Acute Medicine Seminar

1. Acute Medicine Seminar (Diabetic Ketoacidosis) Yeo See Seng, Adrian 19/1/05

2. Diabetic Ketoacidosis Case Study

3. History • 16 year old Malay male • Admitted to A&E to Surgical ward for acute onset of severe epigastric pain associated with vomiting. • No past history of note

4. Examination • Low grade fever, 37.5 degree Celsius • Drowsy • Dehydrated • RR: 28/min • PR: 129/min • BP: 110/60 • Abdomen: epigastric tenderness, otherwise soft, no masses felt. Bowel sounds normal. • No other abnormal findings.

5. Investigations • FBC: TW 20000; Hb, platelet normal • Urine glucose 3+; Acetone 2+ • Blood gas pH: 7.23 pO2: 131mmHg pCO2: 15.1 mmHg HCO3: 6.3mmol/L SaO2: 98.5% Anion gap: 41 =(Na)-(HCO3+Cl)

6. Investigations • Biochemistry Urea: 6.8mmol/L (2.5-7.5) Na+: 132mmol/L (135-150) K+: 4.9mmol/L haemolysed (3.5-5.0) Cl-: 83mmol/L (95-105) CO2: 8mmol/L (22-31) Creatinine: 187umol/L (62-133) Glucose: 61.7mmmol/L (4.0-7.8) Uric acid: 1069 umol/L (149-506) • Serum osmolality: 2(Na)+glu+urea= 333

7. Investigations • Biochemistry Total protein: 88g/L (60-82) Albumin: 48g/L (35-50) Globulin: 40g/L GGT: 512U/L (5-80) ALT: 109U/L (5-55) AST: 167U/L (5-45) ALP: 192U/L (38-126) LDH: 880U/L haemolysed (300-650)

8. Investigations • Biochemistry Bilirubin, unconj: 9umol/L (0-22) Bilirubin, conj: 2umol/L (0-8) Bilirubin, total: 11umol/L (1-33) Anion gap: 46mmol/L (10-18) Amylase: 871U/L (0-110)

9. Biochemical Results • Diabetic ketoacidosis Low pH, HCO3-, high anion gap (metabolic acidosis), ketones+, glucose+, raised amylase, young age • Low pCO2: Hyperventilation due to DKA • Low Cl-: vomiting • Raised Creatinine, uric acid: dehydration

10. Biochemical Results • Raised total protein and liver enzymes: liver impairment due to dehydration? • Low Na+: Pseudohyponatraemia • Raised total white: infection

11. Diabetic Ketoacidosis • A metabolic emergency in which hyperglycaemia is associated with a metabolic acidosis due to greatly raisedketone levels. • Occurs in type 1 diabetes only. • Causes: previously undiagnosed DM, interruption of insulin therapy, stress ofintercurrent illness.

12. Clinical Features • Polyuria • Polydipsia • Lethargy • Anorexia • Hyperventilation • Ketotic breath • Dehydration • Vomitting • Abdominal pain • Coma

13. Clinical Evaluation • Vital signs: BP, HR, conscious level (10% comatose), state of dehydration. • Respiration: Kussmaul breathing, may be depressed in severe acidosis • Pyrexia: <10% despite high incidence of infection. • Look for cause

14. Investigations • Bedside fingerprick glucose and lab estimation of plasma glucose. • U&E, ABG, blood lactate • Serum CK and CKMB (if indicated) • Urine ketones (+plasma ketones if available) • ECG, CXR • Septic workup: FBC, blood and urine culture, sputum culture

15. Management • Replace fluids with normal saline • Replace electrolyte losses • Restore acid base balance • Replace deficient insulin • Monitor blood glucose closely • Replace energy losses • Treat underlying cause

16. Fluids • IV normal saline at 15-20ml/kg/hr (1-1.5L) in 1st hr with recourse to colloids if patient is still hypotensive (caution in cardiac & renal compromised patients) • Subsequent infusion rate (4-14ml/kg/hr) depend on hydration and urine output. • If corrected serum Na+ is low, continue IV normal saline. • If corrected serum Na is high or normal, change to 0.45% NaCl.

17. Fluids • Corrected serum Na = Na+(Glucose-5)/3.5 • 148=132+(61.7-5)/3.5 • Fluid replacement should correct estimated deficit within 1st 24 hr. • Serum osmolality should not decrease more than 3momsm/kg/hr to avoid cerebral oedema. • Monitor strictly hlry fluid input, urine output, BP, pulse rate, with CVP as necessary. Check U&E every 2-4hrs till stable.

18. Insulin • Give bolus IV soluble insulin (SI) 5-10 units, follow with IV SI infusion 0.1unit/kg/hr. (~3-5units/hr) • Repeat IV SI bolus if blood glucose level does not decrease by at least 3mmol/L after 1st hr of IV SI infusion. • Monitor finger prick blood glucose hrly and adjust insulin infusion rate every 1-2hr to reduce blood glucose by 3-6mmmol/hr, until blood glucose is <14mmol/L.

19. Insulin • When blood glucose falls to <12mmol/L decrease IV SI infusion rate to 0.05-0.1unit/kg/hr (~2-4 units/hr) and start IV dextrose infusion. • Keep blood glucose between 8-12mmol/L. Maintain IV SI and dextrose infusion until DKA resolve. • DKA resolution: pH>7.3, anion gap<12, HCO3- >18

20. Insulin • When DKA resolves, stop IV SI, commence SC SI (between 4-14 units) 4 hrly. • Stop IV SI infusion only 1-2 h after 1st SC administration. Maintain IV dextrose till oral feeding is tolerated. Keep blood glucose between 8-12mmol/L. • Monitor blood glucose every hour with bedside meter until it is 12-14mmol/L and every 2-4hr thereafter.

21. Replace Energy Losses • Let patient eat as soon as possible. When oral diet is well tolerated, stop IV dextrose. • Start S/C SI insulin regime before breakfast and dinner. • Monitor glucose premeals and bedtime.

22. Potassium • Insulin therapy, volume expansion and correction of acidosis will lower serum K+ • K+ replacement is given as IV KCL 7.45% mmol/hr • Ensure adequate urine output prior K+ replacement. • Keep serum K+ at 4-5mmol/L • Monitor serum K+ every 2-4 hours till stable.

23. Bicarbonate • Replacement not necessary unless pH<7.0 • If arterial pH<7.0 repeat blood gas after 1 hour of hydration. • If pH still < 7.0, give 8.4% NaHCO3- 50-100mmol in 200ml sterile water over 1 hour as slow infusion. • Check pH 1 hour later, repeat HCO3- if needed till pH rises to 7.1

24. Treat Underying Cause • Treat precipiating factors and co-morbid conditions like AMI and infection.

25. Monitor and Flow Chart • Intensive and continual monitoring of clinical, laboratory and fluid and electrolyte therapy parameters against date/time till DKA has resolved and patient’s condition is stable.