Biomedical subjects
Publications and source records attributed to O Nouel.
Four patients are described, admitted during a three-year period, who recovered from acute fatty liver of pregnancy; vomiting and jaundice were the main manifestations of the disease; coma and anuria were absent. During the same period, we observed one patient who died of acute fatty liver of pregnancy. This experience suggests that the non-fatal form of the disorder may be much commoner than the fatal form.
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Placebo or propranolol was given randomly of two groups of 12 adults with cirrhosis who had recently held from oesophageal or gastric varices or from acute gastric erosions. During three months' follow-up 5 patients in the placebo and none in the propranolol group had recurrent gastrointestinal bleeding.
Asymptomatic hypoglycemia was demonstrated in 15 of 30 cirrhotic patients with septicemia. Blood glucose levels were measured daily in these patients. Severe circulatory failure was present in the 15 patients with hypoglycemia and was absent in the 15 patients with normal blood glucose levels. Hypoglycemia is a common complication of septic shock in patients with cirrhosis, and blood glucose levels should be systematically measured in cirrhotic patients with septicemia or shock. Septicemia should be considered in any cirrhosis patient with a low blood glucose level.
Fifteen patients with a patent shunt after distal splenorenal shunt with gastrosplenic disconnection were prospectively studied by angiography three to 36 months after operation. In all patients a collateral circulation from the portomesenteric to the gastrosplenic system was developed through enlarged venous channels. In all patients the portal flow decreased, as suggested by the angiographically assessed degradation of the portal perfusion of the liver and/or the diminution of the diameter of the portal vein. In two patients the portal vein was thrombotic. We conclude that three months after operation distal splenorenal shunt with gastrosplenic disconnection is not hemodynamically different than portacaval laterolateral shunt.
The suitability was investigated of the segmental perfusion technique under an occluding balloon (which prevents the contamination of the test segment by upper digestive secretions and pancreatic proteolytic enzymes) for measuring immunoglobulin A (IgA) and serum albumin outputs into the jejunal lumen. The influence of the perfusion rate and of the transintestinal water movements in the 40 cm long test segment was studied in 11 healthy subjects. IgA and serum albumin outputs did not differ significantly when the same isotonic solution was perfused at rates of 5 or 10 ml/min, nor when water absorption was stimulated by the presence of glucose. A possible artefact linked to intestinal wall distension by the occluding balloon was evaluated in eight subjects with complete exocrine pancreas insufficiency. IgA and serum albumin outputs obtained under the occluding balloon were compared with those found with the triple non-occlusive method. Care was taken to achieve a similar flow rate and solute composition of the fluid entering the test segments with both techniques in each subject. Under these conditions, IgA and serum albumin outputs measured with both methods did not differ significantly. These findings validate the use of the segmental perfusion technique under an occluding balloon to measure IgA and serum albumin outputs into the human small intestine.
We report the case of a patient with transient hypertension in relation to acute veno-occlusive disease of the liver. Ascites and esophageal varices, both transient, occurred in this patient and a transient elevation of the gradient between wedged and free hepatic venous pressures was observed.
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Continuous, oral administration of propranolol at doses which reduced the heart-rate by 25% produced a sustained decrease in portal venous pressure in cirrhotic patients with portal hypertension. This effect of propranolol might be useful in preventing recurrent bleeding due to ruptured oesophageal varices in patients with portal hypertension.
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Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequences of which are intermingled with those of cardiac insufficiency in most cases. We report the cases of six patients suffering from chronic heart failure in whom an episode of acute circulatory failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure, ie, hepatic encephalopathy, jaundice, and marked increase in prothrombin time, developed after an interval of one to three days, after the episode of acute circulatory failure, while the patiens' hemodynamic condition had returned to the previous basal status.
The gradient between wedged and free hepatic venous pressures were measured in 10 unselected adult patients suffering from fulminant viral hepatitis. The gradient was increased in all the studied patients, ranging from 0.9 to 2.1 kPa; this finding indicates that portal hypertension was present in all these cases. Ascites was present in all the five patients having a gradient about 1.5 kPa and affected only two of the five patients having a gradient below 1.5 kPa; this observation suggests that portal hypertension plays a role in the mechanism of ascites in fulminant viral hepatitis. Portal hypertension in fulminant viral hepatitis is likely to be the consequence of an intrahepatic block due to massive necrosis of the liver cells.
Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.
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A report is given on the results of 12 radiological explorations of the bladder in 12 patients with pseudo-neoplastic sigmoiditis. In all cases the bladder had an abnormal aspect, in two cases there was a pseudotumor, in two an inflammatory aspect, in four conical attraction of the bladder by the sigmoid. In all 12 cases morphological anomalies of the filled bladder were seen. The ureters were either normal or dilated but without true stenoses. These various aspects may contribute to the differential diagnosis between sigmoiditis and cancer. The differential diagnosis of such vesical lesions is discussed.