While the ADA guidelines acknowledge that approximately 10% of patients with DKA present with lower glucose levels, they emphasize that. Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) are the .. In fact, the guidelines for diabetes self-management education were. Med Clin North Am. May;(3) doi: / Management of Hyperglycemic Crises: Diabetic Ketoacidosis and.

Author: Zulumi Gazilkree
Country: Grenada
Language: English (Spanish)
Genre: Music
Published (Last): 7 February 2012
Pages: 172
PDF File Size: 12.96 Mb
ePub File Size: 8.6 Mb
ISBN: 980-8-23496-116-2
Downloads: 61784
Price: Free* [*Free Regsitration Required]
Uploader: Faezragore

Diabetic ketoacidosis DKA and the hyperosmolar hyperglycemic state HHS are the two most serious acute metabolic complications of diabetes. DKA is responsible for more thanhospital days per year 12 at an estimated annual direct medical expense and indirect cost of 2. The triad of uncontrolled hyperglycemia, metabolic acidosis, and increased total body ketone concentration characterizes DKA.

HHS is characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of significant ketoacidosis.

These metabolic derangements result from the combination of absolute or relative insulin deficiency and an increase in counterregulatory hormones glucagon, catecholamines, cortisol, and growth hormone. Most patients with DKA have autoimmune type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness such as trauma, surgery, or infections.

This consensus statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS in adult subjects. It is based on a previous technical review 4 and more recently published peer-reviewed articles sincewhich should be consulted for further information. Data adapted from ref.

Hyperglycemic Crises in Adult Patients With Diabetes

Recent epidemiological studies indicate that hospitalizations for DKA in the U. DKA is the most common cause of death in children and adolescents with type 1 diabetes and accounts for half of all deaths in diabetic patients younger than 24 years of age 56. Death in these conditions is rarely due to the metabolic complications of hyperglycemia or ketoacidosis but relates to the underlying hyperglycemjc illness 49.

The prognosis of both conditions is substantially worsened at the extremes of age in the presence of coma, hypotension, and severe comorbidities 14812 The events leading to hyperglycemia and ketoacidosis are depicted in Fig. In DKA, reduced effective insulin concentrations and increased concentrations of counterregulatory hormones catecholamines, cortisol, glucagon, and growth hormone lead to hyperglycemia and ketosis.

Hyperglycemia develops as a result of three processes: This is magnified by transient insulin resistance due to the hormone imbalance itself as well guideliines the elevated free fatty acid concentrations nyperglycemic FFA, free fatty acid.

Hyperglycemic Crises in Adult Patients With Diabetes

All of these parameters return to near-normal values with insulin therapy and hydration within 24 h. The procoagulant and inflammatory states may be due to nonspecific phenomena of stress and may partially explain the association of hyperglycemic guidelinex with a hypercoagulable state The pathogenesis of HHS is not as well understood as that of DKA, but a greater degree of dehydration due to osmotic diuresis and differences in insulin availability distinguish it from DKA 4 Although relative insulin deficiency is clearly present hhyperglycemic HHS, endogenous insulin secretion reflected by C-peptide levels appears to be greater than in DKA, where it is negligible Table 2.

Insulin levels in HHS are inadequate to facilitate glucose utilization by insulin-sensitive tissues but adequate to prevent lipolysis and subsequent ketogenesis Other precipitating factors include discontinuation of or inadequate insulin therapy, pancreatitis, myocardial infarction, cerebrovascular accident, and drugs 1013 In crisws, new-onset type 1 diabetes or discontinuation of insulin in established type 1 diabetes commonly leads to the development of DKA.

Factors that may lead to insulin omission in younger patients include fear of weight gain with improved metabolic control, fear of hypoglycemia, rebellion against authority, and stress of chronic disease. Before aca, the use of continuous subcutaneous insulin infusion devices had also been associated with an increased frequency of DKA 23 ; however, with improvement in technology and better education of patients, the incidence of DKA hyperglycekic to have reduced in pump users.

Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State.

However, additional prospective studies are needed to document reduction of DKA incidence with the use of continuous subcutaneous insulin infusion devices Underlying medical illness that provokes the release of counterregulatory hormones or compromises the access to water is likely to result in severe dehydration and HHS.

In most patients with HHS, restricted water intake is due to the patient being bedridden and is exacerbated by the altered thirst response of the elderly. Elderly individuals with new-onset diabetes particularly residents of chronic care facilities or individuals with known diabetes who become hyperglycemic and are unaware of it or are unable to take fluids when necessary are at risk for HHS 10 Drugs that affect carbohydrate metabolism, such as corticosteroids, thiazides, sympathomimetic agents, and pentamidine, may precipitate the development of HHS or DKA 4.

  JEPSON 9435 PDF

Recently, a number of case reports indicate that the conventional antipsychotic as well as atypical antipsychotic drugs may cause hyperglycemia and even DKA or HHS 26 An increasing number of DKA cases without precipitating cause have been reported in children, adolescents, and adult subjects with type 2 diabetes.

Observational and prospective studies indicate that over half of newly diagnosed adult African American and Hispanic subjects with unprovoked DKA have hyperglgcemic 2 diabetes 28 — The clinical presentation in such cases is acute as in classical type 1 diabetes ; however, after a short period of insulin therapy, prolonged remission is often possible, with eventual cessation of insulin treatment and maintenance of glycemic control with diet or oral antihyperglycemic agents.

This unique, transient insulin-requiring profile after DKA has been recognized mainly in blacks and Hispanics but has also been reported in Native American, Asian, and white populations Some experimental work has shed a mechanistic light on the pathogenesis of ketosis-prone type 2 diabetes.

At presentation, they have markedly impaired insulin secretion and insulin action, but aggressive management with insulin improves insulin secretion and action to levels similar to guidelunes of patients with type 2 diabetes without DKA 2831 The process of HHS usually evolves over several days to weeks, whereas the evolution of the acute Hyperhlycemic episode in type 1 diabetes or even in type 2 diabetes tends to be much shorter.

Occasionally, the entire symptomatic presentation may evolve or develop more acutely, and the patient may present with DKA with no prior clues or symptoms. For both DKA and HHS, the classical clinical picture includes a history of polyuria, polydipsia, weight loss, vomiting, dehydration, weakness, and mental status change.

Physical findings may include poor skin turgor, Kussmaul respirations in DKAtachycardia, and hypotension. Mental status can vary from full alertness to profound lethargy or coma, with the latter more frequent in HHS.

Focal neurologic signs hemianopia and hemiparesis and seizures focal or generalized may also be features of HHS 4 Although infection is a common precipitating factor for both DKA and HHS, patients can be normothermic guidelinnes even hypothermic primarily because of peripheral vasodilation.

Severe hypothermia, if present, is a poor prognostic sign Caution needs to be taken with patients who complain of abdominal pain on presentation because the symptoms could be either a result of the DKA or an indication of a precipitating cause of DKA, particularly in younger patients or in the absence of severe metabolic acidosis gyperglycemic Further evaluation is necessary if this complaint does not resolve with resolution of dehydration and metabolic acidosis.

The initial laboratory evaluation of patients include determination of plasma glucose, blood urea nitrogen, creatinine, electrolytes with calculated anion gaposmolality, serum and urinary ketones, and urinalysis, as well as initial arterial blood gases and a complete blood count with a differential. An electrocardiogram, chest X-ray, and urine, sputum, or blood cultures should also be obtained.

The severity of DKA is classified as mild, moderate, or severe based on the severity of metabolic acidosis blood hyperglyceemic, bicarbonate, tuidelines ketones and the presence of altered mental status 4. Severe guiidelines and dehydration with altered mental status in the absence of significant acidosis characterize HHS, which clinically presents with less ketosis and greater hyperglycemia huidelines DKA.

This may result from a plasma insulin concentration as determined by baseline and stimulated C-peptide [ Guideelines 2 ] adequate to prevent excessive lipolysis and subsequent ketogenesis but not hypergpycemic 4. The key diagnostic feature in DKA is the elevation in circulating total blood ketone concentration.

Assessment of augmented ketonemia is usually performed by the nitroprusside reaction, which provides a semiquantitative estimation of acetoacetate and acetone levels. Accumulation of criess results in an increased anion gap metabolic acidosis.

The anion gap is calculated by subtracting the sum of chloride and bicarbonate concentration from the sodium concentration: Hyperglycemia is a key diagnostic criterion of DKA; crixes, a wide range of plasma glucose can be present on admission.

Elegant studies on hepatic glucose production rates have reported rates ranging from normal or near normal 38 to elevated 1215possibly contributing to the wide range of plasma glucose levels in DKA that are independent of the severity of ketoacidosis This could be due to a combination of factors, including exogenous insulin injection en route to the hospital, antecedent food restriction 3940and inhibition of gluconeogenesis.

On admission, leukocytosis with cell counts in guideelines 10,—15, mm 3 range is the rule in DKA and may not be indicative of an infectious process. In ketoacidosis, leukocytosis is attributed to stress and maybe correlated to elevated levels of cortisol and norepinephrine The admission serum sodium is usually low because of the osmotic flux of water from the intracellular to the extracellular space in the presence guidelined hyperglycemia.

  JAN WITOLD SULIGA BIBLIA SZATANA PDF

Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State.

An increased or even normal serum sodium concentration in the presence of hyperglycemia indicates a rather profound degree of free water loss. To assess the severity of sodium and water deficit, serum sodium may be corrected by adding 1.

Studies on serum osmolality and mental alteration have established a positive linear relationship between osmolality and mental obtundation 9 Serum potassium concentration may be elevated because of an extracellular shift of potassium caused by insulin deficiency, hypertonicity, and acidemia Patients with low normal or low serum potassium concentration on admission have severe total-body potassium deficiency and require careful cardiac monitoring and more vigorous potassium replacement because treatment lowers potassium further and can provoke cardiac dysrhythmia.

Pseudonormoglycemia 44 and pseudohyponatremia 45 may occur in DKA in the presence of severe chylomicronemia. The admission serum phosphate level in guidelimes with DKA, like serum potassium, is usually elevated and does not reflect an actual body deficit that uniformly exists due to shifts of intracellular phosphate to the extracellular space 12asa Insulin deficiency, hypertonicity, and increased guivelines all contribute to the movement of phosphate out of cells.

A serum lipase determination may be beneficial in the differential diagnosis of pancreatitis; however, lipase could also be elevated in DKA in the absence of pancreatitis Not all patients with ketoacidosis have DKA.

DKA must also be distinguished from other causes of high—anion gap metabolic acidosis, including lactic acidosis; ingestion of drugs such as salicylate, methanol, ethylene glycol, and paraldehyde; and acute chronic renal failure 4. Because lactic acidosis is more common in patients with diabetes than in nondiabetic persons and because elevated lactic acid levels may occur in severely volume-contracted patients, plasma lactate should be measured on admission.

A clinical history of previous drug abuse should be sought. Measurement of serum salicylate and blood methanol level may be helpful. Ethylene glycol antifreeze is suggested by the presence of calcium oxalate and hippurate crystals in the urine.

Paraldehyde ingestion is indicated by its characteristic strong odor on the breath.

Because these intoxicants are low—molecular weight organic compounds, they can produce an osmolar gap in addition to the anion gap acidosis A recent report states that active cocaine use is an independent risk factor for recurrent DKA Recently, one case report has shown that a patient with diagnosed acromegaly may present with DKA as the primary manifestation of the disease In addition, an earlier report of hyperglycenic gigantism was presented with two episodes of DKA with complete resolution of diabetes after pituitary apoplexy Successful treatment of DKA hyperglyfemic HHS requires correction of dehydration, hyperglycemia, and electrolyte imbalances; identification of comorbid precipitating events; and above all, frequent patient monitoring.

Bwt, body weight; IV, intravenous; SC, subcutaneous. Initial fluid therapy is directed toward expansion of the intravascular, interstitial, and intracellular volume, all of which are reduced in hyperglycemic crises 53 and restoration of renal perfusion.

In the absence of cardiac compromise, isotonic saline 0. Guideljnes choice for fluid replacement depends on hemodynamics, the state of hydration, serum electrolyte hypergpycemic, and urinary output. Fluid replacement should correct estimated deficits within the first 24 h.

In patients with renal or cardiac compromise, monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status must be performed during fluid resuscitation to avoid iatrogenic fluid guieelines 41015 Aggressive rehydration with subsequent correction of the hyperosmolar state has been shown to result in a more robust response to low-dose insulin therapy During treatment of DKA, hyperglycemia is corrected faster than ketoacidosis.

The mainstay in the treatment of DKA involves the administration of regular insulin via continuous intravenous infusion or by frequent subcutaneous or intramuscular injections 4 tuidelines, 56 Randomized controlled studies in patients with DKA have shown that insulin therapy is effective regardless of the route of administration The administration of continuous intravenous infusion of regular insulin is the preferred route because of its short half-life and easy titration and the delayed onset of action and prolonged half-life of subcutaneous regular insulin 3647 Numerous prospective randomized studies have demonstrated that use of hypergllycemic regular insulin by intravenous infusion is sufficient for successful recovery of patients with DKA.

Until recently, treatment algorithms recommended the administration of an initial intravenous dose of regular guidelijes 0. A recent prospective randomized study reported that guidelinnes bolus dose of insulin is not necessary if patients receive an hourly insulin infusion of 0.