Safety of multidetector computed tomography pulmonary angiography to exclude pulmonary embolism in patients with a likely pretest clinical probability.

Essentials Safety of computed tomography (CTPA) to exclude pulmonary embolism (PE) in all patients is debated. We analysed the outcome of PE-likely outpatients left untreated after negative CTPA alone. The 3-month venous thromboembolic risk in these patients was very low (0.6%; 95% CI 0.2-2.3). Multidetector CTPA alone safely excludes PE in patients with likely clinical probability. SUMMARY: Background In patients with suspected pulmonary embolism (PE) classified as having a likely or high pretest clinical probability, the need to perform additional testing after a negative multidetector computed tomography pulmonary angiography (CTPA) finding remains a matter of debate. Objectives To assess the safety of excluding PE by CTPA without additional imaging in patients with a likely pretest probability of PE. Patients/Methods We retrospectively analyzed patients included in two multicenter management outcome studies that assessed diagnostic algorithms for PE diagnosis. Results Two thousand five hundred and twenty-two outpatients with suspected PE were available for analysis. Of these 2522 patients, 845 had a likely clinical probability as assessed by use of the simplified revised Geneva score. Of all of these patients, 314 had the diagnosis of PE excluded by a negative CTPA finding alone without additional testing, and were left without anticoagulant treatment and followed up for 3 months. Two patients presented with a venous thromboembolism (VTE) during follow-up. Therefore, the 3-month VTE risk in likely-probability patients after a negative CTPA finding alone was 2/314 (0.6%; 95% confidence interval [CI] 0.2-2.3%). Conclusions In outpatients with suspected PE and a likely clinical probability as assessed by use of the simplified revised Geneva score, CTPA alone seems to be able to safely exclude PE, with a low 3-month VTE rate, which is similar to the VTE rate following the gold standard, i.e. pulmonary angiography.

[Popliteal artery entrapment syndrome]. / Syndrome de l'artère poplitée piégée.

Popliteal entrapment is a rare compression syndrome involving vascular (and neurologic) structures of the popliteal fossa. In this article we review the popliteal artery entrapment syndrome (PAES). PAES is a cause of intermittent claudication that can be, although rarely, complicated with acute limb-threatening ischemia. PAES occurs more often in young adult. Concerning pathophysiology, PAES is provoked by an abnormal relationship between popliteal artery and muscular-tendon structures within the popliteal fossa. A surgical repair is usually required to resolve mechanical compression or vascular damage.

[Prevention of chronic venous disease: which advice for our patients?]. / Prévention de la maladie veineuse chronique: quels conseils donner à nos patients?

Chronic venous disease (CVD) is a major public health problem due to its high prevalence and socioeconomic costs. In absence of adequate care, it can lead to chronic venous insufficiency (CVI). Disturbed venous-flow patterns lead to venous hypertension. Therefore, prevention of CVD involves venous hypertension reduction. In primary prevention, it is essential to inform the patient about necessary lifestyle changes. In case of CVD, it is essential to propose treatment (compression, venoactive drugs, and interventional treatments) to avoid CVI appearance and eventually offer the best therapy solutions for CVI complications.

[Vascular follow up in patients suffering from peripheral arterial disease and undergoing revascularization]. / Suivi angiologique des patients artériopathes après geste de revascularisation.

The rapid evolution of revascularization techniques has allowed an improvement in quality of life of patients with peripheral artery disease. The angiological follow-up aims to insure durable results of revascularization, to diminish risk of amputation and to limit progression of atheroma plaques. The patient history and physical examination are essential in evaluating impact of peripheral artery disease upon quality of life and insuring the appropriate control of cardiovascular risk factors.

Central venous catheter infections: concepts and controversies.

Central venous catheters (CVCs) are widely used in critically ill patients in intensive care units. However, infectious complications are common and may limit their utility. We critically review the literature to determine the impact of CVC design and composition, insertion site selection, insertion procedures, care and removal of temporary CVCs on infectious complications. Relevant articles were identified and selected for review using a database search (Medline and manual of the English language literature) based upon study design and sample size with an emphasis on prospective randomized trials. To minimize infectious complications and maintain a reasonable cost-benefit ratio, we recommend: i) use a single lumen catheter unless clear indications for a multi-lumen catheter exist; ii) insert the catheter via the subclavian vein if no relative contraindication exists (bleeding diathesis, positive pressure ventilation); iii) disinfect the insertion site employing sterile technique; iv) apply a dry, sterile dressing and change the dressing every other day; v) inspect the insertion site for signs of infection and remove the catheter if pus is present; vi) if a catheter-related infection is suspected, change the catheter over a guidewire and culture the distal segment. The replacement catheter should be removed if an original catheter segment culture is positive.

The effects of amrinone and calcium chloride on pulmonary vasculature and biventricular function in ethchlorvynol-induced lung injury in sheep.

The effects of amrinone and CaCl2 on pulmonary vasculature and biventricular function in sheep with acute lung injury (ALI) were studied. Seven sheep were ventilated with a tidal volume of 10-12 ml.kg-1 with end-tidal CO2 of 40 +/- 5 mmHg (5.3 +/- 0.7 kPa) after acute lung injury was induced with up to 30 mg kg-1 of ethchlorvynol (ECV). Biventricular function and hemodynamic profiles were estimated with a rapid computerized thermodilution method and modified pulmonary artery catheters after acute lung injury, following a loading dose (1 mg kg-1) and maintenance dose (5 micrograms kg-1 min-1) of amrinone and after a bolus dose of CaCl2 (20 mg kg-1). ECV successfully induced acute lung damage in sheep, causing significant increases in pulmonary artery pressure (PAP) and pulmonary vascular resistance index (PVRI). Amrinone reversed the unfavorable changes induced by ECV, significantly reducing PAP, PVRI and left ventricular end-diastolic volume (LVEDV). CaCl2, however, reversed the effect of amrinone and increased PAP, PVRI, and LVEDV but decreased left ventricular ejection fraction.

COPD: primary care management with drug and oxygen therapies.

Chronic obstructive pulmonary disease related in most cases to extensive cigarette smoking is a leading cause of morbidity and mortality among patients age 55 and older. Smoking cessation, inhaled anticholinergic therapy, and oxygen supplementation (when indicated) are primary treatment modalities. Nicotine administration via a transdermal system or polacrilex is the pharmacologic method of choice for smoking cessation. Concomitant group psychotherapy increases the likelihood of success. Beta agonists, mucolytics, and antibiotics can be useful in selected subgroups. Steroids and theophylline are controversial in COPD and should be used with caution. Prognostic indicators, such as degree of reversible airway disease, aid in long-term care decisions.

Chronic upper lobe cavitary lung disease.

Chronic upper lobe cavitary lung disease may be caused by infections, emphysema, cystic fibrosis, lung cancer, sarcoidosis and rheumatologic syndromes. The diagnostic evaluation includes a complete history, a physical examination, a chest radiograph, and sputum examination and culture. In some cases, computed tomographic scanning and biopsy are required.

Systemic hemodynamic and cardiac function changes in patients undergoing orthotopic liver transplantation.

The objective of this study was to determine the changes in systemic hemodynamics (systemic vascular resistance [SVR], cardiac output [CO], systemic blood pressure [SBP]) and cardiac function (pulmonary artery pressure [PAP] and pulmonary wedge pressure [PWP]) during the 96 hours following orthotopic liver transplantation (OLT) and correlate these with changes in hepatic and renal function and patient outcome. The study took place in a 12-bed medical respiratory intensive care unit in a large teaching hospital. Twenty-one patients had OLT performed over a 21.5-month period (January 1988 to October 15, 1989) for end stage liver disease (ESLD) from a variety of causes. A flow-directed right heart catheter and an indwelling arterial cannula were inserted for hemodynamic monitoring over a 96-hour postoperative period. Liver and renal function studies, total serum calcium, serum albumin, and fluid balance were determined daily. The SVR increased significantly to 12.8 +/- 0.6 U at 48 hours compared with immediate (less than 8 hours) postoperative levels (p less than 0.05) and remained elevated for 96 hours. The CO fell progressively and was significantly lower than baseline values from 64 to 96 hours. There was significant inverse correlation between the increase in SVR and the fall in CO (r = .85, p less than 0.01). The SBP was stable except for a small, but significant fall at 16 and 24 hours postoperatively. The PWP increased significantly from a baseline value of 12.5 +/- 0.9 mm Hg to 15 +/- 0.9 mm Hg at 32 hours and remained elevated through 96 hours (p less than 0.05). The serum bilirubin level fell progressively postoperatively and the prothrombin time and partial thromboplastin time (PTT) shortened significantly. Bile flow increased progressively from 107 +/- 120 ml/24 hours at the end of the first 24 hours to 188 +/- 125 ml/24 hours by 96 hours postoperatively. Five patients died from nine to 43 days postoperatively. These patients' hemodynamic parameters were not significantly different from the patients who survived. Successful OLT is associated with a rapid increase in SVR and a fall in CO without changes in SBP. These findings tend to parallel the improvement found in results of liver function tests. However, there is no correlation between the improvement in the hemodynamic state and long-term survival.

Relationship between cardiac output and the end-tidal carbon dioxide tension.

STUDY OBJECTIVE: To further define the relationship between cardiac output (CO) and end-tidal carbon dioxide tension (ETCO2) at various levels of systemic flow. DESIGN: Prospective, controlled laboratory investigation. SETTING: Animal laboratory. TYPE OF PARTICIPANTS: Fourteen anesthetized, intubated sheep weighing 23 to 47 kg. INTERVENTIONS: One hundred seventy-two simultaneous measurements of thermodilution CO and ETCO2 were made during controlled arterial hemorrhage. After a 30-minute baseline control period, CO was sampled from approximately 0.6 to more than 8.0 L/min during a 60- to 90-minute period of controlled hemorrhage. MEASUREMENTS: Thermodilution CO; arterial pressure using fluid-filled plastic 14-gauge catheters; ETCO2 using an infrared analyzer. MAIN RESULTS: A plot of CO versus ETCO2 suggested that the relationship was logarithmic rather than linear. Linear regression showed that ETCO2 was significantly related (r = .91; P less than .001) to a logarithmic transformation of the CO. CONCLUSIONS: The relationship between CO and ETCO2 is logarithmic. Decreased presentation of CO2 to the lungs is the major, rate-limiting determinant of the ETCO2 during low flow. As the CO increases during resuscitation from shock or cardiac arrest, respiration becomes the rate-limiting controller of the ETCO2 (after the tissue washout of CO2 has occurred). Under such conditions, the ETCO2 provides useful information about the adequacy of ventilation provided that there is little ventilation/perfusion mismatch.

Fatal Cunninghamella bertholletiae infection in an immunocompetent patient.

The first fatal Cunninghamella bertholletiae infection in a clinically immunocompetent host is reported. This case differs from previously reported cases by the lack of extensive vascular invasion and thrombosis.

Mediastinal pseudocyst associated with chronic pleural effusions.

We present a patient who had chronic, bilateral pleural effusions without evidence of parenchymal, retrocardiac or mediastinal masses. A CAT scan of the abdomen and chest revealed the extension of a large abdominal pseudocyst through the diaphragm into the posterior mediastinum. The pseudocyst resolved with conservative management.

Pulmonary hypertensive response to foreign body microemboli.

Pulmonary hypertension and foreign body granulomas are recognized sequelae of chronic intravenous drug abuse. We have recently described the development of transient pulmonary hypertension and increased permeability pulmonary edema after the intravenous injection of crushed, suspended pentazocine tablets in both humans and dogs. To determine the role of vasoactive substances in the development of this transient pulmonary hypertension, we measured pulmonary hemodynamics and accumulation of arachidonic acid metabolites in dogs during the infusion of indomethacin, a cyclooxygenase inhibitor, diethylcarbamazine (DEC), a lipoxygenase inhibitor, and FPL 55712, a receptor antagonist for leukotriene C4/D4 (LTC4/D4). Following the intravenous administration of crushed, suspended pentazocine tablets (3-4 mg/kg of body weight), mean pulmonary artery pressure increased from 14 +/- 2 mmHg to 30 +/- 6 mmHg (p less than 0.05) at 60 secs with a concomitant increase in plasma concentrations of 6-keto-PGF1 alpha from 187 +/- 92 pg/ml to 732 +/- 104 pg/ml and thromboxane B2 from 206 +/- 83 pg/ml to 1362 +/- 117 pg/ml (both p less than 0.05). Indomethacin prevented the increase in both cyclooxygenase metabolites, but had no effect on the pulmonary hypertension. In contrast, DEC had no effect on the increase in cyclooxygenase products, but blocked the pulmonary hypertension. FPL 55712 did not effect either the increase in cyclooxygenase metabolites or the pulmonary hypertension. We conclude that the transient pulmonary hypertension, induced by the intravenous injection of crushed, suspended pentazocine tablets, is not mediated by cyclooxygenase products but may be mediated by lipoxygenase product(s) other than LTC4/D4.