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Last updated: ACS (Acute Coronary Syndrome)
on September 06, 2010

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)

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


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 Diagnosis

HONK
Hyperglycaemia and other causes metabolic acidosis (eg aspirin overdose and lactic acidosis)

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


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

review 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