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Last updated: Hypothermia
on May 21, 2013

Diabetic Ketoacidosis (DKA)

Key facts:

Authors: Kate Outterside, Sailesh Sankar, Ateeq Syed
Top Tip: Give a lot of fluids, but don't cause cerebral oedema

Key Differential Diagnoses

  • HONK
  • Hyperglycaemia + other causes of metabolic acidosis (eg lactic)
  • Hyperglycaemia + other causes of drowsiness

Key Investigations

  • Glucose (BM) + Capillary Blood Test for ketones
  • FBC, ESR, CRP
  • U+E, LFT, Bone, Glucose, HbA1C ± Troponin T
  • ECG, CXR
  • ABG, BC
  • Urinalysis (ketones?) ± MSU

Key Treatment

  • INSULIN (ACTRAPID, 50 units in 50 mls N saline), start infusion at 0.1 units/kg/hr
  • SC ENOXAPARIN 40 mg od
  • IV + FLUIDS + K

Key Management Decision

  • ITU

Background

80-90% patients are already known to have DM1; for the rest, it may the the first presentation

Introduction

  • DKA is one of the most important acute complications of DM (mainly Type 1; occasionally Type 2) and can be the first presentation of Type 1 DM (10-20%); ie more usually patient is known to have Type 1
  • Blood glucose does not have to be high (ie euglycaemic DKA can occur) 
  •  Diagnosis requires ketosis and acidosis. To establish a diagnosis, you need to demonstrate: glucose >11.1, ketonuria 2+, pH <7.3, and HCO3 <15
  • But, milder metabolic disturbance may be present 'on the way' to 'full DKA'
  • Either way, patients are water, sodium and potassium depleted; and acidotic. It can present over hours, though more usually 1-3 days
  • Aim for gradual fall in glucose
  • Watch out for cerebral oedema esp in pts <30y, with Na that fails to rise with rehydration
  • Prognosis: with modern fluid management, mortality rate is about 2%. Before the discovery of insulin in 1922, the mortality rate was 100%
  • People with diabetes also have CVAs, take overdoses and have head injuries

Pathophysiology

DKA pathophysiology

Definition

  • (Ketoacidotic) hyperglycemia, that mainly occurs in Type 1 DM

Aetiology

  • 1st presentation of Type 1 DM (10-20%)
  • Genetic
  • Autoimmune

Precipitants

  • Infection
  • Surgery
  • MI
  • Pancreatitis
  • Non-compliance

Symptoms

  • Polyuria/polydipsia
  • Weight loss
  • Vomiting/abdominal pain (can present as 'acute abdomen')
  • Genital candida
  • Visual blurring
  • Confusion

Key Questions

  • "Have you stopped taking/changed your insulin recently?"
  • "Have you had an infection recently?"

Signs

  • Fever, dehydration (low BP, tachycardic?)
  • Smell of ketosis on breath
  • Hyperventilation (Kussmaul's breathing; appears as SOB)
  • Genital candida
  • Reduced level of consciousness

Investigation

Note: patients with Type 2 DM can also have DKA; ketonuria does not equate with ketosis

Blood

  • Glucose (BM) + Capillary Blood Test for ketones (separate ketone test strip)
  • FBC (WC can be raised in absence infection), ESR, CRP
  • U+E, LFT, Bone, Glucose
    Note: glucose usually > 11 mmol/L; but DKA can occur with glucose <10 mmol/L; euglycaemic DKA can even occur
  • HbA1C, Troponin T (myocardial infarction can precipitate DKA)
  • Consider BHCG in women
  • BC
  • Amylase
    Note: pancreatitis can precipitate DKA but amylase can be raised in the absence of pancreatitis (salivary origin?)
  • ABG (need to make diagnosis; to make diagnosis pH <7.3 ± serum bicarbonate <15 mmol/L)
    Note: serial blood gases can be venous blood

Other

  • Urinalysis: ketones?; these are notoriously unreliable, with a significant false positive rate; ie there are a lot of old/frail patients with DM, who come in with ketonuria 1+ or 2+ who do not have DKA
    Note: ketonuria does not equate with ketoacidosis
  • ± MSU (infection?)
  • ECG (silent MI?; if abnormal, do Troponin T)
  • CXR (infection?)

Key Investigations

  • Glucose
  • Urinalysis
  • ABG
  • To establish a diagnosis: Glucose >11.1, Ketonuria 2+, pH <7.3, HCO3 <15

Differential Diagnoses

  • HONK
  • Hyperglycaemia + other causes of metabolic acidosis (eg lactic, salicylate OD)
  • Hyperglycaemia + other causes of drowsiness

Treatment

Principles: replace fluid, correct electrolytes, give insulin, look for+Rx infection

Treatment (first line)

Drugs

  • INSULIN (ACTRAPID, 50 units in 50 mls N saline)
    Start infusion at 0.1 units/kg/hr = 7 units/hr for 70kg person
    Blood gluc (mmol/L)                    Insulin infusion (units/h)
    0-4.0                                            0.5
    4.1-7                                            1
    7.1-10                                          2
    10.1-12                                        3
    12.1-16                                        4
    >16.1                                           6
    Measure BM hourly and titrate insulin accordingly
    Note: aim for fall in glucose > 3mmol/L/h; and, do not stop insulin infusion, until SC insulin re-established
    Note: if on basal bolus regime, continue basal long acting insulin (such as glargine); if patient on an insulin pump, contact diabetologist
  • SC ENOXAPARIN 40 mg od
  • ± BROAD SPECTRUM AB (according to local policy), if infected

Procedures

  • BM (hourly), VBG hourly until normal then 2 hrly, lab bloods twice daily, K 2-4 hrly
  • NG tube, if drowsy (prevent aspiration)
  • IV + FLUIDS + K (N Saline ± K; until BG < 15, then use 5% dextrose)
  • 1L in 30 mins; 1L in 1h; 1L in 2h; then 4 hourly until rehydrated (aim approx 8-10L over 48h); keep IV fluids going whilst on insulin infusion
    Serum K                                      K added to each litre
    <3.5                                           40 mmol
    <3.5-5.0                                     20 mmol
    <5.0, or anuric                            No supplements
    Note: aim to replace approx 8-10L in 48h (less in elderly, or patients with CCF)

Key management decision

  • ITU/not

Treatment
(second line)

Drugs

  • If cerebral oedema, IV MANNITOL 0.25-2 g over 30-60 mins (usually 100 mls 20%), if cerebral oedema; repeated 1-2x after 4-8 hrs

Procedures

  • If hypotensive, start with IV colloids
    If unwell, urinary catheter, CVP, arterial line

Prescribing issues

  • Keep IV going whilst on insulin infusion

Admit?

  • Always

Bed plan

  • Medical admission ward
  • ± Endocrine
  • ± ITU

Referrals

Medical

  • Endocrine
  • ± ITU

Other

  • Hospital DM nurse ± Community DM nurse)

The Rest

Community follow-up is important: ring GP or community DM nurse, or both

Complications

  • Of infection
  • Hypoglycaemia (over-zealous use insulin)
  • Hypokalaemia (insulin causes shift of K into cells)
  • Cerebral oedema (especially children; Rx mannitol/dexamethasone)
  • Phosphate/magnesium may decrease
  • Thromboembolism

Follow-up

  • Hospital DM nurse ± Community DM nurse + GP

Prognosis

  • With modern fluid management, mortality rate is about 2%. Before the discovery of insulin in 1922, the mortality rate was 100%
  • Poorer if shock, oliguria, first presentation Type 1 DM, severe acidosis (pH <7.1), cerebral oedema

2° Prevention
+ Health promotion

  • Education
  • Encourage compliance
  • Seek help if cannot give themselves insulin (or run out), or BG > 20 mmol/L, or if infected

Don't forget

  • K may fall rapidly
  • Aim for gradual fall in glucose
  • Exclude MI and infection

Red flags

  • Reduced level of consciousness (cerebral oedema?)
  • Severe sepsis/shock
  • Severe acidosis (pH <7.1)
    Note: if so, manage on ITU

References

international guidelines US/ADA: Hyperglycemic crises in adult patients with diabetes: A consensus statement from the American Diabetes Association. Kitabchi AE et al. Diabetes Care; 29: 2739-48, 2006

national guidelines UK: Emergency management of diabetic ketoacidosis in adults. R D Hardern RD et al. EMJ; 20: 210–213, 2003

UK/DoH: National Service Framework for Diabetes: Standards, 2001

reviews Diabetic ketoacidosis (DKA) in Birmingham, UK, 2000-2009: an evaluation of risk factors for recurrence and mortality. Wright J et al. British Journal of Diabetes & Vascular Disease; 9: 278-282, 2009

Type 1 Diabetes. Daneman D. Lancet; 367: 847–58, 2006 (pdf)

Endocrine emergencies. Savage MW et al. Postgrad Med J; 80: 506-515, 2004

Kitabchi AE et al, Endotext.com, 2008