Diabetic emergencies and insulin class.pptx

insulin class

1. Diabetic emergencies and insulin class

2. Diabetic ketoacidosis

3. Diabetic ketoacidosis The most serious acute complications of T2DM. The overall mortality is <1%, but a mortality rate >5% in the elderly has been reported. Mortality in patients with DKA is frequently related to the underlying aetiological prepitant rather than the metabolic sequelae of hyperglycaemia or ketoacidosis.

4. Principles of management Correction of dehydration Correction of electrolyte imbalance Insulin therapy Treatment of precipitating factor Prevention of complications

5. Initial assessment History and physical examination Look for precipitating causes Infection Missed therapy Non-adherence ACS CVA Surgery and drugs Investigations Capillary and venous plasma glucose VBS Blood or urinary ketones BUSE and Creatinine FBC Urinalysis If indicated: Blood cultures, CXR and ECG

6. Diagnostic criteria Capillary plasma glucose >11 mmol/L Capillary ketones >3 mmol/L or urine ketones >= 2+ Venous pH <7.3 and/ or bicarbonate <15 mmol/L High risk factors Elderly Pregnancy Heart and kidney failure Other serious co-morbidities

7. Clinical parameters for severe DKA Venous HCO3 <5 mmol/L Plasma ketones >6 mmol/L Venous pH <7.1 Hypokalaemia <3.5 mmol/L GCS <12 SpO2 <92% on air SBP <90 mmHg HR >100 bpm Anion gap >16

8. Aim of treatment Rate of fall of ketones of at least 0.5 mmol/L/hr OR HCO3 rise of 3 mmol/L//hr Plasma glucose fall of at least 3 mmol/L/hr Maintain serum K+ within normal range

9. Hyperglycemic Hyperosmolar State

10. Hyperglycemic hyperosmolar state ● A life-threatening emergency and should be suspected in patients with T2DM who are very ill with significant hyperglycaemia. ● Elderly with multiple comorbidities are more prone ● Has higher mortality rate than DKA and more vascular complications like ○ Myocardial infarction ○ Stroke ○ Peripheral arterial thrombosis ● unlike DKA which progress within hours, HHS progress over days ○ severe dehydration and metabolic disturbances

11. ● Severe dehydration (hypovolemia) ● Marked hyperglycaemia (plasma glucose >30 mmol/L) ● Serum osmolality >320 mosmol/kg Diagnostic criteria There is no significant ketonaemia (<3.0 mmol/L) or acidosis (pH >7.3, HCO3 - >15 mmol/L). When significant acidosis is present, a mixed picture of HHS and DKA should be considered. However, other causes of acidosis (lactic acidosis, sepsis and poisoning) should be excluded.

12. Precipitating factors Infection Poor adherence to treatment omission of insulin or OGLDs Presence of acute concomitant illness A cardiovascular insult like stroke, angina pectoris, and myocardial infarction can also trigger a stress response. This leads to the release of counterregulatory hormones with the resultant effect of an increased level of blood glucose, causing osmotic diuresis and dehydration, with the final result being HHS. Medication thiazide diuretics, beta-blockers, glucocorticoids, and some atypical antipsychotics Clinical features Mental changes, such as confusion, delirium or experiencing hallucinations . Loss of consciousness. Dry mouth profound dehydration and extreme thirst Frequent urination , polyuria Blurred vision or loss of vision.. Coma, Unconscious drowsiness

13. Treatment goals in HHS › correction of dehydration, › correction of electrolyte imbalance, › control of hyperglycaemia, › treatment of precipitating factors, › prevention of complications.

14. Insulin initiation

15. Insulin initiation Insulin therapy should be considered in the following situations: inadequate glycaemic control on optimal dose and number of OGLD as initial therapy in newly diagnosed T2DM in presence of symptomatic hyperglycaemia when HbA1c >10% or FPG >13.0 mmol/L as short-term use in the following acute illness or surgery Pregnancy Breast-feeding severe metabolic decompensation (DKA, HHS)

16. Insulin initiation Initially to start at low dose to prevent hypoglycemia to perform self monitoring blood glucose (SMBG) 6 point (pre and post each meal) Then gradually, safely and promptly titrate according SMBG level Basal: 10U a day or 0.1-0.2U/kg/day. Increase by 2U every 3 days to reach target FPG without hypoglycemia Adjust 2U every week based on 3 days glucose readings The main advantage of insulin over other GLDs is that insulin lowers glucose in a dose-dependent manner to almost any glycaemic target. The main limitation of insulin is hypoglycaemia.

17. Types of insulin Prandial insulin administered pre-meal Controls postprandial glucose Basal insulin administered once or twice daily C overs the basal insulin requirements in between meals and through the night Premixed insulin short/rapid-acting insulin with intermediate-acting insulin covers both postprandial glucose excursion as well as basal insulin needs Co-formulation insulin combination of a rapid acting and basal insulin existing separately in one formulation. Components do not interact with each other

18. Insulins pics

19. INSULIN PHARMACOKINETICS AND PHARMACODYNAMICS Biochemical action: Diminish hepatic glycogenolysis inhibit glycogen phosphorylase Promote hepatic glucose glycogen storage (glycogen synthethase) Inhibit hepatic gluconeogensis Inhibit lipolysis-inhibit hormone-sensitive lipase Promote active transport of amino acid into cell

20. References CPG Management of T2DM 6th edition Sarawak Handbook of medical emergencies