Acid-Base Disturbances in Patients With Cirrhosis of the Liver

Mulhausen, Robert; Eichenholz, A.; Blumentals, A.

doi:10.1097/00005792-196703000-00010

Cited by 63 publications

(17 citation statements)

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“…When the acid-base status of these patients was evaluated ( fig. I) the majority exhibited uncompensated metabolic alkalosis or mixed metabolic-respiratory alka losis, situations, in which the elevations of L and P are primarily found in those patients with lower PaC02 [21]. However, elevations in L and P were also observed in some of our patients with normal PaCCX.…”

Section: Discussionmentioning

confidence: 60%

Red Blood Cell Transketolase Activity and Blood Lactate and Pyruvate in Patients with Cirrhosis of the Liver

Presser¹,

Farmer²,

Shoberg³

et al. 1971

Digestion

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Red blood cell transketolase activity, before and after addition of thiamine pyrophosphate, was the same in 17 cirrhotic patients and in 31 normal volunteers and chronically ill noncirrhotic patients receiving an adequate thiamine intake. Blood lactate and pyruvate levels and L/P ratios were higher in the cirrhotics. Thiamine supplementation did not alter these results. PaO₂ was lower in the cirrhotic group. pHa and PaCO₂ were not different from controls. Although thiamine dependent enzymes were not evaluated in ether tissues, the red blood cell data suggest that these patients can utilize thiamine normally. Factors other than thiamine deficiency (circulatory changes, hyperventilation, cellular damage) may explain the alteration in lactate-pyruvate metabolism observed in these patients.

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Section: Discussionmentioning

confidence: 60%

Red Blood Cell Transketolase Activity and Blood Lactate and Pyruvate in Patients with Cirrhosis of the Liver

Presser¹,

Farmer²,

Shoberg³

et al. 1971

Digestion

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“…We believe that the lactic acidosis and liver hypoxia are not incompatible with the elevated arterial blood pO 2 observed in the IR animals; Bihari et al (1985) and other authors (Mulhausen et al 1967;Tonsgard et al 1982) have reported that liver hypoxia in several hepatic diseases that develop with portal hypertension may occur despite adequate systemic blood pressure and oxygenation.…”

Section: Discussionmentioning

confidence: 71%

Acid-base disturbances in the rabbit during experimental hepatic parasitosis

Fernández

Domingo

Cava³

et al. 1996

Parasitology Research

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Acid-base disturbances were examined during experimentally induced infection in the rabbit with Eimeria stiedai, a parasite that profoundly modifies liver morphology and physiology, resulting in anatomical and functional alterations similar to those appearing in different human hepatic diseases. Over 28 days of infection, bicarbonate and lactate concentrations, partial pressures of O2 and CO2, and pH values were determined in the blood and bile of infected animals and compared with the values obtained in noninfected rabbits. The plasma activity of several liver-indicator enzymes was also evaluated. Under our experimental conditions we observed an uncompensated metabolic acidosis that developed with elevated levels of lactate and reduced concentrations of bicarbonate in blood and bile and tended to be compensated by respiratory and biliary mechanisms.

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“…Nevertheless, hypocapnia and hypoxia may contribute. Hypocapnia causes a rise in lactate and pyruvate in proportion to the fall in PCo2 (Mulhausen et al, 1967) and may stimulate lactate production by erythrocytes and muscle. In the presence of hypoxia hepatic anaerobic glycolysis may occur, resulting in lactate production rather than removal (Berry and Scheuer, 1967).…”

Section: Commentmentioning

confidence: 99%

“…The data of Mulhausen et al (1967) show that once established in liver failure lactic acidosis is often irreversible. We feel that fructose is contraindicated in the treatment of liver failure and suggest that ethanol-fructose mixtures should be used with caution if hepatic function is disturbed, since ethanol can also induce lactic acidosis by altering the proportion of NADH to NAD in the liver cell.…”

Section: Commentmentioning

confidence: 99%

Lactic acidosis complicating liver failure after intravenous fructose.

Craig¹,

Crane²

1971

BMJ

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procedure she complained of the sudden onset of pain in the chest, shortness of breath, and haemoptysis. A lung scan showed lage areas of impaired perfusion in both lung fields typical of pulmonary embolism. There were no physical signs in her legs but testing with the ultrasound flow detector showed an impairment of venous flow in the left popliteal and lower femoral vein. Peripheral ascending phlebography was carried out as an emergency procedure and showed extensive recent, non-adherent thrombus in most of the calf veins, the popliteral vein, and lower femoral vein of the left side (see Fig.).It was considered advisable to protect her against a further and CommentThis case shows that thrombus can propagate along a vein very quickly. Within an hour the risk to this patient of developing a massive, as opposed to a minor, pulmonary embolus was seriously increased, because the potential embolus had doubled in size. Anticoagulants had not been given because of the recent episode of haemorrhage from the cerebral artery aneurysm and it may be that they would have prevented the growth of the thrombus. Normally we find at operation that the thrombus fits the phlebogram perfectly, but most of these patients are already anticoagulated with heparin as the first line of treatment of their pulmonary embolus.If thrombus can grow so quickly then the value of any routine screening procedure, such as ultrasound flow detection or the labelled fibrinogen uptake test, in the prophylaxis of sudden massive embolism is open to doubt.This case emphasises the urgency with which any procedure must be carried out when attempting to prevent recurrent pulmonary embolism.

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Acid-Base Disturbances in Patients With Cirrhosis of the Liver

Cited by 63 publications

References 0 publications

Red Blood Cell Transketolase Activity and Blood Lactate and Pyruvate in Patients with Cirrhosis of the Liver

Red Blood Cell Transketolase Activity and Blood Lactate and Pyruvate in Patients with Cirrhosis of the Liver

Acid-base disturbances in the rabbit during experimental hepatic parasitosis

Lactic acidosis complicating liver failure after intravenous fructose.

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