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D Perrin

Publications and source records attributed to D Perrin.

113 records · Page 7Linked to original sources
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[Is portacaval anastomosis still valid treatment for portal hypertension in alcoholic cirrhotic patients?].

Mortality and quality of survival after portacaval anastomosis in cirrhotic patients are such that the validity of the operation was investigated during a retrospective study of 242 cases, operation being for hemorrhage and involving emergency or delayed surgery. Operative mortality was higher in emergency cases, but was improved by stricter selection criteria, particularly of pathological features. Cause of death from secondary factors varied during the two years following anastomosis, with perhaps a high frequency of hepatic failure. Recurrence of hemorrhage was a serious complication often related to hepatic insufficiency, while the onset of combined jaundice-edema-ascites (1 out of 4 patients) was frequently the result of continued alcohol abuse. Portacaval encephalopathy (24,4%) did not worsen the vital prognosis, and was severe in only 3 cases. Alcohol intoxication was very frequent in minor forms. Edema of the lower limbs (34,4% of cases), a frequent complication, appeared to result mainly from hemodynamic causes. A return to work was not possible in 20% of patients, but in only 12% was this due to the anastomosis. Portacaval anastomosis would not, therefore, appear to alter survival of patients from complications of cirrhosis. It suppresses the hemorrhagic risk, however, and the course of the disease is then related only to the cirrhosis and to its stability if abstinence is maintained.

Adult↗
PubMedDate not supplied

Tissue iron storage patterns in fetal hydrops associated with congestive heart failure.

To learn whether fetal congestive heart failure causes a characteristic tissue iron storage pattern, we selected 15 neonatal autopsy cases of hydrops fetalis in which both the clinical and gross autopsy findings suggested intrauterine congestive heart failure. The latter appeared to be due to functional causes in 10 (3 nonhemolytic anemia, 4 cardiac dysrhythmia, 3 dilated cardiomyopathy) and was associated with cardiac malformation in 5. We graded the amount of hepatocellular siderosis, reticuloendothelial siderosis, and renal tubular siderosis in Perls-stained microscopic sections of liver, spleen, and kidney and compared the iron storage pattern with that in 15 normally developed neonatal autopsy controls (4 preterm, 11 term) and a further 7 with hemolytic anemia (5 alpha-thalassemia, 2 parvovirus B19 infection). Liver cell siderosis was absent in the three cases with nonhemolytic anemia. It was increased in 11 of the remaining 12 cases, as in hemolytic anemia controls. Among the five cardiac malformation cases, three had proximal renal tubular siderosis (as in hemolytic anemia controls) attributed to turbulent blood flow through the heart. Among the five, hydrops appeared to be due to prenatal closure of the foramen ovale in one and to prenatal constriction of the ductus arteriosus in another. In one of the five, and despite complex malformation of the heart, hydrops appeared to be due to complete heart block. We concluded that, although clinical information and morphologic assessment of the heart were basic to identifying a cardiac cause of fetal hydrops, histologic assessment of the pattern of iron storage helped confirm the pathologic diagnosis. Analysis of the pathologic findings led to a scheme for categorizing cardiogenic fetal hydrops.

Female↗
PubMedDate not supplied

Alveolar capillary dysplasia: lung biopsy diagnosis, nitric oxide responsiveness, and bronchial generation count.

Alveolar capillary dysplasia, a rare cause of neonatal pulmonary hypertension characterized by a developmental abnormality in the pulmonary vasculature, was diagnosed by lung biopsy in a male newborn maintained on nitric oxide therapy for 18 days. Autopsy confirmed the pulmonary vascular defect and demonstrated deficient airspace formation. In addition, a bronchial generation count was low, suggesting that the abnormal lung vascular development in this condition represents a special form of pulmonary hypoplasia that starts in early fetal life.

Biopsy↗