A case of recurrent renal failure associated with metabolic alkalosis induced by protracted vomiting

We describe a case of recurrent deterioration of renal function in a 54-year-old man who was found to have metabolic alkalosis, with a maximum PaCO₂ of 73.9 mmHg and a bicarbonate concentration of 55.3 mmol/l. He had a gradual exacerbation of nausea and vomiting due to atrophic gastritis, with a scarred, deformed pyloric part of the stomach and a duodenal bulb secondary to chronic peptic ulcer. His metabolic alkalosis and deteriorated renal function were corrected by intravenous saline with or without potassium chloride. However, his recovered creatinine clearance was at most 60 l/day (41.6 ml/min). A renal biopsy revealed cellular infiltration of mononuclear cells and atrophic change in the tubulointerstitium, suggesting chronic interstitial nephritis. Latent renal insufficiency and dehydration induced by protracted vomiting may easily induce a rapid and recurrent deterioration of renal function, and control of vomiting seemed to be the cardinal measure. Initially, his nausea and vomiting seemed to be successfully controlled by medication, however, they later became persistent and surgical correction of the stomach was carried out. Postoperative recovery was smooth, and the patient's vomiting and recurrent deterioration of renal function finally settled.     

Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman

The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. Triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course.     

Hypokalemic alkalosis in patients with pyloroduodenal stenosis

The work presents an analysis of results of examinations and treatment of 56 patients with Darrow hypokalemic alkalosis resulting from stenosis of the pylorus. In 45 of them the stenosis was caused by ulcer disease of the stomach and duodenum. The timely diagnosis, admission to the hospital and adequate therapy in 53 patients facilitated successful surgical interventions. In 3 patients the therapy was ineffective.     

A case of the milk-alkali syndrome with a small amount of milk and magnesium oxide ingestion--the contribution of sustained metabolic alkalosis induced by hypertonic dehydration

We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.     

A mixed acid-base disorder revealing a cystic dystrophy of aberrant pancreatic tissue

We report about a patient presenting with a mixed acid-base disorder. His blood gas analysis showed a metabolic acidosis caused by renal failure and lactic acidosis combined with a hypochloraemic alkalosis. The underlying pathology was a cystic dystrophy of aberrant pancreatic tissue leading to excessive vomiting, extracellular dehydration with a renal failure and hypochloraemia.     

Cystic fibrosis presenting as metabolic alkalosis in a boy with the rare D579G mutation.

We report on a 10-month-old boy with hypotonic dehydration and metabolic alkalosis. Sweat test was borderline and genetic analysis was negative for common mutations. Analysis of the whole coding regions of the CFTR gene revealed the rare mutation D579G in homozygosity.     

Vagotomy in perforated duodenal ulcers complicated by peritonitis

Perforated ulcers of the duodenum complicated by peritonitis, its terminal phases excluded, should be treated by the same radical surgical interventions as other complications of the disease. The intervention must consist of vagotomy and draining operations on the stomach, its risk being not higher than risk of palliative operation of suturing the perforation.     

Carbon Dioxide Elimination after Acetazolamide in Patients with Chronic Obstructive Pulmonary Disease and Metabolic Alkalosis

Acetazolamide, an inhibitor of carbonic anhydrase, which catalyzes hydration/dehydration of carbon dioxide, has been used for correction of metabolic alkalosis in patients with chronic obstructive pulmonary disease (COPD). Animal experiments have shown that the gradient between tissue and the alveolar CO2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO2. In order to determine the true degree of carbon dioxide retention after total inhibition of carbonic anhydrase, 10 patients with COPD and pronounced metabolic alkalosis (base excess above 6) under controlled mechanical ventilation were studied. The study showed that there was a statistically significant increase in tissue PCO2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that PaO2 and PVO2 increased significantly after inhibition of carbonic anhydrase, which could, at least partly, explain the improvement seen in patients with COPD and metabolic alkalosis after treatment with acetazolamide.     

Nature of metabolic alkalosis in the postoperative period in patients with pulmonary tuberculosis]

Sixty five patients with pulmonary tuberculosis subjected to extensive and traumatic surgical interventions were investigated. Metabolic alkalosis to the end of the 1st--2d postoperative day would develop in patients, who showed acid-base balance disorders toward acid aspect during the operation. In the mechanism of development of a grave decompensated postoperative metabolic alkalosis the role of a trigger factor is played by a massive intraoperative blood loss with marked hemodynamic disturbances in the immediate postoperative period.     

Neonatal Bartter syndrome

A pre-term baby girl was born following a pregnancy complicated by severe polyhydramnios at a gestational age of 36 weeks. She was initially suffering from respiratory distress consistent with idiopathic respiratory distress syndrome, and altered electrolyte imbalance with hyponatremia, hypokalemia and hypochloremic metabolic alkalosis. However, during the third week of life when she had dehydration along with significant electrolyte imbalance, Bartter's syndrome was considered which was supported by findings of high renin and aldosterone levels. Treatment was done by correction of electrolytes and dehydration along with indomethacin. The drug was well tolerated. The infant showed correction of electrolyte imbalance. The features of this case suggest an extreme form of Bartter's syndrome presenting from the early days of life. The syndrome is reported because of it's rarity and alerts pediatricians to the antenatal and neonatal variant of Bartter's syndrome.     

Omeprazole in post-gastrocystoplasty metabolic alkalosis and aciduria.

The use of segments of stomach for bladder augmentation is gaining popularity in pediatric urology due to favorable muscular and secretory properties. However, in a renal failure patient who underwent gastrocystoplasty a high level of acid production within the bladder associated with persistent hypergastrinemia was noted leading to severe systemic metabolic alkalosis. This condition was unresponsive to standard acid-inhibiting or neutralizing therapies but it was treated successfully with omeprazole, a proton-pump inhibitor recently introduced for treatment of peptic ulcer disease.     

Experience in the surgical treatment of patients with cancer of the proximal stomach

The results of surgical treatment of 116 patients with cancer of the proximal part of the stomach are analysed; in 63 of the patients the tumor had spread to the esophagus. Combined gastrectomy was performed in 87 patients, combined proximal resection of the stomach--in 2 patients. In 73 patients the operation was carried out through a transperitoneal approach. The authors describe an original method of compression esophago-intestinal anastomosis established through a transperitoneal approach with a suturing apparatus of their design. The operation was performed on 14 patients. Comparative analysis of the results of surgical treatment with the use of different methods for creating the anastomosis allows the suggested method to be recommended when a transpleural approach is contraindicated.     

Postoperative metabolic alkalosis following general surgery: Its incidence and possible etiology

A prospective clinical study was performed on 293 patients, in order to elucidate the abnormalities in acid-base balance following general surgery. Six arterial blood gas and pH determinations were taken from each patient before surgery and on postoperative days zero, one, three, five and seven. A total of 1699 determinations were obtained. Although the majority of patients (87.5 per cent) had a normal acid-base balance before surgery, a postoperative metabolic alkalosis was seen in 50.5 per cent of the patients. However, there was an extremely low incidence of other postoperative acid-base abnormalities, apart from a transient increase in metabolic acidosis on the operative day. A significantly high mortality rate (32.3 per cent) was observed in 31 patients who had continuous metabolic alkalosis during the postoperative period. An excessive bicarbonate load resulting from the administration of fresh frozen plasma following surgery was strongly suggested as one of the major causes of postoperative metabolic alkalosis. Further investigation is required to elucidate the mechanism of the generation of metabolic alkalosis induced by the postoperative bicarbonate load in surgical patients.     

Metabolic alkalosis after pediatric cardiac surgery.

OBJECTIVE: To determine occurrence, causes and associated mortality of postoperative metabolic alkalosis in pediatric cardiac surgery. METHODS: We retrospectively analyzed clinical and biochemical variables of 186 consecutive cardiac operations other than ductal ligations on children less than 2 years old during the years 1999 and 2000. Metabolic alkalosis was defined as a pH>7.48 corrected for PCO2, with a base excess > or =5 on two or more consecutive measurements during an 8h period. RESULTS: Median age was 15 weeks [range 2 days-95 weeks] and median weight 4.5 kg [range 2.1-15.7 kg]. In 157 cases, cardiopulmonary bypass was used. In 92 [49%] procedures, metabolic alkalosis occurred with the highest corrected pH 24.3h after operation. Multivariate regression analysis associated age [P<0.001], cardiopulmonary bypass [P<0.001] and preoperative ductal dependency [P=0.04] with postoperative metabolic alkalosis. Of the surgical procedures the arterial switch for transposition of the great arteries [n=19] was strongly associated with metabolic alkalosis [100%, P<0.001]. Hemodilution appeared to enhance the development of alkalosis: those who experienced alkalosis had been hemodiluted to a greater extent [P=0.007]. Nearly 95% of patients experienced some increase in bicarbonate, but patients with metabolic alkalosis experienced more than those without [5.9 versus 3.5 mmol/l, P<0.001]. There were four postoperative deaths, only one coincidental with metabolic alkalosis. CONCLUSIONS: Metabolic alkalosis has a high incidence after pediatric cardiac surgery, strongly associated with younger age, cardiopulmonary bypass, preoperative ductal dependency and perioperative hemodilution. Early recognition allows for timely therapeutic intervention.     

Severe episodes of extra cellular dehydration: an atypical adult presentation of cystic fibrosis

Cystic fibrosis (CF) is usually diagnosed during childhood by respiratory or gastro-intestinal symptoms. Hyponatremic hypochloremic dehydration with metabolic alkalosis is a rare but typical presentation of CF in infants. In contrast, only 3 cases have been described in adults. We report a case of CF in a 33-year-old Caucasian female presenting with a severe sodium and chloride depletion caused by inappropriate sweating. She experienced three episodes of severe dehydration before the diagnosis was suspected. Sweat chloride test was pathological and mild pulmonary involvement was found on CT scan. Delta F508 mutation and a rare mutation (3849+40 A/G) on the intron 19 of CFTR gene were found. Interestingly, our patient has a heterozygote twin sister, carrier of the same mutations of CFTR gene who also developed CF but with a different phenotype. We suspect modifier genes to be implicated in the differences observed between the two phenotypes. We discuss the physiopathology of electrolyte disturbance and review the other similar adults cases.     

Concealed administration of frusemide simulating Bartter syndrome in a 4.5-year-old boy

A 4.5-year-old boy was admitted to three different hospitals because of a tendency towards dehydration and polyuria, along with normal blood pressure, hypochloraemia, hypokalaemia, metabolic alkalosis and an impaired urinary concentrating ability. A renal biopsy failed to reveal juxtaglomerular hyperplasia. The clinical and laboratory findings failed to improve despite supplementation with potassium chloride and treatment with indomethacin. The urine was found to contain frusemide. The parents denied any drug administration to the boy. The child is now doing well more than 1 year after separation from his mother. Since ingestion of diuretic cannot be differentiated from true Bartter syndrome by blood and urinary electrolyte measurements alone, a diuretic screen is warranted in children with findings consistent with Bartter syndrome.     

Surgical treatment of ulcer disease in arterio-mesenterial compression of the duodenum

Experience in surgical treatment of 124 patients with gastric and duodenal ulcers associated with chronic duodenal obstruction due to arterio-mesenterial compression of the duodenum is analyzed. This combination occurred in 12% of all patients with ulcers over 20-year period. Special methods of examination were used for diagnosis: probe duodenography with duodeno-manometry, hepato-bili-scintigraphy. Differential approach to choice of surgical method was developed, and two original methods of surgery are presented: selective proximal vagotomy and resection of the stomach in combination with duodeno-jejuno-anastomosis. Long-term results were studied in 75 patients, and in 93% of them they were assessed as excellent and good. Quality of life of patients after surgery depends on severity of chronic duodenal insufficiency.     

Paradoxical reaction of intracellular pH values during therapy of acid-base imbalance with arginine hydrochloride

A well known complication following surgical intervention is metabolic alkalosis. In general this acid-base disturbance is treated in our intensive care units by application of arginine-hydrochloride. In an experimental study on rats in vivo we determined the influence of this substance on the acid-base status of the extra- and intracellular body compartment. It was found that the extracellular bicarbonate decreases but there is nearly no influence on intracellular buffering. The "mean whole body pHi", an overall estimate of the intracellular pH as complementary to the in vivo determined extracellular plasma pH, was determined with DMO (5,5-dimethyl-2,4-oxazolidinedione) and shown to increase significantly after application of arginine-HCl. From this result it is concluded that arginine-hydrochloride should no longer be used for clinical therapy of metabolic alkalosis.     

Hypocapnia prolongs bradycardia induced by bupivacaine or levobupivacaine in isolated rat hearts

Purpose: Systemic alkalinization is recommended for resuscitation from local anesthetic-induced cardiotoxicity. It has been suggested that inducing hypocapnic alkalosis, prior to exposure to toxic concentrations of local anesthetics, may minimize cardiotoxicity. However, it remains unclear whether inducing severe hypocapnic alkalosis after administration of local anesthetics will minimize the duration of bradycardia. We used isolated rat hearts to investigate the effects of hypocapnic alkalosis on heart rate (HR) recovery from bupivacaine or levobupivacaine-induced bradycardia. Methods: We measured the time required for the HR in 24 isolated rat hearts, respectively, to attain 90% of the baseline HR (recovery time) following bradycardia induced by 1µg·mL^?1 and 10µg·mL^?1 concentrations of either bupivacaine or levobupivacaine. Normal pH perfusate (bupivacaine or levobupivacaine with normal pH washout groups) or severe hypocapnic alkalosis perfusate (bupivacaine or levobupivacaine with hypocapnic alkalosis washout groups) were reperfused after exposure to the local anesthetics. Results: Severe hypocapnic alkalosis prolonged the recovery time from 273 ± 122 sec, at the 1µg·mL^?1 bupivacaine concentration with normal pH washout, to 1203 ± 540 sec, in the bupivacaine with hypocapnic alkalosis washout (P=0.029). Severe hypocapnic alkalosis also prolonged the recovery time from 1 153 ± 644 sec, at a 10µg·mL^?1 bupivacaine concentration in the normal pH washout group, to 2065 ±617 sec, in the bupivacaine with hypocapnic alkalosis washout group (P=0.032). With levobupivacaine 10µg·mL^?1 in the normal pH washout group, HR recovery time increased from 863 ± 186 sec to 1565 ± 567 sec, compared to the hypocapnic alkalosis washout group (P=0.045). Conclusions: Severe hypocapnic alkalosis prolonged the recovery time from bupivacaine or levobupivacaine-induced bradycardia in isolated rat hearts. When bradycardia occurs after intravascular bupivacaine or levobupivacaine administration, maintenance of normocapnia may minimize the duration of bradycardia.     

Anesthésie-réanimation des craniosténoses et dysmorphies craniofaciales de l'enfant

Craniosynostosis occurs in one out of 2,000 births. It results in primary skull deformations requiring surgical repair, in infants with a body weight of less than 10 kg. Pure craniosynostosis is the most frequent situation, where the risk for cerebral compression during brain development is the lowest. Therefore the aim of surgical correction in this case is mainly cosmetic. Conversely, in syndromic craniosynostosis, associated malformations are more common and cerebral, visual and respiratory consequences of complex facio-craniosynostosis are usually severe. Current surgical techniques consist of a total skull vault reconstruction which carry a high risk of sudden and major blood losses. Intraoperatively, whatever the type of craniosynostosis, mean blood losses corresponding to 90% of estimated red cell mass have to be anticipated. These blood losses vary according to the type of skull deformation and the type of surgery. Accurate evaluation is usually difficult and must be based more on calculation of red cell mass variations than on simple monitoring of surgical drainage. Invasive haemodynamic monitoring is always required. To reduce the amount of homologous blood transfusion, peroperative haemodilution seems to be the most suitable technique, due to unresolved technical difficulties in autotransfusion practice in infants. Severe facial deformities are associated with chronic hypoxaemia and cerebral compression representing major risk for these children in poor condition undergoing such major surgical procedures. With experienced teams, this high-risk surgery carries a low peroperative mortality (less than 1%) and morbidity rate. The latter includes essentially transient peroperative hypotension. The excellent final cosmetic and functional results justify the practice of this surgery in children with a bodyweight of less than 10 kg.