Diagnosis of

1
Diagnosis of Diabetic Ketoacidosis

• Diabetic Ketoacidosis (DKA)
• State of absolute or relative deficiency
• Aggravated by hyperglycaemia, dehydration
• acidosis
• Most common causes
• Underlying infection (18)
• Disruption of insulin treatment (25)
• New onset of diabetes (15)
• Other (20)
• Typically characterised
• Hyperglycaemia gt300mg/dL
• Bicarbonate lt15mEq/L
• Acidosis pH lt7.30
• Ketonemia Ketonuria

• Case Details
• 36 year old female
• Presented to Emergency with
• ? lethargy, ? thirst
• ? appetite for 4/7
• Coated dry tongue and occasional vomiting
• Afebrile, no septic symptoms
• Clinically dehydrated, ? perfusion to lower limbs
• History
• Obese patient
• Mother type 2 diabetic
• Cholecystectomy 2 years prior

Further investigative testing
Results Initial Biochemistry Results

• HbA1C
• Glucose binds to HbA forming subtype A1C
• HbA1C level represents past 4 weeks of blood
  glucose level
• Diabetics have elevated HbA1C levels

Fig. 1 Glycerol fatty acid metabolism

• Urine blood cultures
• Consider cause of precipitating event which lead
  to diabetic condition
• Serum GAD Abs IA-2 Abs
• Markers for autoimmune diabetes
• Radioimmunoassay
• GAD Abs have a high predictive value for insulin
  dependency in diabetic patients
• C-Peptide
• Measures level of peptide (inactive amino acid)
  released in equal amounts to insulin
• Type 1 diabetes displays ?insulin C-peptide
• Type 2 diabetes displays normal or ?C-peptide

• Ketones in urine
• ? serum glucose
• HCO3 lt5nmol/L
• ? CRP (possible concurrent infection)
• FBC slightly ?Hb, Hct RCC
• (consistent with pts hydration status)
• pH 7.06 life threatening

Fig. 2 Blood glucose regulation
Dipstick urinalysis done in DEM

• Conclusion
• Although Abs GAD IA-2 from the patient were
  negative, a diagnosis of type 1 diabetes was
  determined based on the extreme presentation of
  marked ketoacidosis, and hugely elevated glucose,
  as well as a borderline normal/low C-peptide
  level.
• Patient management
• Sent to a nutritionalist
• Informed of need for long term insulin therapy
  glucose monitoring

• Suspected diagnosis of Ketoacidosis
• DKA caused by ? insulin availability, causing
  transition from glucose to lipid oxidation
  metabolism.
• Pt becomes dehydrated.
• Goals for treatment are
• Rapid fluid volume expansion to treat dehydration
• Correction of hyperglycaemia hyperketonemia
• Prevention of hypokalemia
• ID/treatment of any associated bacterial infection

Acknowledgements Thanks goes to the staff at the
Royal Hobart Hospital Pathology Unit,
particularly the core lab staff.
Fig. 3 Insulin secretion
References 1. Tachtenbarg DE. Diabetic
Ketoacidosis. American Family Physician. 2005
91705-1714 2. National Diabetes Data Group,
Diabetes in America, 2nd Edition 1995 3. Author
unknown, http//images.google.com/ accessed
07/05/2006 4. The Merek Manual, Diabetic
Ketoacidosis. http//www.merek.com/ accessed
27/03/2006