Ventilación mecánica no invasiva en la lesión pulmonar aguda hipoxémica / Noninvasive mechanical ventilation in acute hypoxemic lung injury (AHLI)

Objetivos. Evaluar los efectos de la ventilación mecánica no invasiva (VMNI), la incidencia de intubación orotraqueal (IOT), de complicaciones asociadas al procedimiento y la mortalidad. Pacientes y método. Se incluyen 27 pacientes con lesión pulmonar aguda hipoxémica, sin antecedentes de enfermedad pulmonar obstructiva crónica o asma y que no mejoraban su situación clínica y gasométrica con las medidas convencionales. Se utilizó VMNI con presión de soporte ventilatoria (PSV), aplicando presión positiva al final de la espiración (PEEP) cuando era necesario, administrada con mascarillas faciales. Resultados. Un total de 17 enfermos eran varones (63 por ciento). El promedio de edad fue de 50,7 (20,7) años. El Acute Phisiology And Chronic Health Evaluation (APACHE) y el score de lesión pulmonar aguda a la admisión fueron de 13,7(3,7) y 2,2 (0,4), respectivamente. Siete pacientes debieron ser intubados (25 por ciento) y todos ellos fallecieron. Las causas de la intubación orotraqueal fueron: agotamiento muscular y empeoramiento de la disnea (2 pacientes), escasa mejoría en el intercambio gaseoso con excesivo trabajo respiratorio (4 casos) e intolerancia a la máscara (un caso). Los pacientes con IOT presentaron un score de lesión pulmonar aguda significativamente superior al compararlos con los no intubados [2,5 (0,3) frente a 2,0 (0,4); p = 0,02]. Obtuvimos una mejoría estadísticamente significativa en la relación PaO2FiO2 [116,1(23,5) frente a 232 (63,8); p < 0,05]; frecuencia respiratoria [38,4 (5,5) frente a 26,2 (7,2); p < 0,05] y frecuencia cardíaca [125,4 (17,5) frente a 105 (17,7); p < 0,05] comparados al ingreso a la UCI y después de 6 h de ser asistidos con VMNI. En 3 pacientes (11 por ciento) se observó lesión sobre el tabique nasal. Conclusión. Un 75 por ciento de los pacientes asistidos con VMNI no necesitaron intubación orotraqueal, mejorando el intercambio gaseoso, y fue útil para estabilizar clínicamente al paciente colaborativo con este tipo de enfermedad (AU)

Wegener's granulomatosis in a patient with apparent drug-induced acute interstitial nephritis.

We describe a patient whose clinical presentation was suggestive of drug-induced acute interstitial nephritis (AIN). A renal biopsy and serologic testing led instead to the diagnosis of Wegener's granulomatosis (WG) with necrotizing crescentic glomerulonephritis. Treatment with corticosteroids and cyclophosphamide resulted initially in complete recovery of renal function, and an exacerbation of acute renal failure after doses of these agents had been tapered responded to resumption of the original regimen. We report this case to emphasize the potentially identical presentations of AIN and WG. Since the two conditions are treated differently, we suggest that the diagnosis of AIN should be accepted only after biopsy confirmation.

Nephrotic-range proteinuria in renal atheroembolic disease: report of four cases.

The protean clinical manifestations of atheroembolic disease (AED) mimic systemic disorders with kidney involvement. Acute or chronic renal failure develops spontaneously or more frequently after an inciting event in patients with AED. Significant proteinuria and nephrotic syndrome, however, constitute uncommon findings. We present four patients with AED documented histopathologically who developed nephrotic-range proteinuria. The mechanisms of proteinuria are discussed, and it is suggested that AED be considered in the differential diagnosis of nephrotic syndrome in elderly patients with serious vascular disease.

Hemolytic uremic syndrome: current pathophysiology and management.

The combination of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure, referred to as hemolytic uremic syndrome (HUS), is one of the main causes of acute renal failure in children. In most patients, infection with verotoxin-producing E. coli (VTEC, serotype O157:H7) precedes the development of bloody diarrhea (D+) characteristic of enteropathic HUS cases. In a minority, however, neither the enteropathogenic bacteria nor bloody diarrhea (D-) are documented. Despite that the pathogenesis of the two varieties remains unclear, clinical differentiation between D+ and D- HUS is extremely important to the final outcome. A more severe course, which may result in end stage renal disease, is frequently observed in the D- group.

Drug poisoning patterns: the Albany experience, 1978 and 1988.

This study retrospectively compares the demography and patterns of poisonings and their local variations among patients admitted to Albany Medical Center Hospital in the years 1978 and 1988. An increase in the number of admissions during this period of time, and an apparent substantial change in the pattern of poisonings was observed; in addition, the gender difference observed in 1978 disappeared. Although street drugs were a common source of poisoning, the resulting morbidity and mortality was low. The use of extracorporeal drug removal procedures appears to have declined in this institution in the two years evaluated.

[New concepts about hemolytic-uremic syndrome]. / Nuevos conceptos acerca del síndrome hemolítico urémico.

According to the heterogenous nature of hemolytic uremic syndrome in relation to the etiology, pathophysiology, treatment and diagnosis, we wish to draw attention to the main characteristics about its epidemiological clinical and immunopathological aspects. The HUS's distributes through all the world, but in Argentina, North of Europe, South Africa and west of USA the incidence is higher than the rest of the countries. The immunopathological studies shows thrombotic angiopathic lesion, consisting in generalized alteration of the capillary and arteriolar epithelium. Decreased levels of PGI2, Von Willebrand's factor and bacterial toxins are apparently involved among mechanism that are able to produce HUS. Dialysis is one of the main helps in the treatment of HUS, and in spite of our continued advances in knowledge about this disease, still further developments are needed in pathophysiology and therapeutics to enlight its intimate mechanisms.

Glomerulitis induced by cationized bovine serum albumin in the rat.

The effects of injected native and cationized bovine serum albumin (BSA- and BSA+ respectively) were evaluated in rats which subsequently received anti-BSA. Thrombocytopenia, low creatinine clearance (Ccr), increased proteinuria, capillary swelling, mild tuft necrosis and BSA+ deposits in glomeruli resulted within 24 h of BSA+ injection. Later BSA+ produced mesangial expansion glomerular capillary wall (GCW) thickening and deposits of BSA+ accompanied by rabbit anti-BSA and rat anti-BSA which correlated well with small mesangial, subendothelial and subepithelial electron-dense granular accumuli. These latter enlarged considerably after the injection of anti-BSA. BSA- controls showed minimal or no lesions. The disappearance from the blood (t1/2) of a single dose of immune complexes (IC) prepared with chromatography-purified, radioiodinated anti-BSA - BSA- and BSA+ was determined in another group of rats. The t1/2 of BSA- anti-BSA was 42.8 h (95% confidence: 39.8-46.2) while that of BSA+ anti-BSA was 52.5 h (48.1-57.8). These results suggested that serum sickness glomerulitis developed only in rats injected with BSA+, due to in situ IC which presumably grew by accretion of foreign anti-BSA. Circulating IC may have developed and colocated with the latter, with dissociation and recombination at these sites. It is postulated that the functional-immunomorphological changes and the slow removal of cationized IC reported herein could be explained by the highly positive net charge of the injected antigen.

Disseminated intravascular coagulation (DIC) induced by liquoid (polyanetholsulfonate) in the rat. V. Effects on circulating fibronectin.

Levels of plasma fibronectin (Fn) were 63% lower than normal 15 min after the intravenous injection of liquoid (P less than 0.01); 3 h later they were still low but rebounded to 35% above normal (P less than 0.01) by 24 h. Concurrently microthrombi containing fibrinogen, Fn and Factor VIII related-antigens (VIII:Ag) were detected in the kidneys and lungs by immunohistopathological studies. Ultrastructurally, thrombi were composed of dense granular and occasional fibrillar non-striated material. In liquoid-injected rats 125I-fibrinogen mainly localized in kidneys and lungs, especially in the latter (P less than 0.01), and the lungs had a higher wet-to-dry weight ratios than did controls (P less than 0.01). It is concluded that the polyanion (liquoid)-induced intravascular coagulation-like reaction sequestered Fn concomitantly with the precipitation of fibrinogen and VII:Ag in the microclots. The reduced concentration of plasma Fn may have impaired the disposal of coagulation products thus enhancing the expression of the coagulopathy-mediated renal and pulmonary histopathology. It is suggested that the liquoid-related coagulopathy may have resulted in enzymatic lysis of Fn.

Age-related renal, hematologic, and hemostatic abnormalities in FH/Wjd rats.

This longitudinal study compared the renal morphologic changes and hemostatic defects of FH/Wjd rats at different ages. A second aim was to determine whether the bleeding tendency becomes intensified in older animals by the concomitant renal disease. Results indicated that reduced capacity for platelet 14C-serotonin release (P less than 0.01) was found for each age group studied in comparison with Wistar controls. The nephropathy of old FH/Wjd male rats was more severe than that in either FH/Wjd females or age-matched Wistars of both sexes. The mesangial lesions showed abundant deposits of factor VIII-related antigen, fibronectin, and immunoglobulins, but not C3, along with tightly packed or loose electron-dense material. Polyethylene glycol precipitation and platelet aggregation tests detected small amounts of circulating immune complex-like material. Old FH/Wjd rats did not develop edema, and the glomerular filtration rate remained normal despite the persistent proteinuria, hematuria, and arterial hypertension characteristic of this strain. Our data indicated that the congenital platelet dysfunction does not become more severe in older animals and that the nephropathy seems unrelated, does not appear to be mediated by immune complexes, and, in contrast to the focal segmental glomerulosclerosis of persons, the lesions progress without a parallel impairment of renal function.