Diabetic Ketoacidosis
Diabetic Ketoacidosis (DKA) potentially life-threatening complication of diabetes mellitus resulting from the consequences of insulin deficiency
Precipitants for DKA
- commonly
- Inadequate insulin in a child or adolescent with known diabetes (eg missed insulin doses, insulin pump failure).
- First presentation of Type 1 diabetes mellitus.
Common triggers of DKA include:
- Absolute insulin deficiency:
- Insulin nonadherence.
- Inadequate dosing of basal insulin.
- Insulin pump failure.
- New diagnosis of diabetes.
- Infection (e.g., gastroenteritis, pneumonia, urinary tract infection, diabetic foot infection).
- Pancreatitis.
- Pregnancy.
- Trauma, surgery.
- Substance abuse or alcoholism.
- Medications:
Ketosis-Prone Type 2 Diabetes (KPD)
- Traditional View: Diabetic ketoacidosis (DKA) has been classically associated with type 1 diabetes, not type 2.
- Emerging Evidence: Increasing cases of DKA are seen in patients with type 2 diabetes, especially among African and African-American populations.
- South African Study: About half of the DKA presentations were due to type 2 diabetes.
- Descriptions: This condition is also known as “ketosis-prone type 2 diabetes,” “type 1.5 diabetes,” or “Flatbush diabetes.”
- Presentation Characteristics:
- Middle-aged, obese, hypertensive.
- Signs of insulin resistance (e.g., acanthosis nigricans).
- Often a positive family history of type 2 diabetes.
- Mechanism: A combination of insulin insensitivity and a transient loss of insulin secretion capacity.
- During Hospital Admission:
- Insulin resistance decreases.
- No autoantibodies typical of type 1 diabetes.
- Insulin secretion recovers, indicated by rising C-peptide levels.
- Long-term Management: These patients often maintain good glycaemic control without insulin injections after recovery.
Evaluation for the cause of DKA
- History and physical examination are the key here. If there is clear history of nonadherence, a big workup isn’t necessary.
- Infectious trigger?
- DKA itself may cause leukocytosis, so a WBC elevation alone is nonspecific.
- Infection is suggested by fever, marked left-shift, or severe leukocytosis (>20,000-25,000).(3101715)
- Primary abdominal problem?
- DKA itself can cause abdominal pain. This creates diagnosis confusion – we must sort out whether the pain is due to DKA, or whether the pain represents an underlying problem (appendicitis, cholecystitis, etc). This may be sorted out in two ways:
- (#1) Severe pain with only mild ketoacidosis argues against DKA causing the pain.(12040551)
- (#2) When in doubt about the need for an abdominal CT scan, aggressively treat the DKA and follow serial abdominal examinations. If the abdominal pain is due to DKA, it will resolve as the ketoacidosis improves. If pain fails to resolve or gets worse, then further investigation is warranted.
- Primary neurologic problem?
- DKA itself may cause mental status changes, but this usually occurs when the calculated serum osmolality is >320 mOsm/kg. Abnormal mental status despite normal serum osmolality should trigger suspicion for a primary neurologic problem (e.g., meningitis, intracranial hemorrhage).(25905280)
- Another sign of a primary neurologic problem is if the mental status doesn’t improve with treatment of the DKA. (Noting also that if mental status deteriorates during therapy, the possibility of cerebral edema should also be considered.)
Diagnostic criteria
- pH < 7.3
- ketosis (ketonemia or ketonuria)
- HCO3 <15 mmol/L due to high anion gap metabolic acidosis (HAGMA)
- hyperglycemia (may be mild; euglycemic DKA can occur)
PATHOGENESIS
- increased glucagon, cortisol, catecholamines, GH
- decreased insulin
- hyperglycaemia
- hyperosmolality + glycosuria
- electrolyte loss
- ketone production from metabolism of TG
- acidosis
HISTORY
- dehydration
- weakness
- fatigue
- abdominal pain (particularly in children).
- glycosuria, leading to:
- Urinary frequency
- Polyuria
- Polydipsia
- Cereberal Signs
- Early: Headache, irritability, lethargy, vomiting
- Later: depressed consciousness, incontinence, thermal instability
- Very late: bradycardia, increased BP, respiratory impairment
- risk factors: non-compliance, illness, newly diagnosed
- ROS to rule find out possible precipitant (infection, MI, pneumonia, GI illness)
- normal insulin regime
- diabetic control
- previous DKA / admissions
- previous ICU admissions
EXAMINATION
- volume assessment
- hypotension
- tachycardia
- Kussmaul respirations – deep fast breathing (tachypnea and hyperpnea)
- fruity breath
- signs of cause e.g. (infection)
- GCS
INVESTIGATIONS
- ABG
- electrolytes
- osmolality
- urinalysis: ketones
- pregnancy test
- standard investigations to rule out cause: FBC, ECG, CXR
MANAGEMENT
- establish precipitant and treat
- assess severity of metabolic derangement
- cautious fluid resuscitation with replacement of body H2O
- provision of insulin
- replacement of electrolytes
Resuscitate
- intubation for airway protection if required
- O2 as required
- IV access
- fluid boluses (20mL/kg boluses of NS/HMN)
- urinary catheter
Acid-base and Electrolyte abnormalities
- will have a severe metabolic acidosis with probable incomplete respiratory compensation
- K+ may be normal but patient will have a whole body K+ deficiency -> needs to be replaced once < 5mmol/L -> use KH2PO4
- Na+ may be deranged
- acidaemia rarely requires HCO3- therapy and will respond to other treatments
Specific therapy
- start insulin infusion (avoid bolus) 0.1u/kg/hr
- aim to lower glucose by 1-2mmol/L/hr
- balanced salt solution fluid resuscitation
- once glucose < 15mmol/L -> provide dextrose (5%) 100mL/hr
- monitor urinary ketones or BE clearance
- correct osmolality by 3mosmol/kg/hr
Underlying cause
- treat infection
- review compliance
- ischaemia (ACS, CVA, PVD, mesenteric ischaemia)
- pregnancy
COMPLICATIONS
- hypoglycaemia
- hyponatraemia
- hyperchloraemic acidosis
- cerebral oedema
- arrhythmias
- venous thrombosis
- infection
- hyperchloraemia