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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the incidence of normal (50.4%), increased (46.7%), and decreased (2.9%) anion gap among hospitalized patients in a retrospective study. The mean and range of increased anion gaps were 25 and 19-28 mmol/L. Values exceeding 30 mmol/L were uncommon and may indicate either acidosis or laboratory error. The most common causes of the increased anion gap among patients were chronic renal failure, congestive heart failure, malignant neoplasm, and diabetes mellitus. Increased anion gap in this study may be due to excess acids along with decreases in sodium, chloride, and carbon dioxide. The mean and range of decreased anion gap were 6 and 3-8 mmol/L. Anion-gap values less than 3 mmol/L were uncommon (one of 500 cases), and a high incidence of such values may indicate laboratory error. Nephrotic syndrome, liver cirrhosis, intestinal obstruction, and severe hemorrhage were the common disorders associated with decreased anion gap, which resulted from hypoalbuminemia and hyponatremia. Although most patients with decreased anion gap had hypoalbuminemia, hypoalbuminemic patients did not necessarily have decreased anion gap.
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PMID:Value of the anion gap in clinical diagnosis and laboratory evaluation. 682 31

In 17 patients, breathing room air and pure oxygen, with histologically proven cirrhosis of the liver and portocaval encephalopathy grade I, static and dynamic lung volumes, closing capacity and arterial blood gases were determined. Furthermore, CO2, response curves were provided and mouth occlusion pressure measurements were carried out. The residual volume was found to be increased (130 +/- 8% of predicted) which resulted in decreased vital capacity (79 +/- 2% of predicted) with total lung capacity being normal (94 +/- 2% of predicted). Closing capacity was increased to 134 +/- 5% of the predicted value. Gas exchange for oxygen was impaired (AaDO2 = 262 +/- 30% of predicted). Arterial PO2, however, was within normal range PaO2 = 84 +/- 3.6 mm Hg) due to hyperventilation (PaCO2 = 28.1 +/- 0.8 mm Hg). Hypoxic ventilatory stimulation could be excluded because inspiration of pure oxygen caused no change of PaCO2 (PaCO2 = 27.3 + 0.7 mm Hg and PaO2 = 465 + 16.9 mm Hg with FIO2 = 1.0). The slope of the CO2 response curves was normal, the mouth occlusion pressures, however, were higher than the predicted value: up to PaCO2 of 55 mm Hg. The slope of these curves being smaller than predicted. The results show that in patients with portocaval encephalopathy the lung function is disturbed due to premature airway closure with consequently decreased regional ventilation: perfusion ratios and that regulation of ventilation is impaired by a loss of sensitivity for CO2 with high basal output of the respiratory centers not related to CO2.
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PMID:[Lung function, gas exchange and regulation of ventilation in patients with portocaval encephalopathy (author's transl)]. 742 66

Impairment of cerebral blood flow (CBF) autoregulation may have serious implications for patients with cirrhosis if arterial hypotension occurs during coma, anesthesia, bleeding, or sepsis. In this study, CBF autoregulation was investigated in patients with cirrhosis with no or mild encephalopathy. Ten patients (median age, 45 years; range, 30 to 61 years) and six healthy volunteers (median age, 30 years; range 21 to 61 years) were included. Catheters were placed in a radial artery and in the internal jugular veins. Baseline CBF was measured using single-photon emission computed tomography (SPECT) with concomitant measurements of cerebral arteriovenous oxygen content differences (AVDO2). CBF autoregulation was evaluated using the AVDO2 method and changes in mean flow velocity in the middle cerebral artery (Vmean) as determined by transcranial Doppler (TCD). Mean arterial pressure (MAP) was increased by 30 mm Hg by intravenous norepinephrine, and subsequently decreased by a combination of lower body negative pressure and ganglion blockade, whereas AVDO2 and Vmean were measured at each 5 mm Hg change in MAP. CBF was 61 (range, 45 to 78) mL 100 g-1 min-1 in patients with cirrhosis and 65 (range < 53 to 88) mL 100 g-1 min-1 in volunteers (not significant [NS]). There were no regional differences in CBF between the two groups. Arterial carbon dioxide tension was 31 (23 to 35) mm Hg in patients with cirrhosis and lower, compared with 36 (range, 34 to 47) mm Hg in the volunteers (P < .01). For evaluation of autoregulation, MAP was raised to 116 (range, 100 to 145) and then decreased to 39 (range, 34 to 50) mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral blood flow autoregulation and transcranial Doppler sonography in patients with cirrhosis. 765 76

This paper introduced a technique of portal vein embolization by injection of ethanol via fine needle under guidance of angio-echography. First introportal ethanol injection were done in 28 dogs to evaluate its embolic efficacy and safety. The result showed if a dose of injected ethanol was chosen properly, expected embolization could be obtained with slight toxicity to hepatic parenchyma and function. For clinical application, selective portal vein puncture was percutaneous transhepatic under echo guidance. Ultrasound angiography by injecting carbon dioxide (CO2) into portal vein was introduced initially. After confirmed that the injected branch was that supplied the tumor and there was no retrograde overflow of portal blood, ethanol was injected at a dose no more than 10ml. Eighteen patients with hepatocellular carcinoma and underlying liver cirrhosis underwent the procedure preoperatively. Of 14 cases who received hepatectomies, portal vein embolization developed in 12. Since the procedure was guided by angio-echography it could be used for indicated cases with satisfactory embolic effect and not harmful to liver. The procedure had advantages of simple manipulation and made selective embolization easier compared to interventional transcatheter portal vein embolization.
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PMID:[Portal vein embolization via a fine needle guided by angio-echography: experimental and clinical study]. 777 2

Arterial oxygen tension (Pao2), carbon dioxide tension (PaCO2), and vital capacity were measured preoperatively and one day postoperatively in patients with chronic hepatic cirrhosis having elective oesophageal injection sclerotherapy under general anaesthesia. The results were compared with the same measurements made in patients with chronic cirrhosis anaesthetised and scheduled to have injection sclerotherapy under general anaesthesia but who, because of variceal obliteration, only had an oesophagogastroscopy. In the injected group PaO2 decreased by 9.3 (3.0) mm Hg (1.2 (0.4) kPa) (mean (SEM)) (p < 0.02) but in the controls did not change. The difference between the two groups was significant (p < 0.02). Vital capacity decreased by 0.39 (0.08) litres (BTPS) (p < 0.01) after injection sclerotherapy but in the controls did not change. Again the difference between the two groups was significant (p < 0.02). In the injected group there was a significant correlation between the change in PaO2 and the percentage change in vital capacity (r = 0.787, p < 0.01) but no such relation was seen in control subjects. These results suggest that oesophageal injection sclerotherapy is associated with a restrictive defect in respiratory function one day after the injection caused, possibly, by sclerosant embolising to the lung.
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PMID:Respiratory function after injection sclerotherapy of oesophageal varices. 795 5

Urease is an enzyme found in plants and bacteria, but not mammals. It catalyzes the conversion of urea to carbon dioxide and ammonia. Ammonia shortens the life span of cells; and higher concentrations cause tissue necrosis and cytolysis. Twenty percent of total body urea is converted to ammonia by bacterial urease in the colon. Small injections of urease immunize animals by producing antiurease, a gamma globulin, which inactivates urease. Immunization eliminates the colonic conversion of urea to ammonia. Injection of urease produces ammonia intoxication making immunization hazardous. Although previously impossible, a non enzymatic urease antigen was synthesized by covalently bonding jack bean urease with glutaraldehyde. This antigen stimulated the production of antiurease that inactivates native urease. Helicobacter pylori, a potent urease producer, has been implicated in peptic ulcer, gastritis and other inflammatory bowel lesions. The pathogenicity of H pylori is dependent on its urease production. Immunization to urease can render H pylori non pathogenic. Cirrhotics develop encephalopathy and hyperammonemia because their livers fail to convert all the ammonia in portal venous blood to urea and collaterals develop by passing the liver. Colonic ammonia increases the turnover rate of colonic mucosa. Ammonia absorbed into the portal venous system is transported to the liver where it is reconverted to urea. Absorbed ammonia adversely influences liver function. Infections with urease producing organisms destroy the renal parenchyma and produce struvite stones. Urease immunization aids colonic healing and prevents uremic colitis. Absorbed ammonia is a noxious influence on the liver. Animals immunized to urease regenerate the liver faster and are less susceptible to hepatotoxins. Immunization to urease ameliorates cirrhosis. Proteus and other urease producers become non toxic and do not damage the renal parenchyma. Urease is responsible for the pathogenicity of infections with urease producing organisms. Immunization to urease renders urease producing organisms non pathogenic.
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PMID:Awakenings to the pathogenicity of urease and the requirement for continuous long term therapy. 799 80

Deep hypothermic circulatory arrest has been widely used as an adjunct for surgery of the aortic arch to protect the brain and other vital organs. We introduced the use of continuous retrograde cerebral perfusion via the superior vena cava during deep hypothermic circulatory arrest in 1987 and have used it in 33 patients. Continuous retrograde cerebral perfusion times ranged from 10 to 89 minutes (mean 40.2 +/- 22.5), and minimal nasopharyngeal temperatures ranged from 14 to 25 degrees C (mean 17.4 +/- 2.0). Two patients with a ruptured aneurysm died during operation due to bleeding and two other patients, with continuous retrograde cerebral perfusion time of 24 and 35 minutes, died 1 month postoperatively due to preoperative liver cirrhosis and sepsis. Two patients suffered from stroke. The remaining 27 patients, including 6 with from 60 to 82 minutes of continuous retrograde cerebral perfusion, had no complications related to continuous retrograde perfusion. During continuous retrograde cerebral perfusion, 66 pairs of blood samples from the perfusate and from the drainage back to the arch vessels were obtained. Analysis of these samples revealed that partial pressure of oxygen, saturation of oxygen, and oxygen content significantly decreased (p < 0.001), and partial pressure of carbon dioxide (CO2) and CO2 content significantly increased (p < 0.001). The nasopharyngeal temperature gradually increased at the rate of 0.01 to 0.03 degree C/min, but was maintained below 20 degrees C. These results reflect the fact that the aerobic metabolism of the brain is maintained during continuous retrograde cerebral perfusion due to oxygen and substrate availability. This technique offers the potential of metabolic support to the brain during deep hypothermic circulatory arrest and prolongs the safe time limits of deep hypothermic circulatory arrest in surgery of the aortic arch.
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PMID:Protective effect of continuous retrograde cerebral perfusion on the brain during deep hypothermic systemic circulatory arrest. 799

Herein, we present the diagnostic efficacy of various imaging diagnostic techniques for small liver cancer(HCC) and HCC occurrence predictability by ultrasonography during the follow-up period of chronic liver diseases. During the recent 4 years, 78 nodules of small liver cancer measuring 2 cm or less in diameter were found in 50 patients with liver cirrhosis. In this study, the tumor size was divided into 2 groups; 1.5 cm or less in maximal diameter (group A) and 1.6 to 2 cm (group B). The tumor detectability of ultrasound (US), computed tomography (CT), magnetic resonance imaging (MRI), angiography and lipiodol CT in group A vs group B was 96% vs 97%, 68% vs 88%, 65% vs 94%, 12% vs 78% and 38% vs 89%, respectively. Therefore, angiography and lipiodol CT were not effective for detection of small HCCs smaller than 1.5 cm. Recently, helical CT scanning has been induced in the diagnosis of HCCs and the tumor detectability was enhanced to 82% even in group A. Additionally, helical-dynamic CT has some advantages in evaluating vascularity, especially arterial feeding which is a specific finding to HCCs. In comparison with contrast-enhanced US using CO2-microbubbles, helical-dynamic CT had equivalent accuracy in diagnosing hypervascular tumors, while hypovascular masses were observed in about 30% of group A. With respect to prediction of HCC occurrence in cirrhotic liver, sonographic evaluation of liver parenchyma seemed to be an important parameter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Integrated diagnosis of small hepatocellular carcinoma with imaging diagnosis]. 799 12

Postoperative pulmonary complications are often fatal in patients with oesophageal cancer. The influence of various preoperative and perioperative risk factors in the prediction of such complications was analysed. Some 170 oesophageal resections performed through a thoracotomy between January 1977 and December 1991 were reviewed. Twenty-two parameters generated from various medical risk categories were studied. Six variables were significant (P < 0.05) on univariate analysis: vital capacity, serum albumin level, partial pressure of carbon dioxide in arterial blood, presence of liver cirrhosis, presence of chronic obstructive airway disease and clinical stage of the tumour. Multivariate discriminant analysis of these six factors identified three as significant, namely vital capacity (P < 0.0001), liver cirrhosis (P = 0.01) and tumour stage (P = 0.01), yielding an equation for assessment of the risk of postoperative pulmonary complications. Calculation of the risk score showed that 42 of 53 patients with pulmonary complications had scores of 0 or more and that 74 of 102 without had scores below 0. The mean risk score was 0.34 for patients with complications and -0.26 for those without. The equation predicted pulmonary complications after transthoracic oesophagectomy with 74.8 per cent accuracy, 79.2 per cent sensitivity and 72.5 per cent specificity. It is concluded that the risk of postoperative pulmonary complications can be accurately assessed in individual patients by calculation of a risk score based on vital capacity, liver cirrhosis and tumour stage.
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PMID:Prediction of pulmonary complications after transthoracic oesophagectomy. 804 3

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.
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PMID:Arterial and mixed venous acid-base status in patients with cirrhosis. Influence of liver failure. 845 22


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