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Sudden cardiopulmonary arrest due to a defective respiratory reflex is observed in diabetic patients. Impaired ventilatory response in diabetic patients to acute hypoxia or hypercapnia induced by the inhalation of an artificial gas has been reported. Little is known regarding the respiratory compensatory ability for mild to moderate metabolic acidosis due to renal failure in insulin-dependent diabetic subjects. Arterial blood pH, HCO3-, PaCO2 and PaO2 were measured in 13 insulin-dependent diabetic subjects with advanced nephropathy and in 33 non-diabetic subjects with end-stage renal failure. The diabetic group consisted of six predialysis patients and seven on regular hemodialysis (HD) and the non-diabetic group, ten predialysis patients and 23 on HD. Differences between measured partial arterial pressure of carbon dioxide (PaCO2) and predicted PaCO2 determined from HCO3- were examined. PaCO2 was significantly higher in the diabetic than in non-diabetic group (40.0 +/- 7.4 versus 31.1 +/- 5.1 mmHg, p < 0.05 in predialysis, 42.0 +/- 6.4 versus 36.0 +/- 2.6 mmHg, p < 0.05 in HD), though plasma pH was essentially the same for either. Differences in measured PaCO2 and predicted PaCO2 were significantly larger in the diabetic group than in non-diabetic group. Ventilatory response to uremic acidosis may thus be considered impaired in subjects with advanced diabetic nephropathy.
In five members of three generations in a family studied in 1972, 3 nephrological disorders occurred concurrently: distal renal tubular acidosis (dRTA), polycystic kidney and nephrogenic diabetes insipidus (with the exception of a five-year-old child in whom polycystic kidney was not detectable--yet?). Chromosoma studies revealed an increased rate of the occurrence of variations. The youngest patient was reinvestigated in 1993; the other four affected members of the family were already not alive. 7 offsprings in two generations of the 3 healthy members of the third "patient generation" were healthy. The autosomal dominant way of inheritance characteristic to both dRTA and polycystic kidney disease was obvious in this family. On the other hand the same degree of the concentrating defect found both in the patients of the familial dRTA and in 11 control patients with non familial (acquired) dRTA suggested that the nephrogenic diabetes insipidus as an acquired disorder was associated with the two congenital abnormalities. The clinical picture of the combined disease was dominated by the symptoms of polydipsia and polyuria. The vasopressin resistance with a variation in the degree interindividually seemed to be responsible for the nephrogenic diabetes insipidus. Functional insufficiency of the loop of Henle was excluded on the basis of normal responses to a "loop diuretic".
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All patients admitted with severe lactic acidosis to a university teaching hospital during a 17-month period were taking phenformin hydrochloride. Serum phenformin concentration was measured in one patient and found to be four to nine times the usual therapeutic concentration. Prerenal azotemia was present at the time of admission in all but one of these patients, but renal function was normal at the time of discharge in those patients with phenformin-associated lactic acidosis who survived. Phenformin-associated lactic acidosis accounted for 7% of the episodes of metabolic acidosis and 27% of deaths due to metabolic acidosis in diabetics.
Transitory blindness is described in a diabetic patient with typical ethanol- and phenethylbiguanide induced lactic acidosis. The blindness developed in the course of 8 hours, but the vision returned during treatment with iv bicarbonate, insulin and glucose. The condition is discussed in relation to a presumed inhibition of the oxidative metabolism in the retina.
A survey of the literature leads to the conclusion that lactic acidosis should be considered as a side effect of therapy with biguanides. Essential for the development of lactic acidosis seems to be the preexistence or the acute development of renal insufficiency. However, the over-dosage (for instance in the case of attempted suicide) causes acidosis (lactic acidosis) in healthy persons also. Using the experimental animal lactic acidosis is demonstrated following biguanide application. Diagnosis of lactic acidosis is substantiated by acidosis with lactic acid concentrations higher than 8-10 meq/l (= 72-90mg/100 ml) and with considerably increased lactate/pyruvate ratios (50-150). Generally a non ketotic acidosis of diabetic patients (especially under biguanide-therapy) should be considered to be a lactic acidosis. On the other hand the existence of lactic acid concentrations higher than 8-10 meq/l ist characteristic for a lactic acidosis. The prognosis of lactic acidosis induced by biguanides is not too good. Therapy of the acidosis using bicarbonate is not sufficient in most cases. The intravenous application of glucose (or glucose substitutes), perhaps with additional insulin, might be indicated by hypoglycemia. However, this therapy might cause an additional increase in lactic acid concentration. Treatment of choice might be dialysis, effecting the elimination of the biguanides. If peritoneal dialysis is performed acetate containing solutions should be used. Biguanide induced lactic acidosis is prevented by a very cautious selection of patients suited for biguanide therapy. The performance of renal function tests is absolutely necessary if therapy with biguanides is intended. Additionally, periodical control of renal function is required in patients treated with biguanides (at least twice a year). Biguanide therapy should be performed only with extreme caution, because decrease in renal function is very common in older patients.
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Acid-base derangements are encountered frequently in clinical practice and many have life-threatening implications. Treatment is dependent on correctly identifying the acid-base disorder and, whenever possible, repairing the underlying causal process. Bicarbonate is the agent of choice for the treatment of acute metabolic acidosis. Controversy surrounds the use of alkali therapy in lactic acidosis and diabetic ketoacidosis, but bicarbonate should clearly be administered for severe acidosis. In most patients with mild to moderate chloride-responsive metabolic alkalosis, providing an adequate amount of a chloride salt will restore acid-base balance to normal over a matter of days. In contrast, therapy of the chloride-resistant metabolic alkalosis is best directed at the underlying disease. When alkalemia is severe, administering hydrochloric acid or a hydrochloric acid precursor may be necessary. Treatment of respiratory acidosis should be targeted at restoring ventilation; alkali should be administered only for superimposed metabolic acidosis. The therapy of respiratory alkalosis is centred on reversal of the root cause; short of this goal, there is no effective treatment of primary hypocapnia. The coexistence of more than one acid-base disorder (i.e. a mixed disorder) is not uncommon. When plasma bicarbonate concentration and arterial carbon dioxide tension (paCO2) are altered in opposite directions, extreme shifts in pH may occur. In such cases, it is imperative that the nature of the disturbance is identified early and therapy directed at both disorders.
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We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.
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