DIABETIC KETOACIDOSIS (DKA)
Essentials to diagnosis
- Decreased venous bicarbonate
- Ketonuria (urinalysis) - not always
present
- Hyperglycaemia (dextrostix)
+ metabolic acidosis (Venous Blood gas is
sufficient)
Differential Diagnosis - altered mental state and metabolic acidosis
See Coma
See Poisonings
and metabolic acidosis
- Nonketotic hyperosmolar coma
- Alcoholic ketoacidosis
- Lactic acidosis
- Methanol, ethylene glycol or salicylate ingestion
Pathogenesis
Relative insulin deficiency causes:
- Ketonaemia/Ketacidosis - vomiting
- Hyperglycaemia - osmotic diuresis/polyuria
resulting in:
- Metabolic acidosis
- Water Depletion/Dehydration/Shock
- Electrolyte abnormalities/Altered mental status
Clinical Manifestations
|
EARLY |
MIDDLE |
LATE |
HISTORY |
Malaise
Nausea
Polydipsia
Polyuria
Polyphagia |
Vomiting
Abdominal pain
Dyspnoea |
Drowsiness (proportional to the serum osmolality)
Coma |
EXAMINATION |
Dehydration
Acetone breath |
Deep, rapid, and intense breathing
Tachycardia
Fever/Hypothermia (suggests underlying infection)
Abdominal tenderness (resolves with treatment otherwise consider surgical abdomen) |
Kussmaul pattern consisting of deep, sighing respirations
Depressed sensorium
Hypotension |
Resuscitation
- Intubate and ventilate (if comatose)
- 2 X IV lines
- 500ml Normal Saline bolus (if significant tachycardia,
hypotensive, oliguria) repeated every 10 min till signs improve
- Insert IDC
Investigations
- Increased anion gap: [Na (Cl + HCO3)] > 25: (due to ketone
bodies)
- ABG - Metabolic acidosis with respiratory compensation
- Glycosuria/Ketonuria
- Leucocytosis (due to infection or ketosis)
- Low Sodium (may be artifactual due to lipidaemia)
- Normal or Elevated Potassium (but total body depletion)
- Increased plasm osmolality. [2(Na + K) + urea+ BSL]
Consider CXR, ECG, CK, blood cultures looking for precipitants
Definitive Management
Treat Cause
Infection is commonest cause
(fever not always present)
- Infection
- Myocardial infarction
- Stroke
- Trauma
Fluid management
- If Na+ < 155 mmol/L use Normal Saline, If Na+ > 155
mmol/L use 1/2 Normal Saline
- Measure and replace urine output hourly (i.e. replace
previous hour's loss over the following hour)
- Once BSL < 15 mmol/L then calculate degree of
dehydration and replace remaining fluid over next 48 hours in addition to
maintenance
requirements
- Once BSL < 15 mmol/L change from normal saline to 5%
dextrose infusion and continue sliding scale
Unproven association between excess fluid administration
and development of cerebral oedema
Treat acidosis
- 50 units actrapid insulin in 50 mls normal saline in
syringe pump.
- Commence at 4 mls/hr (4 units/hour) on sliding scale (see
below)
- Monitor BSL hourly
- Aim for a fall in glucose of not greater
than 5 mmol/hr.
Glucose (mmol/L) |
Insulin (Units/hr) |
0 - 5 |
Nil |
5.1 10 |
1 |
10.1 15 |
2 |
15.1 20 |
4 |
> 20 |
8 |
- Aim of insulin therapy is to treat acidosis NOT to resolve
hyperglycaemia. There is no urgency to normalise hyperglycaemia for the next 24
hours.
- There is no indication for bicarbonate therapy
Unproven association between excess insulin administration
and development of cerebral oedema
Potassium replacement
- Requires eventual replacement despite initially normal/high
serum levels
- Commence once urine output established or if K+ is
initially low
- Give 5-10 mmol/hr
Phosphate/Magnesium replacement
- Important later but not required in the ED management
Treat complications
- Cerebral oedema - head up, mannitol, intubate/controlled
ventilation
DVT - heparin prophylaxis
- Paralytic ileus/Gastroparesis - NGT
Monitoring
- 1/24 hrly urine output (may require IDC)
- 1/24 hrly BSL (NB 'HI' = BSL > 33 mmol/L)
- 2-4/24 hrly Na+, K+ and venous
blood gases (consider sampling line e.g. large bore cannule in cubital fossa with 3 way
tap instead of repeated venipuncture)
Poor Prognostic Factors
- Renal failure
- Altered mental state
- Hypotension
- Related to underlying disease and pulmonary thromboembolism
Disposal
- Admit all under endocrine unit
- Admit ICU if
- coma
- pH < 7.1
- BSL > 60 mmol/L