patient’s full recovery was yet to be realized.The cardiothoracic nurses in the cardiac surgical care unit applied their skills and expertise to provide care for this new mother, whose story had touched them deeply. Many of the nurses who took care of Shelby were parents themselves and felt a personal connection to her, her new baby, and her family. Although Shelby was not alert, by postoperative day 2, her condition had begun to improve. She demonstrated normal reflexes and appropriate withdrawal from painful stimuli, which reassured the physicians and nurses who were caring for her.The nurses relayed the encouraging news to her vigilant husband and family. A room close to the intensive care unit was obtained for the family, serving as a place for them to retreat, shower, and sleep without having to leave the hospital. They were encouraged to talk to Shelby when at the bedside, to touch her hand, and to participate in her care whenever possible.Although the demands of Shelby’s care were great, the nurses were acutely aware of how large a part Shelby’s family played in her recovery. The staff often inquired about the whole family, including Shelby’s newborn and 2 young daughters, when speaking with her husband. The family brought in pictures of Shelby’s children to post at the bedside. These photos warmed the hearts of all who saw them. While providing care for Shelby, the nurses frequently mentioned her children and their well-being in an effort to reorient her. Her neurological status continued to progress, but whether she would be the Shelby her family remembered was still uncertain.Although the responses were minimal at first, the mention of her children’s names seemed to reassure Shelby, quieting her moaning and thrashing in the bed. This response provided hope and encouragement to her family and all who were caring for her. Nursing staff continued to monitor Shelby’s responses and overall neurological status, while caring for her many physical needs.Shelby was successfully weaned off of mechanical ventilation on postoperative day 5; however, she remained encephalopathic, moaning and thrashing in the bed. Shelby’s inability to respond appropriately greatly disturbed her family, and they feared a complete neurological recovery would never occur. The nurses encouraged the family to take it 1 day at a time, reassuring them that hope remained for a full recovery.The nurses reevaluated Shelby’s overall care at different intervals throughout her course, and at this point in her recovery they surmised that the last thing Shelby remembered was the delivery of her daughter. It was thought that she might feel a longing for her baby. In an attempt to reorient Shelby, the cardiac surgery and maternity staff nurses coordinated efforts to bring mother and baby together at regular intervals. Shelby became noticeably calmer as the baby lay next to her. The nurses observed a dramatic reduction in Shelby’s heart rate, blood pressure, and respiratory rate whenever she and the baby were united. The union of mother and baby proved to have a profound effect on Shelby and to be of considerable therapeutic value, reassuring the family and staff of a possible full neurological recovery. Visiting by Shelby’s family had always been permitted and was now strongly encouraged.Shelby regained complete neurological functioning by postoperative day 7, much to the relief of her family. The dedicated team of medical professionals, who had worked hard to see that this family was preserved, was also relieved. Their efforts dramatically improved Shelby’s chance for a complete recovery. The love of family and friends and the group of once-strangers who walked into Shelby’s life to “just do a good job” made a difference. Shelby was cared for and survived this traumatic experience to be reunited with her newborn and family.Shelby was discharged home to her family on postoperative day 9, neurologically intact, just 12 days before Christmas. This patient’s remarkable recovery was a Christmas miracle, an answer to the many silent prayers that helped bring about a successful outcome.Pulmonary embolism is the leading cause of maternal death after a live birth, occurring in 2 out of 100000 live births.1 Pulmonary embolism has an annual incidence of 60 to 70 per 100000 persons within the general population.2 Seven world cases of successful survival after postcesarean pulmonary embolectomy have been reported worldwide, and only 2 of those patients survived without permanent neurological damage.1 Virchow’s triad of venous stasis, hypercoagulability, and vessel wall damage triggers a venous thrombus (clot) to develop in susceptible patients.3 Pulmonary embolism results when fragments detach from a thrombus, travel through the venous system, pass through the right side of the heart, and lodge in the main branches of the pulmonary artery. A pulmonary embolism can also occur as a result of other fluids or material entering the vasculature. Deep vein thrombosis, amniotic fluid, air, and iatrogenic causes are all sources of pulmonary embolism. A venous thrombus most commonly originates in the lower extremities, the pelvis, or the kidneys. The main symptom of pulmonary embolism is often a vague complaint of dyspnea or chest pain, and death commonly occurs within 1 hour of the onset of signs and symptoms4 if the correct diagnosis is not established.Pulmonary embolism may be classified as massive, submassive, or minor, depending on the amount of pulmonary vasculature affected. Massive pulmonary embolism is defined as thrombus occluding more than 50% of the pulmonary vasculature. Thrombus that occludes the bifurcation of the pulmonary artery is termed a saddle embolus.5 When the embolus lodges in the pulmonary vasculature, blood flow to the alveoli beyond the blockage is eliminated.6 The obstruction causes a section of lung to be ventilated but not perfused, thus creating intrapulmonary “dead space.” The blockage acts like a dam, causing blood pressure to increase in the vessels upstream. The right ventricle must then generate tremendous pressure to overcome this obstacle and maintain forward blood flow and perfusion to distal organs.If the right ventricle is unable to maintain adequate forward blood flow, right-sided heart failure develops and leads to hypoxemia, dyspnea, hypotension, and syncope. In a massive pulmonary embolism, cardiac arrest occurs because the left ventricle is unable to maintain adequate cardiac output.7 Pulseless electrical activity is the most common rhythm seen in cardiac arrest. Only 25% of patients with cardiac arrest survive the ordeal, and a preoperative cardiac arrest is the strongest predictor of postoperative mortality.Massive pulmonary embolism with cardiovascular collapse indicates a significant accumulation of thrombus within the pulmonary arteries and carries a grim prognosis if not diagnosed and treated quickly. Although most patients with massive pulmonary embolism do not present in shock, mortality reaches 30% for those who do.8Risk factors for the development of venous thromboembolism center on Virchow’s triad of venous stasis, hypercoagulability, and vessel wall damage. Advanced age, surgery, and prolonged immobility from bed rest or extended confined travel9 are commonly identified risk factors in critically ill patients. Anderson et al10 showed that 88% of patients treated for acute deep venous thrombosis and/or pulmonary embolism were more than 40 years of age. Surgical procedures cause direct damage of vessel walls and often lead to a period of postoperative immobilization. Any abdominal or thoracic surgery lasting more than 30 minutes increases the risk of development of venous thromboembolism.11 The sex of the patient is not an independent risk factor, but many women take oral contraceptives or other forms of hormone therapy that contribute to a hypercoagulable state.3 Pulmonary embolism is 10 times more likely to develop in pregnant and postpartum women than in nonpregnant women. Smoking, pre-eclampsia, and delivery by cesarean section are reported to increase pregnancy-related risk of venous thromboembolism.12 The expanding uterus obstructs venous blood return, posing increased risk for thrombus formation in the venous system of the pelvis or lower extremities. Polycythemia, sickle cell anemia, and inherited or acquired thrombophilia, including antithrombin III deficiency, protein C deficiency, protein S deficiency, and factor V Leiden, also increase the risk for thromboemboli.13 Obesity, trauma, burns, cancer, and cardiac disease are also conditions contributing to the abnormalities that define Virchow’s triad. Our patient’s only risk factor for deep venous thrombosis or pulmonary embolism was her pregnancy (Table 1).The “classic” signs and symptoms of pulmonary embolism, namely dyspnea, hemoptysis, and chest pain, occur in fewer than 20% of patients.14 Acute-onset dyspnea and tachypnea are the most common initial signs and symptoms, and patients often report a feeling of apprehension. In massive pulmonary embolism, 10% to 15% of patients present with syncope,7 which results from obstruction of the pulmonary outflow tract by embolic material. Pressure increases within the right ventricle, causing dilatation and dysfunction.15 Dilatation of the right ventricle causes the tricuspid leaflets to separate, resulting in tricuspid regurgitation and symptoms of right-sided heart failure. The physical findings include distention of the jugular vein, increased central venous pressure, tachycardia, tachypnea, hypotension, a new murmur due to tricuspid regurgitation, and decreased oxygen saturation shown by pulse oximetry (Table 2). Hypoxemia results from a mismatch between regional alveolar ventilation and pulmonary blood flow. Therefore, early recognition and diagnostic investigation of signs and symptoms are paramount for avoidance of a catastrophe.Chest pain and dyspnea are vague symptoms associated with many disease processes. Acute coronary syndrome, aortic dissection, pneumothorax, acute asthma or exacerbation of chronic obstructive pulmonary disease, pneumonia, pericarditis, rib fracture, and musculoskeletal pain must be quickly excluded from the list of possible diagnoses.When a patient complains of chest discomfort, an electrocardiogram is usually the first test ordered. This test may eliminate other causes of chest pain such as myocardial infarction or aortic dissection. Anterior T-wave inversion is evident in 85% of cases of pulmonary embolism.16 This abnormality reflects inferoposterior ischemia that results from pressure overload.17(p1902) A pattern of acute right ventricular strain is highly suggestive of pulmonary embolism but is present in only 20% of the cases. This pattern is evidenced by an S wave in lead I, a Q wave in lead III, and a T-wave inversion in lead III (Figure 1). Tall peaked P waves, tachycardia, new incomplete right bundle branch block, and right-axis deviation are the most common abnormalities noted in patients with pulmonary embolism. This test was not performed on Shelby because she never complained of chest pain. Her rapid deterioration from acute dyspnea to cardiac arrest with pulseless electrical activity precluded the opportunity to obtain an electrocardiogram.Chest radiographs are not diagnostic for pulmonary embolism but can exclude other diseases that may mimic pulmonary embolism. Pleural effusions are noted in 48% of patients with pulmonary embolism. The Hampton hump, a triangular wedge-shaped pleural infiltrate, is a rare finding of an embolus resulting in pulmonary infarction (Figure 2).The Westermark sign is dilatation of the pulmonary vasculature near the embolus in contrast to decreased vascular markings in the affected regions14 (Figure 3). This finding, if present, may point clinicians toward the possibility of pulmonary embolism. Shelby’s chest radiograph did not include any of these findings.Arterial blood gas analysis is not diagnostic for pulmonary embolism but typically shows PaO2 less than 80 mm Hg and PaCO2 less than 36 mm Hg on room air. Hypoxia is an indicator of metabolic derangement and should prompt critical care nurses to consider probable causes and pursue further diagnostic workup. Respiratory alkalosis and hypoxemia with a widened alveolar-arterial difference in PaO2 develop.18(p463) Increased physiological dead space and muscle fatigue then lead to respiratory acidosis. Finally, metabolic acidosis results from tissue hypoxemia and shock. It is vital to remember that a normal PO2 does not exclude pulmonary embolism.The D-dimer assay is a sensitive but nonspecific test to detect the presence of venous thromboembolism. D-dimers are produced during the degradation of fibrin clot by plasmin. The D-dimer level may be elevated in other conditions, such as infection, cancer, pregnancy, surgery, renal failure, or heart failure.2 The D-dimer assay has a negative predictive value of 90% when results are less than 500 mg/L.3 In essence, the nurse is virtually assured that pulmonary embolism is excluded from the list of possible diagnoses when the D-dimer level is less than 500 mg/L. This test was not performed because Shelby’s recent pregnancy would have elevated her D-dimer levels.Duplex ultrasonography of the lower extremity is a noninvasive imaging study used to detect deep venous thrombosis. Although its sensitivity and specificity for deep venous thrombosis above the knee exceeds 95%, duplex ultrasonography is not accurate in detecting deep venous thrombosis in pelvic vessels or small vessels in the calf. About 50% of patients with a documented pulmonary embolism have no evidence of deep venous thrombosis. Critical care nurses must carefully assess patients’ extremities for unilateral increase in size, warmth, redness, or pain that may be present in patients with deep venous thrombosis. Because of Shelby’s urgent situation, investigation for a source of the emboli was suspended.If clinical suspicion for pulmonary embolism remains high, a noninvasive scintigraphic lung scan (ventilation/perfusion scan) is done to calculate pulmonary air flow and blood flow. Pulmonary embolism is suspected when areas of adequate lung ventilation exhibit decreased perfusion (getting the air but not the blood flow). A normal ventilation/perfusion ratio is reported as 0.8:1. A high-probability result is defined as 2 or more segmental perfusion defects in the presence of normal ventilation and is associated with an 85% to 90% likelihood of pulmonary embolism. A low- or intermediate-probability result does not exclude a diagnosis of pulmonary embolism and is not an acceptable end point if clinical suspicion of pulmonary embolism is high. In the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study of 1990, investigators concluded that a scan with a high-probability result usually indicates pulmonary embolism, but that only a small percentage of patients with pulmonary embolism have a scan with a high-probability result19(p1084); therefore, further testing is mandatory. Patients with previous pneumonia, atelectasis, or pulmonary embolism may show a persistent mismatch between ventilation and perfusion for several months following the event (Figure 4).Helical (spiral) computed tomography (Figure 5) is highly accurate for direct visualization of large emboli in the main or lobar pulmonary arteries, but it requires a 20- to 30-second breath-hold, which may not be feasible in patients who are in unstable condition.20(pp78–79) This diagnostic imaging technique is replacing the ventilation/perfusion scan in some institutions.Echocardiography is performed to identify structural causes of chest discomfort (Figure 6). This imaging technique is not diagnostic for pulmonary embolism, but evidence of right ventricular hypocontractility and dysfunction is seen in 95% of patients who are in unstable condition. This test is useful in differentiating between massive pulmonary embolism and other causes of hemodynamic compromise. Transthoracic echocardiography can visualize intra-cardiac thrombi, and transesophageal echocardiography can show thrombi within the central pulmonary artery.21Moderate to severe tricuspid regurgitation due to right ventricular pressure overload leads clinicians to suspect pulmonary embolism. The finding of severe tricuspid regurgitation on Shelby’s transthoracic echocardiogram provided the first clue to the diagnosis of pulmonary embolism. Nurses should inform nonintubated patients that a transthoracic echocardiogram is a surface ultrasound image obtained by placing a probe over the chest to identify cardiac chambers, valves, and the pulmonary artery. The patient will feel pressure as the technician glides the probe over the chest wall. If a nonintubated patient is scheduled for transesophageal echocardiography, the nurse should explain that the patient will be lightly sedated and a probe will be passed into the esophagus to assess the heart and pulmonary artery more accurately. Reassure the patient that he or she will not recall the procedure.Pulmonary angiography or aortography is the reference standard test for diagnosing pulmonary embolism. Catheterization of the right side of the heart with injection of contrast dye allows direct visualization of the pulmonary vasculature and identification of areas of obstruction. This test must be performed when pulmonary embolism cannot be reliably diagnosed or excluded by means of non-invasive testing22 (Table 3). The nurse explains that a catheter is inserted into the femoral or brachial artery and dye is injected thorough the catheter in order to visualize the pulmonary arteries and identify areas of obstructed blood flow.The goals of medical and/or surgical interventions (Table 4) are to relieve pulmonary obstruction, stop clot propagation, regain or maintain hemodynamic stability, prevent clot recurrence, and prevent pulmonary hypertension.Medical interventions for treating massive pulmonary embolism are aimed at preserving circulatory support by maintaining blood pressure, managing the airway, and preventing new thrombus formation. Airway management and oxygen administration are paramount in the treatment of pulmonary embolism. Mechanical ventilation is often required to maximize oxygen delivery to the patient with circulatory collapse. Cautious use of sedatives during induction is warranted as these drugs can blunt the catecholamine response that the patient depends on to maintain blood pressure through peripheral vasoconstriction. Hypotension is initially treated with judicious volume resuscitation of 1 to 2 L of crystalloid infused over 1 hour. If hypotension persists, the addition of a vasopressor such as norepinephrine, epinephrine, dopamine, or phenylephrine is warranted.Patients in stable condition are treated with anticoagulation alone, but thrombolytics are the treatment of choice in hemodynamically unstable patients. Thrombolytics convert plasminogen to plasmin and directly lyse the clot. Plasminogen activation interferes with coagulation by inactivating fibrinogen and factors II, V, and VII. Clot lysis results in faster improvement in pulmonary perfusion, hemodynamic alterations, and gas exchange, which rapidly reduces right ventricular afterload and dysfunction. The thrombolysis process is nonselective and can cause a major bleeding event. Bleeding complications occur in 20% of patients, and intracranial hemorrhage occurs in 3% of patients.Contraindications to use of thrombolytics include pregnancy and obstetric delivery, recent major or minor trauma including cardiopulmonary resuscitation, recent surgery (within past 10 days), acute internal bleeding (within past 6 months), hemorrhagic retinopathy, uncontrolled hypertension (systolic blood pressure >200 mm Hg or diastolic blood pressure >100 mm Hg), recent stroke (within past 2 months), active intracranial disease (aneurysm, arteriovenous malformation, neoplasm), puncture of a noncompressible vessel, organ biopsy, infective endocarditis, pericarditis, and aneurysm.23In the United States, 3 thrombolytics have been approved for treatment of pulmonary embolism. Streptokinase, a bacterial protein derivative, is produced from streptococcal bacteria and often causes febrile reactions. Streptokinase is administered as an intravenous infusion of 250000 IU over 30 minutes, followed by 100000 IU/h intravenously for 24 to 72 hours. This product is highly antigenic and may be administered only once during a 6-month period. Febrile reactions respond to treatment with acetaminophen (Tylenol).24Urokinase is produced from cultures of human source materials and thus has a small potential to transmit infectious agents. Urokinase is administered as an intravenous bolus of 4400 U/kg over 10 minutes, followed by 4400 U/kg per hour intravenously for 12 hours.24The third choice, alteplase, uses recombinant DNA technology and is synthesized by a human melanoma cell line. This enzyme binds to fibrin in a thrombus, causing conversion of plasminogen to plasmin. Alteplase is administered as a 100-mg intravenous infusion over 2 hours27 (Table 5).Anticoagulation with unfractionated heparin and warfarin is the standard treatment for pulmonary embolism in stable patients.Heparin acts as a catalyst to activate prothrombin, which inhibits factor Xa and thrombin. Heparin is unable to dissolve existing thrombus because of the inability to inhibit thrombin bound to fibrin. The activated partial thromboplastin time (aPTT) is maintained at 60 to 100 seconds or according to institutional policy. The nonspecific binding of unfractionated heparin to other plasma proteins contributes to a variable dose response among patients.Low-molecular-weight heparin is a heparin-based product used in patients with submassive pulmonary embolism and deep venous thrombosis, but it remains an unproven treatment option for patients with massive pulmonary embolism. Low-molecular- weight heparin is also contraindicated in patients with heparin-induced thrombocytopenia (HIT).Warfarin (Coumadin) therapy should overlap with heparin therapy for 4 days to avoid transient hypercoagulability that may occur with isolated administration of warfarin. The warfarin-induced decline in levels of coagulation factors is a function of the half-life of each factor, which varies from 5 hours for factor VII to 72 hours for factor II. The half-life of warfarin is 36 to 42 hours; therefore, an increase in the international normalized ratio (INR) is not seen until 2 days after the first dose is administered. The goal for the INR is 2 to 2.5 for 3 to 6 months.8 Warfarin may be initiated after 48 hours of direct thrombin inhibitor therapy as long as the platelet count is greater than 100 × 109/L.25 Warfarin is contraindicated in pregnancy because it crosses the placenta. Warfarin is safely used in lactating patients because it is not excreted in breast milk.HIT or “heparin allergy” is an important complication of heparin therapy and can result in severe venous and arterial thrombosis.26 This autoimmune disorder occurs in 1% to 3% of patients who receive heparin-based products. HIT results from the development of heparin-associated antibodies. These antibodies induce platelet aggregation in the presence of heparin. Thrombosis may occur in both arterial and venous circulation. All patients who receive heparin are at risk for HIT, because no known characteristics of patients can be used to predict the development of HIT.HIT occurs in 2 forms: HIT-1, also known as heparin-associated thrombocytopenia, is a nonimmune disorder that occurs 2 to 3 days after initiation of heparin therapy. This disorder may occur in up to 15% of patients exposed to heparin. The thrombocytopenia is transient, and platelet counts rarely decrease to less than 100 × 109/L. Patients are not at risk for development of significant thrombosis. HIT-2 is an immune-mediated disorder that occurs in 1% to 3% of patients who receive heparin and is frequently associated with life-or limb-threatening thromboembolic complications (deep venous thrombosis, pulmonary embolism, cerebrovascular accident, myocardial infarction, extremity ischemia, gangrene, and death). This disorder causes a significant decrease in platelet count. Thrombocytopenia manifests 5 to 10 days after the start of heparin therapy, and platelet count decreases 30% to 50%, to less than 100 × 109/L.27HIT is a clinical diagnosis supported by confirmatory laboratory work. The C-serotonin release assay combines serum from patients with suspected HIT with serum from healthy donors and adds this to therapeutic concentrations of heparin. A positive result detects the C-serotonin released from the serum of the patient with suspected HIT.The treatment for HIT is immediate cessation of use of all heparin-based products, including heparin-coated catheters and heparin flushes. Patients with HIT who require anticoagulation for deep venous thrombosis or pulmonary embolism are treated with a direct thrombin inhibitor, such as lipirudin or argatroban. The direct thrombin inhibitor is administered until the platelet count has increased to 100 × 109/L. Lipirudin is administered as an intravenous bolus of 0.4 mg/kg followed by infusion of 0.15 mg/kg per hour for an aPTT 1.5 to 2.5 times the
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