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Diabetic Ketoacidosis. Introduction Diabetes mellitus is a syndrome of disturbed energy homeostasis caused by a deficiency of insulin or of its action.

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Presentation on theme: "Diabetic Ketoacidosis. Introduction Diabetes mellitus is a syndrome of disturbed energy homeostasis caused by a deficiency of insulin or of its action."— Presentation transcript:

1 Diabetic Ketoacidosis

2 Introduction Diabetes mellitus is a syndrome of disturbed energy homeostasis caused by a deficiency of insulin or of its action resulting in abnormal metabolism of carbohydrate, protein, and fatDiabetes mellitus is a syndrome of disturbed energy homeostasis caused by a deficiency of insulin or of its action resulting in abnormal metabolism of carbohydrate, protein, and fat Diabetes mellitus is the most common endocrine-metabolic disorder of childhood and adolescenceDiabetes mellitus is the most common endocrine-metabolic disorder of childhood and adolescence

3 Introduction Individuals affected by insulin-dependent diabetes confront serious burdens that include an absolute daily requirement for exogenous insulin, the need to monitor their own metabolic control, and the need to pay constant attention to dietary intakeIndividuals affected by insulin-dependent diabetes confront serious burdens that include an absolute daily requirement for exogenous insulin, the need to monitor their own metabolic control, and the need to pay constant attention to dietary intake

4 Introduction Morbidity and mortality stem from metabolic derangements and from long- term complications that affect small and large vessels and result in retinopathy, nephropathy, neuropathy, ischemic heart disease, and arterial obstruction with gangrene of the extremitiesMorbidity and mortality stem from metabolic derangements and from long- term complications that affect small and large vessels and result in retinopathy, nephropathy, neuropathy, ischemic heart disease, and arterial obstruction with gangrene of the extremities

5 Classification Type I Diabetes (insulin-dependent diabetes mellitus, IDDM)Type I Diabetes (insulin-dependent diabetes mellitus, IDDM) –characterized by severe insulinopenia and dependence on exogenous insulin to prevent ketosis and to preserve life –onset occurs predominantly in childhood –probably has some genetic predisposition and is likely autoimmune-mediated

6 Classification Type II Diabetes (non-insulin-dependent diabetes mellitus, NIDDM)Type II Diabetes (non-insulin-dependent diabetes mellitus, NIDDM) –patients are not insulin dependent and rarely develop ketosis –generally occurs after age 40, and there is a high incidence of associated obesity –insulin secretion generally adequate; insulin resistance is present –no associated genetic predisposition

7 Classification Secondary DiabetesSecondary Diabetes –occurs in response to other disease processes: exocrine pancreatic disease (cystic fibrosis)exocrine pancreatic disease (cystic fibrosis) Cushing syndromeCushing syndrome poison ingestion (rodenticides)poison ingestion (rodenticides)

8 Type I Diabetes Mellitus: Epidemiology Prevalence of IDDM among school-age children in the US is 1.9 per 1000Prevalence of IDDM among school-age children in the US is 1.9 per 1000 The annual incidence in the US is about new cases per 100,000The annual incidence in the US is about new cases per 100,000 Male to female ratio is equalMale to female ratio is equal Among African-Americans, the occurrence of IDDM is about % of that seen in Caucasian-AmericansAmong African-Americans, the occurrence of IDDM is about % of that seen in Caucasian-Americans

9 Type I Diabetes Mellitus: Epidemiology Peaks of presentation occur at years of age and at adolescencePeaks of presentation occur at years of age and at adolescence Newly recognized cases appear with greater frequency in the autumn and winterNewly recognized cases appear with greater frequency in the autumn and winter Definite increased incidence of IDDM in children with congenital rubella syndromeDefinite increased incidence of IDDM in children with congenital rubella syndrome

10 Type I Diabetes Mellitus: Etiology and Pathogenesis Basic cause of clinical findings is sharply diminished secretion of insulinBasic cause of clinical findings is sharply diminished secretion of insulin The mechanisms that lead to failure of pancreatic  -cell function are likely autoimmune destruction of pancreatic isletsThe mechanisms that lead to failure of pancreatic  -cell function are likely autoimmune destruction of pancreatic islets IDDM is more prevalent in persons with Addison’s disease, Hashimoto’s thyroiditis, and pernicious anemiaIDDM is more prevalent in persons with Addison’s disease, Hashimoto’s thyroiditis, and pernicious anemia

11 Type I Diabetes Mellitus: Etiology and Pathogenesis % of newly diagnosed patients with IDDM have anti-islet cell antibodies % of newly diagnosed patients with IDDM have anti-islet cell antibodies

12 Type I Diabetes Mellitus: Pathophysiology

13 Progressive destruction of  -cells leads to a progressive deficiency of insulinProgressive destruction of  -cells leads to a progressive deficiency of insulin As IDDM evolves, it becomes a permanent low-insulin catabolic state which feeding does not reverseAs IDDM evolves, it becomes a permanent low-insulin catabolic state which feeding does not reverse Secondary changes involving stress hormones accelerate the metabolic decompensationSecondary changes involving stress hormones accelerate the metabolic decompensation

14 Type I Diabetes Mellitus: Pathophysiology With progressive insulin deficiency, excessive glucose production and impairment of its utilization result in hyperglycemia with glucosuria when the renal threshold of ~ 180 mg/dL is exceededWith progressive insulin deficiency, excessive glucose production and impairment of its utilization result in hyperglycemia with glucosuria when the renal threshold of ~ 180 mg/dL is exceeded The resultant osmotic diuresis produces polyuria, urinary losses of electrolytes, dehydration, and compensatory polydipsiaThe resultant osmotic diuresis produces polyuria, urinary losses of electrolytes, dehydration, and compensatory polydipsia

15 Type I Diabetes Mellitus: Pathophysiology Hyperosmolality as a result of progressive hyperglycemia contributes to cerebral obtundation in DKAHyperosmolality as a result of progressive hyperglycemia contributes to cerebral obtundation in DKA Serum osmolality:Serum osmolality: –{Serum Na + + K + } x 2 + glucose + BUN 183

16 Type I Diabetes Mellitus: Pathophysiology DKA results in altered lipid metabolismDKA results in altered lipid metabolism –increased concentrations of total lipids, cholesterol, triglycerides, and free fatty acids –free fatty acids are shunted into ketone body formation due to lack of insulin; the rate of formation exceeds the capacity for their peripheral utilization and renal excretion leading to accumulation of ketoacids, and therefore metabolic acidosis

17 Type I Diabetes Mellitus: Pathophysiology With progressive dehydration, acidosis, hyperosmolality, and diminished cerebral oxygen utilization, consciousness becomes impaired, and the patient ultimately becomes comatoseWith progressive dehydration, acidosis, hyperosmolality, and diminished cerebral oxygen utilization, consciousness becomes impaired, and the patient ultimately becomes comatose

18 Type I Diabetes Mellitus: Clinical Manifestations Classic presentation of diabetes in children is a history of polyuria, polydipsia, polyphagia, and weight loss, usually for up to one monthClassic presentation of diabetes in children is a history of polyuria, polydipsia, polyphagia, and weight loss, usually for up to one month Laboratory findings include glucosuria, ketonuria, hyperglycemia, ketonemia, and metabolic acidosis. Serum amylase may be elevated. Leukocytosis is commonLaboratory findings include glucosuria, ketonuria, hyperglycemia, ketonemia, and metabolic acidosis. Serum amylase may be elevated. Leukocytosis is common

19 Type I Diabetes Mellitus: Clinical Manifestations Keotacidosis is responsible for the initial presentation of up to 25% of childrenKeotacidosis is responsible for the initial presentation of up to 25% of children –early manifestations are mild and include vomiting, polyuria, and dehydration –More severe cases include Kussmaul respirations, odor of acetone on the breath –abdominal pain or rigidity may be present and mimic acute appendicitis or pancreatitis –cerebral obtundation and coma ultimately ensue

20 Type I Diabetes Mellitus: Diagnosis Diagnosis of IDDM is dependent on the demonstration of hyperglycemia in association with glucosuria with or without ketonuriaDiagnosis of IDDM is dependent on the demonstration of hyperglycemia in association with glucosuria with or without ketonuria DKA must be differentiated from acidosis and coma due to other causes:DKA must be differentiated from acidosis and coma due to other causes: –hypoglycemia, uremia, gastroenteritis with metabolic acidosis, lactic acidosis, salicylate intoxication, encephalitis

21 Type I Diabetes Mellitus: Diagnosis DKA exists when there is hyperglycemia (> 300 mg/dL), ketonemia, acidosis, glucosuria, and ketonuriaDKA exists when there is hyperglycemia (> 300 mg/dL), ketonemia, acidosis, glucosuria, and ketonuria

22 Type I Diabetes Mellitus: Treatment Treatment is divided into 3 phasesTreatment is divided into 3 phases –treatment of ketoacidosis –transition period –continuing phase and guidance

23 Type I Diabetes Mellitus: Treatment Goals of treatment of DKAGoals of treatment of DKA –intravascular volume expansion –correction of deficits in fluids, electrolytes, and acid-base status –initiation of insulin therapy to correct catabolism, acidosis

24 Type I Diabetes Mellitus: Treatment Intravascular volume expansionIntravascular volume expansion –dehydration is most commonly in the order of 10% –initial hydrating fluid should be isotonic saline this alone will often slightly lower the blood glucosethis alone will often slightly lower the blood glucose Treatment of electrolyte abnormalitiesTreatment of electrolyte abnormalities –serum K + is often elevated, though total body K + is depleted

25 Type I Diabetes Mellitus: Treatment –K + is started early as resolution of acidosis and the administration of insulin will cause a decrease in serum K + Phosphate is depleted as well. Phosphate may be added as KPO 4 especially if serum chloride becomes elevatedPhosphate is depleted as well. Phosphate may be added as KPO 4 especially if serum chloride becomes elevated “Pseudohyponatremia” is often present“Pseudohyponatremia” is often present –Expect that the Na level will rise during treatment –Corrected Na = Measured Na + {(glucose - 100) x 0.016}. –If Na does not rise, true hyponatremia may be present (possibly increasing cerebral edema risk) and should be treated

26 Type I Diabetes Mellitus: Treatment BICARBONATE IS ALMOST NEVER ADMINISTEREDBICARBONATE IS ALMOST NEVER ADMINISTERED –bicarbonate administration leads to increased cerebral acidosis HCO 3 - combines with H + and dissociated to CO 2 and H 2 O. Whereas bicarbonate passes the blood- brain barrier slowly, CO 2 diffuses freely, thereby exacerbating cerebral acidosis and cerebral depressionHCO 3 - combines with H + and dissociated to CO 2 and H 2 O. Whereas bicarbonate passes the blood- brain barrier slowly, CO 2 diffuses freely, thereby exacerbating cerebral acidosis and cerebral depression

27 Type I Diabetes Mellitus: Treatment Indications for bicarbonate administration include severe acidosis leading to cardiorespiratory compromiseIndications for bicarbonate administration include severe acidosis leading to cardiorespiratory compromise Increasing evidence suggests that subclinical cerebral edema occurs in the majority of patients treated with fluids and insulin for DKAIncreasing evidence suggests that subclinical cerebral edema occurs in the majority of patients treated with fluids and insulin for DKA

28 Type I Diabetes Mellitus: Treatment Cerebral edema is the major life-threatening complication seen in the treatment of children with DKACerebral edema is the major life-threatening complication seen in the treatment of children with DKA –usually develops several hours after the institution of therapy –manifestations include headache, alteration in level of consciousness, bradycardia, emesis, diminished responsiveness to painful stimuli, and unequal or fixed, dilated pupils

29 Type I Diabetes Mellitus: Treatment Therapy of cerebral edema includes treatment with mannitol and hyperventilationTherapy of cerebral edema includes treatment with mannitol and hyperventilation Excessive use of fluids, use of bicarbonate, and large doses of insulin have been linked to the increased formation of cerebral edemaExcessive use of fluids, use of bicarbonate, and large doses of insulin have been linked to the increased formation of cerebral edema –fluids are limited to ~ 3 L/m 2 /24 hours

30 Type I Diabetes Mellitus: Treatment Insulin TherapyInsulin Therapy –continuous infusion of low-dose insulin IV (~ 0.1 U/kg/hr) is effective, simple, and physiologically sound –goal is to slowly decrease serum glucose (< 100 mg/dL/hr –frequent laboratory and blood gas analyses are obtained to ensure ongoing resolution of metabolic acidosis

31 Type I Diabetes Mellitus: Treatment “Maintenance” IV fluid at a rate of cc/m 2 /day consists of 2/3 NS (0.66%) or NS“Maintenance” IV fluid at a rate of cc/m 2 /day consists of 2/3 NS (0.66%) or NS –5% Dextrose is added to IVF when blood glucose is ~ 300 mg/dL –10% Dextrose is added when blood glucose is ~ 200 mg/dL

32 Type I Diabetes Mellitus: Treatment Insulin is used to treat acidosis, not hyperglycemiaInsulin is used to treat acidosis, not hyperglycemia –insulin should never be stopped if ongoing acidosis persists When the acidosis is corrected, the continuous insulin infusion may be discontinued and subcutaneous insulin initiatedWhen the acidosis is corrected, the continuous insulin infusion may be discontinued and subcutaneous insulin initiated With the regimen, DKA usually is usually fully corrected in 36 to 48 hoursWith the regimen, DKA usually is usually fully corrected in 36 to 48 hours

33 Type I Diabetes Mellitus: Treatment Hypoglycemic Reactions (Insulin Shock)Hypoglycemic Reactions (Insulin Shock) –symptoms and signs include pallor, sweating, apprehension, trembling, tachycardia, hunger, drowsiness, mental confusion, seizures and coma –management includes administration (if conscious) of carbohydrate-containing snack or drink –glucagon 0.5 mg is administered to an unconscious or vomiting child


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