Diabetic Ketoacidosis

is an acute, major, life-threatening complication of diabetes mainly occurs in patients with type 1 diabetes is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosisproducing derangements in intermediary metabolism

Diabetic Ketoacidosis
defined clinically as an acute state of severe uncontrolled diabetes associated with ketoacidosis that requires emergency treatment with insulin and intravenous fluids Biochemically, as an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level greater than 250 mg/dL, and a blood pH less than 7.3. Ketonemia and ketonuria are characteristic, as is a serum bicarbonate level of 18 mEq/L or less

Precipitating factors include

medications and drugs that affect carbohydrate metabolism such as corticosteroids, thiazides, loop diuretics, sympathomimetics, antihypertensives, anti-histamines, tricyclic antidepressants, alcohol, cocaine and ecstasy Often DKA develops because of an acute illness or infection such as pneumonia or urinary tract infection Pregnancy, gastroenteritis, trauma, burns, surgery, sepsis, pancreatitis, stroke and silent myocardial infarction

Risk Factors Include

Age; preschoool children are most at risk Stress due to co-existing illness or infection Inadequate insulin use or poor management of blood glucose during periods of illnesses are also risk factors
In children, the most common cause of DKA is poor compliance with insulin and/or diet.

In adolescents, eating disroders may contribute in up to 20% of recurrent DKA cases There is no predilection for sex in DKA

4 main characteristics of DKA

1. 2. 3. 4. Hyperglycemia Ketosis and acidosis Dehydration Electrolyte imbalance

Pathophysiology

Clinical Presentation
Feeling unwell for a short period, often less than 24 hours Polydipsia and increased thirst Polyuria/ nocturia Polyphagia Weight loss Nausea and vomiting, vomitus can have coffee-ground colour due to haemorrhagic gastritis Abdominal pain, due to dehydration and acidosis Weakness Neurologic signs: restlessness, agitation, lethargy and drowsiness, coma. Increased osmolality is the main factor that contributes to altered mental status

Clinical Presentation
Deep and rapid breathing, known as Kussmaul breathing, may have acetone odour on breath. Signs of dehydration due to fluid loss through polyuria, vomiting and breathing: reduced skin turgor, dry mucous membranes Signs of hypovolaemia: tachycardia, hypotension, postural hypotension due to fluid loss over 3 litres Mild hypothermia due to acidosis-induced peripheral vasodilation, warm dry skin. Fevers are rare despite infection. Severe hypothermia is a poor prognostic sign.

Diagnostics
Complete blood count Leukocytosis is suggested to be associated with ketosis. Leukocytosis of 10,000-20,000 attributed to dehydration or stress. 30,000+ suggests an infection Blood gas analysis This is done through VBG. This is done to assess pH and bicarbonate status.
Elevated anion gap Computed as [(Na+K) (Cl+HCO3)]. Mild >10 mM, moderate >12 mM, severe >16 mM

Diagnostics
BUN and Creatinine May reveal the presence of renal failure Serum electrolytes K is particularly important. Hyperkalemia may relfect extracellular shift of K due to insulin deficiency and acidosis. Later hypokalemia may reflect depletion of K. Urinalysis to detect ketonuria and glucosuria

Management
1. Oxygenation/ ventilation
1. 2.
3. 4.

1st priority, maintain airway and breathing. If patients GCS<8, consider intubation, else, use an oxygen mask Insert NGT and open to drain if patient regularly vomits Airway, breathing and sensorium have to be constantly monitored
pNSS is most appropriate initially Give 20 mL/kg of pNSS for 2 hr. Then, give 10 mL/kg/hr plain 0.45% NaCl, for the rest, 0.3% NaCl for 5 mL/kg/hr The goal is to decrease serum osmolality by <3mOsm/L/hr

2. Fluid replacement
1. 2. 3. 4.

Management
1. Electrolyte replacement
1. Giving insulin can cause hypokalemia as glucose is transported into cells with K. 2. If K < 3.3 mM, replace with KCl at 10 mM/hr until serum K > 4.4 mM. Place patient on a cardiac monitor while infusing to detect arrhythmias. 3. No need to correct Na abnormalities

2. Insulin therapy
1. Give insulin only when patient has been hydrated 2. Give bolus of 0.1 U/kg then IV drip of 0.1 U/kg/hr 3. Do not reduce glucose by > 4mM/hr or this may cause cerebral edema

Management