Severe Diabetic Ketoacidosis (Diabetic “Coma”): 482 Episodes in 257 Patients; Experience of Three Years

Beigelman, Paul M.

doi:10.2337/diab.20.7.490

Cited by 140 publications

(44 citation statements)

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“…3 the acutely ketotic alloxan diabetic rat is severely ill with marked hypoglycemia and hyperketonemia. The initial plasma glucose concentrations in the three groups of animals at zero time clustered around 1,000 mg/100 ml, a figure much higher than that found in pancreatectomized diabetic rats (19) but very close to values seen in severe human disease (20). Mean plasma ketone levels were greater than 1,500 /mol/100 ml.…”

Section: Resultsmentioning

confidence: 51%

Acute Reversal of Experimental Diabetic Ketoacidosis in the Rat with (+)-Decanoylcarnitine

McGarry¹,

Foster²

1973

J. Clin. Invest.

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A B S T R A C T The effect of (+) -decanoylcarnitine, a potent inhibitor of long-chain acylcarnitine transferase, was tested for its ability to inhibit hepatic ketogenesis both in the isolated perfused liver and in vivo in severely ketotic alloxan diabetic rats. In vitro the inhibitor caused an almost complete block in ketone body production. In vivo (+) -decanoylcarnitine caused a rapid reversal of ketosis under conditions where large doses of insulin had little effect. A combination of the two agents produced an even more striking fall in plasma ketone levels.While (+) -decanoylcarnitine alone had no effect on plasma glucose levels it enhanced the hypoglycemic effect of insulin in anesthetized animals. Loss of this effect was noted in nonanesthetized animals, possibly as a result of increased muscle activity.Studies in the isolated perfused liver indicated that the blockade of fatty acid oxidation and ketogenesis produced by (+) -decanoylcarnitine was rapidly reversible upon removal of the inhibitor.

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Section: Resultsmentioning

confidence: 51%

Acute Reversal of Experimental Diabetic Ketoacidosis in the Rat with (+)-Decanoylcarnitine

McGarry¹,

Foster²

1973

J. Clin. Invest.

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“…Although it has previously been noted that haemostatic problems are frequently seen in patients with DKA [40,41], studies related to the haemostatic system in these patients are rare and not sufficient in content. Beigelman [40] found that 25% of all mortalities during severe DKA were caused by coronary artery thrombosis, which was the most common cause of death together with infections.…”

Section: Discussionmentioning

confidence: 97%

Evaluation of the Haemostatic System during Ketoacidotic Deterioration of Diabetes mellitus

Ileri¹,

Büyükaşık²,

Karaahmetoğlu³

et al. 1999

Pathophysiol Haemos Thromb

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Clinical observations have indicated the frequent development of thrombotic complications during diabetic ketoacidosis (DKA). This study aimed to examine whether haemostatic changes that could lead to a thrombotic tendency occur during ketoacidosis. Plasma levels of in vivo haemostatic markers reflecting activation degrees of the coagulation system, fibrinolytic system, platelets and endothelium were assayed in 34 patients with DKA, both at diagnosis and 1 week after recovery. We found coagulation system and platelet activation and endothelial injury/activation in the patients at diagnosis of DKA. Although significant improvements were observed after recovery, only platelet activity was completely normalized. Fibrinolytic activity was also increased, both at diagnosis and after recovery, compared to the control group. However, although coagulation activity was prominently increased at diagnosis compared to the recovery period, there was no change in fibrinolytic activity in the same periods; on the contrary, the fibrinolytic capacity of the endothelium was diminished at diagnosis of DKA compared to the recovery period, suggesting the presence of relative hypofibrinolysis during DKA. Indications for a role of hyperglycaemia in the emergence of haemostatic disturbances during DKA were observed.

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“…Excessive urinary potassium losses, which occur as a result of osmotic diuresis with increased delivery of fluid and sodium to potassium secretory sites in the distal nephron, are ultimately responsible for the development of potassium depletion (177)(178)(179)(180). Secondary hyperaldosteronism and urinary ketoanion excretion, as potassium salts, further augment potassium losses.…”

Section: Potassiummentioning

confidence: 99%

“…Table 2 shows typical potassium deficits, which represent mainly intracellular losses, in both DKA and HHS. Extracellular hyperosmolarity, secondary to hyperglycemia, causes a shift of water and potassium from the intracellular to the extracellular space, resulting in normal or elevated serum potassium concentrations despite total-body potassium deficits of 500-700 mEq/l (44,(177)(178)(179). This potassium shift is further enhanced by insulin deficiency and the presence of acidosis and accelerated breakdown of intracellular protein (180).…”

mentioning

confidence: 99%

Management of Hyperglycemic Crises in Patients With Diabetes

et al. 2001

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Abbreviations: AaO 2 , alveolar-to-arteriolar oxygen; AKA, alcoholic ketoacidosis; ARDS, adult respiratory distress syndrome; BUN, blood urea nitrogen; CPT, carnitine palmitoyl-transferase; CSF, cerebrospinal fluid; DKA, diabetic ketoacidosis; FFA, free fatty acid; HHS, hyperosmolar hyperglycemic state; IRI, immunoreactive insulin; PaO 2 , arteriolar partial pressure of oxygen; RDKA, recurrent DKA.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Management of Hyperglycemic Crises in Patients With Diabetes T E C H N I C A L R E V I E R e v i e w s / C o m m e n t a r i e s / P o s i t i o n S t a t e m e n t s 132DIABETES CARE, VOLUME 24, NUMBER 1, JANUARY 2001Technical Review noted in newly diagnosed obese type 2 diabetic patients (5,26,31). Therefore, the concept that the presence of DKA in type 2 diabetes is a rare occurrence is incorrect.The most common types of infections are pneumonia and urinary tract infection, accounting for 30-50% of cases (Table 4). Other acute medical illnesses as precipitating causes include alcohol abuse, trauma, pulmonary embolism, and myocardial infarction, which can occur both in type 1 and 2 diabetes (6). Various drugs that alter carbohydrate metabolism, such as corticosteroids, pentamidine, sympathomimetic agents, and ␣-and ␤-adrenergic blockers, and excessive use of diuretics in the elderly may also precipitate the development of DKA and HHS.The recent increased use of continuous subcutaneous insulin infusion pumps that use small amounts of short-acting insulin has been associated with an incidence of DKA that is significantly increased over the incidence seen with conventional methods of multiple daily insulin injections, in spite of the fact that most of the mechanical problems with insulin pumps have been resolved (6,(32)(33)(34). In the Diabetes Control and Complications Trial, the incidence of DKA in patients on insulin pumps was about twofold higher than that in the multipleinjection group over a comparable time period (35). This may be due to the exclusive use of short-acting insulin in the pump, which if interrupted leaves no reservoir of insulin for blood glucose control.Psychological factors and poor compliance, leading to omission of insulin therapy, are important precipitating factors for recurrent ketoacidosis. In young female patients with type 1 diabetes, psychological problems complicated by eating disorders may be contributing factors in up to 20% of cases of recurrent ketoacidosis (36,37). Factors that may lead to insulin omission in younger patients include fear of weight gain with good metabolic control, fear of hypoglycemia, rebellion against authority, and stress related to chronic disease (36). Noncompliance with insulin therapy has been found to be the leading precipitating cause for DKA in urban African-Americans and medically indigent patients (5,26). In addition, a recent study showed that diabetic patients without health insurance or with Medicaid alone had hospitali...

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Severe Diabetic Ketoacidosis (Diabetic “Coma”): 482 Episodes in 257 Patients; Experience of Three Years

Cited by 140 publications

References 0 publications

Acute Reversal of Experimental Diabetic Ketoacidosis in the Rat with (+)-Decanoylcarnitine

Acute Reversal of Experimental Diabetic Ketoacidosis in the Rat with (+)-Decanoylcarnitine

Evaluation of the Haemostatic System during Ketoacidotic Deterioration of Diabetes mellitus

Management of Hyperglycemic Crises in Patients With Diabetes

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