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PubMed2000

[A rapidly fatal case of severe falciparum malaria complicated with high-level metabolic acidosis].

A 67-year-old male was admitted with consciousness disturbance (JCS, III-200) after completing a 12-day tour to east Africa without malaria chemoprophylaxis. When he visited the hospital one day prior to the admission complaining of fever and a slightly sore throat, he did not mention the travel history. Soon after his travel history was revealed, blood films were prepared which showed abundant ring forms accompanied with a small number of trophozoites and schizonts of Plasmodium falciparum, with the parasitemia of 26%. Despite intravenous quinine infusion, first that of loading dose, his consciousness state (JCS, III-300), renal and hepatic functions and anemia (Hb, 5.8 g/dL) deteriorated progressively. Moreover, metabolic acidosis worsened with pH of 6.954, HCO3- of 3.4 mEq/L, BE of--27.0 mEq/L, PCO2 15.5 mmHg by arterial blood gas analysis, although he received a large volume of sodium bicarbonate solution. The patient died on the 4th day of his illness. According to the literature, it is suggested that the treatment of metabolic acidosis in severe faciparum malaria with sodium bicarbonate is sometimes harmful, since it can result in sodium overloading, which may then precipitate pulmonary edema/ARDS. However, alternative treatment regimens have not yet been established. Future investigation on the etiology and the proper treatment of metabolic acidosis associated with severe falciparum malaria is highly needed.

Acidosis↗
PubMed1985

Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis.

Lactic acidosis, a clinical syndrome caused by the accumulation of lactic acid, is characterized by lactate concentration in blood greater than 5 mM. Therapy usually consists of intravenous sodium bicarbonate (NaHCO3), but resultant mortality is greater than 60 percent. The metabolic and systemic effects of NaHCO3 therapy of hypoxic lactic acidosis in dogs were studied and compared to the effects of sodium chloride or no therapy. Sodium bicarbonate elevated blood lactate concentrations to a greater extent than did either sodium chloride or no treatment. Despite the infusion of NaHCO3, both arterial pH and bicarbonate concentration decreased by a similar amount in all three groups of dogs. Additional detrimental effects of NaHCO3 were observed on the cardiovascular system, including decreases in cardiac output and blood pressure that were not observed with either sodium chloride or no treatment. Thus there is evidence for a harmful effect of NaHCO3 in the treatment of hypoxic lactic acidosis.

Acidosis↗
PubMed1988

Effects of the ionophores monensin and tetronasin on simulated development of ruminal lactic acidosis in vitro.

A continuous coculture of four ruminal bacteria, Megasphaera elsdenii, Selenomonas ruminantium, Streptococcus bovis, and Lactobacillus sp. strain LB17, was used to study the effects of the ionophores monensin and tetronasin on the changes in ruminal microbial ecology that occur during the onset of lactic acidosis. In control incubations, the system simulated the development of lactic acidosis in vivo, with an initial overgrowth of S. bovis when an excess of glucose was added to the fermentor. Lactobacillus sp. strain LB17 subsequently became dominant as pH fell and lactate concentration rose. Both ionophores were able to prevent the accumulation of lactic acid and maintain a healthy non-lactate-producing bacterial population when added at the same time as an excess of glucose. Tetronasin was more potent in this respect than monensin. When tetronasin was added to the culture 24 h after glucose, the proliferation of lactobacilli was reversed and a non-lactate-producing bacterial population developed, with an associated drop in lactate concentration in the fermentor. Rises in culture pH and volatile fatty acid concentrations accompanied these changes. Monensin was unable to suppress the growth of lactobacilli; therefore, in contrast to tetronasin, monensin added 24 h after the addition of glucose failed to reverse the acidosis. Numbers of lactobacilli and lactate concentrations remained high, whereas pH and volatile fatty acid concentrations were low.

Acidosis, Lactic↗
PubMed1980

D-Lactic acidosis in a boy with short bowel syndrome.

Metabolic acidosis in a 3-year-old child with short bowel syndrome led to the discovery of massive D-lactic aciduria. After normalisation of the intestinal bacterial flora, D-lactate disappeared together with the acidosis. Dysbacteriosis with excessive production of D-lactate by intestinal bacteria (unidentified) and subsequent absorption explains this unusual cause of metabolic acidosis.

Acidosis↗
PubMed1980

Renal tubular acidosis and nerve deafness.

Two brothers are described with renal tubular acidosis and nerve deafness: the elder also had rickets and hypokalaemia. The parents were unaffected. Studies of urinary acidification and bicarbonate excretion were consistent with a distal tubular abnormality. This report strengthens the view previously proposed in similar cases that nerve deafness and renal tubular acidosis constitute a genetic entity. Examination for nerve deafness is indicated in any child with renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed1977

Metabolic acidosis and infant feeding.

Most cows' milk based formulae for infant feeding present a greater acid load to the infant than breast milk. To determine the effect of this difference the acid base state of 180 healthy term infants was measured on the sixth day of life and related to the type of feed. Those infants fed on cows' milk formula (SMA) had a mean pH of 7-34 +/- 0-05 and a base deficit of 8-8 +/- 3-1, while those fed on breast milk had a mean pH of 7-38 +/- 0-05 and a base deficit of 5-6 +/- 3-1. The difference between the two groups of infants was significant for both these measurements. Metabolic acidosis was defined as a base deficit greater than 10 mmol/l. Seventy-four per cent of the 34 infants who were acidotic at six days were bottle-fed. There was a significant correlation between the pH of the feed and the degree of acidosis in the infant as measured by the base deficit. The findings suggest that when breast milk is not available a pH-adjusted milk formula would be desirable for preventing and treating neonatal metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1970

Fibrosing alveolitis associated with renal tubular acidosis.

The discovery of a case of renal tubular acidosis and fibrosing alveolitis led to the investigation of 19 further patients. Abnormal pulmonary function tests were found in a further four patients with overt renal tubular acidosis and in four out of eight patients with "incomplete" renal tubular acidosis. The response to an ammonium chloride test in seven patients with cryptogenic fibrosing alveolitis was normal. Those patients with a defect of both renal acidification and pulmonary gas transfer had concurrent autoimmune diseases such as Sjögren's syndrome and primary biliary cirrhosis. It is suggested that the renal and pulmonary abnormalities may be part of a systemic disorder capable of affecting many organs. Moreover, hyperglobulinaemia and autoantibodies in these patients further suggests that immunological mechanisms are concerned in the pathogenesis of these abnormalities.

Acidosis, Renal Tubular↗
PubMed1975

Lactic acidosis complicating treatment of ketosis of labour.

Hypertonic glucose, fructose, and sorbitol solutions were given intravenously to women in the first stage of labour who had ketonuria and ketonaemia as evidenced by a raised blood acetoacetate and 3-hydrosybutyrate. There was no difference in the antiketogenic action of these, which was rapid and effective, but when compared with a control group who were given normal saline they had a high incidence of hyperlactataemia, and nine out of 28 patients developed lactic acidosis after the infusions. The "lactatogenic" effect was shared by all three substrates, and when they are used in the treatment of ketosis of labour, and the mother develops lactic acidosis, they might exacerbate pre-existing lactic acidosis and precipitate fetal distress.

Acetoacetates↗
PubMed2002

Recovery from pH 6.38: lactic acidosis complicated by hypothermia.

Survival after extreme arterial acidosis is uncommon. A case of metformin induced lactic acidosis is described where the presenting pH was 6.38 exacerbated by hypothermia (29 degrees C). Increased anion gap acidosis, its varied aetiology, potential reversibility, and the role of hypothermia are discussed. Early liaison with a medical toxicology unit is recommended when this rare condition is suspected.

Acidosis, Lactic↗
PubMed1998

Complement and contact activation in term neonates after fetal acidosis.

AIMS: To evaluate complement and contact activation after fetal acidosis. METHODS: Fifteen term neonates with hypoxic-ischaemic encephalopathy after umbilical arterial pH < 7.10 were compared with 15 healthy neonates with umbilical arterial pH > 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22-28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay. RESULTS: Median complement function (46 vs 73%), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 micrograms/l), C5a (5.0 vs 0.6 micrograms/l), and factor XIIa (3.2 vs 1.3 micrograms/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor. CONCLUSIONS: Complement and contact activation occurred in the newborns with hypoxic-ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.

Acidosis↗
PubMed1988

Lactic acidosis due to metformin therapy in a low risk patient.

A 55 year old diabetic women treated with chlorpropamide and metformin for three years presented with acute oliguric renal failure and lactic acidosis from which she died. The plasma metformin level was very high suggesting that the lactic acidosis was caused by the drug. There were no contraindications to metformin therapy and renal function was normal three months previously. This case demonstrates that lactic acidosis can occur as a result of metformin therapy in the absence of pre-existing risk factors.

Acidosis, Lactic↗
PubMed1989

Severe, self-limiting lactic acidosis and rhabdomyolysis accompanying convulsions.

A 26 year old man with no previous history of convulsions presented in status epilepticus and severe lactic acidosis. He regained consciousness and the acidosis resolved after several hours of conservative management without intravenous bicarbonate, but he developed severe myalgia associated with marked elevation of creatine kinase and moderate raised plasma creatinine levels which resolved spontaneously after 3 days. Severe lactic acidosis and rhabdomyolysis may accompany status epilepticus, although they appear to be self-limiting without important sequelae.

Acidosis, Lactic↗
PubMed1986

Distal renal tubular acidosis in a cat with pyelonephritis.

A four-year-old castrated male domestic shorthair cat with recent onset of lethargy and depression was found to have hypokalaemia, low plasma bicarbonate concentration and a urine pH of 7. Subsequent findings of hyperchloraemic metabolic acidosis with failure to produce acid urine led to a diagnosis of distal renal tubular acidosis. Pyelonephritis associated with Escherichia coli infection of the urinary tract was also diagnosed. The urinary tract infection was eliminated by antibiotic treatment. For two years subsequently, the clinical effects of distal renal tubular acidosis have been controlled by oral administration of potassium bicarbonate, although some biochemical abnormalities have persisted.

Acidosis, Renal Tubular↗
PubMed1992

Ruminal lactic acidosis in sheep and goats.

The clinical findings in 37 sheep and goats with acute ruminal lactic acidosis included a disturbed general condition characterised by anorexia, apathy, teeth grinding and muscle twitching, ruminal stasis, and the excretion of soupy or watery faeces. The ruminal fluid of affected animals was milky, had a sour odour and a low pH. There was a predominance of Gram-positive bacteria in smears of ruminal fluid. In comparison with 10 control animals, the rumen fluid of 23 sheep with ruminal lactic acidosis had higher lactic acid and lower volatile fatty acid concentrations. In addition, the affected animals often had haemoconcentration and metabolic acidosis. Treatment included single or repeated transfer of ruminal fluid from healthy cows and, depending on the severity, the administration of antacids, yeast and chlortetracycline, and the intravenous infusion of isotonic sodium chloride and 5 per cent sodium bicarbonate solutions. Of the 37 treated sheep and goats, four died within 24 hours, and three others were euthanased after one, two and three days because their condition rapidly deteriorated. Thirty animals were discharged one to nine days after treatment. Twenty-nine of them (78.4 per cent) recovered completely but one was euthanased later.

Acetates↗
PubMed1993

Diagnosis and treatment of metabolic acidosis in calves: a field study.

The history and results of a clinical examination were recorded for 32 spring-born suckler calves which were hospitalised for intravenous fluid therapy. Blood samples were taken before treatment, during treatment and before discharge and analysed for colostral status, total carbon dioxide as an indication of acid-base status, and haematocrit. All the calves were given intravenously 5 to 10 litres of electrolyte solution containing 144 mmol/litre sodium, 4 mmol/litre potassium, 113 mmol/litre chloride and 35 mmol/litre bicarbonate, supplemented, in 24 calves, with up to 450 ml of 1M sodium bicarbonate. Nearly all the calves were recumbent but less than half were dehydrated on admission. The signs of dehydration were well correlated with each other and with the haematocrit. Neither the history nor the clinical signs were useful predictors of acidosis. There was no relationship between the severity of acidosis and the degree of dehydration. Acidosis was more prevalent in older calves (P < 0.01). For the severely acidotic calves, supplementary intravenous fluid with sodium bicarbonate significantly (P < 0.05) improved the total blood carbon dioxide at discharge. All 32 calves recovered. It is possible to treat acidotic calves with intravenous fluid therapy effectively, economically and according to their individual needs. The Harleco apparatus is a simple, useful, cost-effective adjunct to the diagnosis and treatment of this life-threatening condition.

Acidosis↗
PubMed1982

Role of acidosis in the protein wasting of fasting in the rat and the rabbit.

The purpose of these experiments was to determine if augmented renal ammoniagenesis in chronic metabolic acidosis could increase the negative nitrogen balance during prolonged fasting. To explore this question, rats and rabbits were fasted for up to 10 days because acidosis would markedly augment ammonium excretion in the rat but not in the rabbit. Since the ketoacidosis of fasting was mild in both species (less than 2 mM) and ketonuria virtually absent, a hydrochloric acid load was given to stimulate renal ammoniagenesis. Under these conditions, nitrogen balance was significantly more negative during acidosis in the rat but not in the rabbit. This increment in nitrogen excretion appeared as ammonium with no detectable difference in urea nitrogen excretion. Therefore, it appears that if more nitrogen is excreted as ammonium, net protein breakdown increases to furnish the substrate for ammoniagenesis rather than reducing the excretion of the other nitrogenous waste component urea. The implications of these findings will be discussed.

Acid-Base Equilibrium↗
PubMed1984

Pathogenesis and management of lactic acidosis.

This chapter reviews the current concepts concerning the pathogenesis and treatment of lactic acidosis. The biochemistry of lactic acidosis and the physiology of lactate homeostasis, particularly as it relates to interorgan lactate flux and the role of the liver, are stressed. Limitations of bicarbonate therapy and the potential benefits of a new drug, dichloroacetate, in the treatment of lactic acidosis are discussed.

Acidosis↗
PubMed2003

Polymodal regulation of hTREK1 by pH, arachidonic acid, and hypoxia: physiological impact in acidosis and alkalosis.

Expression of the human tandem P domain K+ channel, hTREK1, is limited almost exclusively to the central nervous system, where ambient Po2 can be as low as 20 Torr. We have previously shown that this level of hypoxia evokes a maximal inhibitory influence on recombinant hTREK1 and occludes the activation by arachidonic acid; this has cast doubt on the idea that TREK1 activation during brain ischemia could facilitate neuroprotection via hyperpolarizing neurons in which it is expressed. Using both whole cell and cell-attached patch-clamp configurations, we now show that the action of another potent TREK activator and ischemia-related event, intracellular acidification, is similarly without effect during compromised O2 availability. This occlusion is observed in either recording condition, and even the concerted actions of both arachidonic acid and intracellular acidosis are unable to activate hTREK1 during hypoxia. Conversely, intracellular alkalinization is a potent channel inhibitor, and hypoxia does not reverse this inhibition. However, increases in intracellular pH are unable to occlude either arachidonic acid activation or hypoxic inhibition. These data highlight two important points. First, during hypoxia, modulation of hTREK1 cannot be accomplished by parameters known to be perturbed in brain ischemia (increased extracellular fatty acids and intracellular acidification). Second, the mechanism of regulation by intracellular alkalinization is distinct from the overlapping structural requirements known to exist for regulation by arachidonic acid, membrane distortion, and acidosis. Thus it seems likely that hTREK1 regulation in the brain will be physiologically more relevant during alkalosis than during ischemia or acidosis.

Acidosis↗