Diabetic Ketoacidosis

Diabetic Ketoacidosis
Aim(s) and objective(s)
This guideline aims to provide information on how to recognise, diagnose and manage Diabetic
Ketoacidosis, a life threatening, medical emergency associated with Type 1 Diabetes. Use of the
supporting documentation should improve consistency in approach to the management of this
condition in the acute setting, improving record keeping and information governance.
Author(s)
Dr Susan Arnott, Lead Clinician, Diabetes MCN, NHS Lanarkshire
User group
Primary Care
Scottish Ambulance Staff
Accident and Emergency clinicians
Acute physicians
Diabetes specialist staff
This guideline is not intended to serve as a protocol or standard of care. This is best based on all
clinical data available for an individual case and may be subject to change as scientific knowledge
and technology advances and patterns of care evolve. Adherence to guideline recommendations will
not ensure a successful outcome in every case, nor should it be construed as including all proper
methods of care or excluding other acceptable methods of care aimed at the same result. Ultimately
a judgement must be made by the appropriate healthcare professional(s) responsible for a particular
clinical procedure or treatment plan following discussion with the patient, covering the diagnostic
and treatment options available. It is advised that any significant departure from the guideline
should be documented in the patient’s medical record at the time the decision is taken.
This guideline relates to treatment of Diabetic Ketoacidosis in ADULTS.
Guideline
This is a general guide for adults. Fluid volumes and insulin doses may not be
appropriate for every patient e.g. in young or very small
Diabetic ketoacidosis (DKA) is a medical emergency, usually seen in Type 1 Diabetes, with a
significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA
is characterised by hyperglycaemia, acidosis, and ketonaemia. It may present at diagnosis (20%).
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Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is
not a reliable indicator of diabetic ketoacidosis and the blood glucose may rarely be normal or
only slightly elevated in DKA)
Metabolic acidosis - Bicarbonate (HCO3) below 18 mmol/L and H+>45mmol/L
Significant ketonuria (more than 2+ on standard urine sticks) or ketonaemia (3mmol/L and
over)
Severe DKA = HCO3 <5mmol/L or H+>80mmol/L
Precipitating conditions
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Infection, e.g. pneumonia, urinary tract infection
Inadequate insulin or non-compliance
Other illnesses, e.g. pancreatitis, pulmonary embolism, hypothyroidism
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Cardiovascular disease, stroke, myocardial infarction
Cause unknown (4-33%)
Physiological stress – menstruation, pregnancy, trauma or surgery
Drugs – corticosteroids, sympathomimetics, α- and β-blockers and diuretics
Presentation
Taking a history should not delay the time to treatment. Check capillary blood
glucose and blood gases promptly. If these suggest diabetic ketoacidosis (DKA) then
immediately begin resuscitation and management.
History
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The most common early symptoms of DKA are:
o An insidious onset of increased thirst (polydipsia)
o Worsening polyuria
o Weight loss (especially if first presentation)
o Nausea and vomiting
o Nonspecific abdominal pain
o Lassitude, weakness
o Breathlessness due to an increase in respiratory rate, attempting to compensate by
blowing off CO2
Global cerebral symptoms (e.g. confusion, disorientation), which may progress to comatose
state
Enquire about:
o Symptoms of the common precipitants, e.g. fever, dyspnoea, chest pain, palpitations,
abdominal pain
o Recent changes in medication
o Recent alcohol intake
Recent insulin regimen and dietary patterns
Examination
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Unwell, dehydrated with a tendency for rapid deterioration.
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Dry mucous membranes
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Decreased skin turgor/skin wrinkling
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Sunken eyes
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Slow capillary refill
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Tachycardia with weak pulse
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Hypotension
Check temperature, pulse and blood pressure
Smell the breath for the characteristic fruity/musty odour of ketones - the smell is akin to
pear drops or nail-polish remover
Respiratory compensation of acidosis can lead to tachypnoea or Kussmaul's respiration (very
deep, slowly rhythmic breathing)
Examine the chest for signs of pneumonic consolidation
Check cardiovascular system for signs of cardiac failure, pericardial rub and murmurs
Examine the abdomen to identify any intra-abdominal precipitant
Assess mental status and orientation
Perform a screening neurological examination (assess Glasgow Coma Scale)
Check the skin surface for evidence of abscesses, boils or other rashes
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Differential diagnosis
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Alcoholic ketoacidosis
Hyperosmolar hyperglycaemic non-ketotic state
Lactic acidosis
Other causes of metabolic acidosis e.g. aspirin overdose, methanol/ethylene glycol ingestion
Acute pancreatitis
Septicaemia without ketoacidosis
Acute abdomen
Ketoacidosis due to starvation
Investigations
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Capillary blood glucose (remember to send a plasma glucose also)
Urine dipstick testing shows marked glycosuria and ketonuria (also send urine for microscopy
and culture)
Assay of blood ketones is more sensitive and specific in detecting ketonaemia but is not
always available
Blood tests:
o Plasma glucose is usually elevated, normoglycaemic DKA can occur but is rare
o Full blood count (FBC) - raised white cell count (WCC) is often seen but this does not
necessarily indicate sepsis as it may occur in diabetic ketoacidosis (DKA)
o Electrolytes – Sodium (Na+) may be high due to dehydration, low due to interference
of glucose/ketones with assay, or normal; Potassium (K+) may be high due to the
effect of acidosis, normal or occasionally low but overall there is cell depletion of K+
o Urea and creatinine - elevated due to prerenal failure or where renal impairment is
the primary cause. Creatinine can also be falsely elevated by ketonaemia
o Blood gases (Venous not arterial blood gases should be checked unless suspect
hypoxia eg abnormal CXR, low O2 sats or patient extremely unwell) - metabolic
acidosis with low pH and low HCO3; pCO2 usually low due to respiratory compensation
o Blood cultures
12 lead ECG (Troponin levels - if myocardial ischaemia/infarction suspected)
CXR
Other investigations as indicated by history, examination and response to treatment e.g.
creatine kinase – if rhabdomyolysis is suspected (also increased in myocardial infarction),
Amylase - if pancreatitis is suspected
MANAGEMENT
Assessment of severity
Patients should initially be managed in “rescus.” area in A&E and once stabilized in a medical high
dependency ward (where available).
The presence of one or more of the following may indicate severe DKA. Consider admission to
intensive care/referral for review by ITU team.
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Bicarbonate level below 5 mmol/L
Hypokalaemia on admission (below 3.5 mmol/L)
Glasgow coma scale (GCS) less than 12
Oxygen saturation below 92% on air (assuming normal baseline respiratory function)
Systolic blood pressure below 90 mm Hg
Pulse rate over 100 or below 60 beats per minute
Blood ketones above 6 mmol/L – if available
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Initial management and monitoring
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Immediate resuscitation as required
Put patient on SaO2 monitor, continuous ECG monitor and blood pressure/heart rate monitor
Obtain 2 large-bore peripheral intravenous (IV) access or insert central venous catheter
Urinary catheterisation is usually carried out to monitor urine output, will also allow urinalysis
Prophylactical dose low molecular weight heparin unless contraindication
In unconscious, drowsy or vomiting patients, consider passing a nasogastric tube
Contact the Diabetes Specialist Team at an early stage
Correct dehydration
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The main aims for fluid replacement are to restore circulatory volume, clearance of ketones
and correction of electrolyte imbalance
The fluid deficit should be replaced as crystalloid (0.9% sodium chloride solution is the
recommended fluid of choice). In patients with kidney failure or heart failure, as well as the
elderly and adolescents, the rate and volume of fluid replacement may need to be modified
Insulin therapy
• Insulin is required for suppression of ketogenesis, reduction of blood glucose and correction
of electrolyte imbalance
• IV insulin infusion should be commenced. Soluble human insulin should be used (i.e. actrapid
or humulin S). For usual adult protocol this would be at a rate of 6 units per hour until blood
glucose <15 then reduce to 3 units per hour
• Aim to reduce capillary blood glucose by 3 mmol/L/hour (rapid reduction of glucose causes
rapid changes in serum osmolality and may precipitate cerebral oedema)
• A priming dose (bolus) of insulin should not be used
• Long-acting insulin analogues should be continued as normal (fast acting insulins and
mixed/biphasic insulins should be discontinued until DKA resolved)
• Introduction of 10% glucose is recommended when the blood glucose falls below 14 mmol/L.
It is important to continue 0.9% sodium chloride solution to correct circulatory volume.
Glucose should not be discontinued until the patient is eating and drinking normally
• Convert back to an appropriate subcutaneous regime when biochemically stable i.e. acidosis
resolved (including normal bicarbonate) and the patient is ready and able to eat. If
patients long acting/biphasic insulin has been discontinued (i.e. patient has no long acting
insulin on board) then IV insulin must not be stopped until patient has had subcutaneous
long acting insulin with at least 30 minute overlap and done around the time of a meal so
subcutaneous short acting insulin will also be given. This is because IV soluble insulin has a
half life of approximately 10-15 minutes and DKA can rapidly recur in patients with type 1
diabetes who have no endogenous insulin. Contact diabetes team for advice if unsure
Metabolic treatment
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The recommended targets are (if these rates are not achieved then the fixed-rate IVII rate
should be increased):
o Increasing the venous bicarbonate by 3 mmol/L/hour
o Potassium being maintained between 4.0 and 5.0 mmol/L:
Hypokalaemia and hyperkalaemia are potentially life-threatening conditions during
the management of diabetic ketoacidosis (DKA)
Because of the risk of prerenal acute kidney injury associated with severe
dehydration, it is recommended that no potassium be prescribed with the initial fluid
resuscitation or if the serum potassium level remains above 5.5 mmol/L
Potassium will almost always fall as the DKA is treated with insulin, and so 0.9%
sodium chloride solution with potassium 20 mmol/L should be used as long as the
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serum potassium level is below 5.5 mmol/L and the patient is passing urine
If the serum potassium level falls below 3.5 mmol/L, the potassium regimen needs
review (see protocol re potassium replacement)
Bicarbonate administration is not routinely recommended
Phosphate should not be supplemented routinely
Reduction of the blood ketone concentration by 0.5 mmol/L/hour (if available)

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Treat any precipitating illness
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Measures to actively detect a precipitating cause should be pursued
One clue to the possibility of an unrecognised underlying cause is if the pH fails to improve
despite the aforementioned measures. In this case, review insulin therapy and consider
other further investigations, e.g. serial ECGs in silent cardiac ischaemia
If an underlying cause is identified then it should also be treated, as appropriate.
If there are reasonable clinical grounds to suspect infection as the precipitant then
appropriate antibiotic therapy should be given (usually broad-spectrum blind treatment);
routine antibiotics are not advised
Monitoring
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Patients should ideally be managed in an HDU setting, or even ITU if they are severely unwell
Electrolytes and venous bicarbonate must be checked at least every 1-2 hours for the first 24 hours, then 2- to 4-hourly thereafter (frequency dependent on individual clinical scenario)
Monitor hourly fluid balance
Monitor capillary blood glucose every hour with an aim to reduce plasma glucose by 3-5
mmol/hour
Plasma glucose should also be checked regularly (at the same time as the U&E), as capillary
blood glucose may be inaccurate in diabetic ketoacidosis (DKA)
If capillary/plasma glucose has not fallen by at least 4 mmol/L in the first hour after
commencing insulin therapy, then check adequacy of rehydration and patency of infusion
lines; if these are not at fault then increase insulin infusion rate will need to be increased.
Consider seeking expert advice and review response
Venous and not arterial blood should be used to monitor bicarbonate
Blood ketone and glucose meters should be used for near patient testing when available
Electrolyte measurements can be obtained from most modern blood gas analysers and can
be used to monitor sodium, potassium and bicarbonate levels - with intermittent laboratory
confirmation
COMPLICATIONS
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Cerebral oedema:
o This is a life threatening emergency. Request senior review and CT brain immediately
if suspected but do not need to wait for confirmation prior to starting treatment if high
level of suspicion. Treatment is with IV dexametasone or mannitol
o Cerebral oedema causing symptoms is relatively uncommon in adults during diabetic
ketoacidosis (DKA), although asymptomatic cerebral oedema may be common
o Cerebral oedema usually occurs within a few hours of the initiation of treatment. It
presents in the first 24 hours with headache, behavioural changes and urinary
incontinence, progressing to abrupt neurological deterioration and coma
Pulmonary oedema:
o Pulmonary oedema has only been rarely reported in DKA. Pulmonary oedema usually
occurs within a few hours of the initiation of treatment
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Elderly patients and those with impaired cardiac function are at particular risk, and
monitoring of central venous pressure should be considered
Iatrogenic hypoglycaemia: severe hypoglycaemia is also associated with cardiac arrhythmias,
acute brain injury and death
Iatrogenic hypokalaemia
Cardiac dysrhythmia due to electrolyte disturbance (particularly K+) or metabolic acidosis
Myocardial suppression due to metabolic acidosis
Venous thromboembolism
Myocardial infarction (may be a cause or a complication of DKA)
Diabetic retinopathy changes may be seen prior to or after therapy for DKA
Hypophosphataemia - rarely has significant clinical effects. Although there is a large loss of
total body phosphate in DKA, there is no evidence of benefit of phosphate replacement but
phosphate measurement and replacement should be considered in the presence of
respiratory and skeletal muscle weakness
Adult respiratory distress syndrome
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Prognosis
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Mortality rate = 0.67%
Prognosis worsens with age and the nature and severity of the underlying precipitating
pathology (particularly myocardial infarction, sepsis and pneumonia)
The presence of coma at presentation, hypothermia or persistent oliguria are poor prognostic
indicators
The main causes of mortality in the adult population include severe hypokalaemia, adult
respiratory distress syndrome, cerebral oedema and comorbid states such as pneumonia,
acute myocardial infarction and sepsis
FURTHER MANAGEMENT
Patient should have review by the diabetes team prior to discharge from hospital. Ideally contact the
diabetes team as early into the admission as possible, especially if there are concerning features or
not responding to treatment as expected.
Prevention
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Education programmes for diabetic patients, particularly concerning what to do in cases of
illness ('sick day rules')
Provision of urine ketostix or handheld ketone meters and education on management of
ketonuria/ketonaemia
Patients with diabetes who are admitted with diabetic ketoacidosis (DKA) should be
counselled about the precipitating cause and early warning symptoms of DKA by a diabetes
presentation and early management of DKA, in the medical/allied healthcare professions
Summary/Flow Chart
Appendix 1- NHS Scotland (2010) Diabetic Ketoacidosis Care Pathway 1
Appendix 2 - NHS Scotland (2010) Diabetes Ketoacidosis Care Pathway 2
Appendix 3 - Diabetic ketoacidosis care pathway 1and 2 NHSL v2 (2013)
Diabetes MCN endorsement
May 2014
Review Date
May 2017
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