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Failure to thrive and metabolic alkalosis. Adverse effects of a chloride-deficient formula in two infants.

This report concerns two infants with failure to thrive and hypochloremic metabolic alkalosis. Both infants were fed exclusively with a soybean-based formula, which, as a result of a manufacturing error, was severely deficient in chloride. When an alternative formula containing an adequate amount of chloride was prescribed, the electrolyte abnormality was corrected, and the infants resumed their normal weight gain.

Alkalosis↗

Primary metabolic alkalosis.

Primary metabolic alkalosis is a disorder caused by both precipitating and perpetuating mechanisms. Correction of the abnormality requires intervention at both levels. Diuretic therapy and prolonged nasogastric suctioning are the major precipitating events, while volume depletion is the most common aggravating factor. Treatment is directed toward correction of dehydration and removal of the precipitating cause when possible. If this does not suffice, hemodialysis with a high chloride dialysate, with or without hydrochloric acid infusion, is the treatment of choice.

Alkalosis↗

Alkalosis and hypomagnesaemia: unwanted effects of a low-calcium CAPD solution.

We studied 43 CAPD patients for 4 months during the change from a high-calcium dialysis fluid (Baxter PD1) to a low-calcium fluid (Baxter PD4), which also contained low magnesium (0.25 mmol/l) and high lactate concentrations (40 mmol/l). Serum calcium fell significantly as did the incidence of hypercalcaemia, whilst the proportion of patients taking calcium-containing phosphate binders increased. There was a non-significant increase in serum i-PTH levels but the proportion with i-PTH > 150 pg/ml (normal range 10-65 pg/ml) increased significantly. There was a significant fall in serum magnesium level and seven patients developed hypomagnesaemia. Serum bicarbonate increased significantly and progressively and 17 patients were alkalotic at 4 months, five severely (bicarbonate 35-40 mmol/l). One patient developed recurrent episodes of painful subcutaneous and periarticular calcification, which may have been related to the alkalosis. Initial serum bicarbonate levels correlated significantly with dialysis adequacy assessed by daily Kt/V (r = 0.458, P = 0.002). The relationship to adequacy was abolished during the period of use of the high-lactate dialysis fluid. Use of low-magnesium CAPD fluids must be supported by regular monitoring of serum magnesium levels. The high lactate concentration in such fluids may not be appropriate and is potentially hazardous when individualization of dialysis dose demands the use of relatively high exchange volumes. Low serum bicarbonate levels in CAPD patients reflect inadequate dialysis, which use of these fluids serves to mask.

Adult↗

Evaluation of abomasal outflow diversion as an experimental model of hypochloremic, hypokalemic metabolic alkalosis in lactating cows.

Four adult, lactating dairy cows were subjected to diversion (loss) of gastric contents through a T-shaped cannula placed in the cranial part of the duodenum just distal to the pylorus. Diversion was continued for 10 to 12 hours, at which point the cows were very weak and depressed. The volume of effluent during this period ranged from 37.3 to 46.8 L, with the largest volume being produced during the first four hours. All cows became dehydrated, with mean packed cell volume and total plasma protein concentration increasing 30% and 19.6%, respectively, but with only a slight increase in plasma creatinine concentration. Plasma Cl- concentrations decreased from a mean of 97.3 mEq/L at the beginning of diversion to a mean of 87.2 mEq/L at eight hours. This was followed by a plateau or slight increase in concentrations over the final hours of diversion. Plasma K+ concentration followed a similar pattern, decreasing from a mean of 3.9 mEq/L to a mean of 2.94 mEq/L at six hours, followed by increasing values until termination of diversion. No changes in plasma Na+ concentration were noted, except for a mild decrease in one cow. Plasma calcium concentrations decreased significantly, reaching 6.6 +/- 0.6 mEq/L at the end of diversion. Venous pH, plasma HCO3- concentration, and plasma base excess concentration increased during the first four to eight hours of diversion, followed by a gradual decline. Although a mild hypochloremic metabolic alkalosis resulted from diversion of abomasal outflow in all cows, substantiated by a mild increase in plasma strong ion difference, the changes observed were not as great as expected.(ABSTRACT TRUNCATED AT 250 WORDS)

Abomasum↗

Severe acute metabolic alkalosis.

We have presented the case of a 34 year old male patient who was admitted with severe metabolic alkalosis (MA). Peak serum HCO3 was 96 mg/dl and compensatory PCO2 was 95 which, to our knowledge, has never been reported before in a patient with MA. MA was probably generated by consumption of high amount of NaHCO3 and renal impairment and maintained by impaired renal function due to volume depletion hypokalemia and hyochloremia. The patient was successfully treated with IV administration of saline and KCL.

Adult↗

[Chronic metabolic alkalosis in a newborn infant caused by congenital chloride diarrhea].

The case of a female preterm infant (gestational age 36 weeks) is described, who presented with abdominal distension, diarrhoea, dehydration and metabolic alkalosis at the fifth day of life. After different diagnostic tests had been performed, congenital chloride diarrhoea was suspected and chloride supplementation was started. However, this diagnosis could not be confirmed, until the measurement of electrolytes in faeces had been improved. Then, we found the typically elevated fecal chloride concentration (130-153 mmol/l) which exceeded the sum of the fecal concentration of sodium (64-90 mmol/l) and potassium (28-35 mmol/l). The chloride supplementation was increased to 6 mmol/kg/d NaCl and 2 mmol/kg/d KCl. The most recent examination at the age of 1 year revealed the girl to be in good clinical condition, with normal growth and psychomotor-development and with no evidence of renal impairment.

Alkalosis↗

Blood lactate and ammonia in short-term anaerobic work following induced alkalosis.

This study was designed to investigate the effect of an induced metabolic alkalosis on a 300 m sprinting time in six elite 400 m runners. The subjects competed as pairs, on two separate occasions, in a standard racing format, three hours after ingestion of either an alkaline (sodium citrate, 0.5 g.kg-1 body weight) or a placebo solution (calcium carbonate, 0.5 g.kg-1 body weight). The results showed that following alkaline ingestion mean sprinting time was not improved. Peak blood lactate during recovery was higher after sodium citrate administration than after placebo (19.88 +/- 2.09 vs 18.82 +/- 1.84 mmol.l-1, p < 0.01). No difference was observed in peak blood ammonia between the alkaline and placebo treatments (187.0 +/- 37.0 vs 188.8 +/- 49.0 mumol.l-1). The absence of effects on performance confirms that when exercise of short duration (30 to 40 s) is used, alkaline agents have minor or no effects on performance. The altered relationship observed between blood lactate and ammonia under placebo and buffering loading conditions suggests that the regulation of lactate and ammonia metabolism is unrelated.

Adult↗

[Renovascular hypertension due to unilateral renal artery stenosis with hypokalemic alkalosis, the salt-losing syndrome and reversible hyperechogenicity of the contralateral kidney. A study of 2 infants].

This report describes two infants with severe arterial hypertension secondary to unilateral renal artery stenosis which was manifested by polyuria, polydipsia, hypokalemic alkalosis, hyponatremia, increased natriuresis and increased plasma values of rennin and aldosterone. On sonographic examination, the contralateral non-stenotic kidney of both patients appeared enlarged and hyperechogenic mimicking parenchymal lesion. When the patients became normotensive, their sodium and potassium balance became normal and their contralateral non-stenotic kidney also became normal in size and echogenicity. The increase of the filtration and the natriuresis observed in the contralateral non-stenotic kidney of the patients with renovascular hypertension due to renal artery stenosis might be responsible for the hyperechogenicity. When the patients became normotensive, the filtration and excretion of sodium of the contralateral kidney also became normal and the increase of echogenicity also disappeared. The reversibility of the sonographic findings suggest a functional origin.

Alkalosis↗

[Postoperative respiratory alkalosis as a complication of neuroendoscopy].

Endoscopic neurosurgery is a minimally invasive technique that has been developing rapidly. It is mainly indicated for the treatment of hydrocephaly due to ventriculocisternostomy, biopsies of cerebral ventricular lesions, evacuation of cerebral hematomas and spinal surgery. Hemorrhage, infection and spinal fluid fistula are known complications. We report the appearance of symptomatic postoperative respiratory alkalosis in a patient who underwent ventriculocisternostomy by endoscopic neurosurgery. The underlying disease was obstructive hydrocephaly secondary to partial stenosis of the Silvius aqueduct.

Adult↗

[Metabolic alkalosis. Relation between bicarbonate load and the behavior of blood lactic acid in the light of the intra-erythrocyte indices of the acid-base balance].

The plasma an intra-erythrocyte acid-base balance in man was studied, along with blood pyruvate and lactate levels, in acute metabolic alkalosis induced by i.v. infusion of bicarbonate. It was found that the red cell offers a satisfactory expression of the phenomena that occur in the intracellular space. The bicarbonate ion has difficulty in crossing the red cell membrane, while the production of lactate is seen as a fundamental compensation mechanism for rapid buffering of the extra base.

Acid-Base Equilibrium↗

Hypercalcemia and alkalosis due to the milk-alkali syndrome: a case report and review.

At one time, when antacids were the primary medical means of treating peptic ulcer disease, the milk-alkali syndrome was not an uncommon cause of hypercalcemia. The simultaneous occurrence of hypercalcemia, alkalosis, and renal failure, in conjunction with the appropriate history of ingestion fof antacids, was suggestive of the syndrome. With the advent of antisecretory therapy, however, the milk-alkali syndrome has become an uncommon diagnosis. I report a case of milk-alkali syndrome and review the history of this syndrome as reported in the medical literature. Contemporary reports have focused on understanding the pathophysiology of the syndrome. Recent series have identified a shifting demographic profile, as increasing numbers of elderly women consume calcium carbonate as an anti-osteoporosis measure.

Aged↗

[Acid-base equilibrium of the arterial blood of subjects with grave hypercapnia subjected to mechanical ventilation with the iron lung (concerning 2 cases of post-hypercapnic alkalosis)].

Two cases of severe chronic respiratory insufficiency in severely acute phase with disturbances in acid base balance characterized by serious gaseous acidosis are reported. Therapy was based essentially on controlled ventilotherapy using an iron lung and considerable improvements were achieved clinically with practically total normalization of the acid base imbalance after only a few hours of treatment. In the following days, however, a picture of metabolic alkalosis established itself and this is discussed and interpreted as an expression of post-hypercapnic hypochloraemia.

Acid-Base Equilibrium↗

Alkalosis monitored by 31P NMR in a human glioma cell line exposed to the anti-tumor drug 1,3-bis(2-chloroethyl)-1-nitrosourea.

A transient alkalosis of similar magnitude to that observed in vivo has been observed using 31P NMR and 2-deoxy-D-glucose-6-phosphate as a pH marker in a human glioma cell line, SKI-1, with demonstrated sensitivity to 1,3-bis(2-chloroethyl)-1-nitrosourea. At an effective dose of 5 +/- 1 x 10 micrograms/ml, an increase of 0.13 +/- 0.05 pH units was observed within 4 +/- 1 x 10 min of introducing the drug into the perfusion chamber. Although the in vitro response is of a time course much faster than that in vivo, these results suggest that this immediate pH change could be an indicator of the cytotoxic action of the drug.

Carmustine↗

The influence of metabolic alkalosis upon exercise metabolism in the thoroughbred horse.

Six thoroughbred horses exercised on a motorised treadmill on two separate occasions at a speed of 11 or 12 m.s-1 for up to 2 min. 4 h prior to exercise each horse was given a 21 test solution of sodium bicarbonate (NaHCO3; 0.6 g.kg-1 body mass) or a control solution of water by nasogastric intubation, the order of administration of the two solutions was randomised. Blood samples (n = 15) were obtained before and during the 4 h after intubation, during exercise and for 30 min after exercise. NaHCO3 ingestion resulted in changes in pre-exercise acid-base status. The changes in blood lactate and base excess with exercise were greater after NaHCO3 administration; after 1 min of exercise in the case of lactate (P less than 0.05) and immediately after exercise in the case of base excess (P less than 0.05). Plasma ammonia levels were lower during (P less than 0.05) and immediately after (P less than 0.05) exercise following NaHCO3 ingestion. The peak change in plasma ammonia with exercise was also lower after NaHCO3 ingestion (P less than 0.05). Following exercise after NaHCO3 ingestion, five horses demonstrated lower muscle adenosine 5-triphosphate loss (P less than 0.05) and inosine 5-monophosphate formation (P = 0.05) and higher glycerol 3-phosphate formation (P less than 0.05). There is evidence to suggest that metabolic alkalosis may delay the onset of fatigue by decreasing the extent of adenine nucleotide loss during high-intensity exercise.

Acid-Base Equilibrium↗

Metabolic alkalosis during immobilization in monkeys (M. nemestrina).

We studied the systemic and renal acid-base response of monkeys during ten weeks of immobilization. By three weeks of immobilization, arterial pH and bicarbonate concentrations were elevated (chronic metabolic alkalosis). Net urinary acid excretion increased in immobilized animals. Urinary bicarbonate excretion decreased during the first three weeks of immobilization, and then returned to control levels. Sustained increases in urinary ammonium excretion were seen throughout the time duration of immobilization. Neither potassium depletion nor hypokalemia was observed. Most parameters returned promptly to the normal range during the first week of recovery. Factors tentatively associated with changes in acid-base status of monkeys include contraction of extracellular fluid volume, retention of bicarbonate, increased acid excretion, and possible participation of extrarenal buffers.

Acid-Base Equilibrium↗

Gitelman's variant of Bartter's syndrome, inherited hypokalaemic alkalosis, is caused by mutations in the thiazide-sensitive Na-Cl cotransporter.

Maintenance of fluid and electrolyte homeostasis is critical for normal neuromuscular function. Bartter's syndrome is an autosomal recessive disease characterized by diverse abnormalities in electrolyte homeostasis including hypokalaemic metabolic alkalosis; Gitelman's syndrome represents the predominant subset of Bartter's patients having hypomagnesemia and hypocalciuria. We now demonstrate complete linkage of Gitelman's syndrome to the locus encoding the renal thiazide-sensitive Na-Cl cotransporter, and identify a wide variety of non-conservative mutations, consistent with loss of function alleles, in affected subjects. These findings demonstrate the molecular basis of Gitelman's syndrome. We speculate that these mutant alleles lead to reduced sodium chloride reabsorption in the more common heterozygotes, potentially protecting against development of hypertension.

Amino Acid Sequence↗

Cell alkalosis elevates cytosolic Ca2+ in rabbit resident alveolar macrophages.

Disruption of cellular acid-base status alters the host defence functions of alveolar macrophages (m phi). These pH effects might be mediated by pH-sensitive changes in the signalling pathways of the effector functions of m phi. The present study examined the effects of intracellular pH (pH(i)) on the free cytosolic calcium concentration ([Ca(2+)](i)), an important second messenger for cell functions. [Ca(2+)](i) and pH(i) of rabbit resident alveolar m phi were measured using fluorescent dyes. With extracellular pH (pH(o)) of 7.4, the steady-state pH(i) and [Ca(2+)](i) were approx. 7.14 and 123 nM respectively. Incubation at pH(o) 6.8 caused a sustained cytosolic acidosis, but did not affect [Ca(2+)](i). Likewise, [Ca(2+)](i) was unchanged when m phi at pH(o) 7.4 were acidified using bafilomycin A(1) or sodium propionate. In contrast, [Ca(2+)](i) was markedly sensitive to cytosolic alkalosis. Exposure to NH(4)Cl at pH(o) 7.4 caused transient increases in both pH(i) and [Ca(2+)](i). The Ca(2+) response was mediated by release of intracellular Ca(2+) from thapsigargin-sensitive stores and was potentiated by capacitative entry of extracellular Ca(2+). Incubation at high pH(o) values (>7.4) produced sustained increases in pH(i) and [Ca(2+)](i). The sustained elevation of [Ca(2+)](i) was consistent with pH-sensitive inhibition of plasma-membrane Ca(2+)-ATPase. The response to high pH(o) was unaffected by blockade of L-type or receptor-operated Ca(2+) channels with nifedipine or SKF-96365, and was independent of extracellular Na(+). The findings indicate that pH impacts cytosolic Ca(2+) homoeostasis at multiple levels. The data suggest that cellular acid-base status can influence Ca(2+)-dependent signalling events in resident alveolar m phi, especially during alkaline disruptions of pH(i).

Ammonium Chloride↗