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

1. The ventilatory responses to transient and steady-state hypoxia were measured in ten patients with hepatic cirrhosis and in ten healthy control subjects. Successive measurements of these responses were also obtained in six goats before and after the experimental production of liver failure. Changes in the effect of steady-state hypoxia on the ventilatory response to hypercapnia were evaluated by successive studies in another goat. 2. In spite of a respiratory alkalosis during liver failure, the response to transient hypoxia was greater in the patients than in the control subjects. This response was increased after the onset of liver failure in all the goats. 3. In healthy humans and goats the responses to transient and steady-state hypoxia were similar in magnitude. During liver failure there was a disparity between the size of these responses, since the ventilatory increment evoked by steady-state hypoxia was unchanged in spite of the increase in response to transient hypoxia. Steady-state hypoxia consistently enhanced the ventilatory response to hypercapnia in a healthy goat, but frequently depressed the response to hypercapnia during liver failure. 4. The findings suggest that liver failure heightens the sensitivity of the peripheral chemoreceptors to the hypoxic stimulus, but may increase the tendency of the medullary centres to become depressed in hypoxia.
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PMID:Effect of liver failure on the ventilatory response to hypoxia in man and the goat. 0 6

This contribution presents data from the literature as well as our own results concerning the mechanisms of hepatic encephalopathy (HE). 1. Blood chemistry: In patients with liver cirrhosis, the plasma levels of ammonia, phenylalanine, tyrosine, phenolic acids, and octopamine correlated with the stages of HE. Methionine and free tryptophan concentrations were increased only in stages 2-4. Further, branched chain amino acids were below the normal range. Experimental findings in animals elucidated some mechanisms of these changes. 2. Effects of administered substances: With ammonia, methionine, methanethiol, tryptophan, phenolic substances, and fatty acids central nervous disturbances were observed. 3. Interactions: Anemia, methanethiol, and fatty acids favored ammonia toxicity. Alkalosis diminished cerebral symptoms. 4. Neurotransmitters: HE was accompanied by an enhanced turnover of serotonin and by increased amounts of false neurotransmitters (like octopamine) in the brain. 5. Oxydative brain metabolism: Disorders of cerebral oxygen and glucose utilization were mainly documented in cases of long term HE with EEG alterations. 6. Structural changes of the brain: Most of them are irreversible.
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PMID:[Pathogenesis of hepatic encephalopathy (author's transl)]. 1 66

In a series of 68 cirrhotics subjected to portacaval anastomosis for digestive haemorrhage, alterations in the acid base balance, 3, 6, 12, 24 and 48 weeks after anastomosis, were examined. Following operation, an increase in the incidence of the usual acid base disturbances of liver cirrhosis is observed. Respiratory alkalosis increases with no direct relationship to teh postoperative increase in ammoniemia, the main stimulating agent of the resporatory centres. This is probably because the active fraction on the nerve cells is the non-ionized one only, freely diffusible through the haematoencephalic barrier, the plasma concentration of which is a function of blood pH. Postoperative metabolic alkalosis is secondary to the potassium and chloride depletion consequent on operative trauma, on the malnutrition syndrome and, in the case of potassium, on secondary hyperaldosteronism which, unlike what is observed in the other groups of cirrhotics, is uncorrected by anastomosis. After the shunt, metabolic acidosis may be the expression of an increase in lactates and pyruvates following on further liver function deterioration, and of a functional renal insufficiency which anastomosis makes more manifest.
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PMID:[Acid-base metabolism in patients with hepatic cirrhosis treated with portacaval anastomosis at various intervals after the operation]. 30 8

By observing a group of 20 patients with liver cirrhosis, we have clarified some features concerning the tissue hypoxia, which is often present in such a disease. By determining the levels of the haemoglobin and of the intraerythrocytic 2,3-DPG, and by evaluating the acid-base state of such patients, we have emphasized the increased output of the 2,3-DPG as mechanism of adaptation to hypoxia associated with hepatic cirrhosis, both in subjects with anemia and alkalosis and in subjects without anemia but with alkalosis.
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PMID:[Adaptation to hypoxia in liver cirrhosis: the role of 2,3-DPG (author's transl)]. 55 61

In a group of 23 patients suffering from liver cirrhosis, metabolic acidosis was always observed, in most cases corrected by respiratory alkalosis. In 8,6% of cases a tubular renal acidosis (type I), in 8,6% (type II) and 8,6% a loss of urinary bicarbonate without acidosis were observed.
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PMID:[Renal tubular acidosis during a course of liver cirrhosis]. 59 85

Glomerular filtration rate and renal plasma flow may be normal, reduced or increased in cirrhosis. The mechanism of departures from normal is not known. Other renal functional changes in cirrhosis include avid sodium reabsorption, impaired concentrating and diluting abilities, and partial renal tubular acidosis. Fluid and electrolyte disorders are common. Sodium retention with edema and ascites should generally be treated conservatively because they tend to disappear as the liver heals and because forced diuresis has hazards. The indications for diuretics are (1) incipient or overt atelectasis; (2) abdominal distress; and (3) possibility of skin breakdown. Hyponatremia is common and its mechanism and treatment must be assessed in each patient. Hypokalemia occurs and requires treatment. Respiratory alkalosis and renal tubular acidosis seldom need therapy. The hepatorenal syndrome is defined as functional renal failure in the absence of other known causes of renal functional impairment. The prognosis is terrible and therapy is unsatisfactory. The best approach is not to equate the occurrence of renal failure in cirrhosis with the hepatorenal syndrome. Rather the physician should first explore all treatable causes of renal failure, eg, dehydration, obstruction, infection, heart failure, potassium depletion, and others.
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PMID:Fluid and electrolyte disturbances in cirrhosis. 96 15

The literature data concerning respiratory function in cirrhosis of the liver are cited and reference is made to the results of a spirometric, gas analysis and 133-Xenon investigation of this parameter in 38 patients. Spirometry pointed to slight ventilatory incapacity of the restrictive type. Arterial gas analaysis showed respiratory alkalosis, usually accompanied by metabolic acidosis and slight hypoxyaemia. Examination with 133-Xe indicated that hypoxyaemia was not due to a shunt effect, since there was no excess of perfusion with respect to district ventilation. It was clear, on the other hand, that the pulmonary capillary reserve was almost exhausted. Such complete perfusion of the capillary bed may be due to increased cardiac output and, in part, to reduction of the respiratory surface caused by raising of the diaphragm and hypoventilation of the lung bases.
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PMID:[Respiratory function in liver cirrhosis. Spirometry, blood gas analysis and radioisotope study with Xenon 133]. 111 19

The authors present a series of 72 observations of septic shock. The overall hospital mortality is 51%. Aggravating factors with worst prognosis are a cirrhosis (90% mortality) and wrong antibiotics before shock occurred (88% mortality). Some therapeutic acts (cannulae, venous catheter, urinary catheter, immuno-depressing treatment) increase penetration of gram positive germs of hostipal origin. The germs account for 30% of cases, the most frequent being staphylococcus. Among gram-negative organisms, one finds colibacilli, pseudomonas and last klebsiella. Usual entrance site was respiratory (33%). On clinical grounds we found equal frequency of "warm" shock with vasodilatation (mortality 30%) and "cold" shock (mortality 67%). A certain degree of renal failure sometimes necessitating dialysis is the rule. Intravascular disseminated coagulation occurred 3 times out of 46; 13 had hemorrhage. Finally acid-base disorders were usually of the metabolic acidosis type with respiratory alkalosis. Treatment consists in restauring volemia with abundant perfusions under control of central venous and arterial pressures and diuresis. Antibiotherapy, bactericidal and with wide spectre or specific for the suspected germ, must be immediately started. Importance of surgical debridement when required is evidenced by the low mortality of those cases (2 deaths out of 12). We use steroids systematically at high dosage, intravenous. Vasoactive or tonicardiac drugs are used selectively. Their efficiency and that of steroids are not prooved. Finally a review of the literature concerning the physiopathology and treatment of septic shock and its complications is presented.
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PMID:[Septic shock. Clinical review of 72 cases (author's transl)]. 122 90

Acid-base status was determined in 86 patients with cirrhosis of the liver. Group I comprised 55 patients living more than 3 months after examination (stable). Another 18 stable patients with a surgical porta-caval shunt (p.c.a.) formed group II. Group III consisted of 12 terminal patients without p.c.a. examined within the last week of life. With respect to liver function group II was intermediate between I and III. The most common acid-base disturbance in group I was compensated respiratory alkalosis (20%) followed by compensated metabolic alkalosis (15%). 50% of group II presented compensated respiratory alkalosis. 85% of group III showed metabolic acidosis, which was compensated in only half of the patients. Respiratory alkalosis seemed more related to impairment of liver function than to portasystemic shunting. The genesis of the terminal metabolic acidosis was complex. Renal function was reduced in 92% of group III, and lactic acidosis was found in 36%. In this group hepatic function was most severely impaired, and 60% were hypotensive. These disturbances were not related to aetiology or treatment of the liver disease.
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PMID:Acid-base status in liver cirrhosis. Disturbances in stable, terminal and portal-caval shunted patients. 127 3

Eighty unselected cases of hyponatremia complicating liver cirrhosis were analysed. Of these cases, 20 had sodium levels less than 135 mmol/L, 48 less than or equal to 130 mmol/L and 12 less than or equal to 125 mmol/L. 5 cases developed acute hyponatremic syndrome after abdominal paracentesis and high-dose of diuretics. Of these 5 cases, 1 died and 4 recovered after immediate infusion of 3% sodium chloride (200-300 ml/d intravenously for 7-10 days). Both the crystal and colloid pressure of blood determined in 10 cases were less than normal. The sodium level of the ascitic fluid determined in 5 cases was higher than that of serum. Respiratory alkalosis complicated with metabolic alkalosis or acidosis were the main features of acid-base disorders. These might be due to alkalinizing agents therapy, infection and hepato-renal syndrome. Based on these clinical studies, it was shown that paracentesis and diuretics are the main causes of acute hyponatremic syndrome, so these measures should be taken carefully in patients with hyponatremic state previously, especially in patients with poor general, hepatic and renal conditions.
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PMID:[Hyponatremia in patients with ascites complicating liver cirrhosis]. 158 43


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