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Solvent abuse in adolescents and young adults has been reported to cause a metabolic acidosis with a normal or increased anion gap (Streicher et al., 1981; Voights & Kaufman, 1983, Anonymous, 1988). We report a particularly severe clinical problem produced by the combination of toluene intoxication and diabetic ketoacidosis.
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To determine the respective role of metformin accumulation and tissue hypoxia in triggering metformin-associated lactic acidosis (MALA), we measured plasma (PM) and red blood cell (RM) metformin concentrations in 14 patients with MALA and in 58 diabetic patients on well-tolerated chronic metformin treatment. In this control group RM was 0.9 +/- 0.5 mg/l. In MALA, lactic acidosis was of comparable severity whether there was significant cellular metformin accumulation (9 patients with severe renal failure) or not (5 patients with less severe renal failure). Factors of hypoxia were found in all patients except three with isolated anuria and major metformin accumulation. Early mortality was low in patients with metformin accumulation (no rapid death with the exception of two patients with end-stage hepatic failure) whereas it was high in those with metformin accumulation (4 patients died rapidly). In conclusion, MALA is not always associated with metformin accumulation. The prognosis of MALA depends mainly not upon the degree of metformin accumulation but rather upon the severity of hypoxic factors.
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The aim of this study was to determine the characteristics of metformin elimination by dialysis. For this purpose we report the kinetic parameters during dialysis and the metformin clearance (i.e. dialysance) in four patients presenting with lactic acidosis which occurred on metformin therapy. We also studied metformin elimination in two chronically hemodialyzed diabetic patients inadvertently maintained on metformin therapy and in two chronically hemodialyzed non-diabetic patients who took a single dose of metformin before a dialysis session. Analysis of plasma concentration-time curves showed a biphasic pattern of metformin - elimination, according to a two-compartment model. We demonstrate that metformin may be removed even after reaching an equilibrium between blood and dialysate levels in a recirculating system, suggesting a storage of metformin in a deep compartment with a gradient of concentration between this compartment and the blood. Lastly, metformin dialysance appears satisfactory (68 ml/min) even in the case of relatively low blood flow; this value reached 170 ml/min under good hemodynamic conditions. In conclusion, hemodialysis efficiently removes metformin and corrects metabolic acidosis in patients with metformin-induced lactic acidosis.
Four cases of intravascular coagulation associated with a state of acidosis in diabetics were observed in 57 patients with diabetic acidosis and 19 with lactic acidosis, in a series of 112 cases of consumption coagulopathy admitted to a department of medical resuscitation. In three cases the coagulopathy was found only on investigation; in one there were clinical and anatomic signs. The coagulopathy may be found either during the phase of recovery from ketoacidosis, or during the course of severe lactic acidosis, particularly during a recurrence of this form of acidosis. In spite of the unfavorable outcome in 3 of the 4 cases, the abnormal findings of coagulopathy reverted toward normal along with successful metabolic corrections. The factors responsible for consumption coagulopathy are acidosis, collapse, generalised systemic reactions and alterations of platelet function, of coagulation, of the balance between fibrin deposition and lysis and of lipid levels, all characteristic of diabetes. The clinical effects of this coagulopathy seldom become apparent but provide a possible explanation of some of the complications of diabetic ketoacidosis, particularly certain hemorrhagic or thrombotic events, as well as certain visceral complications, especially those affecting renal, pulmonary and cerebral areas.
The evaluation of gastrointestinal symptoms in patients with diabetic acidosis frequently challenges the physician's clinical acumen. Faced with a seriously ill patient, he must judge whether the abdominal pain, nausea, or vomiting are a consequence of the metabolic decompensation, and hence likely to resolve with correction of the ketoacidosis, or if these symptoms signal a serious underlying intra-abdominal process (e.g., cholecystitis, appendicitis, etc.) which may have precipitated the development of ketoacidosis. The pathogenesis of the reversible gastrointestinal symptoms which frequently accompany diabetic acidosis has not been rigorously defined and may be multifactorial, involving metabolic, humoral, and neural processes. Careful attention to the medical history and abdominal examination greatly facilitates distinguishing patients with intra-abdominal pathology from those with reversible symptoms secondary to ketoacidosis. Similarly, the judicious use of laboratory tests (electrocardiography, blood counts, urinalysis, serum enzyme profile, and abdominal roentgenograms) materially aids in differential diagnosis. Finally, clinical suspicion of an acute abdominal process should prompt early surgical consultation and, if required, surgical intervention as the acidosis is being brought under control.
BACKGROUND/AIMS: The aim of this study was to examine a plausible correlation between venous and arterial blood gas values in acidotic patients with chronic uremia or diabetic ketoacidosis (DKA). METHODS: A total of 152 arterial and 152 venous blood samples from uremic patients (n = 100), DKA patients (n = 21) and healthy controls (n = 31) were analyzed for measurements of blood gas and acid-base status. RESULTS: The means of arterial and venous pH, and arterial and venous HCO(-)(3) values for the uremic patients were 7. 17 +/- 0.14, 7.13 +/- 0.14, 10.13 +/- 4.26 and 11.86 +/- 4.23 mmol/l, respectively. The respective mean differences between arterial and venous pH values and arterial and venous HCO(-)(3) values were 0.04 +/- 0.02 and -1.72 +/- 0.42 mmol/l, respectively, for these patients. The means of the laboratory findings of DKA patients were arterial pH, 7.15 +/- 0.15; venous pH, 7.10 +/- 0.15; arterial HCO(-)(3), 8. 57 +/- 5.71 mmol/l and venous HCO(-)(3), 10.46 +/- 5.73 mmol/l. The respective mean differences between arterial and venous pH and arterial and venous HCO(-)(3) for this group were calculated to be 0. 05 +/- 0.01 and -1.88 +/- 0.41 mmol/l. In the healthy controls, the means of arterial and venous pH, and arterial and venous HCO(-)(3) values were 7.39 +/- 0.02, 7.34 +/- 0.02, 24.91 +/- 0.82 and 26.57 +/- 0.83 mmol/l, respectively. For the healthy controls the mean differences between the respective values in arterial and venous pH, and arterial and venous HCO(-)(3) were 0.05 +/- 0.01 and -1.66 +/- 0. 58 mmol/l. Although in healthy controls the correlation between arterial and venous pH values (r(2): 0.595) and arterial and venous HCO(-)(3) values (r(2): 0.552) were moderate, these correlations were significantly increased in both the acidotic patient group (r(2): 0.979 and 0.990) and the DKA group (r(2): 0.989 and 0.995) CONCLUSION: A venous blood sample can be used to evaluate the acid-base status in uremic and DKA patients.