Effects of large volume abdominal paracentesis combined with plasma volume expansion on portal venous dynamics

The aim of this study was to identify the effects of large volume paracentesis combined with replacement with plasma volume expander on the portal and splenic veins hemodynamics in patients suffering from advanced liver cirrhosis with intractable ascites as well as to investigate the role and the statistical relation between the mechanical factors participating in inducing ascites and the hepatic function studies, blood proteins and electrolytes. Aspiration was simultaneously accompanied with iv infusion of 1000 ml plasma expander. Abdominal sonography was done to determine the volume of spleen and diameters of portal and splenic veins. Color Doppler and pulse wave mode measurements before and after the tap for blood flow velocities in the portal splenic veins were determined

Diagnosis of abdominal masses with percutaneous biopsy guided by ultrasound

Sixty consecutive patients identified as having abdominal masses were subjected to percutaneous biopsy of the masses guided by ultrasound to permit precise localization of the target organ. Biopsy failed in five cases. Adequate histological specimens were obtained in 60 patients with masses in the liver [35], renal systems [10], retroperitoneal lymphadenopathy [5], splenomegaly [2], splenic cyst [1], suprarenal [2], pancreatic [2], epigastric [1], pelviabdominal [1] and subphrenic [1] masses. No complications occurred from biopsy. Malignancy was suspected in 23 patients before biopsy; this was confirmed in sixteen cases, in seven of them confirmation of disseminated metastatic cancer obviated the need for further investigation. Two cases suspected to have benign liver lesion proved to have hepatoma. The overall sensitivity of the technique is 91.6% and the specificity is 84.09%. Percutaneous ultrasound guided biopsy is a safe and accurate method of obtaining a histological diagnosis and has a considerable effect on clinical management

Brain stem auditory evoked potentials [BAEPS] in patients with chronic renal and chronic hepatic failure

This study included 40 subjects divided into 3 groups. Group 1 consisted of 15 uremic patients, group 2 of 15 hepatic patients and group 3 of 10 completely normal control subjects. The brain stem auditory evoked potentials [BAEPs] demonstrated a statistically significant delay in absolute peak latency and in changes which occurred at high repetition rate between the uremic patients, the hepatic patients and the control group. Also, a statistically significant delay in the absolute peak latency and in inter peak latency was demonstrated when the hepatic patients of Child's class B were compared with those of Child's class A. There were no statistically significant changes when the uremic patients with serum creatinine level below 10 mg/dl were compared with those with serum creatinine level above 10 mg/dl. This work suggested that BAEPs can play an early and important role in prediction of metabolic encephalopathy

Gastro-duodenal mucosal changes in relation to portal vein size in patients with portal hypertension

This study was conducted on 48 patients divided into group I10 normal controls group II a 10 cirrhotics without portal hypertension and group II-b 28 cirrhotics with portal hypertension. Clinical examination, liver function abdominal ultrasound examination and upper gastrointestinal endoscopy was done for all patients. There were significant increase in the gastric mucosal changes in group II-b [cirrhotics with portal hypertention] if compared to group II-a [cirrhotics without portal hypertension] Also incidence of gastric mucosal change were significantly higher than incidence of duodenal mucosal change in group II-b. pyloric antrum in group II-b was the main site for gastric mucosal change. These gastric changes seem to be due to portal hypertension which leads to change in gastric vascularization. AIso the morphology of gastric microcirculation is modified in the form of changes in the length and shape of submucosal arties, veins and mucosal capillaries and veins which become larger in diameter and more straight. Moreover the artiovenous shunting, gastric congestion, jaundice, tissue hypoxia and oedema are factors that lower the local resistance of gastric mucosa to acid and pepsin. So normal or even subnormal levels of gastric acid secretions cause injury to gastric mucosa furthermore the local factors influencing mucosal cellular integrity [mucus, bicarbonate, and local prostaglandin] are altered by gastric venous hypertension. Also there was no correlation between the portal vein size in group II-b and the extent of severity of gastric mucosal changes

Role of some vasoregulatory factors in the pathogenesis of vascular complications of diabetes mellitus

This work included 10 normal controls, 10 diabetics without vascular complications and 15 diabetics with acuts macrovascular complications [acte myocardial infarction and/or cerebrovascular accident], 15 diabetics with microvascular complications [retinopathy and/or nephrpathy]. Clinical examination, blood glucose [fasting, 1hr and 2 hrs after oral glucose], blood urea, s creatinine, plasma 6-Keto-PG F1[6-Keto prostaglandin F1], plasma angiotensin-I were done for every patient. There was significant elevation of blood glucose, blood urea, and serum creatinine in all diabetics with or without vascular complications. Also there was significant elevation of thromboxan B2 and angiotensin-I in all diabetics irrespective of the presence or absence of vascular complications. While there was significant elevation of 6-Kete PG F1, in all diabetics but more in diabetics with macroagniopathy and most in diabetics with microangiopathy. Diabeties mellitus itself may be the causative factor in the elevation of plasma rennin activity [measured indirectly as angiotensin-I], prostacyclin [measurd as 6-keto-PGFI Infinity] and thromboxan-A2. elevated plasma rennin activity in diabetes may be harmfull as it can be a Causative factor in vascular complication of diabetes as it is a vasculotoxic agent