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Diabetic Ketoacidosis.pptx
- 1. INTRODUCTION - Diabetic Ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. - Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. - DKA occurs mostly in type 1 diabetes mellitus (DM). - It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. - DKA is diagnosed by detection of hyperglycemia. - Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia.
- 2. DEFINITION - Diabetic Ketoacidosis is a state of absolute or relative insulin deficiency aggravated by ensuring hyperglycaemia, dehydration and acidosis producing derangements in intermediary metabolism. - They are both associated with: • Insulin deficiency (absolute in TlDM and relative in T2DM) and hyperglycemia. • Acid-base abnormalities (ketoacidosis) • Severe volume depletion.
- 3. DEFINITION - Diabetic Ketoacidosis is a state of absolute or relative insulin deficiency aggravated by ensuring hyperglycaemia, dehydration and acidosis producing derangements in intermediary metabolism. - They are both associated with: • Insulin deficiency (absolute in TlDM and relative in T2DM) and hyperglycemia. • Acid-base abnormalities (ketoacidosis) • Severe volume depletion.
- 4. Other hyperglycemic states Diabetes mellitus Hyperosmolar hyperglycemic state Impaired glucose tolerance Stress hyperglycemia Other ketotic states Ketotic hypoglycemia Alcoholic ketosis Starvation ketosis H yper glycemia O K A Ket-. Acidosis Other metabolic acidosis states lactic acidosis Hyperchloremic acidosis Salicylism Uremic acidosis Drug-induced acidosis
- 5. ROLE OF INSULIN Insulin Skeletal m usc le Liver i glycogenesis J. gluconeogenesis i glycogenesis T protein synthesis Tissue metabolic spectrum Adipose t issue i adipogenesis J. lipolysis INSULIN- . Cat abolism Anabolism Tissue breakdown Glycogenolysis, gluconeogenesis, protein catabolism, lipotysis Tissue b uildup Glycogen, protein, fat synthesis
- 6. - - - - ' I I
- 7. CAUSES CAN TRIGGER OKA: - New diagnosis of diabetes. - Drugs: • Antipsychotic agents • Others: Corticosteroids, sympathomimetic agents, thiazide diuretics... - Inf ection :Pneumonia, sepsis, urinary tract infection (UTI) - Lack of insulin - Most common cause of DKA. • Insulin pump failure. • Nonadherence to insulin treatment plans:body image issues, financial problems, psychological factors. • Umecognized symptoms of new-onset diabetes mellitus. - Other physiologic stressors: MI, Stroke, Pancreatitis, Trauma.
- 8. PATHOPHYSIOLOGY f c o u n te r r e e u la t o r y h o r m o n e s J. In s u l in f t;Or U=>ol f GH Tc • t c h ola11111 :. T l{lu c RO•• I + + + ... g lu c o l protein syrH h es1s IS + • - t FrA t o th live r t g luc o ne o genosls + - Tk to I 1J [ H y pe r a ly c e m la - H YPo n a tr o ml a Wnt r shifts out from colls 2 to T 1 a1ucose1cr K e t o u r la Keto c1do Is 1 H yp .·ralyr omt ::!. Jt.ld U H • • K t n m i L c t 1 c nc1dosls ( vory T 3.5 p,tucoso P o ly u r lo 2 lo osrnot1c diuresis 1 1 Na G lu c o u r1Cl D o h y d r t lo n/ h y p o v o l r n la Po ly d lp s la ttypovotomm -sumul n1stho thirst r coptors i n th CNS
- 9. PATHOPHYS IOLOGY Acetoacetate P-hydroxyl bu tyrate D-p-hydroxyl bu tyrate dehydrogenase NADH + H + NAO + • Acetone isn't an acid. • In DKA, the dominant ketoacid is p-hydroxylbu tyric acid, especially in cases of poor tissue perfusion/ lactic acidosis . • During recovery, the balance shifts to acetoacetic acid.
- 10. PATHOPHYS IOLOGY - Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuriacauses an osmotic diuresis, leading to water & solutes loss. - In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead ketosis (acetoacetate & -hydroxyl butyrate) - The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by lactic acidosis caused by dehydration & poor tissue perfusion. - Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydration. - Electrolyte abnormalities are secondary to their loss in urine and trans membrane alterations fallowing acidosis & osmotic diuresis.
- 11. PATHOPHYS IOLOGY - Because of acidosis, K+ions enter the circulation leading to hyperkalemia, this is aggravated by dehydration and renal failure. - So, depending on the duration of DKA, serum K at diagnosis may be high, normal or low, but the intracellular K stores are always depleted. - Na+loss occurs secondary to the hyperosmotic state & the osmotic diuresis. - The dehydration can lead to decreased kidney perfusion and acute renal failure. - Accumulation of ketone bodies contributes to the abdominal pain and vomiting. - P-hydroxyl butyrate can serve as an energy source in the absence of insulin-mediated glucose delivery, and is a protective mechanism in case of starvation.
- 12. PATHOPHYSIOLOGY Dehydration: 6 liters or more, 15-20%of their weight. Osmotic Diuresis: Blood glucose exceeds the renal threshold (160-180mg/ dL) • Vomiting • Hyperventilation . • Impaired consciou sness- Decreased intake. Metabolic acidosis: Initially due to the excess ketones. Compensatory mechanisms: • Respiratory compensation • Intracellular buffering- excess H+goes into cells in exchange for potassium. • Bicarbonate buffering system. Ionic changes: • A general loss of electrolytes due to osmotic diuresis. • Potassiu1n:intracellular bufferin g mechanism shifts potassium out of cells so even if there decreased total potassium in the body, serum potassium may initially be normal or even high. This potassium is further lost through the kidneys. Paradoxes of OKA Hyperglycemin despite decreased intake Polyuria despite dehydration Catabolic state despite hyperglycemia
- 13. THOROUGH HISTORY is imperative! • New onset diabetes Recent history of Polyuria, polydipsia, polyphagia, weight loss Pass medical history Family history of diabetes History/Du ration of syn1 ptoms • Headache • Blurry vision • Nausea/ Vomiting/ Abdominal pain. • Difficulty in breathing • Changes in behavior Precipitatingfactor : • Concurrent illness or infection • Preexisting diabetes History of diabetes and duration: • Last meal/ Carbohydrate intake • Current and routine blood glucose levels - Standard insulin regimen • Last insulin dose • Type of insulin and route - Past hospitalization history - Duration of sy1nptoms • Nausea/vomiting/ abdominal pain - Precipitatingfactors: • Physical exertion • Change in eating habits/ diets • Stress, missed insulin dose, illness
- 14. condition can develop in afew hours. Early symptoms include the following: • Thirst or a very dry mouth. • Frequent urinary • High blood glucose level. • High levels of ketones in the urine. Then, other symptoms appear: • Constantly feeling tired. • Dry or flushed skin. • Nausea, vomiting, or abdominal pain . • Difficulty breathing . • Fruity odor on breath . • Confusion THE WARNING SIGNS DKA usually develops slowly. But when vomiting occurs, this life-threatening nouseo ond vomit1,,s r o ''"'_ d1 abet1 c ketoac1 dosis 1ncreosed ur1 not10" -
- 15. LABORATORY EVALUATION - Initial Labs: • Blood glucose • Urine ketones • Venous blood gas • Basic blood chemistry: Electrolytes, BUN, creatinine, Magnesium, Calcium, Phosphorus. - Ad ditional labs: • CBC • Osmolality • Serum P-hydroxyl butyrate (p-OH) • Hemoglobin AlC (HbAlC) • Pancreatic antibodies. • Additional testing as indicated: CXR, non-contrast head CT, cultures (blood, urine, throat) UfOfflL , . . . . . . . . ......... fM i C • . . .. . . . .. 11MU. . - e 4 Mt t t•...: II II 11 . . • . .
- 16. LABORATORY EVALUATION - Blood Gases: • ABG - artery blood sample or VBG - V enous blood sample are both adequate to determine blood pH . • VBG is sufficient who are hemodynamically stable and without respiratory failure. ); ; >Metabolic acidosis is defined as a low pH and decreased HC0 3- ); ; >Metabolic alkalosis is defined as a high pH and increased HC0 3-
- 17. LABORATORY EVALUATION Calculations for the Evaluation of Diabetic Ketoacidosis Value Purpose Formula Normal value
- 18. DIAGNOSIS ADA Diagnostic Criteria for DKA IParameter I IPlasma glucose, mg/ dL IArterial pH !Serum bicarbonate (mmol/ L) Serum ketones Urine ketones I : I Effective serum osmolality(mOsm/ kg) IAlteration in sensoria or mental >250 >250 >250 7.25-7.3 7.0-7.24 <7.0 15-18 Positive Positive 10 to <15 Positive Positive <10 Positive Positive Variable Variable Variable Alert Alert/ Drowsy Stupor/ Coma I . ..? .? . . ?............................................................................................ .... ......." " " "" " ''''"'''" " " '"'''" '" " '" " " " " " " '" '''" " " " '" '" "''" " " " " " " " " ''" " " " " '" " " '''" " " " " " '" '" ''" " " " " '" " " ''" " '" " "" '" ''"''" " " " '
- 19. MANAGEMENT - Initial Hospital Management: • Fluid Replacement • Potassium Replacement • IV insulin therapy • Bicarbonate and Metabolic Acidosis • Phosphate Depletion • Close Monitoring • Watch for complications - Once Resolved: • • Convert to home insulin regimen Prevent recurrence
- 20. BICARBONATE THERAPY Bicarbonateadministration is also controversial. Several potential harmful effects: If bicarbonate infusion successfully increases the blood bicarbona te concentration, this can reduce the hyperventilatory drive, which will raise the blood pC0 2 . Increase blood C 02 tension is more qu ickly reflected across the blood brain barrier than the increased arterial bicarbona te. This may cause a paradoxical fall in cerebra l pH. Although neurologic deterioration has been attributed to this mechanism, it rema ins a very controversia l effect and, if it occurs, is rare. The ad ministra tion of alkali may slow the rate of recovery of the ketosis Alkali administration can lead to a posttrea tment metabolic alkalosis since metabolism of ketoacid anions with insulin results in the generation of bicarbonate and spontaneous correction of most of the meta bolic acidosis. Source: Uptodate.com Benef it from cautious alkali therapy: Patients with an arterial pH 6.9 in whom d ecreased card iac contractility and vasodila tation can impair tissue perf usion. At an arteria l pH above 7.00, most experts agree that bicarbonate therapy is not necessary, since therapy w ith insu lin and volume expansion will largely reverse the metabolic acid osis. Patients with potentially life-threatening hyperkalemia, since bicarbonate administra tion in academic patients may d rive potassium into cells, thereby lowering the seru m potassium concentration. Source: Up todate.com • • • • • Waiting fortpc.googlesyndication.com...