La tomografía computarizada multidetector en la hemoptisis amenazante / Multidetector computed tomography in life-threatening hemoptysis

La hemoptisis amenazante es una situación grave que precisa de un diagnóstico y tratamiento rápidos. Uno de los tratamientos de elección es la embolización. La evaluación inicial se dirige a localizar el origen y la causa del sangrado. El avance tecnológico de la TC multidetector (TCMD) ha supuesto un cambio en el manejo de estos pacientes. La angio-TCMD permite evaluar la causa rápida e incruentamente, y localizar los vasos implicados; es particularmente útil para detectar arterias bronquiales ectópicas, arterias sistémicas no bronquiales o seudoaneurismas pulmonares. Hacer sistemáticamente una angio-TCMD antes de la embolización permite planificar mejor el tratamiento. En este artículo revisamos la fisiopatología y las causas de la hemoptisis amenazante (incluyendo la hemoptisis criptogenética), la técnica del estudio de la angio-TCMD y describimos cómo evaluar sistemáticamente las imágenes (parénquima pulmonar, vía aérea y estructuras vasculares) (AU)

Life-threatening hemoptysis is a severe condition that requires rapid diagnosis and treatment. One of the treatments of choice is embolization. The initial assessment aims to locate the origin and cause of bleeding. The technological advance of the development of multidetector computed tomography (MDCT) has changed the management of patients with life-threatening hemoptysis. MDCT angiography makes it possible to evaluate the cause of blee- ding and locate the vessels involved both rapidly and noninvasively; it is particularly useful for detecting ectopic bronchial arteries, nonbronchial systemic arteries, and pulmonary pseudoaneurysms. Performing MDCT angiography systematically before embolization enables better treatment planning. In this article, we review the pathophysiology and causes of life-threatening hemoptysis (including cryptogenic hemoptysis) and the MDCT angiography technique, and we review how to systematically evaluate the images (lung parenchyma, airways, and vascular structures) (AU)

Multidetector computed tomography in life-threatening hemoptysis.

Life-threatening hemoptysis is a severe condition that requires rapid diagnosis and treatment. One of the treatments of choice is embolization. The initial assessment aims to locate the origin and cause of bleeding. The technological advance of the development of multidetector computed tomography (MDCT) has changed the management of patients with life-threatening hemoptysis. MDCT angiography makes it possible to evaluate the cause of bleeding and locate the vessels involved both rapidly and noninvasively; it is particularly useful for detecting ectopic bronchial arteries, nonbronchial systemic arteries, and pulmonary pseudoaneurysms. Performing MDCT angiography systematically before embolization enables better treatment planning. In this article, we review the pathophysiology and causes of life-threatening hemoptysis (including cryptogenic hemoptysis) and the MDCT angiography technique, and we review how to systematically evaluate the images (lung parenchyma, airways, and vascular structures).

Hemostatic variables in nephrotic patients.

The paper reviews data in the literature as well as the authors' own investigations, performed during the last seven years, concerning the hemostatic balance in nephrotic patients. The obviously increased plasma levels of fibrinogen, fibronectin, fibrin-stabilizing factor XIII, clotting factors V and VIII, von Willebrand factor as well as the enhanced platelet aggregability of such patients, associated with a decreased plasma antithrombin III, are compatible with a thrombotic tendency. On the other hand the increased plasma protein C may provide a compensative antithrombotic mechanism. A rather complex behaviour of the fibrinolytic system was noted in the nephrotic syndrome. Actually the enhanced release of tissue plasminogen activator (t-PA) from the endothelia of nephrotic patients is accompanied by an accelerated lysis of dilute blood clots, although the inhibitors of fibrinolysis such as alpha 2-macroglobulin and alpha 2-antiplasmin are increased. Failure or exhaustion of the compensative antithrombotic mechanisms would accentuate the hemostatic imbalance and favour the occurrence of thrombotic events. It is considered that increased urinary loss of antithrombin III and the enhanced hepatic synthesis of clotting factors would represent the main mechanisms involved in the production of this precarious hemostatic balance of nephrotic patients.

Plasma von Willebrand factor antigen and activity and platelet aggregability in patients with proteinuria.

Using a complex stimulating mixture containing ADP, epinephrine and collagen, a significantly (p less than 0.002) enhanced platelet aggregability, expressed as platelet sensitivity factor (PSF) was noted in platelet rich plasma of patients with proteinuria (PSF = 472 +/- 125), as against normal weight normolipidemic control subjects (PSF = 32.76 +/- 2.67). A significantly negative correlation (r. -0.579; p less than 0.001) was found between serum albumin concentration and the logarithmic values of platelet sensitivity factor. Plasma von Willebrand factor activity expressed as a percentage of normal was also significantly (p less than 0.001) higher in proteinuric patients (287% +/- 25.8) than in control subjects (99% +/- 5.02), but this hemostatic variable did not correlate with the logarithm of platelet sensitivity factor. Platelet aggregability was higher in hyperlipidemic nephrotic patients than in proteinuric patients with normal serum lipids, while renal failure led to a decrease of platelet function. The raised plasma levels of von Willebrand factor noted in proteinuric patients were not influenced by either hyperlipidemia or by chronic renal failure. It is concluded that changes affecting platelet function in the nephrotic syndrome are produced by other mechanisms than these leading to an increase of endothelia-derived von Willebrand factor. Both changes may, however, contribute to the thrombotic tendency of nephrotic patients.

Tissue-type plasminogen activator (t-PA) and dilute blood clot lysis time in nephrotic patients.

When compared to normal weight normolipidemic control subjects, dilute blood clot lysis time was found to be obviously (p less than 0.001) prolonged in hypertriglyceridemic patients without proteinuria and slightly (p less than 0.05) accelerated in hyperlipidemic nephrotic patients in spite of their very high levels of plasma fibrinogen. As a result the ratio plasma fibrinogen (mg/dl) per clot lysis time (minutes) was 1.241 +/- 0.08 (X +/- SEM) in control subjects, 0.574 +/- 0.07 in hypertriglyceridemic patients and 2.69 +/- 0.172 in nephrotic patients. This finding suggesting that a larger amount of fibrin is rather readily dispersed from dilute blood clots of nephrotic patients was associated with higher levels of plasma t-PA:Ag (9.45 ng/ml +/- 1.18 in nephrotic patients versus 5.8 ng/ml +/- 1.23 in controls before venous occlusion and respectively 33.1 ng/ml +/- 3.83 versus 20.3 +/- 3.40 in controls after venous occlusion). Plasminogen activator activity of the euglobulins as assessed by the bovine fibrin-agarose plate was significantly higher in nephrotic patients only after venous occlusion. Plasma samples of nephrotic patients exerted a more potent inhibition of fibrinolysis in a urokinase activated system. This effect was, however, mainly due to the high levels of alpha 2 macroglobulin in nephrotic plasma which apparently have little influence on dilute blood clot lysis time.

Behaviour of fibrinolysis in the nephrotic syndrome.

When compared to 39 normal-weight normolipidemic control subjects, the dilute blood clot lysis time was found to be slightly (p less than 0.05) accelerated in the 49 investigated nephrotic patients, although their plasma fibrinogen, factor XIII as well as the inhibitors of fibrinolysis, are markedly increased. These findings indicate that the fibrinolytic system as a whole is not markedly depressed in the nephrotic syndrome. Although the fibrinolytic activity of euglobulins tested on agarose-fibrin plates was not significantly increased in nephrotic patients, one cannot definitely preclude an enhanced secretion of plasminogen activators in this pathological condition. A different quality of the inhibitors which may be less active in retarding dilute blood clot lysis time could also be considered.

Plasma fibronectin and factor XIII in nephrotic syndrome.

When compared to control subjects plasma fibronectin and factor XIII as well as plasma fibrinogen, factor VIII-related antigen and serum cholinesterase were found to be significantly increased in nephrotic patients. Factor XIII activity was positively correlated with serum cholinesterase, while plasma fibronectin displayed weak correlations with plasma fibrinogen and factor VIII-related antigen. It is considered that increased levels of factor XIII and fibronectin should be related to the intensity of the liver's compensative response to proteinuria, although their turnover rates and the signals triggering this response may differ. It is however difficult to assess possible consequences of the above-mentioned changes for the evolution of the nephrotic syndrome.