Acidosis and coma in adult diabetic maintenance dialysis patients with extreme hyperglycemia (original) (raw)
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Hyperosmolar Nature of Diabetic Coma
Diabetes, 1975
Stupor in patients with nonketotic hyperglycemia has been ascribed to hyperosmolarity, but the cause of depressed consciousness in patients with ketoacidosis has been puzzling. In this study, blood pH, serum glucose and sodium concentrations, and serum osmolality were measured in eighty-five consecutive episodes of diabetic ketoacidosis and forty-seven of nonketotic hyperglycemia. In the acidotic patients, as in those with nonketotic hyperglycemia, stupor closely paralleled hyperosmolarity and not the severity of acidemia. Indeed, the mean elevations of serum osmolarity were almost the same in the ketotic and in the nonketotic patients who were deeply obtunded. It seems likely that depression of consciousness in patients with severely uncontrolled diabetes mellitus, if not due to a nonmetabolic disorder, such as acute stroke, is attributable to hyperosmolarity, whether or not ketoacidosis is present. DIABETES 24:594-99, June, 1975.
Seminars in Dialysis, 2008
The mechanisms of fluid and solute abnormalities that should be considered in any patient with severe hyperglycemia include changes in the total amount of extracellular solute, osmotic diuresis, intake of water driven by thirst, and influences from associated conditions. The absence of osmotic diuresis distinguishes dialysis-associated hyperglycemia (DH) from hyperglycemia with preserved renal function (HPRF). Mainly because of this absence, comparable degrees of hyperglycemia tend to produce less hypertonicity and less severe intracellular volume contraction in DH than in HPRF, while extracellular volume is expanded in DH but contracted in HPRF. Ketoacidosis can develop in both DH and HPRF. Among DH patients, hyperkalemia appears to be more frequent when ketoacidosis is present than when nonketotic hyperglycemia is present. Among HPRF patients, the frequency of hyper-
BMC Endocrine Disorders, 2011
Background: There is limited literature on hypernatreamia in the setting of hyperglycaemic crisis. This is despite the fact that the presence of hypernatreamia may impact on the classification of hyperglycaemic crisis and its management particularly with regards to the nature of fluid therapy. We determined the prevalence of hypernatreamia and its associated factors at presentation for hyperglycaemic crisis. Methods: This was a retrospective review of data for hyperglycaemic crisis admissions in Nelson Mandela Academic Hospital, Mthatha, South Africa. The prevalence of hypernatreamia (uncorrected Serum Sodium at presentation >145 mmol/L) was determined. Hyperosmolality was defined by calculated effective osmolality >320 mosmols/Kg. Multivariate logistic regression was undertaken using variables that were statistically significant in univariate analysis to ascertain those that were independently associated (Odds Ratio (OR) with 95% Confidence Interval (CI)) with hypernatreamia. Results: The prevalence of hypernatreamia in our admissions for hyperglycaemic crisis was 11.7% (n = 32/273 including 171 females and 102 males). All admissions with hypernatreamia met the criteria for hyperosmolality. Age ≥ 60 years (OR = 3.9 95% CI 1.3-12.3; P = 0.018), Altered level of consciousness (OR = 8.8 95% CI 2.3-32.8; P < 0.001) and a new diagnosis of diabetes (OR = 3.7 95%CI 1.2-11.5; P = 0.025) were independently associated with hypernatreamia. Conclusion: The prevalence rate of hypernatreamia in hyperglycaemic admissions was high with all hypernatreamic admissions meeting the criteria for hyperosmolality. Advanced age, altered conscious level and a new diagnosis of diabetes were independently associated with hypernatreamia.
DIABETIC KETOACIDOSIS: A COMPREHENSIVE REVIEW OF PATHOPHYSIOLOGY, MANAGEMENT AND NEUROLOGICAL IMPACTS IN THE EMERGENCY SETTING (Atena Editora), 2024
Diabetic ketoacidosis (DKA) is a critical medical emergency associated with diabetes mellitus, especially type 1, which requires immediate treatment to avoid serious complications. The condition results from insulin deficiency, leading to uncontrolled hyperglycemia, excessive production of ketone bodies and metabolic acidosis. Initial treatment focuses on rapid correction of dehydration with isotonic saline solutions, blood glucose control and insulin administration, followed by a switch to glucose-containing solutions. Studies indicate that DKA can cause significant cognitive decline, especially in children, and suggest that factors such as cerebral hypoperfusion and neuroinflammation may be more relevant to brain damage than the rate of fluid administration. The review also highlights the importance of biomarkers, such as metalloproteinases, in understanding blood-brain barrier dysfunction. Effective treatment must consider both metabolic and neurological aspects to improve clinical outcomes.
A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate
Endocrinologia japonica, 1991
We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a ...
Journal of Critical Care, 2011
Purpose: The aim of this study was to characterize the first 48-hour evolution of metabolic acidosis of adult patients with diabetic ketoacidosis admitted to the intensive care unit. Materials and Methods: We studied 9 patients retrieved from our prospective collected database, using the physicochemical approach to acid-base disturbances. Results: Mean (SD) age was 34 (13) years; mean (SD) Acute Physiology and Chronic Health Evaluation II score was 16 (10); mean (SD) blood glucose level on admission was 480 (144) mg/dL; mean (SD) pH was 7.17 (0.18); and mean (SD) standard base excess was −16.8 (7.7) mEq/L. On admission, a great part of metabolic acidosis was attributed to unmeasured anions (strong ion gap [SIG], 20 ± 10 mEq/L), with a wide range of strong ion difference (41 ± 10 mEq/L). During the first 48 hours of treatment, 297 ± 180 IU of insulin and 9240 ± 6505 mL of fluids were used. Metabolic improvement was marked by the normalization of pH, partial correction of standard base excess, and a reduction of hyperglycemia. There was a significant improvement of SIG (7.6 ± 6.2 mEq/L) and a worsening of strong ion difference acidosis (36 ± 5 mEq/L) in the first 24 hours, with a trend toward recuperation between 24 and 48 hours (38 ± 6 mEq/L). Conclusion: Initial metabolic acidosis was due to SIG, and the treatment was associated with a significant decrease of SIG with an elevation of serum chloride above the normal range.
The International Journal of Artificial Organs, 2005
We analyzed the changes in serum potassium concentration ([K]) and acid-base parameters in 43 episodes of dialysis-associated hyperglycemia (serum glucose level > 33.3 mmol/L), 22 of which were characterized as diabetic ketoacidosis (DKA) and the remaining 21 as nonketotic hyperglycemia (NKH). All episodes were treated with insulin therapy only. Age, gender, initial and final serum values of glucose, sodium, chloride, tonicity and osmolality did not differ between DKA and NKH. At presentation, serum values of [K] (DKA 6.2 ± 1.3 mmol/L; NKH 5.2 ± 1.5 mmol/L) and anion gap [AG] (DKA 27.2 ± 6.4 mEq/L; NKH 15.4 ± 3.5 mEq/L) were higher in DKA, whereas serum total carbon dioxide content [TCO2] (DKA 12.0 ± 4.6 mmol/L; NKH 22.5 ± 3.1 mmol/L), arterial blood pH (DKA 7.15 ± 0.09; NKH 7.43 ± 0.07) and arterial blood PaCO2 (DKA 26.2 ± 12.3 mm Hg; NKH 34.5 ± 6.7 mm Hg) were higher in NKH. At the end of insulin treatment, serum values of [K] (DKA 4.0 ± 0.7 mmol/L, NKH 4.0 ± 0.5 mmol/L), [AG] ...