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The case history

The case history.

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The case history

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  1. The case history Mr CB, aged 40, has had type 1 diabetes since he was a child. He was brought in to the A & E confused & lethargic. One week ago he had an URTI & also developed polyuria, nausea & abdominal pain. His regular medications include Insulin & Ramipril. For the past three days he has been off his food. To compensate, he stopped injecting his insulin, despite increasing BSL levels ranging from 7.9 to 12.5 mmol/L. On examination he was lethargic, postural hypotension, HR 100, RR 30 & febrile. His mucous membranes were dry, skin trugor was poor, his breath was fruity in odour, disorientated & confused. Clinical Pathology B Case A Acute Diabetes

  2. What is DKA? • DKA: Metabolic disorder • 3 concurrent abnormalities: • Hyperglycemia, Hyperketonemia & Metabolic acidosis. • Generally caused by either: • Absolute deficiency of insulin OR • Relative deficiency: • Excess of counterregulatory hormones: • Glucagon, Catecholamines, Cortisol & GH. Clinical Pathology B Case A Acute Diabetes

  3. Pathophysiology of DKA • Hyperglycemia = osmotic diuresis • ’s tubular reabsorption of fluid • Draws H2O, Na, K, Mg, Ca & P from circulationurine. • Large losses of fluid in urine & vomiting leads to both intracellular & extracellular dehydration. Clinical Pathology B Case A Acute Diabetes

  4. …Pathophysiology DKA • KA results from ed ketone synthesis & release. • ’s in both acetoacetate & [beta]- hydroxybutyratehyperketonemia induces metabolic acidosis respiratory compensation. • Acetoacetic acidAcetone accumulates & slowly disposed of by respiration. Clinical Pathology B Case A Acute Diabetes

  5. Clinical Presentation • Polydipsia, polyuria,fatigue & weakness osmotic diuresis • Abdominal pain & vomiting ketoacidosis • Lethargy & alterations in consciousness serum osmolality Clinical Pathology B Case A Acute Diabetes

  6. …Clinical Presentation • Tachypnea & Kussmaul’s respiration's compensate for metabolic acidosis • Fruity odor of acetone in breath • Signs of dehydration on physical examination • skin, mucous membranes Clinical Pathology B Case A Acute Diabetes

  7. Laboratory Assessment • Urea 17 mmol/L 3-8 • Creat 0.225 mmol/L 0.05-0.12 • pH 7.15 7.36-7.44 • Bicarb 9 mmol/L 24-32 • Glucose 38 mmol/L 3-8 • Osmolality 220 mmol/L 265-285 • Ketones Very high (multistix) Clinical Pathology B Case A Acute Diabetes

  8. Explain the likely precipitating factors for DKA in this case. ? Clinical Pathology B Case A Acute Diabetes

  9. The case history Mr CB, aged 40, has had type 1 diabetes since he was a child. He was brought in to the A & E confused & lethargic. One week ago he had an URTI & also developed polyuria, nausea & abdominal pain. His regular medications include Insulin & Ramipril. For the past three days he has been off his food. To compensate, he stopped injecting his insulin, despite increasing BSL levels ranging from 7.9 to 12.5 mmol/L Clinical Pathology B Case A Acute Diabetes

  10. What causes DKA? HYPERGLYCEMIA Clinical Pathology B Case A Acute Diabetes

  11. Precipitating factors Mr CB, aged 40, has had type 1 diabetes since he was a child. He was brought in to the A & E confused & lethargic. One week ago he had an upper respiratory tract infection & also developed polyuria, nausea & abdominal pain. His regular medications include Insulin & Ramipril. For the past three days he has been off his food. To compensate, he stopped injecting his insulin, despite increasing BSL levels ranging from 7.9 to 12.5 mmol/L Clinical Pathology B Case A Acute Diabetes

  12. Lack of insulin leads to ketoacidosis because insulin has inhibitory effect on ketogenesis. • Free fatty acids are released from adipose tissue & oxidised. Long chain fatty acid CoA transporter facilitates uptake of the fatty acids in to the mitochondria. Insulin directly inhibits this transporter. • The ketoacids that are formed have the function of providing the body with energy when glucose isn’t available. Clinical Pathology B Case A Acute Diabetes

  13. Can DKA occur in type 2 diabetes? YES rarely… Clinical Pathology B Case A Acute Diabetes

  14. Type 2 diabetes • Glucotoxicty vs Insulin deficiency • Type 2 diabetics have insulin available to inhibit ketogenesis. • Thus ketoacids are not formed & there is no consequent acidity. Clinical Pathology B Case A Acute Diabetes

  15. Sick Day Management • General Protocol • Continue Usual Insulin • Eat As Per Usual • If Not Have 15g Cho’s • If Not Fluids Every Few Minutes • Monitor Ketones & BSL • Test Urine for Ketones Every Time Urine Is Passed Clinical Pathology B Case A Acute Diabetes

  16. What To Do With BSL Results • BSL -Check BSL every 2-4 hours if: >12mmol/L <12mmol/L Unsweetened Fluids Sweetened Fluids Clinical Pathology B Case A Acute Diabetes

  17. Other Checks • Body Temp - elevated above 37.5º • Breathing rate -  • Pulse -  • Bodyweight -  • Contact Dr or go to hospital if: • your BSL remains > 17mmol/L • Mod. to large ketones present in urine • Vomiting any food or fluids  Clinical Pathology B Case A Acute Diabetes

  18. Implementation Avoids… • DKA - Diabetic ketone Acidosis • Dehydration • Coma Clinical Pathology B Case A Acute Diabetes

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