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PubMed1977

[Blood picture in lactate acidosis. Part 2: acid-base equilibrium and lactate].

A differentiation between lactate emia (lactic acid emia) and lactate acidosis (lactic acidosis) is made. The normal value for blood lactate concentration is 1-2 mmol/1. The term lactate emia is used for lactate values between 2-6 mmol/1. The limiting value for the diagnosis of lactate acidosis should be more than 7-8 mmol/1 for the blood lactate concentration. Furthermore the different buffer mechanisms are evaluated in respect to their influence on the pH of the blood and to lactate metabolism. Especially the mechanism of respiratory compensation for metabolic acidosis is discussed. It is stated that for the diagnosis of lactate acidosis the blood-pH and the bicarbonate concentration should be measured.

Acid-Base Equilibrium↗
PubMedDate not supplied

Congenital lactic acidosis in children--differential diagnosis in 44 cases.

The purpose of the study was differential diagnosis of lactic acidosis in 44 children aged from 2 weeks to 4 years. In all of them the lactate level in repeated determinations exceeded 27 mg/100 ml. From the point of view of clinical manifestations the children were divided into three groups: 26 with hepatomegaly and hypoglycaemia (I), 6 with ataxia and retardation of somatic development (II), 12 with mental retardation and muscular hypotonia (III). Together with basic biochemical studies other tests were done, if necessary, including glucose and alanine loading, lactate determination in cerebrospinal fluid, analysis of urinary organic acids by the GC-MS method, morphological examinations of muscle biopsy material, enzymatic determinations in liver biopsy material. In group I glycogenosis was suspected and its type was finally established after biochemical and enzymatic tests (types I, Ib, III, VI, VIa, XI). In one case fructose-1,6-diphosphatase deficiency was suspected. In group II the clinical manifestations resembled Leigh's syndrome. The tests demonstrated an inhibition of glucose formation from alanine, and lactate level in the cerebrospinal fluid was evidently raised above that in the serum. Gasometric index showed the presence of respiratory alkalosis with metabolic compensation rather than primary lactate acidosis. In group III, with considerable clinical variety of signs, in only nine out of 12 children the cause of lactate acidosis could have been established (pathological changes of mitochondria in 4 cases, secondary increase of lactate without pathogenetic importance in 4, and 3-hydroxy-3-methylglutaric acidosis in 1 case. In conclusion it is thought that this combination of diagnostic methods is useful in differential diagnosis of congenital lactate acidosis in children.

Acidosis, Lactic↗
PubMed1977

[Chronic metabolic acidosis in dairy cows].

Complex clinical and clinico-biochemical examination of the blood, urine and rumen liquor in a herd of dairy cows revealed chronical metabolic acidosis accompanied by rumen dysfunction and by a reduced butterfat content of milk. During the first examination of the acid-base state of the blood was almost at a standard level. An increased level of urea in blood plasma and a higher GOT transaminase activity testified to an excessive load on the liver. Urine pH was considerably deviated towards the acidic side and inorganic phosphorus was present in urine in a greater concentration. The pH of rumen liquor was slightly shifted towards alkalinity owing to the release of NH3 from urea in the food ration. The diagnosis--suspect chronical metabolic acidosis--was determined on the basis of the first examination. Chronical metabolic acidosis was definitely proved by the second examination when urea had been excluded from the feed ration. Repeated examinations revealed chronical metabolic acidosis which had originally been accompanied by a higher rumen liquor pH. On the basis of case histories and mechanisms of chronical acidosis, measures were proposed, resulting in an increase of the butterfat content of milk. Chronical metabolic disorders often follow a long-lasting latent pattern, manifesting themselves as a reduced milk yield and lower resistance; the clinical form of disease appears only at a later stage. The system of preventive diagnostics provides information on the changes in the composition of internal medium and of the faeces before a drop occurs in milk and fat production. These measures prevent metabolic disorders and high losses of produce which otherwise remain hidden for a long time.

Acidosis↗
PubMed1990

[Non-lactic metabolic acidosis].

The definition of metabolic acidosis (MA) is a primary decrease in plasma bicarbonate concentration. The visceral consequences are largely dependent on the degree of acidosis and the rapidity of its onset; they have been studied mainly in animal studies and therefore, extrapolation to the clinical situation should be cautious. The MA can be classified in two groups according to whether the anionic serum gap is increased or normal (hyperchloremic acidosis). The etiologies of the first group are lactic acidosis, the cetoacidoses and renal failure. The hyperchloremic acidoses usually result from gastro-intestinal bicarbonate losses; the biochemical diagnosis of rarer causes of hyperchloremic acidosis is facilitated by measuring the serum potassium, urinary pH and the urinary anionic gap. Although all causes of MA must be treated, the use of bicarbonate should be discussed in each individual case.

Acid-Base Equilibrium↗
PubMed1990

Severe metabolic acidosis and "muti" (traditional herbal medicine) ingestion in young children.

Twenty infants and young children admitted with severe metabolic acidosis and a positive history of 'muti' ingestion were investigated. All had accompanying gastroenteritis and significant dehydration. Biochemical data was diagnostic of high anion/gap metabolic acidosis in the majority (70 per cent). Further biochemical data indicated that lactic acidosis and pre-renal azotaemia resulting from severe hypovolaemia were likely causes of the high anion GAP metabolic acidosis. There was no evidence to suggest that the ingested muti per se was associated directly with the acidosis or acute renal failure seen in these children.

Acidosis, Lactic↗
PubMed1986

[Ruminal acidosis complex--new observations and experiences (2). A review].

By "Rumen acidosis" until recently only the acute indigestion with intoxication caused by excessive production of lactic acid was understood. Meanwhile, however, it has become evident that further pathologic changes can take place in the acid-base status of the rumen contents which may also be referred to as "Rumen acidosis". Basing on new literature and own experiences the paper gives a review of that "Rumen acidosis complex": Fundamentals of the regulation of pH in the rumen; chronic latent rumen acidosis (hyper- and parakeratosis, chronic hyperplastic rumenitis, rumenitis-liver abscess complex, hyperlipodeposition, low milk fat syndrome, atypical ketosis, chronic laminitis, cerebrocortical necrosis, acid-base metabolism); acute lactic acidosis (etiology, pathogenesis, therapy, prophylaxis).

Acid-Base Equilibrium↗
PubMed1988

Patterns of metabolic acidosis in patients with chronic renal failure: impact of hemodialysis.

The type of metabolic acidosis in patients with chronic renal failure was studied prospectively over a three-month period in 32 stable patients on chronic hemodialysis using acetate. All patients had pre-dialysis metabolic acidosis (mean TCO2 = 16.6 +/- 0.4 mEq/l, range 10 to 23 mEq/l). The patterns of metabolic acidosis were defined using the ratio: delta AG/delta TCO2 where delta AG is the increment in plasma anion gap above normal and delta TCO2 the decrement in plasma bicarbonate below normal. The group as a whole showed a mixed hyperchloremic and high anion gap pattern with a mean delta AG/delta TCO2 ratio of 53.3 +/- 7.1%. The individual distribution of patterns ranged from a pure hyperchloremic acidosis (24%) to a pure high anion gap acidosis (30%) with the mixed pattern being the most frequent (46%). An inverse correlation between the TCO2 change (y) during the dialysis procedure and the TCO2 (x) prevailing at the start of dialysis was found by linear regression analysis: y = -0.51x + 11, r = -0.54, p less than 0.01. Thus, before acetate conversion to bicarbonate was fully completed, patients gained bicarbonate during dialysis if TCO2 was less than 21 mEq/l and lost it when the pre-dialysis TCO2 was above this level. On average, the delta AG was reduced to a greater extent than the delta TCO2 so that the delta AG/delta TCO2 ratio fell significantly (from 53 +/- 7.1 to 11 +/- 8.8%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1985

[The rumen acidosis complex--recent knowledge and experiences (1). A review].

By "Rumen acidosis" until recently only the acute indigestion with intoxication caused by excessive production of lactic acid was understood. Meanwhile, however, it has become evident that further pathologic changes can take place in the acid-base status of the rumen contents which may also be referred to as "Rumen acidosis". Basing on new literature and own experiences the paper gives a review of that "Rumen acidosis complex": Fundamentals of the regulation of pH in the rumen; chronic latent rumen acidosis (hyper-and parakeratosis, chronic hyperplastic rumenitis, rumenitis-liver abscess complex, hyperlipodeposition, low milk fat syndrome, atypical ketosis, chronic laminitis, cerebrocortical necrosis, acid-base metabolism); acute lactic acidosis (etiology, pathogenesis, therapy, prophylaxis).

Acid-Base Equilibrium↗
PubMed1985

Acidosis in the vigorous newborn.

Simultaneous measurements of maternal arterial and umbilical cord blood pH, PCO2, and base deficit at delivery were studied in 168 live-born infants and their mothers. The correlations between maternal and umbilical parameters were highly significant (P less than .001) and were greater in vigorous than in depressed newborns. Mothers of vigorous acidotic infants had a lower pH and a higher base deficit than those of vigorous nonacidotic infants (P less than .001). However, the maternal-fetal differences were wider in the vigorous acidotic than in the vigorous nonacidotic newborns for all three parameters, and in both umbilical vein and umbilical artery (P less than .001). The data indicate that maternal acidosis accounts only partially for the acidosis observed at the time of delivery in the apparently normal fetus. With neonatal depression, the degree of acidosis is not dependent on maternal pH but on other factors. These factors may be influenced by maternal acidosis, but they are the major reasons for the neonatal depression, not the maternal acidosis.

Acidosis↗
PubMed1985

Anorexia nervosa, laxative abuse, hypopotassemia and distal renal tubular acidosis.

A case of anorexia nervosa in a 28-year-old woman with laxative abuse, hypopotassemia and severe metabolic acidosis, is described. The diagnosis of classical renal tubular acidosis, Type I, was confirmed by our inability to decrease urinary pH beyond 5.5 and to increase ammonia excretion during an ammonium chloride loading test. A bicarbonate loading test and normal plasma aldosterone with high renin activity excluded proximal renal tubular acidosis, hyporeninemic-hypoaldosteronemic renal tubular acidosis and Bartter's syndrome. The inability to increase ammonium excretion during severe metabolic acidosis following ammonium chloride loading did not favor the possibility of a transient physiological adaptation of ammoniagenesis at the tubular cell level, related to potassium depletion. Although mental disorder, laxative abuse, abstinence from food intake and severe potassium depletion intermingled in a vicious cycle, we assume that one of the following possibilities may explain the clinical presentation in our patient: either two separated and unrelated disorders, or laxative abuse as the cause of renal tubular acidification impairment.

Acidosis, Renal Tubular↗
PubMed1985

Significant metabolic acidosis induced by acetazolamide. Not a rare complication.

Blood gas and serum electrolyte levels were measured in 27 elderly patients (mean age +/- SD, 63.3 +/- 13.5 years) who were receiving acetazolamide (250 to 1,000 mg/day) for glaucoma. Eleven glaucomatous patients (mean age, 69.1 +/- 7.4 years) who were not receiving acetazolamide served as a control group. In the acetazolamide-treated group, four patients (14.8%) had mild acidosis (7.29 greater than pH less than or equal to 7.31), ten (37%) had moderate acidosis (7.20 greater than pH less than or equal to 7.29), and one patient (3.7%) had severe acidosis (pH, 7.15). None of the patients in the control group had acidosis. It is concluded that moderate metabolic acidosis of potential clinical significance is common among glaucomatous elderly patients who receive acetazolamide. The exact clinical significance of our observations is yet to be determined.

Acetazolamide↗
PubMed1980

[Urinary-blood delta PCO2 in renal tubular acidosis (author's transl)].

A state of renal tubular acidosis has been produced in rats by the administration of sodium maleate or acetazolamide (proximal tubular acidosis) and of lithium chloride of amiloride (distal tubular acidosis). During progressive alkaline diuresis, delta PCO2 (urine minus blood PCO2) increases significantly in rats presenting proximal tubular acidosis. Delta PCO2 is significantly depressed in rats presenting distal tubular acidosis. In well defined conditions of bicarbonate or phosphate excretion, delta PCO2 is a valuable index of distal ion secretion.

Acetazolamide↗
PubMedDate not supplied

[Renal disorders in cirrhotic patients: functional renal failure and metabolic acidosis (author's transl)].

A study of renal tubular acidification in two cirrhotic patients with functional renal failure and partly compensated metabolic acidosis. Unlike renal distal tubular acidosis, but alike what is seen in organic renal failure, renal acidification was nearly normal and could not account per se for the development of metabolic acidosis. The multiple cause of the association in the cirrhotic of hyperchloremia and hypobicarbonatemia are reviewed (respiratory alkalosis, metabolic acidosis due to renal failure, distal tubular acidosis) and the diagnostic procedures outlined.

Acidosis↗
PubMed1983

Renal tubular acidosis in a patient with recurrent metabolic alkalosis.

A 7-month-old infant with failure to thrive and recurrent episodes of vomiting and metabolic alkalosis was evaluated. Urine pH, serum bicarbonate, and urine PCO2-blood PCO2 studies were consistent with the diagnosis of distal renal tubular acidosis (RTA-type I). Analysis of serum potassium and chloride levels during periods of alkalosis and acidosis revealed that potassium depletion and hypochloremic volume contraction served to maintain the alkalotic state despite the presence of an underlying chronic acidosis. This case represents an unusual presentation for renal tubular acidosis and suggests that, under certain conditions, renal tubular acidosis may predispose to the maintenance of a metabolic alkalosis.

Acidosis, Renal Tubular↗
PubMed1982

[Studies on the mechanism of metabolic acidosis observed in the children treated with anticonvulsants].

Clinical and experimental studies were performed on the mechanisms of metabolic acidosis observed in the children with epilepsy who had long been treated with anticonvulsants such as phenobarbital (PB) or diphenylhydantoin (DPH). The effect of the anticonvulsants was studied on the erythrocyte carbonic anhydrase isozymes (CA-B and CA-C) and on the calcium ion metabolism. The results obtained were as follows: (1) Ten cases with metabolic acidosis were found in 37 cases of epilepsy (27%). Hypocalcemia and high alkaline phosphatase activity in the serum were observed in the acidotic cases. The specific activity of erythrocyte CA-B isozyme was significantly lower in the acidotic cases as compared to those in nonacidotic cases or normal individuals, suggesting that the metabolic acidosis may bring about an inhibition of this enzyme. (2) In vitro experiments were performed to further study the effect of DPH on the erythrocyte CA-B and CA-C. Incubation of the enzymes with DPH resulted in an inhibition of their activities. Affinity binding of DPH to the enzymes was studied using a gel filtration method. The binding of DPH was not replaced by the presence of salicylate, indicating that the binding is non-specific. The addition of ethylenediamine tetraacetic acid did not show any influence on the binding, suggesting that the binding is not chelate-bound with zinc ion which locates at the active center of the enzyme. The binding of DPH was not competitive with respect to acetazolamide which is known to have an affinity for the active center of the enzyme. These results suggest that the binding site of DPH for the enzyme is in the vicinity of its active center, however definitely different from those of acetazolamide. PB was supposed to behave in the same manner as DPH for carbonic anhydrases. (3) This study lead to the conclusion that a long term treatment with PB or DPH specifically inhibits the activity of carbonic anhydrases in erythrocytes. The inhibition of the enzyme activity may result in the metabolic acidosis. Imbalanced calcium ion metabolism was supposed to be induced by the acidosis. The considerable care is requisite for a long-term treatment of anticonvulsants.

Acidosis↗
PubMed1981

The adaptation of neonatal blood to metabolic acidosis and its effect on cisternal oxygen tension.

In eight newborn lambs, the adaption of blood to acidosis was studied by sequential measurements of P50 in vitro (pH 7.4; 37 degrees C) and P50 in vivo (animal's pH and temperature, 39 degrees C) during the course of HCl-induced metabolic acidosis. The benefit of the change in both P50 on tissue oxygen tension was studied by the change in O2 partial pressure at the level of the cisterna magna. Eight hr of acidosis caused a significant (P less than 0.01) decrease in P50 in vitro which fell from 29.0 to 24.4 torr. Nonetheless, because of pH effect on the hemoglobin affinity, the corresponding P50 in vivo was increased from 32.4 to 36.3 torr. This latter rise in the in vivo O2 affinity contributed to increase (P less than 0.01) the cisternal O2 tension. It is concluded that the hemoglobin of the newborn is capable of adaption to metabolic acidosis by displacing the in vivo O2 dissociation curve to the right favouring a greater unloading of O2 at the tissue level and thus preventing tissue hypoxia during metabolic acidosis.

Acidosis↗
PubMed1981

[Systemic and coronary haemodynamic effects of dobutamine and norepinephrine during metabolic acidosis].

The effects of clinical doses of dobutamine (5 microgram/kg x min) and norepinephrine (0.2 microgram/kg x min) on systemic haemodynamics and coronary circulation were studied during normal pH and during metabolic acidosis (pH 7.0) induced by hydrochloric acid in 9 anaesthetized closed chest dogs. Metabolic acidosis per se failed to show any significant depression of cardiac function, indicating that animals with intact sympathoadrenal system are highly resistant to acidaemia. Our results further demonstrated that a significant circulatory response to clinical doses of dobutamine and norepinephrine was still present during metabolic acidosis. However, the increase in cardiac output, max dp/dt and mean arterial pressure after dobutamine was found to be significantly reduced at low pH-values, whereas the vasopressor response to norepinephrine was not affected. From these results it may be speculated that metabolic acidosis differently influences the responsiveness of alpha- and beta-adrenergic receptors. Finally our results show that metabolic acidosis did not compromise the coronary adjustment to catecholamine-induced increases in myocardial oxygen demand.

Acidosis↗
PubMed1995

Proximal renal tubular acidosis secondary to FK506 in pediatric liver transplant patients.

We hereby report our experience with an index case of a pediatric liver transplant patient in whom FK506 administration was associated with the development of proximal renal tubular acidosis (RTA), as well the prevalence of acidosis and renal dysfunction in all pediatric liver transplant patients in our institution followed long term during a 6-year period. Data were grouped according to immunosuppressant regime: cyclosporine (CsA) only, FK506 only, or CsA with conversion to FK506. A 23-month-old female treated with FK506 after orthotopic liver transplantation (OLT) performed 15 months earlier presented with a 1-wk history of fever, watery diarrhea and metabolic acidosis. Although the acidosis did not improve following correction of her hydration status, administration of oral bicarbonate was effective. Discontinuation of this therapy resulted in acidosis. Since other indirect measurements of renal tubular function were normal, the patient was judged to have an isolated proximal RTA. In our group of pediatric liver transplant patients converted from CsA to FK506, FK506 administration was associated with a decline in serum bicarbonate (19 +/- 1 vs. 16 +/- 1 mEq/l, p < 0.02); neither blood urea nitrogen nor serum creatinine differed between the two groups. The number of rejection episodes/patient/month was comparable, allowing clinically relevant comparison of relative drug nephrotoxicities. We conclude that proximal RTA may be a relatively common treatable complication of FK506 administration in children.

Acidosis, Renal Tubular↗