Post-traumatic pulmonary embolism in the intensive care unit
Department of Intensive Care, Hedi Chaker, University Hospital Sfax, Tunisia.
Annals of thoracic medicine
10/2011; 6(4):199-206. DOI: 10.4103/1817-1737.84773
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.
Figures in this publication
Available from: Rana Arslan
- "Intravascular arterial thrombosis causes multiple types of cardiovascular damage such as ischemia, myocardial infarction, and angina (Gross & Weitz, 2009; Kumaran et al., 2011; Lands, 2003). Venous thrombosis, which causes deep vein thrombosis and pulmonary embolism, is one of the most common vascular disorders after heart attack and stroke (Bahloul et al., 2011; Gross & Weitz, 2009). Antithrombotic agents have been extensively used to prevent or treat thrombus formation. "
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ABSTRACT: Context: Crataegus species are widely used as herbal medicines for preventing cardiovascular diseases (CVDs). However, there are no studies on the effects of Crataegus monogyna Jacq. (Rosaceae) and C. davisii Browicz on thrombosis, which is an important mechanism in CVDs. Objective: The purpose of this study was to investigate the antithrombotic effects of ethanol extracts of Crataegus monogyna (CMEx) and C. davisii (CDEx) leaves by using the carrageenan-induced tail thrombosis model. Materials and methods: The hind paw of each mouse was injected with 1% Type I carrageenan to induce thrombosis. CMEx was tested at the doses of 100, 200, and 300 mg/kg and CDEx at the dose of 50, 100, 200, and 300 mg/kg in comparison with heparin. The lengths of tail thrombosis were measured at the 24, 48, and 72 h. Results: Does of 200 and 300 mg/kg CMEx showed significant effects (p < 0.01; p < 0.001) at 24 h when compared with the control group. The antithrombotic activity of 200 and 300 mg/kg CMEx showed a decrease at 48 and 72 h but the activity of 300 mg/kg dose of CMEx was still significant (p < 0.01). The activities of 50 and 100 mg/kg doses of CDEx were significant (p < 0.001; p < 0.01) between 24 and 72 h whereas 200 and 300 mg/kg CDEx did not show any significance. Discussion and conclusions: CMEx and CDEx significantly inhibited the carrageenan-induced mouse tail thrombosis. Based on these results, it was concluded that CDEx and CMEx may potentially be used as therapeutic agents or complementary treatments against thrombosis.
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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.
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ABSTRACT: : To estimate the rate of pulmonary embolism among mechanically ventilated patients and its association with deep venous thrombosis.
: Prospective cohort study.
: Medical intensive care unit of a university-affiliated teaching hospital.
: Inclusion criteria: mechanically ventilated patients requiring a thoracic contrast-enhanced computed tomography scan for any medical reason. Exclusion criteria: a diagnosis of pulmonary embolism before intensive care unit admission, an allergy to contrast agents, and age younger than 18 yrs.
: All the mechanically ventilated patients requiring a thoracic computed tomography underwent the standard imaging protocol for pulmonary embolism detection. Therapeutic anticoagulation was given immediately after pulmonary embolism diagnosis. All the included patients underwent a compression ultrasound of the four limbs within 48 hrs after the computed tomography scan to detect deep venous thrombosis.
: Of 176 included patients, 33 (18.7%) had pulmonary embolism diagnosed by computed tomography, including 20 (61%) with no clinical suspicion of pulmonary embolism. By multiple logistic regression, independent risk factors for pulmonary embolism were male gender, high body mass index, history of cancer, past medical history of deep venous thrombosis, coma, and high platelet count. Previous prophylactic anticoagulant use was not a risk factor for pulmonary embolism. Of the 176 patients, 35 (19.9%) had deep venous thrombosis by compression ultrasonography, including 20 (57.1%) in the lower limbs and 24 (68.6%) related to central venous catheters. Of the 33 pulmonary embolisms, 11 (33.3%) were associated with deep venous thrombosis. The pulmonary embolism risk was increased by lower-limb deep venous thrombosis (odds ratio 4.0; 95% confidence interval 1.6-10) but not upper-limb deep venous thrombosis (odds ratio 0.6; 95% confidence interval 0.1-2.9). Crude comparison of patients with and without pulmonary embolism shows no difference in length of stay or mortality.
: In mechanically ventilated patients who needed a computed tomography, pulmonary embolism was more common than expected. Patients diagnosed with pulmonary embolism were all treated with therapeutic anticoagulation, and their intensive care unit or hospital mortality was not impacted by the pulmonary embolism occurrence. These results invite further research into early screening and therapeutic anticoagulation of pulmonary embolism in critically ill patients.
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