Search PubMed⌕ Search

Biomedical subjects

T Soupison

Publications and source records attributed to T Soupison.

29 records · Page 2Linked to original sources
PubMed1994

[Relationships between plasma concentrations of endothelin and the severity of liver cirrhosis].

OBJECTIVES: Results of studies on plasma endothelin concentrations in patients with cirrhosis are conflicting. Moreover, the relationships between plasma endothelin concentrations and the severity of cirrhosis have not yet been studied. The aim of this study was to measure plasma endothelin concentrations in controls and in patients with cirrhosis. In addition, this study examined the relationships between plasma endothelin concentrations, and the severity of liver disease, splanchnic and systemic hemodynamics. METHODS: Plasma endothelin concentrations (in the hepatic vein and the right atria), hepatic venous pressures, arterial pressure, cardiac output, pulmonary pressures and plasma concentrations of sodium and creatinine were measured in 7 controls and 28 patients with cirrhosis. RESULTS: Plasma endothelin concentrations in the hepatic vein and the right atria were significantly higher in patients with cirrhosis (18.9 +/- 2.9 and 20.2 +/- 3.1 pg/mL, respectively) than in controls (6.1 +/- 1.1 and 7.2 +/- 1.1 pg/mL, respectively). In these patients, hepatic venous plasma endothelin concentrations were significantly correlated with Pugh's score (r = 0.49), hepatic venous pressure gradient (r = -0.44), and plasma sodium concentrations (r = -0.46). No significant correlation was found between plasma endothelin concentrations and systemic hemodynamics. CONCLUSION: Plasma endothelin concentrations are increased in patients with cirrhosis. Moreover, this increase is more marked in patients with severe liver disease than in patients with no or moderate impairment of liver function.

Blood Chemical Analysis↗
PubMed1993

Arterial and mixed venous acid-base status in patients with cirrhosis. Influence of liver failure.

Although it has been established that liver failure is associated with arterial hypocapnia and alkalaemia (i.e., respiratory alkalosis), the influence of liver failure on mixed venous acid-base status has not yet been studied. Thus, arterial and mixed venous acid-base status were simultaneously measured in controls and in a large series of patients with cirrhosis. Grade B patients (n = 28) or Grade C patients (n = 21) had significantly lower arterial and mixed venous carbon dioxide tensions than controls (n = 29). Grade B or Grade C patients also had significantly higher arterial, mixed venous pH, and lower mixed venous bicarbonate concentrations than controls. Among Grade A patients (n = 27), those with the lowest Pugh's score (i.e., equal to five) had significantly lower mixed venous carbon dioxide tension than controls. The other arterial and mixed venous acid-base values did not differ significantly between Grade A patients with the lowest Pugh's score and controls. Grade A patients with a Pugh's score equal to six and Grade B patients had similar acid-base disorders. No significant differences were found between groups concerning the anion gap and plasma chloride concentrations. In conclusion, this study shows that in Grade B or C patients, respiratory alkalosis was responsible for mixed venous hypocapnia, alkalaemia and hypobicarbonataemia. In addition, in Grade A patients with the lowest Pugh's score (equal to five), analysis of arterial and mixed venous blood revealed that mixed venous hypocapnia was the sole anomaly of the acid-base status. This last finding suggests that mixed venous hypocapnia might be an early event preceding the onset of arterial hypocapnia.

Alkalosis, Respiratory↗
PubMed1992

Septic shock in patients with cirrhosis: hemodynamic and metabolic characteristics and intensive care unit outcome.

OBJECTIVES: To examine the hemodynamic and metabolic characteristics and ICU outcome of septic shock in patients with cirrhosis. DESIGN: Prospective, comparative study. Measurements performed in the first 24 hrs of septic shock. SETTING: A general hospital ICU. PATIENTS: Twelve patients with cirrhosis and 23 patients without cirrhosis admitted for septic shock. MEASUREMENTS AND MAIN RESULTS: Arterial pressure was measured using an arterial catheter. Pulmonary arterial and right atrial pressures were measured by using a pulmonary artery catheter. Cardiac output was determined by using the thermodilution method. Pulmonary arterial L-lactate plasma concentrations were measured using an automated spectrophotometer, and blood temperature was measured using a cardiac output computer. Arterial and mixed venous PO2, PCO2, and pH values were measured by using specific electrodes. Oxygen saturations and hemoglobin concentrations were measured using a hemoximeter. Patients with cirrhosis had decompensated liver disease (grade C of the Child-Pugh classification). The number of Gram-negative infections and therapeutic interventions were similar in both groups. Patients with cirrhosis had higher cardiac indices (5.14 +/- 0.52 [SE] vs. 3.91 +/- 0.30 L/min/m2, p less than .05), plasma lactate concentrations (9.0 +/- 2.0 vs. 5.2 +/- 0.7 mmol/L, p less than .05) and ICU mortality rates (100% vs. 43%, p less than .05), and lower blood temperatures (35.5 +/- 0.6 vs. 37.6 +/- 0.2 degrees C, p less than .05) than patients without cirrhosis. Systemic vascular resistance, arterial pressure, pulmonary arterial pressure, oxygen delivery and consumption, and arterial and mixed venous acid-base status were not significantly different between the two groups. CONCLUSIONS: In patients with cirrhosis, septic shock was characterized by severe liver dysfunction, low blood temperature, marked increases in cardiac index and lactic acidemia, and a 100% ICU mortality rate. These findings should be taken into account if patients with cirrhosis are to be included in controlled studies on septic shock.

Acid-Base Equilibrium↗
PubMed1990

Abnormal pressor response to vasopressin in patients with cirrhosis: evidence for impaired buffering mechanisms.

In patients with cirrhosis, vasopressin infusion induces sustained vasoconstriction and elevation of arterial pressure. The vasopressor effect could be caused by impairment of mechanisms normally aimed at buffering increases in arterial pressure (reflex bradycardia and decreases in arteriolar resistance). We studied the acute effects of continuous vasopressin infusion (0.4 IU/min) on systemic hemodynamics in seven patients with cirrhosis and in six patients without cirrhosis (controls). Vasopressin effects on systemic O2 consumption were also studied. In both groups, vasopressin infusion induced similar peak increases in arterial pressure, followed by similar decreases in heart rate and cardiac output. However, cirrhotic patients and controls differed 30 min after the start of vasopressin infusion. At 30 min, mean arterial pressure, diastolic arterial pressure and systemic vascular resistance remained significantly higher than preinfusion values in patients with cirrhosis. No decrease in systemic O2 consumption occurred in cirrhotic patients. In controls, at 30 min, mean arterial pressure and diastolic arterial pressure had returned to baseline. Systemic vascular resistance was not significantly higher than the preinfusion value and systemic O2 consumption had significantly decreased to below preinfusion values. We conclude that the vasopressor effect of vasopressin is abnormally sustained in patients with cirrhosis. This might be caused by insufficient buffering of vasopressin-induced arteriolar constriction rather than by abnormal vagal control of heart rate. In turn, as suggested by the lack of a decrease in systemic O2 consumption, persistent arteriolar constriction might be related to abnormally sustained sympathetic vascular tone in patients with cirrhosis.

Adult↗
PubMed1989

Occult gastrointestinal bleeding in high-risk intensive care unit patients receiving antacid prophylaxis: frequency and significance.

Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding (GB) and receiving antacid prophylaxis (gastric pH greater than 3.5). Of the present patients, 27% (11/41) had at least one episode of occult GB (three consecutive positive determinations; a total of 14 episodes). Endoscopy identified acute gastroduodenal mucosal lesions (stress ulcers) as the most frequent lesion in this group (eight patients). Sepsis was the most frequent underlying condition associated with occult GB due to stress ulcer. Hematemesis occurred in 36% (4/11) of patients with occult GB and was due to stress ulcer in three patients and to benign gastric tumor in one. No overt GB occurred in the absence of previous occult GB. We conclude that: a) risk of GB persists in critically ill ICU patients in spite of antacid prophylaxis (gastric pH greater than 3.5); b) high-risk patients can be identified through periodic testing for the presence of blood in gastric juice using the reagent; c) when occult GB occurs, treatment should be based on the endoscopy results. In the absence of acute gastroduodenal mucosal lesions, antacid prophylaxis should not be modified, and specific treatment of the identified lesion(s) should be initiated. In the presence of stress lesions, antacid prophylaxis should be reinforced if the pH of the gastric content is less than 3.5 and a septic complication should be actively sought if the pH is greater than 3.5.

Adult↗
PubMed1989

Comparison of two simplified severity scores (SAPS and APACHE II) for patients with acute myocardial infarction.

The Simplified Acute Physiology Score (SAPS), the Acute Physiology and Chronic Health Evaluation II (APACHE II), the Acute Physiology Score (APS), and the Coronary Prognostic Index (CPI), calculated within the first 24 h of ICU admission, were compared in 76 patients with acute myocardial infarction (AMI). Sixteen (21%) patients subsequently died in the ICU. The nonsurvivors had significantly higher SAPS, APACHE II, and CPI scores than the survivors. ROC curves drawn for each severity index were in a discriminating position. There were no significant differences either between the areas under the ROC curves drawn for SAPS, APACHE II, and CPI, or between the overall accuracies of these indices. APS provided less homogeneous information. We conclude that SAPS and APACHE II, two severity indices which are easy to use, assess accurately the short-term prognosis, i.e., the ICU outcome, of patients with AMI.

Aged↗
PubMed1989

[Fulminant hepatitis induced by disulfiram in a patient with alcoholic cirrhosis. Survival after liver transplantation].

Fulminant hepatitis was observed in a 44-year-old patient with cirrhosis, 38 days after the beginning of a treatment by disulfiram. Hepatitis was associated with fever and hypereosinophilia. Liver transplantation was performed with success. We reviewed 15 previously published cases of disulfiram-induced hepatitis. They occurred from 10 to 180 days after the beginning of the treatment by disulfiram, aminotransferases were increased whereas alkaline phosphatases were not markedly changed; there was either focal or widespread necrosis. Fulminant hepatitis was observed mainly in patients with alcoholic chronic liver disease or in patients who continued to ingest disulfiram while jaundice was already present. An immunoallergic mechanism is thought to be responsible for disulfiram-induced hepatitis.

Adult↗
PubMed1988

Abnormal tissue oxygenation in patients with cirrhosis and liver failure.

Systemic haemodynamic and hepatic venous pressures, arterial and mixed venous gases and arterial lactate concentration were measured in 35 patients with histologically proven alcoholic cirrhosis who had been classified into three groups (A, B and C). Eight alcoholic patients without cirrhosis on liver biopsy were also studied. Compared with group A patients, group C patients had significantly higher hepatic venous pressure gradient, cardiac index, O2 transport and arterial lactate concentration and significantly lower systemic vascular resistance, arteriovenous O2 content difference and O2 uptake. In group B patients, corresponding values fell between those of groups A and C. Group A patients, unlike group C patients, were not significantly different from patients without cirrhosis with respect to cardiac index, systemic vascular resistance, O2 uptake and arterial lactate concentration. Our results suggest that in patients with cirrhosis, liver failure-associated hyperdynamic circulation may be accompanied by an abnormal tissue oxygenation.

Acid-Base Equilibrium↗