Post-traumatic pulmonary embolism in the intensive care unit
ABSTRACT To determine the predictive factors, clinical manifestations, and the outcome of patients with post-traumatic pulmonary embolism (PE) admitted in the intensive care unit (ICU).
During a four-year prospective study, a medical committee of six ICU physicians prospectively examined all available data for each trauma patient in order to classify patients according to the level of clinical suspicion of pulmonary thromboembolism. During the study period, all trauma patients admitted to our ICU were classified into two groups. The first group included all patients with confirmed PE; the second group included patients without clinical manifestations of PE. The diagnosis of PE was confirmed either by a high-probability ventilation/perfusion (V/Q) scan or by a spiral computed tomography (CT) scan showing one or more filling defects in the pulmonary artery or its branches.
During the study period, 1067 trauma patients were admitted in our ICU. The diagnosis of PE was confirmed in 34 patients (3.2%). The mean delay of development of PE was 11.3 ± 9.3 days. Eight patients (24%) developed this complication within five days of ICU admission. On the day of PE diagnosis, the clinical examination showed that 13 patients (38.2%) were hypotensive, 23 (67.7%) had systemic inflammatory response syndrome (SIRS), three (8.8%) had clinical manifestations of deep venous thrombosis (DVT), and 32 (94%) had respiratory distress requiring mechanical ventilation. In our study, intravenous unfractionated heparin was used in 32 cases (94%) and low molecular weight heparin was used in two cases (4%). The mean ICU stay was 31.6 ± 35.7 days and the mean hospital stay was 32.7 ± 35.3 days. The mortality rate in the ICU was 38.2% and the in-hospital mortality rate was 41%. The multivariate analysis showed that factors associated with poor prognosis in the ICU were the presence of circulatory failure (Shock) (Odds ratio (OR) = 9.96) and thrombocytopenia (OR = 32.5).Moreover, comparison between patients with and without PE showed that the predictive factors of PE were: Age > 40 years, a SAPS II score > 25, hypoxemia with PaO(2)/FiO(2) < 200 mmHg, the presence of spine fracture, and the presence of meningeal hemorrhage.
Despite the high frequency of DVT in post-traumatic critically ill patients, symptomatic PE remains, although not frequently observed, because systematic screening is not performed. Factors associated with poor prognosis in the ICU are the presence of circulatory failure (shock) and thrombocytopenia. Predictive factors of PE are: Age > 40 years, a SAPS II score > 25, hypoxemia with PaO(2)/FiO(2) < 200, the presence of a spine fracture, and the presence of meningeal hemorrhage. Prevention is highly warranted.
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ABSTRACT: Venous thromboembolism (VTE) remains a major challenge in the care of critically ill patients. Subjects in the intensive care unit (ICU) are at high risk for both deep-vein thrombosis (DVT) and pulmonary embolism (PE). Pulmonary embolism (PE) is the major complication of VTE. Pulmonary embolism is a cardiovascular emergency. By occluding the pulmonary arterial bed it may lead to acute life-threatening but potentially reversible right ventricular failure. The diagnosis of PE is usually suspected by the presence of common symptoms (include difficulty breathing, chest pain on inspiration, and palpitations) and clinical signs include low blood oxygen saturation (hypoxia), rapid breathing (tachypnea), and rapid heart rate (tachycardia). However in ICU, the most of patients required sedation and mechanical ventilation. The clinical manifestations usually observed in this condition (PE) cannot be exhibited by theses patients and clinical presentation is usually atypical. While the gold standard for diagnosis is the finding of a clot on pulmonary angiography, CT pulmonary angiography is the most commonly used imaging modality today. Pulmonary embolism causing hemodynamic instability is termed massive; once it is suspected, a diagnostic plan and supportive measures are essential. Oxygen supplementation, intubation, and mechanical ventilation are instituted as necessary for respiratory failure. If saline is infused for hypotension, it should be done with caution. Vasopressor therapy (e.g., dopamine, norepinephrine) should be considered if the blood pressure is not rapidly restored; there is little information about the use of inotropic agents in general. Anticoagulant treatment plays a pivotal role in the management of patients with PE. Heparin, low molecular weight heparins (such as enoxaparin and dalteparin), or fondaparinux is administered initially. Severe cases may require thrombolysis with drugs such as tissue plasminogen activator (tPA) or may require surgical intervention via pulmonary thrombectomy. Prevention is highly warranted.02/2012; 2(1):25–29. DOI:10.1016/j.tacc.2011.11.005
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ABSTRACT: Background Venous thromboembolism events are common in trauma patients. Immediate acute inflammation following injury triggers coagulation cascade and may increase the risk of pulmonary embolism (PE) in this population. Objective We aimed to evaluate whether early low-dose steroids prevent symptomatic PE onset in multiple trauma patients. Setting The medical surgical intensive care unit of Habib Bourguiba University Hospital (Sfax-Tunisia). Methods Comparative study of two cohorts: a retrospective cohort of patients who didn't receive early low-dose steroids (steroid (-) group) and a prospective cohort of patients who received hydrocortisone with a dose of 100 mg/8 h for a scheduled period of 7 days (steroid (+) group). All adult patients admitted in our intensive care unit (ICU) for multiple trauma with predicted duration of mechanical ventilation over 48 h were included. Main outcome measure Evaluation of the impact of low-dose steroids on the incidence of symptomatic PE. Results We included 175 patients: 92 in the steroids (-) group and 83 in the steroids (+) group. PE was diagnosed in 15 patients (8.5 %). The incidence of PE was significantly lower in steroid (+) group (3.6 vs 13 %; p = 0.013). In multivariate analysis, independent factors predicting PE onset were meningeal hemorrhage [OR = 14.7; 95 % CI (2.2-96.3); p = 0.013] and pelvic ring trauma [OR = 8; 95 % CI (1.8-36.4); p = 0.007] whereas low-dose steroids were significantly associated with a protective effect [OR = 0.2; 95 % CI (0.05-0.77); p = 0.019]. There was no significant difference between steroids (+) and steroids (-) groups neither in terms of mean ICU length of stay (LOS) (respectively 11 ± 9.7 and 12.3 ± 10.7 days; p = 0.372) nor in terms of ICU mortality (respectively 29.3 and 24.1 %; p = 0.434). Conclusion Steroids are effective in reducing the incidence of PE in multiple trauma patients. However, no significant benefice was found on ICU mortality.04/2013; DOI:10.1007/s11096-013-9775-y
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ABSTRACT: Although early acute traumatic coagulopathy has received much recent attention, the procoagulopathy that often follows appears less appreciated. Thromboembolic disease following trauma is common and lethal, but very effective prophylactic strategies are available. These strategies are variably implemented because of the difficulty in quantifying the magnitude of procoagulopathy in individual patients. The principal mechanisms of the procoagulopathy of trauma include inflammation and disseminated intravascular coagulation, tissue factor and thrombin dysregulation, and circulating microparticles and phospholipids. Quantification of these factors may allow better risk assessment in individual patients, but as yet none of these tests is in routine practice. Viscoelastic measurement of developing clot strength identifies a procoagulant state in many trauma patients, and may be a guide to the best choice of the many options for thromboembolic prophylaxis. The logical next step following from the improved pathophysiological understanding of the procoagulopathy of trauma should be a simultaneous clinical trial of procoagulopathy diagnosis and thromboembolic prophylaxis.Current opinion in critical care 12/2013; 19(6):578-86. DOI:10.1097/MCC.0000000000000032 · 3.18 Impact Factor