Diabetic Ketoacidosis (DKA)

Description

Life-threatening acute Cx of DM characterised by dehydration, hyperglycaemia, glycosuria,

ketonaemia, ketonuria& acidosis. [Biochem: BSL>11, pH <7.3, HCO3

-<15mmol/L, ketonuria/aemia].

Pathophysiology

Inadequate insulin→progressivehyperglycaemia→'cellular starvation'→ ↑release of

glucagon, catecholamines, cortisol and GH → glycogenolysis& gluconeogenesis, ↑BSL

The stress response →proteolysis and lipolysis, forming free fatty acids, which are then

converted to the ketoacids acetoacetate, beta-hydroxybutyrate and acetone.

The high glucose levels cause a huge osmotic diuresis and gross dehydration which may

reduce tissue perfusion and further derange metabolism by causing lactic acidosis

Epidemiology

1-5% T1DM (20% new).T2DM unusual (HONK more likely).Esp young adults or children. 2F:1M.

Precipitating conditions:

Infection (19–56%) e.g. pneumonia, UTI

Inadequate insulin/non-compliance (15–41%)

Undiagnosed diabetes (10–22%)

Other medical illness (10–12%) e.g. hypothyroidism, pancreatitis, inborn errors of metab

Cardiovascular disease (3–6%) e.g. PE, stroke, MI

Other physiological stress e.g. pregnancy, surgery

Drugs e.g. corticosteroids, sympathomimetics, α- and β-blockers and diuretics

Cause unknown (4–33%)                                                                 

Presentation

History

Insidious onset of ↑thirst (polydipsia), worsening polyuria, & weight loss. (Rarely ↑hunger)

Nausea and vomiting are common } non-specific abdominal pain

Lassitude, weakness and fatiguability often occur

Global cerebral symptoms such as confusion and disorientation may be present

Note focal symptoms of infection, dyspnoea, chest pain, palpitations, abdominal pain,

recent changes in medication, episodes of overdose/ingestion of poisons, and EtOH use

If on insulin note regimen and compliance

Examination

Check vitals (T,HR, BP, RR, SaO2, GCS)

Signs of gross dehydration

Ketoticfoetor (pear drops or nail-polish remover)

Respiratory compensation of acidosis can lead to tachypnoea or Kussmaul's respiration

Assess mental status and orientation & neurology

Examine the chest, abdomen, skin for signs of infective precipitant

Check cardiovascular system for signs of cardiac failure, pericardial rub and murmurs

Differential Diagnosis

Alcoholic ketoacidosis

HONK

Lactic acidosis

Causes of metabolic acidosis, e.g. OD

Acute pancreatitis

Septicaemia without ketoacidosis

Acute abdomen

Ketoacidosis due to starvation

Investigations

Bloods: FBC, UEC, Glucose, ABG, anion gap, plasma osmolarity, Trop/CK, amylase, cultures. Note:

Assay of blood ketones is more sensitive and specific but is not always available

GAD, IAA, IA-2 autoantibodies if new T1DM suspected

WCC, Trop/CK, amylase may all be ↑ by DKA itself rather than by a precipitant

Na+ may ↑(dehydration), normal or ↓( pseudohypoNa: Corr.Na=Na + (glu-5.5)/2.75 )

K+ may ↑(acidosis), normal or occ. ↓, but overall there is depletion of body K+;

Cr & Ur rise with pre-renal RF; bicarbonate ↓.

Plasma Osmolarity = 2([Na] + [K]) + [Ur] + [glucose]. >290mOsm/L in cases of DKA.

Consider HONK if >320 mOsm/l and lack of ketonuria or glu>30mmol/L.

Anion Gap = ([Na] + [K]) – ([Cl] + [HCO3] )>13 mEq/l in DKA

Urine: urinalysis for glycosuria and ketonuria. Send for M, C & S

Radiology: CXR (?pneumonia or cardiac failure), CT/MRI (if LOC, ?CVA), LP (if ?meningitis)

Other: ECG

Management

General:           

Triage to resuscitation/acute area. Attach continuous monitoring, weigh if possible

ABCD. Give O2, consider intubation and ventilation if ↓LOC

Obtain large-bore peripheral IV access + sampling line or insert central venous catheter

Consider urinary catheterisation } NG

Intravenous fluid and electrolyte replacement:

Adult: may be sig. dehydrated (10%) can give: 1L NS stat, q1h, q2h unless concern of CCF.

Child: 10-20mL/kg if shocked, beware cerebral oedema. Maintenance+deficit over 48hrs.

Give potassium replacement when K+<5.5 and urine output established &chk UEC q2–4h

Insulin therapy:

Initially 6U/hr (child: 0.05/kg/hr if<5y else 0.1U/kg/hr) short-acting soluble insulin

In adults use a sliding scale for hourly insulin dose based. In children do not ↓insulin.

Hourly BSL. Aim is to reduce plasma glucose by 3–5 mmol/hr after initial fluid bolus.

When BSL<15mmol/l add 5%D (child: 0.45% NaCl+5%D) so BSL 8-12 til pH/ketone norm

Further measures:

HCO3 in rare cases (pH≤6.9) - 0.15 x wt x base deficit mmol (give over 1 hr & reassess)

DKA leads to phosphate depletion but this rarely causes significant clinical problems.

Any precipitating illness should be managed optimally as per current guidance

Progression:

When eating dbl infusion rate while eating +1hr (meals) or +30min (snacks)

If stable (pH>7.3, BSL<12, HCO3>15, no ketonuria) & eating – convert to an sc insulin

regime and wean off infusion 90min after sc dose.

Give this dose before breakfast, lunch, dinner & about half this dose at midnight

Dietician, education, blood testing, and conversion to home insulin