Diabetic ketoacidosis

Straight to the point of care

Last updated: Apr 22, 2024

 Table of Contents
Overview 3
Summary 3
Definition 3

Theory 5
Epidemiology 5
Risk factors 5
Aetiology 7
Pathophysiology 7
Classification 8
Case history 9

Diagnosis 10
Recommendations 10
History and exam 22
Investigations 27
Differentials 32
Criteria 33
Screening 33

Management 35
Recommendations 35
Treatment algorithm overview 56
Treatment algorithm 59
Primary prevention 101
Patient discussions 101

Follow up 103
Monitoring 103
Complications 105
Prognosis 106

Guidelines 107
Diagnostic guidelines 107
Treatment guidelines 108

References 109

Images 119

Disclaimer 125
Diabetic ketoacidosis Overview

Summary
Diabetic ketoacidosis (DKA) is characterised by a biochemical triad of hyperglycaemia (or a history of
diabetes), ketonaemia, and metabolic acidosis, with rapid symptom onset.

OVERVIEW
Common symptoms and signs include increased thirst, polyuria, weight loss, excessive tiredness, nausea,
vomiting, dehydration, abdominal pain, hyperventilation, and reduced consciousness.

Successful treatment includes correction of volume depletion, ketogenesis, hyperglycaemia, electrolyte

imbalances, and comorbid precipitating events, with frequent monitoring.

Complications of treatment include hypoglycaemia, hypokalaemia, pulmonary oedema, and acute respiratory
distress syndrome.

Cerebral oedema, a rare but potentially rapidly fatal complication, occurs mainly in children. It may be
prevented by avoiding overly rapid fluid and electrolyte replacement.

Definition
DKA is an acute metabolic complication of diabetes that is potentially fatal and requires prompt medical
attention for successful treatment. It is characterised by absolute or relative insulin deficiency and is the most
common acute hyperglycaemic complication of type 1 diabetes mellitus.[1] [2]

Triad of DKA
Adapted with permission from Kitabchi AE, Wall BM. Diabetic ketoacidosis. Med Clin North Am. 1995;79:9-37.

This topic covers diabetic ketoacidosis in adults. Bear in mind that people aged 16 to 18 years may be
managed by either a paediatric team or an adult medical team according to local arrangements. The Joint

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 Diabetic ketoacidosis Overview
British Diabetes Societies for Inpatient Care guideline recommends following paediatric guidelines if the
patient is being managed by a paediatric team, and following adult guidance if they are being managed by an
adult team.[2] [3]
OVERVIEW

In the UK, the British Society for Paediatric Endocrinology and Diabetes publishes guidance for the
management of DKA in children.[3]

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Diabetic ketoacidosis Theory

Epidemiology
In England, the incidence of hospital admissions for DKA among adults with type 2 diabetes increased
4.24% annually between 1998 and 2013; hospitalisations for DKA in adults with type 1 diabetes increased

THEORY
from 1998 to 2007, and remained static until 2013.[10]

In Denmark, the annual incidence of DKA in the general population was estimated to be 12.6/100,000
during the period 1996 to 2002, and was higher in men than in women (14.4 versus 11.4 per 100,000,
p<0.0001).[11] Twelve percent of patients, typically those aged over 50 years, were diagnosed with type 2
diabetes. Overall mortality was 4%.[11] In Brazil, DKA was reported in 32.8% of patients at diagnosis of type
1 diabetes.[12] DKA at diagnosis was more common in non-white than in white people.[12]

In the US from 2000 to 2009, the rate of hospitalisations for DKA decreased overall, from 21.9 to 19.5 per
1000 persons with diabetes, but then increased in the period 2009 to 2014 to 30.2 per 1000 persons with
diabetes.[13] In 2014, rates of hospitalisation for DKA were highest among people aged <45 years (44.3 per
1000 persons with diabetes), and decreased with age (5.2 per 1000 persons with diabetes aged 45 to 64
years; 1.6 per 1000 persons aged 65 to 74 years; and 1.4 per 1000 persons aged ≥75 years).[13] During the
period 2000 to 2014, in-hospital mortality rates among people with DKA consistently decreased, from 1.1%
to 0.4%.[13] In 2014, about 207,000 accident and emergency department visits for people aged 18 years or
older in the US were for hyperglycaemic crises (e.g., DKA, hyperglycaemic hyperosmolar state).[14]

Risk factors
Strong
inadequate or inappropriate insulin therapy
Reduction in the net effective concentration of insulin leads to impaired carbohydrate, lipid, and
ketone metabolism in DKA. Decreased insulin results in increased gluconeogenesis, accelerated
glycogenolysis, and impaired glucose utilisation by peripheral tissues.[1]

Non-compliance with insulin therapy has been found to be the leading precipitating factor in black
people,[26] and is present in over 30% of patients with DKA.[16] Psychological and social factors
may impact on glycaemic control, and low socio-economic status is correlated with a higher risk for
DKA.[27] [28]

infection
The most common precipitating factor in DKA is infection. Increased counter-regulatory hormones,
particularly adrenaline, as a systemic response to infection lead to insulin resistance, increased
lipolysis, ketogenesis, and volume depletion, which may contribute to the development of
hyperglycaemic crises in patients with diabetes.[1]

myocardial infarction
Underlying cardiovascular events, particularly myocardial infarction, provoke the release of counter-
regulatory hormones likely to result in DKA in patients with diabetes.[1] [29]

Weak

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 Diabetic ketoacidosis Theory
pancreatitis
Medical conditions such as pancreatitis, characterised by increased levels of counter-regulatory
hormones and compromised access to water and insulin, may contribute to the development of
hyperglycaemic crises.[1] [30]
THEORY

stroke
Acute medical events such as stroke, with increased levels of counter-regulatory hormones and
compromised access to water and insulin, may contribute in the development of hyperglycaemic
crises.[1]

acromegaly
Hormonal derangements in some endocrine glands lead to increased counter-regulatory hormones
and development of DKA in patients with concomitant diabetes.[31]

hyperthyroidism
Hormonal derangements in some endocrine glands lead to increased counter-regulatory hormones
and development of DKA in patients with concomitant diabetes.[32]

drugs (e.g., corticosteroids, thia zides, pentamidine, sympathomimetics,

second-generation antipsychotics, cocaine, immune check point inhibitors,
or SGLT2 inhibitors)
Drugs that affect carbohydrate metabolism may precipitate hyperglycaemic crises.[18] [33] [34] [35] A
recent report suggests that cocaine abuse is an independent risk factor associated with recurrent
DKA.[36] [37]

Sodium-glucose co-transporter-2 (SGLT2) inhibitors (e.g., canagliflozin, dapagliflozin, empagliflozin),

used for glycaemic control of type 2 diabetes, have been the subject of a US Food and Drug
Administration warning about a risk for DKA.[38]

Immune checkpoint inhibitor therapy for cancer (PD-1 and PD-L1 blocking antibodies such as
nivolumab, pembrolizumab and avelumab) appears to be associated with a risk for DKA and type 1
diabetes mellitus.[39] [40] [41]

Cushing's syndrome
Hypercortisolism leads to insulin resistance and may occasionally precipitate DKA in patients with
concomitant diabetes; it more commonly precipitates hyperosmolar hyperglycaemic state.

Hispanic or black ancestry

Ancestry plays a role in ketosis-prone diabetes, with DKA a presenting manifestation of undiagnosed
type 2 diabetes in young adults. Approximately 80% of obese black patients with DKA have type 2
diabetes, characterised by higher insulin secretion, the absence of autoimmune markers, and a lack of
HLA genetic association compared with lean patients with type 1 diabetes.[6]

bariatric surgery
DKA has been reported in patients with type 1 diabetes who have had bariatric surgery.[42]

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Diabetic ketoacidosis Theory

Aetiology
In DKA, there is a reduction in the net effective concentration of circulating insulin along with an elevation of
counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These alterations

THEORY
lead to the extreme manifestations of metabolic derangements that can occur in diabetes. The two
most common precipitating events are infection and discontinuation of, or inadequate, insulin therapy.
Underlying medical conditions, such as myocardial infarction or pancreatitis, that provoke the release of
counter-regulatory hormones are also likely to result in DKA in patients with diabetes.[15] Drugs that affect
carbohydrate metabolism, such as corticosteroids, thiazides, sympathomimetic agents (e.g., dobutamine
and terbutaline), second-generation antipsychotics, immune checkpoint inhibitors, cocaine, and cannabis
may contribute to the development of DKA.[1] [16] [17] The use of sodium-glucose co-transporter 2 (SGLT2)
inhibitors has also been implicated in the development of DKA in patients with both type 1 and type 2
diabetes.[18] [19] [20] [21] [22]

Pathophysiology
Reduced insulin concentration or action, along with increased insulin counter-regulatory hormones, leads to
the hyperglycaemia, volume depletion, and electrolyte imbalance that underlie the pathophysiology of DKA.
Hormonal alterations lead to increased gluconeogenesis, hepatic and renal glucose production, and impaired
glucose utilisation in peripheral tissues, which results in hyperglycaemia and hyperosmolarity. Insulin
deficiency leads to release of free fatty acids from adipose tissue (lipolysis), hepatic fatty acid oxidation,
and formation of ketone bodies (beta-hydroxybutyrate and acetoacetate), which result in ketonaemia
and acidosis. Studies have demonstrated the elevation of pro-inflammatory cytokines and inflammatory
biomarkers (e.g., C-reactive protein [CRP]), markers of oxidative stress, lipid peroxidation, and cardiovascular
risk factors with hyperglycaemic crises. All of these parameters return to normal following insulin and
hydration therapies within 24 hours of hyperglycaemic crises. Elevation of pro-inflammatory cytokines,
and markers of lipid peroxidation and oxidative stress, have also been demonstrated in people without
diabetes with insulin-induced hypoglycaemia.[23] The observed pro-inflammatory and pro-coagulant states in
hyperglycaemic crises and hypoglycaemia may be the result of adaptive responses to acute stress, and not
hyperglycaemia or hypoglycaemia per se.[1] [23] [24] It has also been postulated that ketosis-prone diabetes
comprises different syndromes based on auto-antibody status, HLA genotype, and beta-cell functional
reserve.[25]

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THEORY Diabetic ketoacidosis Theory

Pathogenesis of DKA and HHS; triggers include stress, infection, and insufficient
insulin. FFA: free fatty acid; HHS: hyperosmolar hyperglycaemic state
From: Kitabchi AE, Umpierrez GE, Miles JM, et al. Diabetes Care. 2009,32:1335-43; used with permission

Classification
Severe DKA
The presence of one or more of the following may indicate severe DKA:[4]

• Blood ketones >6 mmol/L

• Bicarbonate <5 mmol/L
• Venous/arterial pH <7.0
• Hypokalaemia on admission (<3.5 mmol/L)
• Glasgow Coma Scale <12
• Oxygen saturation <92% on air (assuming normal baseline respiratory function)
• Systolic blood pressure (SBP) <90 mmHg
• Pulse >100 bpm or <60 bpm
• Anion gap >16

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Diabetic ketoacidosis Theory

Case history
Case history #1

THEORY
A 20-year-old man is brought to the accident and emergency department with abdominal pain, nausea,
and vomiting with increasing polyuria, polydipsia, and drowsiness since the previous day. He was
diagnosed with type 1 diabetes 2 years previously. He mentions that he ran out of insulin 2 days ago.
Vital signs at admission are: BP 106/67 mmHg, heart rate 123 beats per minute, respiratory rate
32 breaths per minute, temperature 37.1°C (98.8°F). On mental status examination, he is drowsy.
Physical examination reveals Kussmaul's breathing (deep and rapid respiration due to ketoacidosis) with
acetone odour and mild generalised abdominal tenderness without guarding and rebound tenderness.
Initial laboratory data are: blood glucose 25.0 mmol/L (450 mg/dL), arterial pH 7.24, PCO 2 25 mmHg,
bicarbonate 12 mmol/L (12 mEq/L), WBC count 18.5 × 10⁹/L (18,500/microlitre), sodium 128 mmol/L (128
mEq/L), potassium 5.2 mmol/L (5.2 mEq/L), chloride 97 mmol/L (97 mEq/L), serum urea 11.4 mmol/L (32
mg/dL), creatinine 150.3 micromol/L (1.7 mg/dL), serum ketones strongly positive.

Other presentations
It is now well recognised that new-onset type 2 diabetes can manifest with DKA. These patients are
obese and have undiagnosed hyperglycaemia, impaired insulin secretion, and insulin resistance.
However, after treatment of the acute hyperglycaemic episode with insulin, beta-cell function and
insulin effects improve, so these patients are able to discontinue insulin therapy and may be treated
orally or by diet alone, with 40% remaining insulin-independent 10 years after the initial episodes of
DKA. These patients do not have the typical autoimmune laboratory findings of type 1 diabetes.[5]
This type of diabetes has been labelled as 'type 1 and 1/2' or 'type 1 and a half' diabetes, 'Flatbush'
diabetes, or 'ketosis-prone' diabetes. Conversely, an extreme hyperosmolar state similar to hyperosmolar
hyperglycaemic state (HHS) has been reported in combination with DKA in type 1 diabetes.[6] [7] [8] [9]

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 Diabetic ketoacidosis Diagnosis

Recommendations

Urgent
This topic covers diagnosis and management of DKA in adults.

Consider DKA in:

• Patients with known diabetes who are unwell[4] [17]

• DKA is most common in people with type 1 diabetes but can also present in those with type
2 diabetes.[1] [2] [47]

• Any patient with increased thirst, polyuria, recent unexplained weight loss, or excessive tiredness,
AND any of the following:[17] [48]

• Nausea
• Vomiting
• Abdominal pain[4] [49]
• Hyperventilation (Kussmaul's respiration)[50]
• Dehydration
• Reduced consciousness.

Urgently order a venous blood gas, blood ketones, and capillary blood glucose.[2]

• These tests should be done at the bedside.

Diagnose DKA if:[2] [17] [47] [51]

• Diabetes - blood glucose is >11.0 mmol/L OR known diabetes

DIAGNOSIS

AND
• Ketonaemia - blood ketones are >3.0 mmol/L OR there is ketonuria (2+ or more on standard urine
sticks)

AND
• -
Acidosis - bicarbonate (HCO3 ) is <15.0 mmol/L, AND/OR venous pH is <7.3.

Ensure continuous cardiac monitoring and involve senior or critical care support if:[2] [17]

• There is persistent hypotension (systolic blood pressure <90 mmHg) or oliguria (urine output <0.5
ml/kg/hour) despite intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Potassium <3.5 mmol/L on admission
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16

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Diabetic ketoacidosis Diagnosis
• The patient is pregnant or has heart or kidney failure or other serious comorbidities.

Involve the specialist diabetes team as soon as possible and definitely within 24 hours.[2]

Key Recommendations
Clinical presentation
Other features of DKA are:

• Acetone smell on breath[17]

• Smells like pear drops or nail varnish remover

• Hypothermia[52]

• Suspect sepsis as a precipitant if there is fever as this is not a feature of DKA. Sepsis may
also cause hypothermia, however.

History
Ask about causes of DKA. These are:

• Infection[17] [47]

• The most common causes are pneumonia and urinary tract infection.
• Suspect sepsis as a cause of DKA if there is fever or hypothermia, hypotension, refractory
acidosis, or lactic acidosis.[3]

• Discontinuation of insulin (either unintentional or deliberate)[17] [47]

• Inadequate insulin

DIAGNOSIS
• Due to:

• Malfunctioning insulin pen or pump[53]

• Degradation of insulin due to storage at incorrect temperature.[54]

• New onset of diabetes[17]

• Acute illness

• Common causes include myocardial infarction, sepsis, and pancreatitis.[15] [30] [47]

• Physiological stress

• This includes:

• Pregnancy[17]
• Trauma[55]

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 Diabetic ketoacidosis Diagnosis
• Surgery.[55]

• Drugs[17]

• Corticosteroids[56]
• Thiazides
• Sympathomimetics[26]
• Second-generation antipsychotics[57]
• Immune checkpoint inhibitors[58]
• Cocaine, cannabis, and acute intoxication with alcohol[55] [59]
• Sodium-glucose co-transporter 2 (SGLT2) inhibitors.[21] [22]

Examination
Examine the chest:

• Look for hyperventilation (Kussmaul's respiration).[17]

• Auscultate for crepitations or reduced air entry.

• This may indicate pneumonia as a cause of DKA or pulmonary oedema.

• Monitor for pulmonary oedema. This typically occurs several hours after treatment is started and
can occur even in patients with normal cardiac function.[2] [17]

Assess for signs of dehydration:[17]

• Dry mucous membranes

• Decreased skin turgor or skin wrinkling
• Slow capillary refill
• Tachycardia with a weak pulse
• Hypotension.
DIAGNOSIS

Assess conscious level hourly using the Glasgow Coma Scale to monitor for cerebral oedema.[2]

• Signs include headache, irritability, slowing pulse, rising blood pressure, reducing conscious level.
These may occur several hours after starting treatment.[3] [60]
• Involve immediate critical care input and give mannitol.[61]

Examine the abdomen

• Look for an intra-abdominal cause of DKA such as pancreatitis.[15] [30] [47]

• However, DKA commonly causes abdominal pain and may be mistaken for an acute
abdomen.[62]

Check the patient’s feet to look for new ulceration or infection.[63]

Check the patient’s skin for rashes, signs of cellulitis, or open wounds that may have precipitated
DKA.

Investigations
Always order:

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Diabetic ketoacidosis Diagnosis
• Venous blood gas

• This will show a metabolic acidosis with a raised anion gap. Involve senior or critical
care support if pH is <7.0.[2]
• Check the potassium level. Involve senior or critical care support if it is <3.5 mmol/L.[2]
• Calculate plasma osmolality. This is high (>320 mmol/kg) in patients with DKA.[52] [60]

• Blood ketones

• This will show ketonaemia (ketones >3.0 mmol/L).[2]

• Use urinary ketones if near-patient blood ketone testing is unavailable. This will show
ketonuria (2+ or more on standard urine sticks).[2]

• Blood glucose

• Hyperglycaemia (blood glucose >11.0 mmol/L) is common.[2]

• Be aware that some patients can present with euglycaemic DKA and have a normal blood
glucose.[64] Manage euglycaemic DKA in the same way as hyperglycaemic DKA.[2]

• Urea and electrolytes

• This commonly shows hyponatraemia and hyperkalaemia, but hypokalaemia may also
be present and indicates severe DKA.[1] [2]
• It may also show hypomagnesaemia and hypophosphataemia.[2] [65]

• Full blood count[1]

• Leukocytosis is common.
• Suspect infection if there is a leukocytosis of more than 25 × 10⁹/L (25,000/microlitre).[1]

Full Recommendations

DIAGNOSIS
Clinical presentation
Consider DKA in:

• Patients with known diabetes who are unwell[4] [17]

• DKA is most common in people with type 1 diabetes but can also present in those with type
2 diabetes.[1]

• Any patient with increased thirst, polyuria, recent unexplained weight loss, or excessive tiredness
AND any of the following:[17] [48]

• Nausea
• Vomiting
• Abdominal pain[4] [49]
• Hyperventilation (Kussmaul's respiration)[50]
• Dehydration
• Reduced consciousness.

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 Diabetic ketoacidosis Diagnosis
• This is strongly associated with more severe DKA and a worse prognosis.[66]

Practical tip

Patients with type 2 diabetes who have increased risk of DKA are those with newly diagnosed
diabetes or obesity.[60]

Practical tip

DKA is the initial presentation in up to 25% of patients with newly diagnosed diabetes.[1]
DKA is easily missed, especially when it is the initial presentation of diabetes in infants or older
patients, or when patients present with other acute medical illnesses such as stroke or myocardial
infarction.[60]

Other features of DKA are:

• Acetone smell on breath[17]

• The patient’s breath smells like pear drops or nail varnish remover. This is due to high ketone
levels.
• A significant proportion of people are unable to smell acetone even if it is present.

• Hypothermia

• Severe hypothermia is associated with a mortality rate of 30% to 60%.[67]

• Mild hypothermia may be seen in some patients with DKA due to peripheral vasodilation.[1]

Practical tip

Fever is not a feature of DKA but DKA may be caused by sepsis. Suspect sepsis as a cause of DKA
if there is fever or hypothermia, hypotension, refractory acidosis, or lactic acidosis.[3]
DIAGNOSIS

Ensure continuous cardiac monitoring and involve senior or critical care support if:[2]

• There is persistent hypotension (systolic blood pressure <90 mmHg) or oliguria (urine output <0.5
ml/kg/hour) despite intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Potassium < 3.5 mmol/L on admission
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart or kidney failure or other serious comorbidities.

• DKA in pregnancy can result in significant morbidity and mortality for both the mother and the
fetus.[2] [68]

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Diabetic ketoacidosis Diagnosis
• Pregnant women with suspected DKA must be admitted to the delivery suite or the high
dependency unit and receive care from both the obstetric and medical (or diabetes) teams.[2]

Evidence: Clinical predictors of outcomes in DKA

Prognostic factors for survival in patients with DKA are unclear.

There is limited evidence from a case series of patients with DKA in India for several
favourable prognostic indicators, including being male, having lower APACHE scores,
and having lower serum phosphate levels on presentation.

• A case series assessed 270 patients hospitalised with DKA in India over 2 years.[69]

• It found that survival was more likely among males than females (odds ratio [OR] 7.93,
95% CI 3.99 to 13.51).[69]
• Other favourable prognostic factors in multivariate analysis (adjusting for type of diabetes,
blood pressure, total leukocyte count, urea, serum creatinine, serum magnesium,
serum osmolality, serum glutamic oxaloacetic transaminases, serum glutamic pyruvic
transaminases, and serum albumin) were lower APACHE scores (OR 2.86, 95% CI 1.72
to 7.03) and lower serum phosphate (OR 2.71, 95% CI 1.51 to 6.99) at presentation.[69]
• However, this study reported a high overall mortality rate and may not represent the UK or
European context.[69]

Involve the specialist diabetes team as soon as possible and definitely within 24 hours.[2]

• The specialist diabetes team should also be involved in the assessment of the cause of DKA.
• It is unsafe to manage DKA without the specialist diabetes team and could compromise patient
care.[2]

History
Ask about possible causes of DKA. These include:[1] [2] [26] [33] [35] [36] [52] [70]

DIAGNOSIS
• Infection (most common cause of DKA)[17] [26] [52]

• The most common causes are pneumonia and urinary tract infection.
• Suspect sepsis as a cause of DKA if there is fever or hypothermia, hypotension, refractory
acidosis, or lactic acidosis.[3]

• Discontinuation of insulin (unintentional or deliberate; second most common cause of DKA)[17] [26]
[52]

• Ask sensitively about reasons for deliberate discontinuation of insulin, which may include fear
of weight gain or hypoglycaemia, financial barriers, and psychological factors such as needle
phobia and stress.[4] [17]
• Younger patients with type 1 diabetes may omit insulin due to fear of hypoglycemia, weight
gain, eating disorders, or the stress of having a chronic disease. These factors may account
for 20% of recurrent DKA.[71]

• Inadequate insulin

• Common reasons are:

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 Diabetic ketoacidosis Diagnosis
• Malfunctioning insulin pen or pump[53] [54]
• Degradation of insulin due to storage at incorrect temperature.[54]

• New onset of diabetes[17]

• Acute illness

• Common causes include myocardial infarction, sepsis, and pancreatitis[15] [30]

• Maintain a high level of suspicion for myocardial infarction as patients with diabetes
often present with atypical symptoms.

• Physiological stress

• This includes pregnancy, trauma, and surgery.

• Some women may develop DKA during menstruation.[72] [73]

• Past medical history

• History of diabetes:

• DKA is most common in people with type 1 diabetes but can occur in those with type 2
diabetes.[1]

• Drug history[17]

• Drugs that may cause DKA include:

• Corticosteroids (increase insulin resistance)[56]

• Thiazides (unclear cause but may increase insulin resistance, inhibit glucose uptake,
and decrease insulin release)
DIAGNOSIS

• Sympathomimetics (alter glucose metabolism)[26]

• Second-generation antipsychotics (alter glucose metabolism)[57]
• Immune checkpoint inhibitors (cause insulin deficiency)[58]
• Cocaine, cannabis, and acute intoxication with alcohol (DKA is associated with
cocaine use but the mechanism is unclear)[55] [59]
• SGLT2 inhibitors (prevent reabsorption of glucose and facilitate its excretion in
urine).[21] [22]

Practical tip

Some patients with diabetes may present with a ‘silent myocardial infarction’ with no or minimal
chest pain. This is thought to be due to cardiac autonomic dysfunction.[74] [75]

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Diabetic ketoacidosis Diagnosis
Practical tip

Diagnosis of DKA in pregnancy is often delayed because it can occur at lower blood glucose levels
(including euglycaemic DKA) and faster than in non-pregnant patients.[2] [76]
DKA in pregnancy may present with abdominal pain; always consider as a possible alternative to
pre-term or term labour.[2]
DKA usually occurs in the second and third trimesters due to increased insulin resistance.[76]
Pregnant women suspected of having DKA should receive care from both the obstetric and medical
(or diabetes) teams.[2]

Examination
Examine the chest.

• Look for hyperventilation (Kussmaul's respiration).[17] [50]

• This is a late sign of DKA and occurs with more severe acidosis.
• Characterised by deep sighing respirations at a slow or normal rate.

Auscultate for crepitations or reduced air entry.[77]

• This may be due to pneumonia, which can be caused by aspiration from gastroparesis in
DKA or a primary infection.[78] [79] [80]
• Basal crepitations are also a sign of pulmonary oedema or acute respiratory distress
syndrome (ARDS) secondary to fluid overload. This is an uncommon complication of
treatment for DKA.[2] [81]

Check for signs of dehydration. These are:[17]

• Dry mucous membranes

• Decreased skin turgor or skin wrinkling
• Slow capillary refill
• Tachycardia with a weak pulse

DIAGNOSIS
• Hypotension.

Assess conscious level hourly using the Glasgow Coma Scale to monitor for cerebral oedema.[2]

• Mental status can range from alert in mild DKA to coma in severe DKA.[52]
• Cerebral oedema can develop during treatment of DKA due to rapid correction of
hyperglycaemia.[2]

• Signs include headache, irritability, slowing pulse, rising blood pressure, reducing conscious
level. These may occur several hours after starting treatment.[3] [60]

• Papilloedema is a late sign of cerebral oedema.[3]

• Involve immediate critical care input and give mannitol.[61]

• Cerebral oedema has a mortality rate of 70%. It is most common in children and adolescents
but can occur in adults.[4]

Examine the abdomen for a possible cause of DKA, such as pancreatitis.[15] [30] [47] DKA can both
cause and mimic an acute abdomen.[49] DKA must be excluded prior to any emergency surgery.

• Look for abdominal distension, which may indicate bowel obstruction.[82]

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 Diabetic ketoacidosis Diagnosis
• Palpate the abdomen to check for rebound tenderness and guarding caused by irritation of the
peritoneum.[82]
• Auscultate for bowel sounds.[83]

• Hyperactive ‘tinkling’ bowel sounds may be present in early bowel obstruction.

• Reduced or absent bowel sounds may be present in late bowel obstruction, perforated
viscus, haemoperitoneum, or any cause of peritoneal inflammation.

• Perform a rectal examination.[82]

• Ensure you take a chaperone with you.

• Assess for occult or frank blood, pain, or a mass.

Practical tip

The severity of abdominal pain caused directly by DKA correlates strongly with the severity of the
metabolic acidosis.[49]

Check the patient’s feet to look for new ulceration or infection.[63]

Practical tip

Check the feet for loss of protective sensation in any patient with diabetes.
• Follow your local guidelines, but a quick simple test is the Ipswich Touch Test©#, which involves
lightly touching/resting the tip of the index finger for 1 to 2 seconds on the tips of the first, third,
and fifth toes and the dorsum of the hallux.[84]
• If your patient has reduced sensation, they are at high risk of pressure ulceration. Inform the
nursing staff and provide pressure-relieving devices.

A daily heel check for signs of pressure trauma should be done by nursing or healthcare assistant
staff.
• There is a debate about whether compression stockings should or should not be used in people
with diabetes - do not use them if there is vascular disease.
DIAGNOSIS

Check the patient’s skin for rashes and signs of cellulitis or open wounds.

• Infections such as meningitis or cellulitis may precipitate DKA.[85] [86]

• Periumbilical discolouration (Cullen's sign) or bruising of the flanks (Grey Turner's sign) indicates
haemorrhagic pancreatitis.[87]

Investigations
Diagnose DKA if:[2] [17] [47]

• Diabetes - blood glucose is >11.0 mmol/L OR known diabetes

AND
• Ketonaemia - blood ketones are >3.0 mmol/L OR there is ketonuria (2+ or more on standard urine
sticks)

AND

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Diabetic ketoacidosis Diagnosis
• -
Acidosis - bicarbonate (HCO3 ) is <15.0 mmol/L, AND/OR venous pH is <7.3.

Practical tip

Assessment of glucose, ketones, and electrolytes, including bicarbonate and venous pH, should be
done at or near the bedside.[2]
• Order laboratory measurements in certain circumstances, such as when blood glucose or ketone
meters are ‘out of range’.

Practical tip

Rarely, patients present with euglycaemic DKA (EDKA) and have a normal blood glucose level.[17]
[88] Always use pH and ketones to guide diagnosis and management in patients with known
diabetes (rather than relying solely on a ‘glucose-centric’ approach).[2]
• Exclude other causes of an anion gap metabolic acidosis before confirming EDKA.
• The mechanism of EDKA is unclear but may be due to decreased insulin secretion with
increased counter-regulatory hormone secretion (cortisol, glucagon, catecholamines, and growth
hormone).[19]
• Possible precipitants of EDKA are pregnancy, starvation, alcohol use, insulin pumps, and SGLT2
inhibitors.[19] [88]
• Patients with EDKA secondary to treatment with an SGLT2 inhibitor may have less polyuria
and polydipsia due to a lower glucose level. They may instead present with malaise, anorexia,
tachycardia, or tachypnoea with or without fever.[17]

Always order the following investigations

Venous blood gas[2]

• This will show a metabolic acidosis with a raised anion gap.

• Anion gap >16 indicates severe DKA.

DIAGNOSIS
• Use the pH to determine the severity of DKA.

• pH ≥7.0 indicates mild or moderate DKA.

• pH <7.0 indicates severe DKA. Discuss these patients with critical care.

• Use the potassium level on venous blood gas to replace potassium if ≤5.5 mmol/L. Discuss
with a senior or critical care if potassium is <3.5 mmol/L.
• Calculate the plasma osmolality.

• Plasma osmolality is high (>320 mmol/kg) in DKA and is an indication of dehydration.[52]

[60]

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 Diabetic ketoacidosis Diagnosis

Evidence: Use of a venous versus arterial blood gas

Venous blood gas measurements are widely used instead of arterial blood gas measurements
and evidence from case studies suggests there is sufficient agreement between them, when
combined with other clinical findings, to use a venous blood gas to guide initial treatment.

A clinical review article aimed to answer the question “can venous blood gas analysis
replace arterial blood gas analysis in emergency care? [89]

• Venous blood gas testing may have a lower risk of serious adverse events (e.g., vascular
occlusion or infection), is less painful for the patient, and is technically easier to perform than
arterial blood gas testing.
• There is little difference in pH values between venous and arterial samples (based on 13
studies; 2009 participants, with 3 studies [295 patients] in patients with DKA).[90]
• Bicarbonate values also show close agreement between venous and arterial samples (8
studies; 1211 patients).[90]
• Agreement for PCO 2 is poor and unpredictable (8 studies; 965 patients), but a venous PCO 2
≤45 mmHg (6 kPa) reliably excludes clinically significant hypercarbia (4 studies; 529 patients;
100% sensitivity).[90]
• Agreement on lactate is close enough to categorise as high or normal (3 studies; 338
patients).[91]
• Evidence regarding arteriovenous agreement for base excess is unclear (2 studies; 429
patients; only 1 study reporting close agreement).[92] [93]
• If data from the venous blood gas does not appear to match the patient’s clinical condition, an
arterial blood gas should be performed.[89]

Blood ketones[2]

• This will show ketonaemia (ketones >3.0 mmol/L) in DKA.[2]

• Use urinary ketones if near patient blood ketone testing is unavailable. This will show ketonuria (2+
or more on standard urine sticks).[2]

Practical tip
DIAGNOSIS

Bear in mind that a patient’s medications can cause errors in detecting ketone bodies.[1]
Some drugs, such as the ACE inhibitor captopril, contain sulfhydryl groups that can react with the
reagent in the nitroprusside test (used to test for ketone bodies) to give a false-positive reaction.
Therefore, use clinical judgement and other biochemical tests in patients who are taking these
medications.

Blood glucose

• Hyperglycaemia (blood glucose >11.0 mmol/L) is common.[2] [51]

• Be aware that some patients can present with euglycaemic DKA and have a normal blood
glucose.[64]

• Always use pH and ketones alongside glucose to guide diagnosis and management.
• Manage euglycaemic DKA in the same way as hyperglycaemic DKA.[2]

Urea and electrolytes

• Hyponatraemia is common in DKA.[2]

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Diabetic ketoacidosis Diagnosis
• Hypernatraemia with hyperglycaemia indicates severe dehydration, however.[1]

• Hyperkalaemia is common but hypokalaemia is an indicator of severe DKA.[1] [2]

• Hypokalaemia on arrival indicates severe total-body potassium deficit and is an indicator

of severe DKA.[1] This is because the total body potassium concentration is low due to
increased diuresis.
• Hyperkalaemia is due to an extracellular shift of potassium caused by insulin insufficiency,
hypertonicity, and acidosis.

• Hypomagnesaemia and hypophosphataemia may also be present.[2] [65]

Full blood count

• Leukocytosis is common in DKA and correlates with blood ketone levels.[1]

• However, leukocytosis more than 25 × 10⁹/L (25,000/microlitre) may indicate infection and requires
further investigation.[1]

Consider ordering the following investigations

Urinalysis

• Order if near-patient testing for ketones is unavailable or you suspect a urinary tract infection.[2]
• Shows ketonuria (2+ or more on standard urine sticks) in patients with DKA.[2]
• May be positive for glucose.[95]
• Other findings include leukocytes and nitrites in the presence of infection, and myoglobinuria and/or
haemoglobinuria in rhabdomyolysis.[95] [96] [97]

ECG

• Use to look for cardiac precipitants of DKA such as myocardial infarction.[2]

• Findings may include abnormal T or Q waves or ST segment changes.[98]

DIAGNOSIS
• Look for cardiac effects of electrolyte abnormalities.

• Evidence of hypokalaemia (U waves) or hyperkalaemia (tall ‘peaked’ T waves) may be

present.[99] [100]

Pregnancy test

• Order in all women of childbearing age.[2]

Amylase and lipase

• Amylase is elevated in most patients with DKA.[1]

• Serum lipase is usually normal in patients with DKA.[1]

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 Diabetic ketoacidosis Diagnosis
• This may differentiate DKA from pancreatitis (lipase level will be elevated in patients with
pancreatitis). However, mildly elevated serum lipase level in the absence of pancreatitis has
also been reported in patients with DKA.

Cardiac enzymes

• Order troponin T or I if you suspect myocardial infarction as a precipitant.[101]

Creatinine kinase

• Elevated if rhabdomyolysis is present. This is common in DKA and present in around 10% of
patients.[96]

Chest x-ray

• Order if there are reduced oxygen saturations.[2]

• Signs of pulmonary oedema are pleural effusions, interstitial and alveolar oedema, prominent
superior vena cava, Kerley B lines, and dilated upper lobe blood vessels.[102]
• Consolidation occurs in pneumonia.

Liver function tests (LFTs)

• Use to screen for an underlying hepatic precipitant of DKA. Abnormal LFTs indicate underlying liver
disease (e.g., non-alcoholic fatty liver disease or congestive heart failure).[103] [104]

Blood, urine, and sputum cultures

• Order these if there are signs of infection.

• The most common infections are pneumonia and urinary tract infections.[55]
• Patients with DKA who have an infection are usually normothermic or hypothermic due to
peripheral vasoconstriction, so fever may not be seen.[52]
DIAGNOSIS

Procedural videos

History and exam

Key diagnostic factors
known diabetes or features of diabetes (common)
Consider DKA in:

• Patients with known diabetes who are unwell[2] [4] [17]

• DKA is most common in people with type 1 diabetes but can also present in those with
type 2 diabetes.[1] [2]

• Patients with features of diabetes AND any of the following:[17] [48]

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Diabetic ketoacidosis Diagnosis
• Nausea
• Vomiting
• Abdominal pain[4] [49]
• Hyperventilation (Kussmaul's respiration)[50]
• Dehydration
• Reduced consciousness.

Features of diabetes are increased thirst, polyuria, recent unexplained weight loss, or excessive
tiredness.[17] [48]

nausea and/or vomiting (common)

Suspect DKA if nausea and/or vomiting is present in a patient with known diabetes, increased thirst,
polyuria, recent unexplained weight loss, or excessive tiredness.[17] [48]

abdominal pain (common)

Examine the abdomen for a possible cause of DKA, such as pancreatitis.[15] [30] [47] DKA can both
cause and mimic an acute abdomen.[49] DKA must be excluded prior to any emergency surgery.

• Look for abdominal distension, which may indicate bowel obstruction.[82]

• Palpate the abdomen to check for rebound tenderness and guarding caused by irritation of the
peritoneum.[82]
• Auscultate for bowel sounds.[83]

• Hyperactive ‘tinkling’ bowel sounds may be present in early bowel obstruction.

• Reduced or absent bowel sounds may be present in late bowel obstruction, perforated
viscus, haemoperitoneum, or any cause of peritoneal inflammation.

• Perform a rectal examination.[82]

DIAGNOSIS
• Ensure you take a chaperone with you.
• Assess for occult or frank blood, pain, or a mass.

dehydration (common)
Check for signs of dehydration. These are:[17]

• Dry mucous membranes

• Decreased skin turgor or skin wrinkling
• Slow capillary refill
• Tachycardia with a weak pulse
• Hypotension.

hyperventilation (common)
This is a late sign of DKA and occurs with more severe acidosis.[17] [50]

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 Diabetic ketoacidosis Diagnosis
Characterised by deep sighing respirations at a slow or normal rate.[17] [50]

reduced consciousness (common)

Assess conscious level hourly using the Glasgow Coma Scale to monitor for cerebral oedema.
Reduced consciousness is strongly associated with more severe DKA and a worse prognosis.[2] [66]

• Mental status can range from alert in mild DKA to coma in severe DKA.[52]
• Cerebral oedema can develop during treatment of DKA due to rapid correction of
hyperglycaemia.[2]

• Signs include headache, irritability, slowing pulse, rising blood pressure, reducing
conscious level. These may occur several hours after starting treatment.[3] [60]

• Papilloedema is a late sign of cerebral oedema.[3]

• Involve immediate critical care input and give mannitol.[61]

• Cerebral oedema has a mortality rate of 70%. It is most common in children and
adolescents but can occur in adults.[4]

presence of risk factors (common)

Infection

• This is the most common cause of DKA.[1] [2] [26] [33] [35] [36] [52] [70]

• The most common causes are pneumonia and urinary tract infection.

Discontinuation of insulin (unintentional or deliberate)

DIAGNOSIS

• This is the second most common cause of DKA.[17] [26] [52]

• Ask sensitively about reasons for deliberate discontinuation of insulin, which may include fear
of weight gain or hypoglycaemia, financial barriers, and psychological factors such as needle
phobia and stress.[4] [17]
• Younger patients with type 1 diabetes may omit insulin due to fear of hypoglycemia, weight gain,
eating disorders, or the stress of having a chronic disease. These factors may account for 20%
of recurrent DKA.[71]

Inadequate insulin

• Common reasons are:

• Malfunctioning insulin pen or pump[53] [54]

• Degradation of insulin due to storage at incorrect temperature.[54]

New onset of diabetes[17]

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Diabetic ketoacidosis Diagnosis
• A common cause of DKA.

Acute illness

• Common causes include myocardial infarction, sepsis, and pancreatitis[15] [30]

• Maintain a high level of suspicion for myocardial infarction as patients with diabetes often
present with atypical symptoms.

Practical tip

Some patients with diabetes may present with a ‘silent myocardial infarction’ with no or minimal
chest pain. This is thought to be due to cardiac autonomic dysfunction.[74] [75]

Physiological stress

• This includes pregnancy, trauma, and surgery.

• Some women may develop DKA during menstruation.[72] [73]

Practical tip

Diagnosis of DKA in pregnancy is often delayed because it can occur at lower blood glucose
levels (including euglycaemic DKA) and faster than in non-pregnant patients.[2] [76]
DKA in pregnancy may present with abdominal pain; always consider as a possible alternative to
pre-term or term labour.[2]
DKA usually occurs in the second and third trimesters due to increased insulin resistance.[76]
Pregnant women suspected of having DKA should receive care from both the obstetric and
medical (or diabetes) teams.[2]

Past medical history

DIAGNOSIS
• History of diabetes:

• DKA is most common in people with type 1 diabetes but can occur in those with type 2
diabetes.[1]

Drug history[17]

• Drugs that may cause DKA include:

• Corticosteroids (increase insulin resistance)[56]

• Thiazides (unclear cause but may increase insulin resistance, inhibit glucose uptake, and
decrease insulin release)
• Sympathomimetics (alter glucose metabolism)[26]
• Second-generation antipsychotics (alter glucose metabolism)[57]
• Immune checkpoint inhibitors (cause insulin deficiency)[58]

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 Diabetic ketoacidosis Diagnosis
• Cocaine, cannabis, and acute intoxication with alcohol (DKA is associated with cocaine
use but the mechanism is unclear)[55] [59]
• Sodium-glucose co-transporter 2 (SGLT2) inhibitors (prevent reabsorption of glucose and
facilitate its excretion in urine).[21] [22]

hypothermia (uncommon)
Severe hypothermia is associated with a mortality rate of 30% to 60%.[67] Mild hypothermia may be
seen in some patients with DKA due to peripheral vasodilation.[1]

Practical tip

Fever is not a feature of DKA but DKA may be caused by sepsis. Suspect sepsis as a cause of
DKA if there is fever or hypothermia, hypotension, refractory acidosis, or lactic acidosis.[3]

Other diagnostic factors

acetone smell on breath (common)
The patient’s breath smells like pear drops or nail varnish remover.[17] This is due to high ketone
levels.

Practical tip

A significant proportion of people are unable to smell acetone even if it is present.

DIAGNOSIS

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Diabetic ketoacidosis Diagnosis

Investigations
1st test to order

Test Result
venous blood gas metabolic acidosis with a
Take a venous (rather than arterial) blood gas in all patients with raised anion gap
suspected DKA.[2]
• anion gap >16
• Use the pH to determine the severity of DKA. indicates severe DKA.

• pH ≥7.0 indicates mild or moderate DKA.

• pH <7.0 indicates severe DKA. Discuss these patients
with critical care.

• Hyperkalaemia is common.[1]

• Use the potassium level on venous blood gas to replace

potassium if ≤5.5 mmol/L. Discuss with critical care if
potassium is <3.5 mmol/L.

• Calculate the plasma osmolality.

• Plasma osmolality is high (>320 mmol/kg) in DKA and is

an indication of dehydration.[52] [60]

Practical tip

Assessment of electrolytes should be done at or near the

DIAGNOSIS
bedside.[2]

Evidence: Use of a venous versus arterial blood gas

Venous blood gas measurements are widely used instead

of arterial blood gas measurements and evidence from case
studies suggests there is sufficient agreement between them,
when combined with other clinical findings, to use a venous
blood gas to guide initial treatment.

A clinical review article aimed to answer the question

“can venous blood gas analysis replace arterial blood gas
analysis in emergency care?”. [89]

• Venous blood gas testing may have a lower risk of serious

adverse events (e.g., vascular occlusion or infection), is less
painful for the patient, and is technically easier to perform
than arterial blood gas testing.

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 Diabetic ketoacidosis Diagnosis

Test Result
• There is little difference in pH values between venous and
arterial samples (based on 13 studies; 2009 participants,
with 3 studies [295 patients] in patients with DKA).[90]
• Bicarbonate values also show close agreement between
venous and arterial samples (8 studies; 1211 patients).[90]
• Agreement for PCO 2 is poor and unpredictable (8 studies;
965 patients), but a venous PCO 2 ≤45 mmHg (6 kPa)
reliably excludes clinically significant hypercarbia (4 studies;
529 patients; 100% sensitivity).[90]
• Agreement on lactate is close enough to categorise as high
or normal (3 studies; 338 patients).[91]
• Evidence regarding arteriovenous agreement for base
excess is unclear (2 studies; 429 patients; only 1 study
reporting close agreement).[92] [93]
• If data from the venous blood gas does not appear to match
the patient’s clinical condition, an arterial blood gas should
be performed.[89]

blood ketones ketonaemia (ketones >3.0

mmol/L)[2]
Use urinary ketones if near-patient blood ketone testing is
unavailable.[2]

Practical tip

Assessment of ketones should be done at or near the

bedside.[2]
• Order laboratory measurements in certain circumstances,
such as when blood ketone meters are ‘out of range’.

Practical tip
DIAGNOSIS

Bear in mind that a patient’s medications can cause errors in

detecting ketone bodies.[1]
Some drugs, such as the ACE inhibitor captopril, contain
sulfhydryl groups that can react with the reagent in the
nitroprusside test (used to test for ketone bodies) to give a
false-positive reaction. Therefore, use clinical judgement
and other biochemical tests in patients who are taking these
medications.
blood glucose hyperglycaemia (blood
Hyperglycaemia (blood glucose >11.0 mmol/L) is common.[2] [51] glucose >11.0 mmol/L)

Be aware that some patients can present with euglycaemic DKA

and have a normal blood glucose.[64] Always use pH and ketones
alongside glucose to guide diagnosis and management. Manage
euglycaemic DKA in the same way as hyperglycaemic DKA.[2]

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Diabetic ketoacidosis Diagnosis

Test Result
Practical tip

Assessment of glucose should be done at or near the

bedside.[2]
• Order laboratory measurements in certain circumstances,
such as when blood glucose meters are ‘out of range’.

urea and electrolytes • hyponatraemia

Hyponatraemia is common in DKA.[2] and hyperkalaemia
are common but
• Hypernatraemia with hyperglycaemia indicates severe hypokalaemia is an
indicator of severe
dehydration, however. DKA[1] [2]
• may show
Hyperkalaemia is common but hypokalaemia is an indicator of severe hypomagnesaemia and
DKA.[1] hypophosphataemia[2]
[65]
• Hypokalaemia on arrival indicates severe total-body potassium
deficit and is an indicator of severe DKA. This is because the
total body potassium concentration is low due to increased
diuresis.
• Hyperkalaemia is due to an extracellular shift of potassium
caused by insulin insufficiency, hypertonicity, and acidosis.

Hypomagnesaemia and hypophosphataemia may also be present.[2]

[65]

Practical tip

Assessment of glucose should be done at or near the

bedside.[2]

DIAGNOSIS
full blood count leukocytosis
Leukocytosis is common in DKA and correlates with blood ketone
levels.[1]

However, leukocytosis more than 25 × 10⁹/L (25,000/microlitre) may

indicate infection and requires further investigation.[1]

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 Diabetic ketoacidosis Diagnosis

Other tests to consider

Test Result
urinalysis ketonuria (2+ or more on
standard urine sticks); may be
Order if near-patient testing for ketones is unavailable or you suspect
positive for glucose[95]
a urinary tract infection.[2]
• other findings include
leukocytes and nitrites
in the presence
of infection, and
myoglobinuria and/or
haemoglobinuria in
rhabdomyolysis[95] [96]
[97]

ECG • abnormal T or Q
Use to look for cardiac precipitants of DKA such as myocardial waves or ST segment
infarction and cardiac effects of electrolyte abnormalities.[98] changes in myocardial
infarction[98]
Ensure continuous cardiac monitoring and involve senior or critical • evidence of
care support if:[2] [17] hypokalaemia
(U waves) or
• There is persistent hypotension (systolic blood pressure <90 hyperkalaemia (tall
‘peaked’ T waves) may
mmHg) or oliguria (urine output <0.5 ml/kg/hour) despite
be present[99] [100]
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Potassium <3.5 mmol/L on admission
• Oxygen saturations <92% on air
DIAGNOSIS

• Pulse >100 bpm or <60 bpm

• Anion gap >16
• The patient is pregnant or has heart or kidney failure or other
serious comorbidities.

• DKA in pregnancy can result in significant morbidity and

mortality for both the mother and the fetus.[2][68]
• Pregnant women with suspected DKA must be admitted
to the delivery suite or the high dependency unit and
receive care from both the obstetric and medical (or
diabetes) teams.[2]

pregnancy test positive in pregnancy

Order in all women of childbearing age.
amylase and lipase amylase may be elevated;
serum lipase is usually
Amylase is elevated in most patients with DKA.[1]
normal[1]
Serum lipase is usually normal in DKA.[1]

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Diabetic ketoacidosis Diagnosis

Test Result
• This may differentiate DKA from pancreatitis (lipase level will
be elevated in patients with pancreatitis). However, mildly
elevated serum lipase level in the absence of pancreatitis has
also been reported in patients with DKA.

cardiac enzymes elevated with myocardial

Order troponin T or I if you suspect myocardial infarction as a infarction
precipitant.[101]
creatinine kinase elevated with rhabdomyolysis
Elevated if rhabdomyolysis is present. This is common in DKA and
present in around 10% of patients.[96]
chest x-ray • signs of pulmonary
Order if there are reduced oxygen saturations.[2] oedema are pleural
effusions, interstitial
and alveolar oedema,
prominent superior
vena cava, Kerley B
lines, and dilated upper
lobe blood vessels[102]
• consolidation occurs in
pneumonia

liver function tests elevated with liver disease

Use to screen for an underlying hepatic precipitant of DKA. Abnormal
LFTs indicate underlying liver disease (e.g., non-alcoholic fatty liver
disease or congestive heart failure).[103] [104]
blood, urine, and sputum cultures positive if infection present

DIAGNOSIS
Order these if there are signs of infection. The most common are
pneumonia and urinary tract infections.[55]

Patients with DKA who have an infection are usually normothermic or

hypothermic due to peripheral vasoconstriction so fever may not be
seen.[52]

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 Diabetic ketoacidosis Diagnosis

Differentials

Condition Differentiating signs / Differentiating tests

symptoms
Hyperosmolar • Patients are typically older • Serum glucose is >33.3
hyperglycaemic state than patients with DKA and mmol/L (>600 mg/dL).
(HHS) are usually patients with type Serum osmolality is usually
2 diabetes. Older nursing >320 mmol/ kg (>320
home residents with poor mOsm/kg).
fluid intake are at high risk. • Urine ketones are normal or
• Symptoms evolve insidiously only mildly positive. Serum
over days to weeks. ketones are negative.
• Mental obtundation and • Anion gap is variable but
coma are more frequent. typically <12 mmol/L (<12
Focal neurological mEq/L).
signs (hemianopia and • Total chloride deficit is 5 to
hemiparesis) and seizures 15 mmol/kg (5 to 15 mEq/
are also seen. Seizures may kg).
be the dominant clinical • ABG: arterial pH is typically
features.[1] >7.30, whereas in DKA it
ranges from 7.00 to 7.30.
Arterial bicarbonate is >15
mmol/L (>15 mEq/L).

Lactic acidosis • The presentation is identical • Serum lactate >5 mmol/L.[1]

to that of DKA. In pure
lactic acidosis, the serum
glucose and ketones should
be normal and the serum
lactate concentration should
be elevated.

Starvation ketosis • Starvation ketosis • The blood glucose is usually

results from inadequate normal. Although the urine
DIAGNOSIS

carbohydrate availability can have large amounts of

resulting in physiologically ketones, the blood rarely
appropriate lipolysis and does. Arterial pH is normal
ketone production to provide and the anion gap is at most
fuel substrates for muscle. mildly elevated.[1]

Alcoholic ketoacidosis • Classically, these are people • In isolated alcoholic

with long-standing alcohol ketoacidosis, the metabolic
use disorder for whom acidosis is usually mild
ethanol has been the main to moderate in severity.
caloric source for days to The anion gap is elevated.
weeks. The ketoacidosis Serum and urine ketones
occurs when for some are always present. Blood
reason alcohol and caloric alcohol may be undetectable
intake decreases. and the patient may be
hypoglycaemic.[1]

Salicylate poisoning • Can be differentiated by • The plasma glucose is

history and laboratory normal or low, ketones
investigation. Salicylate are negative, osmolality
intoxication produces an is normal, and salicylates
anion gap metabolic acidosis are positive in blood and/

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Diabetic ketoacidosis Diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
usually with a respiratory or urine. It should be noted
alkalosis. that salicylates may cause
false-positive or false-
negative urinary glucose
determination.[1]

Ethylene glycol/methanol • Methanol and ethylene glycol • Methanol/ethylene glycol

intoxication also produce an anion gap serum levels are elevated.
metabolic acidosis without They can produce an
hyperglycaemia or ketones. increase in the measured
serum osmolality.[1]

Uraemic acidosis • This is characterised by • Elevated urea usually >71.4

markedly elevated serum mmol/L (>200 mg/dL) and
urea and creatinine with elevated creatinine usually
normal plasma glucose. >884 micromol/L (>10 mg/
The pH and anion gap are dL).[1]
usually mildly abnormal.

Criteria
Diagnose DKA if:[2] [17]

• Diabetes - blood glucose is >11.0 mmol/L OR known diabetes

AND
• Ketonaemia - blood ketones are >3.0 mmol/L OR there is ketonuria (2+ or more on standard urine
sticks)

AND
• -
Acidosis - bicarbonate (HCO3 ) is <15.0 mmol/L, AND/OR venous pH is <7.3.

DIAGNOSIS
Rarely, patients present with euglycaemic DKA and have a normal blood glucose level.[17] [88]

Screening
Consider DKA in:

• Patients with known diabetes who are unwell[2] [4] [17]

• DKA is most common in people with type 1 diabetes but can also present in those with type 2
diabetes.[1] [2]

• Any patient with increased thirst, polyuria, recent unexplained weight loss or excessive tiredness, AND
any of the following:[17] [43] [48]

• Nausea
• Vomiting
• Abdominal pain[4] [49]

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 Diabetic ketoacidosis Diagnosis
• Hyperventilation (Kussmaul’s respiration)[50]
• Dehydration
• Reduced consciousness.

Urgently order a venous blood gas, blood ketones, and capillary blood glucose.
DIAGNOSIS

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Diabetic ketoacidosis Management

Recommendations

Urgent
This topic covers management of DKA in adults.

Start intravenous fluids as soon as DKA is confirmed.[2] [17] [43] [47]

• Give a fluid bolus of 500 mL of normal saline (0.9% sodium chloride) over 10 to 15
minutes if the initial systolic blood pressure (SBP) is <90 mmHg. [105]

• Repeat the fluid bolus if SBP remains <90 mmHg and get help from a senior colleague.
• Repeat the fluid bolus, get an immediate senior review and consider involving critical care if
there is no improvement after the second fluid bolus.

• Give 1 L of normal saline over 1 hour if the initial SBP is >90 mmHg OR if SBP is >90 mmHg after
fluid resuscitation.
• Give more cautious fluids and consider monitoring central venous pressure in patients who:

• Are young (aged 18-25 years), elderly, or pregnant

• Have heart or kidney failure or other serious comorbidities.

• Add potassium to the second litre of intravenous fluid if serum potassium is ≤5.5 mmol/L
using pre-mixed normal saline with potassium chloride.

Start a fixed-rate intravenous insulin infusion (FRIII) according to local protocols; continue FRIII
until DKA has resolved.[2] [17] [43] [47] Continue long-acting basal insulin if the patient is already
taking this.[2] Ensure intravenous fluids have already been started before giving a FRIII.

Ensure continuous cardiac monitoring and involve senior or critical care support if:[2]

• There is persistent hypotension (SBP <90 mmHg) or oliguria (urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Potassium <3.5 mmol/L on admission
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart or kidney failure or other serious comorbidities.
MANAGEMENT

Identify and treat any precipitating acute illness.[2]

• Common causes are myocardial infarction, sepsis, and pancreatitis.[30] [47]

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 Diabetic ketoacidosis Management

Key Recommendations
Management of diabetic ketoacidosis in adults

Management of diabetic ketoacidosis 1. Intravenous fluid

by BMJ Knowledge Centre
MANAGEMENT

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Diabetic ketoacidosis Management

Management of diabetic ketoacidosis 2. Potassium

By BMJ Knowledge Centre

MANAGEMENT

Management of diabetic ketoacidosis 3. Insulin

By BMJ Knowledge Centre

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 Diabetic ketoacidosis Management

Management of diabetic ketoacidosis 4. Resolution

By BMJ Knowledge Centre

Additional management during the first hour

Protect the airway.

• Insert a nasogastric tube and aspirate if the patient is unresponsive to commands or is persistently
vomiting.[2] [43]

Insert a urinary catheter if there is incontinence or no urine is passed after 1 hour of starting treatment.[2]
[43]

Give a dose of long-acting insulin to prevent rebound hyperglycaemia when DKA has resolved and the
fixed-rate intravenous insulin infusion (FRIII) is stopped.

• Continue long-acting basal insulin if the patient is already taking this.[2]

• If this is the first presentation of diabetes, start a long-acting basal insulin as soon as possible.

Involve the specialist diabetes team as soon as possible and definitely within 24 hours.[2]

Ongoing management
MANAGEMENT

Give ongoing fluid replacement once the first litre of fluid has been given. Add potassium if serum
potassium is ≤5.5 using pre-mixed normal saline (0.9% sodium chloride) with potassium chloride.[17] [43]

• A typical regimen for a 70 kg patient with no other comorbidities is:[2] [43]

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Diabetic ketoacidosis Management
Volume of normal saline (with potassium chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litre over next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

Continue the FRIII until DKA has resolved. If the blood glucose falls to <14.0 mmol/L: [2] [17] [43]

• Add 10% glucose. Give this concurrently with normal saline to correct the dehydration[47]
• Consider reducing the rate of intravenous insulin infusion to 0.05 units/kg/hour to avoid the risk of
developing hypoglycaemia and hypokalaemia.

Monitor biochemical parameters to ensure these are improving.[2] [43]

• Measure venous bicarbonate, potassium, pH, blood glucose, and blood ketones as follows:

Ketones Glucose Bicarbonate Potassium pH

# # # # #
0 hours

# # # # #
1 hour

# # # # #
2 hours

# #
3 hours

# # # # #
4 hours

# #
5 hours

# # # # #
6 hours

# # # # #
12 hours

Aim for a reduction in blood ketones of 0.5 mmol/L/hour if blood ketone measurement is available.[2]

• Use venous bicarbonate or blood glucose if blood ketone measurement is unavailable. Aim for an
increase in venous bicarbonate of 3.0 mmol/L/hour or a reduction in blood glucose of 3.0 mmol/L/
hour.
MANAGEMENT

• Increase the FRIII according to local protocols if these targets are not met.

Monitor for cerebral and pulmonary oedema.[2]

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 Diabetic ketoacidosis Management
• Assess Glasgow Coma Scale hourly.
• Order a chest x-ray if oxygen saturations fall and consider performing an arterial blood gas.

Resolution of DKA
Involve senior or specialist input if DKA has not resolved within 24 hours. Resolution of DKA is
defined as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies for Inpatient Care guideline advises that the FRIII should
be continued until bicarbonate is >18 mmol/L.[2]

Switch to subcutaneous insulin once DKA has resolved and the patient is eating and drinking. This should
normally be done by the specialist diabetes team.[2]

• Start subcutaneous insulin with a meal and continue the FRIII for 30 to 60 minutes after this.

Continue intravenous fluids and switch to a variable rate intravenous insulin infusion (VRIII) if DKA is
resolved but the patient is not eating and drinking.[2]

Discharge
Ensure the patient has been reviewed by the diabetes specialist team before discharge and has follow
up.[2]

Counsel patients about causes and early warning symptoms of DKA. Provide access to psychological
support.

Full Recommendations
Treatment goals
Treatment should aim to:[2]

• Restore circulatory volume[47]

• Suppress ketogenesis[47]
• Correct electrolyte imbalance[47]
• Normalise blood glucose
• Treat the precipitating cause and prevent complications.
MANAGEMENT

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Diabetic ketoacidosis Management
Practical tip

This topic covers DKA in adults. Bear in mind that people aged 16 to 18 years may be managed
by either a paediatric team or an adult medical team according to local arrangements. The Joint
British Diabetes Societies for Inpatient Care guideline recommends following paediatric guidelines
if the patient is being managed by a paediatric team, and following adult guidance if they are being
managed by an adult team.[2] [3]
In the UK, the British Society for Paediatric Endocrinology and Diabetes publishes guidance for the
management of DKA in children.[3]

Management during the first hour

Protect the airway.

• Insert a nasogastric tube and aspirate if the patient is unresponsive to commands or persistently
vomiting.[2] [43]
• Aspiration is a common complication of DKA due to gastroparesis.[43] [106]

Insert a large bore cannula and start intravenous fluids as soon as DKA is confirmed.[2] [47]

• Seek immediate help from critical care if you are unable to get intravenous access.[2]

Give a fluid bolus of 500 mL normal saline (0.9% sodium chloride) over 10 to 15 minutes if the
initial SBP is <90 mmHg. [2]

• Repeat the fluid bolus if SBP remains <90 mmHg and seek senior help.[2]
• Repeat the fluid bolus, get an immediate senior review and consider involving critical care if there is
no improvement after the second fluid bolus.

• Consider other causes of hypotension (e.g., sepsis, heart failure, acute myocardial
infarction).[2]

Practical tip

Most patients require 500 to 1000 mL of fluid rapidly on arrival.[2]

MANAGEMENT

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 Diabetic ketoacidosis Management

More info: Management of mild/moderate DKA

Check your local protocols for recommendations on the management of mild DKA.

Globally, there are differences in management between countries reflecting access to healthcare
resources, variations in diagnostic criteria, and the lack of published evidence to guide treatment.[1]
[17]

In UK practice, it is likely that all patients with DKA, regardless of severity, will be admitted to hospital.
Some experts suggest that hospital admission may be avoided for patients who are alert, who do not
need critical care input, and who meet other pre-specified criteria (e.g., pH and bicarbonate remaining
within defined thresholds).[17] They suggest that these patients are managed with oral fluids instead of
intravenous fluids, and with subcutaneous rapid-acting insulin instead of intravenous insulin.[17] This
does not represent usual practice in the UK.

Give 1 L of normal saline over 1 hour once SBP >90 mmHg OR if initial SBP is >90 mmHg.[2]

• Typical fluid deficits in DKA are:[2]

• Water - 100 mL/kg

• Sodium - 7 to 10 mmol/kg
• Chloride - 3 to 5 mmol/kg
• Potassium - 3 to 5 mmol/kg.

• The aim of the first few litres of fluid is to:[2]

• Correct any hypotension

• Replenish the intravascular deficit
• Correct any electrolyte disturbance.

Give more cautious intravenous fluids and consider monitoring central venous pressure in patients who:[2]

• Are young (aged 18-25 years) as rapid fluid replacement may increase the risk of cerebral oedema
in these patients
• Are elderly or pregnant
• Have heart or kidney failure or other serious comorbidities.
MANAGEMENT

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Diabetic ketoacidosis Management
Practical tip

Hartmann’s solution (Ringer’s lactate) is not normally used outside of critical care.[2] This is
because it:
• Contains 29 mmol/L of lactate, which can exacerbate the high lactate to pyruvate ratio in DKA
and lead to adverse outcomes[121]
• Raises the plasma lactate, which leads to more glucose being produced[121]
• Contains 5 mmol/L of potassium, which can lead to fatal cardiac arrhythmias such as
bradycardia or asystole if the patient has hyperkalaemia on arrival[121]
• Contains bicarbonate, which can worsen the existing metabolic acidosis[121]
• Is a hypotonic solution. This increases the risk of cerebral oedema in patients who are
hyponatraemic on arrival.[121] [122] [123]

MANAGEMENT

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 Diabetic ketoacidosis Management

Debate: Normal saline versus balanced crystalloid (Hartmann’s solution) for

resuscitation

There is a debate about the benefits of using normal saline (0.9% sodium chloride) over
Hartmann’s solution (Ringer’s lactate) in patients with DKA, as both have advantages and
disadvantages. In the UK, the Joint British Diabetes Societies for Inpatient Care (JBDS-IP)
guideline recommends using normal saline for fluid resuscitation in patients with DKA on the
general ward. [2]

The studies specifically discussed in this JBDS-IP guideline include the following.

• Two randomised controlled trials (RCTs) with small patient numbers comparing balanced
electrolyte solution with normal saline were unable to show clear evidence of a difference in
terms of clinical outcomes.[124] [125]
• One subsequent post-hoc analysis of two cluster RCTs suggested that balanced crystalloid may
lead to faster resolution of DKA than normal saline, but not when given in a general ward (non-
ICU) environment.[126]
• The JBDS-IP guideline authors mention a systematic review on this issue, which at the time of
writing the guideline, was still in progress.[127]

Normal saline for fluid resuscitation in patients with DKA

• Advantages:

• Normal saline is readily available on general wards and clinicians are experienced with
this product.[2]
• Normal saline is available with pre-mixed potassium so it complies with the UK National
Patient Safety Agency (NPSA) recommendations. The NPSA states that commercially
prepared ready to use diluted solutions containing potassium should be used wherever
possible to reduce the risk of misadministration of potassium, so normal saline is
recommended in the UK.[2] [128]
• It is important to avoid the need to add concentrated potassium to resuscitation fluids, as
there is a risk of death from misadministration of concentrated potassium.[129]

• Disadvantages:

• A potential disadvantage of normal saline is that hyperchloraemic metabolic acidosis

is a possible complication, due to the large volume of sodium chloride required for fluid
resuscitation in DKA.[2]
• Hyperchloraemic metabolic acidosis may result in a delay to resolution of the acidosis
because it can cause arterial vasoconstriction in the kidneys and subsequent oliguria.[2]

Hartmann’s solution (Ringer’s lactate) for fluid resuscitation in patients with DKA
MANAGEMENT

• Advantages:

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Diabetic ketoacidosis Management
• Hartmann’s solution has a minimal tendency to cause hyperchloraemic metabolic
acidosis, due to the lower chloride content than normal saline.[2]

• Disadvantages:

• In general, doctors in the UK are less familiar using Hartmann’s solution clinically and it is
not as readily available in clinical areas.[2]
• Hartmann’s solution contains potassium, which could be harmful in early DKA.[121]
• However, it also does not contain enough potassium if used alone once the potassium
levels begin to fall. It is also not commercially available with pre-mixed potassium and
therefore it does not comply with UK NPSA recommendations.[2]
• Hartmann’s solution can further increase the lactate to pyruvate ratio, which is raised in
DKA, worsen acidosis due to the bicarbonate content, and worsen cerebral oedema as it
is hypotonic.[121]

Add potassium to the second litre of intravenous fluids if serum potassium is ≤5.5 mmol/L using
pre-mixed normal saline with potassium chloride. Replace according to the potassium level on a venous
blood gas as follows:[2] [43]

Potassium replacement (mmol/L of

Potassium level (mmol/L) infusion solution)

<3.5 Involve senior or critical care support as

additional potassium needs to be given

3.5 to 5.5 40

>5.5 None

Use normal saline with pre-mixed potassium chloride as the default fluid for resuscitation in DKA.

• Manually adding potassium to intravenous fluids in general clinical areas is unsafe as this can
result in accidental overdose of potassium, which can be fatal.[128]
• Hyperkalaemia and hypokalaemia are life-threatening complications and common in DKA.[2] [17]

• These can precipitate life-threatening cardiac arrhythmias.

• Serum potassium is often high on admission (although total body potassium is low).

Start a FRIII according to local protocols.[2] [17] [47] [43]

• Ensure intravenous fluids have been started before giving a FRIII.

MANAGEMENT

• Seek advice from the diabetes specialist team if >15 units/hour of insulin are required.[2] [53]

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 Diabetic ketoacidosis Management
Practical tip

• Only give an intramuscular bolus of insulin if there is a delay in setting up a FRIII.[2]

• Write out ‘units’ when prescribing insulin. Never use abbreviations such as ‘U’ or ‘IU’.[2]
• Estimate the patient’s weight if necessary.[2]
• If the patient is pregnant, use the current pregnancy weight and call for immediate senior
obstetric help.[2]
• Avoid rapid correction of hyperglycaemia as this increases the risk of cerebral oedema.[60]

Ensure continuous cardiac monitoring and involve senior or critical care support if:[2]

• There is persistent hypotension (SBP <90 mmHg) or oliguria (urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Potassium < 3.5 mmol/L on admission
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart or kidney failure or other serious comorbidities.

• DKA in pregnancy can result in significant morbidity and mortality for both the mother and the
fetus.[2] [68]
• Pregnant women with suspected DKA must be admitted to the delivery suite or the high
dependency unit and receive care from both the obstetric and medical (or diabetes) teams.[2]

Consider giving bicarbonate only if venous pH <6.9 and after discussion with a senior consultant. Monitor
the patient in a critical care environment.[130]

• Bicarbonate has been associated with the development of cerebral oedema.[130]

MANAGEMENT

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Diabetic ketoacidosis Management

Evidence: Intravenous bicarbonate

The UK Joint British Diabetes Societies for Inpatient Care (JBDS-IP) guideline on management
of DKA does not recommend routine use of intravenous bicarbonate for DKA in adults, stating
that acidosis will resolve with adequate fluid and insulin therapy. [2]

The JBDS-IP guideline cites a systematic review that reported data from 44 studies
of bicarbonate treatment for severe acidaemia in patients with DKA, including three
randomised controlled trials (RCTs) in adults (total number: 73 adults). [131]

• Two of the included RCTs in adults showed transient improvement in metabolic acidosis with
bicarbonate within the initial 2 hours, but no evidence of improved glycaemic control or clinical
efficacy [131]
• It found no studies reporting on cerebral oedema in adults or on patients with an admission pH
<6.85 [131]

• Retrospective studies in children receiving bicarbonate for DKA have found an increased
risk of cerebral oedema and prolonged hospitalisation [131]

Seek senior advice if your patient has severe acidosis, or if bicarbonate treatment is being considered.

Practical tip

Do not routinely replace phosphate.[2]

• However, severe phosphate deficiency can worsen respiratory failure, precipitate cardiac
arrhythmias, and cause rhabdomyolysis.[2]
• If any of these clinical features are present, consider phosphate measurement and replacement
as per local guidance.[2]

Discuss severe hypomagnesaemia with a senior; magnesium may need to be replaced but there is no
guidance for cut-off values.

Insert a urinary catheter if there is incontinence or no urine is passed after 1 hour of starting treatment.[2]
[43]

Give a dose of long-acting insulin to prevent rebound hyperglycaemia when DKA has resolved and the
FRIII is stopped.[2]

• Continue long-acting basal insulin if the patient is already taking this.

• If this is the first presentation of diabetes, start a long-acting basal insulin as soon as possible.
MANAGEMENT

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 Diabetic ketoacidosis Management
Practical tip

Never omit insulin in any patient with type 1 diabetes as this can precipitate DKA.[17]
• In a UK survey, more than 7% of cases of DKA were in an inpatient population. It is often
wrongly assumed that patients aged over 50 years have type 2 diabetes and can tolerate periods
of insulin omission when admitted to hospital.
• Continuing long-acting insulin during DKA also prevents rebound hyperglycaemia when the FRIII
is stopped.[2]

Involve the specialist diabetes team as soon as possible and definitely within 24 hours.[2]

• The specialist diabetes team should also be involved in the assessment of the cause of DKA.
• It is unsafe to manage DKA without the specialist diabetes team and could compromise patient
care.[2]

Identify and treat any precipitating acute illness.[2]

• Common causes are myocardial infarction, sepsis, and pancreatitis.[30] [47]

Consider thromboprophylaxis in patients with impaired consciousness, unless it is contraindicated.[2] [43]

See our topic VTE prophylaxis.

Ensure effective handover of patients with DKA.

• Give relevant details on the clinical and biochemical progress of the patient and the plan for further
management.

Practical tip

Handover is a common source of error in managing DKA.

Ongoing management

Management at 1 to 6 hours
Review the patient hourly to ensure clinical and biochemical improvement and continue the FRIII.[2] [43]

• Order hourly blood glucose and hourly blood ketones.

• Perform a venous blood gas for pH, bicarbonate, and potassium at 60 minutes, 2 hours, and 2
hourly thereafter.

• Aim for a reduction in blood ketones of 0.5 mmol/L/hour if blood ketone measurement is
available.
• Use venous bicarbonate or blood glucose measurement if blood ketone measurement is not
MANAGEMENT

available.

• Aim for an increase in venous bicarbonate of 3.0 mmol/L/hour or a reduction in blood

glucose of 3.0 mmol/L/hour.

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Diabetic ketoacidosis Management
• If the target rates for blood ketones, blood glucose, and venous bicarbonate are not
achieved:[2]

• Check the insulin infusion pump is working and connected and that the correct insulin
residual volume is present (to check for pump malfunction)
• Increase the insulin infusion according to local protocols (if there is no insulin pump
malfunction) until the target rates for ketones, glucose, and bicarbonate are achieved.

Practical tip

Monitor all patients with DKA closely:

• DKA is complicated to manage and needs close monitoring and treatment modifications.[17]
• Treatment protocols are often not followed.[17] However, guidelines and protocols should not
replace sound clinical judgement.[17]

Give ongoing fluid replacement after the first litre of fluid has been given. Add potassium if serum
potassium is ≤5.5 mmol/L using pre-mixed normal saline with potassium chloride.

• A typical regimen for a 70 kg adult with no other comorbidities is:[2] [17] [43]

Volume of normal saline (with potassium chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litre over next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

Give more cautious intravenous fluids and consider monitoring central venous pressure in patients who:[2]

• Are young (aged 18-25 years) as rapid fluid replacement may increase the risk of cerebral oedema
in these patients
• Are elderly or pregnant
• Have heart or kidney failure or other serious comorbidities.

Maintain an accurate fluid balance chart.[2]

MANAGEMENT

• Aim for a minimum urine output of 0.5 mL/kg/hour.

Maintain the potassium level between 4.0 and 5.0 mmol/L. Adjust potassium replacement as follows:[2]

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 Diabetic ketoacidosis Management
Potassium replacement (mmol/L of
Potassium level (mmol/L) infusion solution)

<3.5 Involve senior or critical care support as

additional potassium needs to be given

3.5 to 5.5 40

>5.5 None

If the glucose level falls <14.0 mmol/L:[2] [47]

• Give 10% glucose in addition to normal saline and continue until the patient is eating and drinking
normally
• Consider reducing the rate of intravenous insulin infusion to 0.05 units/kg/hour to avoid the risk of
developing hypoglycaemia and hypokalaemia.

Practical tip

A common mistake is to allow hypoglycaemia to develop as the blood glucose level may drop
rapidly as ketoacidosis is corrected.[2]
• This may lead to a rebound ketosis driven by counter-regulatory hormones and lengthen the
duration of treatment.
• Severe hypoglycaemia is associated with cardiac arrhythmias, acute brain injury, and death.

It is important to give glucose and sodium chloride solutions concurrently to correct the
dehydration.[2] Also consider reduction of the insulin infusion rate once the glucose level falls below
14.0 mmol/L.[2]
MANAGEMENT

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Diabetic ketoacidosis Management

Evidence: Reduction of insulin rate when glucose concentrations drop to <14.0 mmol/L

In people with DKA, reducing the insulin rate once blood glucose <14 mmol/L may help reduce
the risk of hypoglycaemia and hyperkalaemia.

In the Joint British Diabetes Societies for Inpatient Care (JBDS-IP) guideline the panel considered
the issue of hypoglycaemia and hypokalaemia, which a UK national survey had identified as a
significant outcome in the management of DKA despite widespread adoption of previous JBDS-IP
recommendations.[2] [132]

• The main cause was the use of insulin.

• Although there was an absence of trial evidence in adults with DKA the panel noted that other
adult guidelines, including the American Diabetes Association 2009 consensus statement,
recommend considering reducing the rate of intravenous insulin infusion when the glucose level
falls.[1] [2]
• One randomised controlled trial (RCT) in children with DKA (n=50) found that a lower rate
of insulin infusion (0.05 units/kg/hour compared with 0.1 units/kg/hour) did not significantly
increase the time to resolution of acidosis but fewer children on the lower dose developed
hypokalaemia (20% vs. 48%) or hypoglycemia (4% vs. 20%).[133] [134]
• A subsequent RCT also in children (n=60) had similar results.[135]
• UK paediatric guidelines on the management of DKA recommend a starting dose of 0.05 units/
kg/hour to reduce the risk of hypoglycaemia, although they note that management in children
with severe DKA and adolescents may be more similar to that in adults, starting at a higher rate
and reducing if required.[2] [3]

Based on the other guidelines, and the indirect evidence from children, the JBDS-IP panel
recommended that in adults with DKA the insulin infusion rate should be reduced to 0.05 units/kg/hour
when blood glucose falls below 14 mmol/L.[2]

Monitor for complications regularly throughout treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to monitor for cerebral oedema.[2]

• If you suspect cerebral oedema, seek immediate senior and critical care support.

• Give mannitol.[61]
• Consider ordering a CT head if the Glasgow Coma Scale score is deteriorating or the
patient has a new or worsening headache.[136]

• Monitor vital signs closely according to local protocols.

• Request a chest x-ray if oxygen saturations fall as this may be a sign of pulmonary oedema.
Consider performing an arterial blood gas.
MANAGEMENT

• Pulmonary oedema and acute respiratory distress syndrome (ARDS) are rare but
significant complications of treatment for DKA and present with fluid overload and low
oxygen saturations.[137] They occur when excess fluid is given, even in patients with
normal cardiac function.

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 Diabetic ketoacidosis Management
• Look for an increased alveolar to oxygen gradient (AaO 2 ) and auscultate for lung
crepitations.
• Pulmonary oedema and ARDS are more common in patients who are severely
dehydrated or with higher glucose levels on arrival.

Practical tip

Other features of cerebral oedema are recurrent vomiting, incontinence, irritability, abnormal
respirations, and cranial nerve dysfunction. These usually occur several hours after starting
treatment.[2] [60]
The exact cause of cerebral oedema is unknown. It occurs most commonly in children and
adolescents, and is rare over the age of 28. It is the most common cause of mortality in DKA.[2] [4]
[60]

Give thromboprophylaxis if indicated.[2] [43]

• See our topic VTE prophylaxis.

Management at 6 to 12 hours
Continue intravenous fluids, potassium correction, and FRIII.[2] [17] Seek senior advice if clinical and
biochemical markers are not improving.

• Check ketones, blood glucose, venous pH, bicarbonate, and potassium at 6 hours.

Assess for resolution of DKA. This is defined as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies for Inpatient Care guideline advises that the FRIII should
be continued until bicarbonate is >18 mmol/L.[2]

Practical tip

Do not rely on bicarbonate alone to assess the resolution of DKA.[2] [60]

• A hyperchloraemic acidosis typically persists secondary to high volumes of normal saline. This
lowers the bicarbonate and leads to difficulty in assessing whether ketosis has resolved.[2] [17]
[60]
MANAGEMENT

• The hyperchloraemic acidosis may cause renal vasoconstriction and oliguria.

Do not rely on urinary ketone clearance to assess resolution of DKA.[2]

• These will still be present when DKA has resolved.

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Diabetic ketoacidosis Management
Management at 12 to 24 hours
Check venous pH, bicarbonate, potassium, ketones, and glucose at 12 hours. Ensure DKA has resolved
within 24 hours.[2] [43]

Request senior or specialist input if DKA has not resolved within 24 hours.[2]

• It is unusual for patients not to respond to treatment so it is important to identify and treat the cause
of DKA.
• Continue the FRIII and intravenous fluids.
• Monitor blood ketones and glucose hourly, and pH, potassium, and bicarbonate every 2 hours to
ensure they fall at the specified target rates.

Start regular subcutaneous insulin when DKA is resolved and the patient is eating and drinking. This
should normally be done by the diabetes specialist team and given with a meal.[2] [60]

• Switch to subcutaneous insulin from intravenous insulin in the morning if possible as most hospitals
have better staffing during daytime, should DKA recur.[106]

Continue intravenous insulin for 30 to 60 minutes after administering subcutaneous insulin to prevent
relapse of DKA.[2]

• It is a common error to stop intravenous insulin either too early or before the timing and doses of
subcutaneous insulin have been sorted out.[17]

If the patient was on basal bolus insulin:[2]

• This should have been continued if they were taking a long-acting insulin analogue[17]
• Restart their normal short-acting subcutaneous insulin at the next meal
• In general, restart the patient’s previous insulin regimen if their most recent HbA1c shows an
acceptable level of control l (i.e., HbA1c 64 mmol/mol [<8.0%])[2]
• Do not stop the intravenous insulin if the long-acting insulin has been stopped in error until a form
of background insulin has been given.[2]

• Give half the usual daily dose of basal insulin (using insulin isophane) in the morning if the
basal analogue was normally taken once daily in the evening and the intention is to convert
to subcutaneous insulin in the morning.
• Check the blood ketone and glucose levels regularly.

If the patient was on twice daily fixed-mix insulin:[2]

• Re-introduce the subcutaneous insulin before breakfast or before the evening meal. Do not change
at any other time.
MANAGEMENT

If the patient was on continuous subcutaneous insulin infusion (CSII):[2]

• Restart the CSII at the normal basal rate

• Continue the intravenous insulin infusion until the meal bolus has been given

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 Diabetic ketoacidosis Management
• Do not restart CSII at bedtime.

Estimate the total daily dose (TDD) of insulin for patients who were not previously taking insulin.[2]

• Take into account the patient’s sensitivity to insulin, degree of glycaemic control, insulin resistance,
and age.
• Calculate TDD by multiplying the patient’s weight (in kg) by 0.5 to 0.75 units. For example: a person
weighing 72 kg would require approximately 72 x 0.5 units (36 units) for a TDD. Use 0.75 units/kg
for people thought to be more insulin resistant (e.g., adolescents, obese people).
• If using a basal bolus regimen:

• Give 50% of the TDD with the evening meal as long-acting insulin and divide the remaining
dose equally between pre-breakfast, pre-lunch, and pre-evening meal.
• Give the first dose of fast acting subcutaneous insulin preferably before breakfast.

• Only give the first dose before the evening meal if monitoring is in place.
• Never convert to a subcutaneous regimen at bed time.

• If using a twice daily pre-mixed regimen:

• Give two-thirds of the TDD at breakfast and give the remaining third with the evening meal.

Practical tip

Use a basal bolus regimen for most patients, especially the young and fit.
Consider a twice daily pre-mixed regimen for older patients as they may not be able to manage a
basal bolus regimen.

Continue intravenous fluids if the patient is not eating and drinking.[2] [17]

• Start a variable rate intravenous insulin infusion (VRIII) for these patients if DKA has resolved.
• Measure blood glucose regularly.

Discharge
Counsel patients about the precipitating cause and early warning symptoms of DKA. Consider:[2] [17]

• Review of their usual glycaemic control

• Review of their injection technique, blood glucose monitoring, equipment, and injection sites
• Prevention of recurrence (e.g., provide written ‘sick day rules’)
• Checking the patient’s insulin prior to reuse (this may be expired or denatured)
• Assessing the need for provision of handheld ketone meters for use at home
MANAGEMENT

• Providing a contact number on how to contact the diabetes specialist team out of hours
• Providing a written care plan which allows the patient to have an active role in their diabetes
management, with a copy of this sent to their GP.

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Diabetic ketoacidosis Management
Be aware that in the UK, all patients with type 1 diabetes mellitus should be offered real-time continuous
glucose monitoring (rtCGM) or intermittently scanned continuous glucose monitoring (isCGM, or ‘flash’
glucose monitoring), based on discussion of a range of factors including whether erratic blood glucose is
affecting their quality of life.[43]

Ensure patients have appropriate follow-up with the diabetes specialist team and access to psychological
support.[2]

Procedural videos

MANAGEMENT

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 Diabetic ketoacidosis Management

Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

Acute ( summary )
initial systolic blood pressure <90
mmHg

serum potassium <3.5 1st intravenous fluids and potassium

mmol/L replacement

plus supportive care and referral to critical care

plus insulin

plus identify and treat any precipitating acute

illness

plus monitor biochemical markers

plus monitor and treat complications

consider sodium bicarbonate

consider thromboprophylaxis

serum potassium 3.5 to 1st intravenous fluids and potassium

5.5 mmol/L replacement

consider supportive care and referral to critical care

plus insulin

plus identify and treat any precipitating acute

illness

plus monitor biochemical markers

plus monitor and treat complications

consider sodium bicarbonate

consider thromboprophylaxis

serum potassium >5.5 1st intravenous fluids

mmol/L

consider supportive care and referral to critical care

plus insulin

plus identify and treat any precipitating acute

illness
MANAGEMENT

plus monitor biochemical markers

plus potassium replacement (once serum

potassium is ≤5.5 mmol/L)

plus monitor and treat complications

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Diabetic ketoacidosis Management

Acute ( summary )
consider sodium bicarbonate

consider thromboprophylaxis

initial systolic blood pressure ≥90

mmHg

serum potassium <3.5 1st intravenous fluids and potassium

mmol/L replacement

plus supportive care and referral to critical care

plus insulin

plus identify and treat any precipitating acute

illness

plus monitor biochemical markers

plus monitor and treat complications

consider sodium bicarbonate

consider thromboprophylaxis

serum potassium 3.5 to 1st intravenous fluids and potassium

5.5 mmol/L replacement

consider supportive care and referral to critical care

plus insulin

plus identify and treat any precipitating acute

illness

plus monitor biochemical markers

plus monitor and treat complications

consider sodium bicarbonate

consider thromboprophylaxis

serum potassium >5.5 1st intravenous fluids

mmol/L

consider supportive care and referral to critical care

plus insulin

plus identify and treat any precipitating acute

illness

plus monitor biochemical markers

MANAGEMENT

plus potassium replacement (once serum

potassium is ≤5.5 mmol/L)

plus monitor and treat complications

consider sodium bicarbonate

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 Diabetic ketoacidosis Management

Acute ( summary )
consider thromboprophylaxis
MANAGEMENT

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Diabetic ketoacidosis Management

Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

Acute
initial systolic blood pressure <90
mmHg

serum potassium <3.5 1st intravenous fluids and potassium

mmol/L replacement

» Start intravenous fluids as soon as DKA is

confirmed.[2] [17] [43]

» Give a fluid bolus of 500 mL of normal

saline (0.9% sodium chloride) over 10 to 15
minutes.

• Repeat the fluid bolus if systolic blood

pressure (SBP) remains <90 mmHg and
get help from a senior colleague.
• Repeat the fluid bolus, get an immediate
senior review and consider involving
critical care if there is no improvement
after the second fluid bolus.

• Consider other causes of

hypotension (e.g., sepsis,
heart failure, acute myocardial
infarction).[2]

» Give 1 L of normal saline over 1 hour

once SBP >90 mmHg. [2]

• Give more cautious intravenous fluids

and consider monitoring central venous
pressure in patients who:[2]

• Are young (aged 18-25 years)

as rapid fluid replacement may
increase the risk of cerebral
oedema in these patients
• Are elderly or pregnant
• Have heart or kidney failure or other
serious comorbidities.
MANAGEMENT

» Add potassium to the second litre of

intravenous fluids using pre-mixed normal
saline with potassium chloride. Involve senior

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 Diabetic ketoacidosis Management

Acute
or critical care support as a high dose of
additional potassium needs to be given. [2]
[43]

• A typical fluid regimen for a 70 kg, well

adult is:[2] [17] [43]

Volume of normal saline (with potassium

chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litre over next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

» Give 10% glucose in addition to normal

saline if the glucose level falls below 14.0
mmol/L. [2] [47]

• Continue this until the patient is eating and

drinking normally.

plus supportive care and referral to critical care

Treatment recommended for ALL patients in
selected patient group
» Protect the airway.

• Insert a nasogastric tube and aspirate if

the patient is unresponsive to commands
or is persistently vomiting.[2] [43]

» Ensure continuous cardiac monitoring and

involve senior or critical care support if:[2] [17]

• There is persistent hypotension (systolic

blood pressure <90 mmHg) or oliguria
(urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
MANAGEMENT

• Venous bicarbonate <5 mmol/L

• Venous pH <7.0
• Potassium <3.5 mmol/L on admission
• Oxygen saturations <92% on air

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Diabetic ketoacidosis Management

Acute
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart
or kidney failure or other serious
comorbidities.

» Insert a urinary catheter if there is incontinence

or no urine is passed after 1 hour of starting
treatment.[2] [43]
plus insulin
Treatment recommended for ALL patients in
selected patient group
Primary options

» insulin neutral: consult local protocols for

dosing guidelines

» Start a fixed-rate intravenous insulin

infusion (FRIII) at a dose of 0.1 units/kg/
hour or according to local protocols; continue
FRIII until DKA has resolved.[2] [17] [43] [47]
Continue long-acting basal insulin if the
patient is already taking this.[2]

• Ensure intravenous fluids have been

started before giving a FRIII.
• Seek advice from the diabetes
specialist team if >15 units/hour of
insulin are required.[2] [53]
• Use the following table as a guide:

Insulin dose per

Weight in kg hour (units)

60-69 6

70-79 7

80-89 8

90-99 9

100-109 10

110-119 11
MANAGEMENT

120-129 12

130-139 13

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 Diabetic ketoacidosis Management

Acute
Insulin dose per
Weight in kg hour (units)

140-149 14

>150 15

» If the blood glucose falls below 14.0 mmol/

L, consider reducing insulin dose rate.[2] See
monitor biochemical markers below for more
information.

» Start regular subcutaneous insulin

when DKA is resolved and the patient is
eating and drinking. This should normally be
done by the diabetes specialist team and given
with a meal.[2] [60]

• Continue intravenous insulin for 30 to 60

minutes after administering subcutaneous
insulin to prevent relapse of DKA.[2]

» Continue intravenous fluids if the patient is not

eating and drinking.[2] [17]

• Start a variable rate intravenous insulin

infusion (VRIII) for these patients if DKA
has resolved.
• Measure blood glucose regularly.

plus identify and treat any precipitating acute

illness
Treatment recommended for ALL patients in
selected patient group
» Common causes of DKA are myocardial
infarction, sepsis, and pancreatitis.[30] [47]
plus monitor biochemical markers
Treatment recommended for ALL patients in
selected patient group
» Monitor biochemical markers as follows:[2] [43]

KetonesGlucoseB icarbonate
Potassium
pH

0 # # # # #
MANAGEMENT

hours

1 # # # # #
hour

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Diabetic ketoacidosis Management

Acute
KetonesGlucoseB icarbonate
Potassium
pH

2 # # # # #
hours

3 # #
hours

4 # # # # #
hours

5 # #
hours

6 # # # # #
hours

12 # # # # #
hours

» Aim for a reduction in blood ketones of 0.5

mmol/L/hour if blood ketone measurement is
available.

• Use venous bicarbonate or blood

glucose measurement if blood ketone
measurement is not available.

• Aim for an increase in venous

bicarbonate of 3.0 mmol/L/hour or
a reduction in blood glucose of 3.0
mmol/L/hour.

• If the target rates for blood ketones, blood

glucose, and venous bicarbonate are not
achieved:[2]

• Check the insulin infusion pump

is working and connected and
that the correct insulin residual
volume is present (to check for
pump malfunction)
• Increase the insulin infusion by 1
unit/hour (if there is no insulin pump
malfunction) until the target rates for
ketones, glucose, and bicarbonate
are achieved.
MANAGEMENT

» If the blood glucose falls to <14.0 mmol/L:[2]

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 Diabetic ketoacidosis Management

Acute
• Add 10% glucose. Give this concurrently
with normal saline to correct the
dehydration[47]
• Consider reducing the rate of
intravenous insulin infusion to 0.05 units/
kg/hour to avoid the risk of developing
hypoglycaemia and hypokalaemia.

Evidence: Reduction of insulin rate

when glucose concentrations drop to
<14.0 mmol/L

In people with DKA, reducing the insulin

rate once blood glucose <14 mmol/L may
help reduce the risk of hypoglycaemia and
hyperkalaemia.

In the Joint British Diabetes Societies for

Inpatient Care (JBDS-IP) guideline the panel
considered the issue of hypoglycaemia
and hypokalaemia, which a UK national
survey had identified as a significant
outcome in the management of DKA despite
widespread adoption of previous JBDS-IP
recommendations.[2] [132]

• The main cause was the use of insulin.

• Although there was an absence of
trial evidence in adults with DKA
the panel noted that other adult
guidelines, including the American
Diabetes Association 2009 consensus
statement, recommend considering
reducing the rate of intravenous insulin
infusion when the glucose level falls.[1]
[2]
• One randomised controlled trial (RCT)
in children with DKA (n=50) found
that a lower rate of insulin infusion
(0.05 units/kg/hour compared with
0.1 units/kg/hour) did not significantly
increase the time to resolution of
acidosis but fewer children on the
lower dose developed hypokalaemia
(20% vs. 48%) or hypoglycemia (4%
vs. 20%).[133] [134]
• A subsequent RCT also in children
(n=60) had similar results.[135]
• UK paediatric guidelines on the
management of DKA recommend a
MANAGEMENT

starting dose of 0.05 units/kg/hour

to reduce the risk of hypoglycaemia,
although they note that management
in children with severe DKA and
adolescents may be more similar to

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Diabetic ketoacidosis Management

Acute
that in adults, starting at a higher rate
and reducing if required.[2] [3]

Based on the other guidelines, and the

indirect evidence from children, the JBDS-IP
panel recommended that in adults with DKA
the insulin infusion rate should be reduced to
0.05 units/kg/hour when blood glucose falls
below 14 mmol/L.[2]

» Assess for resolution of DKA. This is defined

as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies

for Inpatient Care guideline advises
that the fixed-rate intravenous
insulin infusion (FRIII) should be
continued until bicarbonate is >18
mmol/L.[2]

plus monitor and treat complications

Treatment recommended for ALL patients in
selected patient group
» Monitor for complications regularly throughout
treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to

monitor for cerebral oedema.[2]

• If you suspect cerebral oedema,

seek immediate senior and critical
care support.

• Give mannitol.[61]
• Consider ordering a CT
head if the Glasgow Coma
Scale score is deteriorating
or the patient has a new or
worsening headache.[136]

• Monitor vital signs closely according to

MANAGEMENT

local protocols.

• Request a chest x-ray if oxygen

saturations fall as this may be
a sign of pulmonary oedema.

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
65
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
Consider performing an arterial
blood gas.

consider sodium bicarbonate

Treatment recommended for SOME patients in
selected patient group
» Only consider giving bicarbonate if venous
pH <6.9 and after discussion with a senior
consultant. Monitor the patient in a critical care
environment.[130]
consider thromboprophylaxis
Treatment recommended for SOME patients in
selected patient group
» Consider thromboprophylaxis in patients
with impaired consciousness, unless it is
contraindicated.[2] [43] See our topic VTE
prophylaxis.
serum potassium 3.5 to 5.5 1st intravenous fluids and potassium
mmol/L replacement

» Start intravenous fluids as soon as DKA is

confirmed.[2] [17] [43]

» Give a fluid bolus of 500 mL of normal

saline (0.9% sodium chloride) over 10 to 15
minutes.

• Repeat the fluid bolus if systolic blood

pressure (SBP) remains <90 mmHg and
get help from a senior colleague.
• Repeat the fluid bolus, get an immediate
senior review and consider involving
critical care if there is no improvement
after the second fluid bolus.

• Consider other causes of

hypotension (e.g., sepsis,
heart failure, acute myocardial
infarction).[2]

» Give 1 L of normal saline over 1 hour

once SBP >90 mmHg. [2]
MANAGEMENT

• Give more cautious intravenous fluids

and consider monitoring central venous
pressure in patients who:[2]

66 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
• Are young (aged 18-25 years)
as rapid fluid replacement may
increase the risk of cerebral
oedema in these patients
• Are elderly or pregnant
• Have heart or kidney failure or other
serious comorbidities.

» Add 40 mmol/L potassium to the second

litre of intravenous fluids using pre-mixed
normal saline with potassium chloride.[2] [43]

• A typical fluid regimen for a 70 kg, well

adult is:[2] [17] [43]

Volume of normal saline (with potassium

chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litre over next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

» Give 10% glucose in addition to normal

saline if the glucose level falls below 14.0
mmol/L. [2] [47]

• Continue this until the patient is eating and

drinking normally.

consider supportive care and referral to critical care

Treatment recommended for SOME patients in
selected patient group
» Protect the airway.

• Insert a nasogastric tube and aspirate if

the patient is unresponsive to commands
MANAGEMENT

or is persistently vomiting.[2] [43]

» Ensure continuous cardiac monitoring and

involve senior or critical care support if:[2] [17]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
67
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
• There is persistent hypotension (systolic
blood pressure <90 mmHg) or oliguria
(urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart
or kidney failure or other serious
comorbidities.

» Insert a urinary catheter if there is incontinence

or no urine is passed after 1 hour of starting
treatment.[2] [43]
plus insulin
Treatment recommended for ALL patients in
selected patient group
Primary options

» insulin neutral: consult local protocols for

dosing guidelines

» Start a fixed-rate intravenous insulin

infusion (FRIII) at a dose of 0.1 units/kg/
hour or according to local protocols; continue
FRIII until DKA has resolved.[2] [17] [43] [47]
Continue long-acting basal insulin if the
patient is already taking this.[2]

• Ensure intravenous fluids have been

started before giving a FRIII.
• Seek advice from the diabetes
specialist team if >15 units/hour of
insulin are required.[2] [53]
• Use the following table as a guide:

Insulin dose per

Weight in kg hour (units)

60-69 6
MANAGEMENT

70-79 7

80-89 8

68 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
Insulin dose per
Weight in kg hour (units)

90-99 9

100-109 10

110-119 11

120-129 12

130-139 13

140-149 14

>150 15

» If the blood glucose falls below 14.0 mmol/

L, consider reducing insulin dose rate.[2] See
monitor biochemical markers below for more
information.

» Start regular subcutaneous insulin

when DKA is resolved and the patient is
eating and drinking. This should normally be
done by the diabetes specialist team and given
with a meal.[2] [60]

• Continue intravenous insulin for 30 to 60

minutes after administering subcutaneous
insulin to prevent relapse of DKA.[2]

» Continue intravenous fluids if the patient is not

eating and drinking.[2] [17]

• Start a variable rate intravenous insulin

infusion (VRIII) for these patients if DKA
has resolved.
• Measure blood glucose regularly.

plus identify and treat any precipitating acute

illness
Treatment recommended for ALL patients in
selected patient group
» Common causes of DKA are myocardial
MANAGEMENT

infarction, sepsis, and pancreatitis.[30] [47]

plus monitor biochemical markers
Treatment recommended for ALL patients in
selected patient group

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
69
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
» Monitor biochemical markers as follows:[2] [43]

KetonesGlucoseB icarbonate
Potassium
pH

0 # # # # #
hours

1 # # # # #
hour

2 # # # # #
hours

3 # #
hours

4 # # # # #
hours

5 # #
hours

6 # # # # #
hours

12 # # # # #
hours

» Aim for a reduction in blood ketones of 0.5

mmol/L/hour if blood ketone measurement is
available.

• Use venous bicarbonate or blood

glucose measurement if blood ketone
measurement is not available.

• Aim for an increase in venous

bicarbonate of 3.0 mmol/L/hour or
a reduction in blood glucose of 3.0
mmol/L/hour.

• If the target rates for blood ketones, blood

glucose, and venous bicarbonate are not
achieved:[2]

• Check the insulin infusion pump

is working and connected and
that the correct insulin residual
volume is present (to check for
MANAGEMENT

pump malfunction)
• Increase the insulin infusion by 1
unit/hour (if there is no insulin pump
malfunction) until the target rates for

70 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
ketones, glucose, and bicarbonate
are achieved.

» If the blood glucose falls to <14.0 mmol/L:[2]

• Add 10% glucose. Give this concurrently

with normal saline to correct the
dehydration[47]
• Consider reducing the rate of
intravenous insulin infusion to 0.05 units/
kg/hour to avoid the risk of developing
hypoglycaemia and hypokalaemia.

Evidence: Reduction of insulin rate

when glucose concentrations drop to
<14.0 mmol/L

In people with DKA, reducing the insulin

rate once blood glucose <14 mmol/L may
help reduce the risk of hypoglycaemia and
hyperkalaemia.

In the Joint British Diabetes Societies for

Inpatient Care (JBDS-IP) guideline the panel
considered the issue of hypoglycaemia
and hypokalaemia, which a UK national
survey had identified as a significant
outcome in the management of DKA despite
widespread adoption of previous JBDS-IP
recommendations.[2] [132]

• The main cause was the use of insulin.

• Although there was an absence of
trial evidence in adults with DKA
the panel noted that other adult
guidelines, including the American
Diabetes Association 2009 consensus
statement, recommend considering
reducing the rate of intravenous insulin
infusion when the glucose level falls.[1]
[2]
• One randomised controlled trial (RCT)
in children with DKA (n=50) found
that a lower rate of insulin infusion
(0.05 units/kg/hour compared with
0.1 units/kg/hour) did not significantly
increase the time to resolution of
acidosis but fewer children on the
MANAGEMENT

lower dose developed hypokalaemia

(20% vs. 48%) or hypoglycemia (4%
vs. 20%).[133] [134]
• A subsequent RCT also in children
(n=60) had similar results.[135]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
71
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
• UK paediatric guidelines on the
management of DKA recommend a
starting dose of 0.05 units/kg/hour
to reduce the risk of hypoglycaemia,
although they note that management
in children with severe DKA and
adolescents may be more similar to
that in adults, starting at a higher rate
and reducing if required.[2] [3]

Based on the other guidelines, and the

indirect evidence from children, the JBDS-IP
panel recommended that in adults with DKA
the insulin infusion rate should be reduced to
0.05 units/kg/hour when blood glucose falls
below 14 mmol/L.[2]

» Assess for resolution of DKA. This is defined

as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies

for Inpatient Care guideline advises
that the fixed-rate intravenous
insulin infusion should be continued
until bicarbonate is >18 mmol/L.[2]

plus monitor and treat complications

Treatment recommended for ALL patients in
selected patient group
» Monitor for complications regularly throughout
treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to

monitor for cerebral oedema.[2]

• If you suspect cerebral oedema,

seek immediate senior and critical
care support.

• Give mannitol.[61]
• Consider ordering a CT
head if the Glasgow Coma
Scale score is deteriorating
MANAGEMENT

or the patient has a new or

worsening headache.[136]

72 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
• Monitor vital signs closely according to
local protocols.

• Request a chest x-ray if oxygen

saturations fall as this may be
a sign of pulmonary oedema.
Consider performing an arterial
blood gas.

consider sodium bicarbonate

Treatment recommended for SOME patients in
selected patient group
» Only consider giving bicarbonate if venous
pH <6.9 and after discussion with a senior
consultant. Monitor the patient in a critical care
environment.[130]
consider thromboprophylaxis
Treatment recommended for SOME patients in
selected patient group
» Consider thromboprophylaxis in patients
with impaired consciousness, unless it is
contraindicated.[2] [43] See our topic VTE
prophylaxis.
serum potassium >5.5 1st intravenous fluids
mmol/L
» Start intravenous fluids as soon as DKA is
confirmed.[2] [17] [43]

» Give a fluid bolus of 500 mL of normal

saline (0.9% sodium chloride) over 10 to 15
minutes.

• Repeat the fluid bolus if systolic blood

pressure (SBP) remains <90 mmHg and
get help from a senior colleague.
• Repeat the fluid bolus, get an immediate
senior review and consider involving
critical care if there is no improvement
after the second fluid bolus.

• Consider other causes of

hypotension (e.g., sepsis,
heart failure, acute myocardial
MANAGEMENT

infarction).[2]

» Give 1 L of normal saline over 1 hour

once SBP >90 mmHg. [2]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
73
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
• Give more cautious intravenous fluids
and consider monitoring central venous
pressure in patients who:[2]

• Are young (aged 18-25 years)

as rapid fluid replacement may
increase the risk of cerebral
oedema in these patients
• Are elderly or pregnant
• Have heart or kidney failure or other
serious comorbidities.

» Give ongoing fluid replacement after the

first litre of fluid has been given. Do not add
potassium chloride until potassium is ≤5.5
mmol/L.

• A typical fluid regimen for a 70 kg, well

adult is:[2] [17] [43]

Volume of normal saline (with potassium

chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litre over next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

» Give 10% glucose in addition to normal

saline if the glucose level falls below 14.0
mmol/L. [2] [47]

• Continue this until the patient is eating and

drinking normally.

consider supportive care and referral to critical care

Treatment recommended for SOME patients in
selected patient group
MANAGEMENT

» Protect the airway.

74 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
• Insert a nasogastric tube and aspirate if
the patient is unresponsive to commands
or is persistently vomiting.[2] [43]

» Ensure continuous cardiac monitoring and

involve senior or critical care support if:[2]

• There is persistent hypotension (systolic

blood pressure <90 mmHg) or oliguria
(urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart
or kidney failure or other serious
comorbidities.

» Insert a urinary catheter if there is incontinence

or no urine is passed after 1 hour of starting
treatment.[2] [43]
plus insulin
Treatment recommended for ALL patients in
selected patient group
Primary options

» insulin neutral: consult local protocols for

dosing guidelines

» Start a fixed-rate intravenous insulin

infusion (FRIII) at a dose of 0.1 units/kg/
hour or according to local protocols; continue
FRIII until DKA has resolved.[2] [17] [43] [47]
Continue long-acting basal insulin if the
patient is already taking this.[2]

• Ensure intravenous fluids have been

started before giving a FRIII.
• Seek advice from the diabetes
specialist team if >15 units/hour of
insulin are required.[2] [53]
• Use the following table as a guide:
MANAGEMENT

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
75
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
Insulin dose per
Weight in kg hour (units)

60-69 6

70-79 7

80-89 8

90-99 9

100-109 10

110-119 11

120-129 12

130-139 13

140-149 14

>150 15

» If the blood glucose falls below 14.0 mmol/

L, consider reducing insulin dose rate.[2] See
monitor biochemical markers below for more
information.

» Start regular subcutaneous insulin

when DKA is resolved and the patient is
eating and drinking. This should normally be
done by the diabetes specialist team and given
with a meal.[2] [60]

• Continue intravenous insulin for 30 to 60

minutes after administering subcutaneous
insulin to prevent relapse of DKA.[2]

» Continue intravenous fluids if the patient is not

eating and drinking.[2] [17]

• Start a variable rate intravenous insulin

infusion (VRIII) for these patients if DKA
has resolved.
• Measure blood glucose regularly.
MANAGEMENT

plus identify and treat any precipitating acute

illness
Treatment recommended for ALL patients in
selected patient group

76 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
» Common causes of DKA are myocardial
infarction, sepsis, and pancreatitis.[30] [47]
plus monitor biochemical markers
Treatment recommended for ALL patients in
selected patient group
» Monitor biochemical markers as follows:[2] [43]

KetonesGlucoseB icarbonate
Potassium
pH

0 # # # # #
hours

1 # # # # #
hour

2 # # # # #
hours

3 # #
hours

4 # # # # #
hours

5 # #
hours

6 # # # # #
hours

12 # # # # #
hours

» Aim for a reduction in blood ketones of 0.5

mmol/L/hour if blood ketone measurement is
available.

• Use venous bicarbonate or blood

glucose measurement if blood ketone
measurement is not available.

• Aim for an increase in venous

bicarbonate of 3.0 mmol/L/hour or
a reduction in blood glucose of 3.0
mmol/L/hour.

• If the target rates for blood ketones, blood

glucose, and venous bicarbonate are not
MANAGEMENT

achieved:[2]

• Check the insulin infusion pump

is working and connected and
that the correct insulin residual

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
77
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
volume is present (to check for
pump malfunction)
• Increase the insulin infusion by 1
unit/hour (if there is no insulin pump
malfunction) until the target rates for
ketones, glucose, and bicarbonate
are achieved.

» If the blood glucose falls to <14.0 mmol/L:[2]

• Add 10% glucose. Give this concurrently

with normal saline to correct the
dehydration[47]
• Consider reducing the rate of
intravenous insulin infusion to 0.05 units/
kg/hour to avoid the risk of developing
hypoglycaemia and hypokalaemia.

Evidence: Reduction of insulin rate

when glucose concentrations drop to
<14.0 mmol/L

In people with DKA, reducing the insulin

rate once blood glucose <14 mmol/L may
help reduce the risk of hypoglycaemia and
hyperkalaemia.

In the Joint British Diabetes Societies for

Inpatient Care (JBDS-IP) guideline the panel
considered the issue of hypoglycaemia
and hypokalaemia, which a UK national
survey had identified as a significant
outcome in the management of DKA despite
widespread adoption of previous JBDS-IP
recommendations.[2] [132]

• The main cause was the use of insulin.

• Although there was an absence of
trial evidence in adults with DKA
the panel noted that other adult
guidelines, including the American
Diabetes Association 2009 consensus
statement, recommend considering
reducing the rate of intravenous insulin
infusion when the glucose level falls.[1]
[2]
• One randomised controlled trial (RCT)
MANAGEMENT

in children with DKA (n=50) found

that a lower rate of insulin infusion
(0.05 units/kg/hour compared with
0.1 units/kg/hour) did not significantly
increase the time to resolution of
acidosis but fewer children on the

78 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
lower dose developed hypokalaemia
(20% vs. 48%) or hypoglycemia (4%
vs. 20%).[133] [134]
• A subsequent RCT also in children
(n=60) had similar results.[135]
• UK paediatric guidelines on the
management of DKA recommend a
starting dose of 0.05 units/kg/hour
to reduce the risk of hypoglycaemia,
although they note that management
in children with severe DKA and
adolescents may be more similar to
that in adults, starting at a higher rate
and reducing if required.[2] [3]

Based on the other guidelines, and the

indirect evidence from children, the JBDS-IP
panel recommended that in adults with DKA
the insulin infusion rate should be reduced to
0.05 units/kg/hour when blood glucose falls
below 14 mmol/L.[2]

» Assess for resolution of DKA. This is defined

as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies

for Inpatient Care guideline advises
that the fixed-rate intravenous
insulin infusion (FRIII) should be
continued until bicarbonate is >18
mmol/L.[2]

plus potassium replacement (once serum

potassium is ≤5.5 mmol/L)
Treatment recommended for ALL patients in
selected patient group
» Add potassium to intravenous fluids once
serum potassium is ≤5.5 mmol/L using pre-
mixed normal saline with potassium chloride.[2]
plus monitor and treat complications
Treatment recommended for ALL patients in
selected patient group
MANAGEMENT

» Monitor for complications regularly throughout

treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to

monitor for cerebral oedema.[2]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
79
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
• If you suspect cerebral oedema,
seek immediate senior and critical
care support.

• Give mannitol.[61]
• Consider ordering a CT
head if the Glasgow Coma
Scale score is deteriorating
or the patient has a new or
worsening headache.[136]

• Monitor vital signs closely according to

local protocols.

• Request a chest x-ray if oxygen

saturations fall as this may be
a sign of pulmonary oedema.
Consider performing an arterial
blood gas.

consider sodium bicarbonate

Treatment recommended for SOME patients in
selected patient group
» Only consider giving bicarbonate if venous
pH <6.9 and after discussion with a senior
consultant. Monitor the patient in a critical care
environment.[130]
consider thromboprophylaxis
Treatment recommended for SOME patients in
selected patient group
» Consider thromboprophylaxis in patients
with impaired consciousness, unless it is
contraindicated.[2] [43] See our topic VTE
prophylaxis.
initial systolic blood pressure ≥90
mmHg

serum potassium <3.5 1st intravenous fluids and potassium

mmol/L replacement
MANAGEMENT

» Start intravenous fluids as soon as DKA is

confirmed.[2] [17] [43]

» Give 1 L of normal saline (0.9% sodium

chloride) over 1 hour. [2]

80 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
• Give more cautious intravenous fluids
and consider monitoring central venous
pressure in patients who:[2]

• Are young (aged 18-25 years)

as rapid fluid replacement may
increase the risk of cerebral
oedema in these patients
• Are elderly or pregnant
• Have heart or kidney failure or other
serious comorbidities.

» Add potassium to the second litre of

intravenous fluids using pre-mixed normal
saline with potassium chloride. Involve senior
or critical care support as a high dose of
additional potassium needs to be given. [2]
[43]

• A typical fluid regimen for a 70 kg, well

adult is:[2] [17] [43]

Volume of normal saline (with potassium

chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litre over next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

» Give 10% glucose in addition to normal

saline if the glucose level falls below 14.0
mmol/L. [2] [47]

• Continue this until the patient is eating and

drinking normally.

plus supportive care and referral to critical care

MANAGEMENT

Treatment recommended for ALL patients in

selected patient group
» Protect the airway.

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
81
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
• Insert a nasogastric tube and aspirate if
the patient is unresponsive to commands
or is persistently vomiting.[2] [43]

» Ensure continuous cardiac monitoring and

involve senior or critical care support if:[2] [17]

• There is persistent hypotension (systolic

blood pressure <90 mmHg) or oliguria
(urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Potassium <3.5 mmol/L on admission
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart
or kidney failure or other serious
comorbidities.

» Insert a urinary catheter if there is incontinence

or no urine is passed after 1 hour of starting
treatment.[2] [43]
plus insulin
Treatment recommended for ALL patients in
selected patient group
Primary options

» insulin neutral: consult local protocols for

dosing guidelines

» Start a fixed-rate intravenous insulin

infusion (FRIII) at a dose of 0.1 units/kg/
hour or according to local protocols; continue
FRIII until DKA has resolved.[2] [17] [43] [47]
Continue long-acting basal insulin if the
patient is already taking this.[2]

• Ensure intravenous fluids have been

started before giving a FRIII.
• Seek advice from the diabetes
specialist team if >15 units/hour of
insulin are required.[2] [53]
MANAGEMENT

• Use the following table as a guide:

82 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
Insulin dose per
Weight in kg hour (units)

60-69 6

70-79 7

80-89 8

90-99 9

100-109 10

110-119 11

120-129 12

130-139 13

140-149 14

>150 15

» If the blood glucose falls below 14.0 mmol/

L, consider reducing insulin dose rate.[2] See
monitor biochemical markers below for more
information.

» Start regular subcutaneous insulin

when DKA is resolved and the patient is
eating and drinking. This should normally be
done by the diabetes specialist team and given
with a meal.[2] [60]

• Continue intravenous insulin for 30 to 60

minutes after administering subcutaneous
insulin to prevent relapse of DKA.[2]

» Continue intravenous fluids if the patient is not

eating and drinking.[2] [17]

• Start a variable rate intravenous insulin

infusion (VRIII) for these patients if DKA
has resolved.
• Measure blood glucose regularly.
MANAGEMENT

plus identify and treat any precipitating acute

illness
Treatment recommended for ALL patients in
selected patient group

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
83
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
» Common causes of DKA are myocardial
infarction, sepsis, and pancreatitis.[30] [47]
plus monitor biochemical markers
Treatment recommended for ALL patients in
selected patient group
» Monitor biochemical markers as follows:[2] [43]

KetonesGlucoseB icarbonate
Potassium
pH

0 # # # # #
hours

1 # # # # #
hour

2 # # # # #
hours

3 # #
hours

4 # # # # #
hours

5 # #
hours

6 # # # # #
hours

12 # # # # #
hours

» Aim for a reduction in blood ketones of 0.5

mmol/L/hour if blood ketone measurement is
available.

• Use venous bicarbonate or blood

glucose measurement if blood ketone
measurement is not available.

• Aim for an increase in venous

bicarbonate of 3.0 mmol/L/hour or
a reduction in blood glucose of 3.0
mmol/L/hour.

• If the target rates for blood ketones, blood

glucose, and venous bicarbonate are not
MANAGEMENT

achieved:[2]

• Check the insulin infusion pump

is working and connected and
that the correct insulin residual

84 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
volume is present (to check for
pump malfunction)
• Increase the insulin infusion by 1
unit/hour (if there is no insulin pump
malfunction) until the target rates for
ketones, glucose, and bicarbonate
are achieved.

» If the blood glucose falls to <14.0 mmol/L:[2]

• Add 10% glucose. Give this concurrently

with normal saline to correct the
dehydration[47]
• Consider reducing the rate of
intravenous insulin infusion to 0.05 units/
kg/hour to avoid the risk of developing
hypoglycaemia and hypokalaemia.

Evidence: Reduction of insulin rate

when glucose concentrations drop to
<14.0 mmol/L

In people with DKA, reducing the insulin

rate once blood glucose <14 mmol/L may
help reduce the risk of hypoglycaemia and
hyperkalaemia.

In the Joint British Diabetes Societies for

Inpatient Care (JBDS-IP) guideline the panel
considered the issue of hypoglycaemia
and hypokalaemia, which a UK national
survey had identified as a significant
outcome in the management of DKA despite
widespread adoption of previous JBDS-IP
recommendations.[2] [132]

• The main cause was the use of insulin.

• Although there was an absence of
trial evidence in adults with DKA
the panel noted that other adult
guidelines, including the American
Diabetes Association 2009 consensus
statement, recommend considering
reducing the rate of intravenous insulin
infusion when the glucose level falls.[1]
[2]
• One randomised controlled trial (RCT)
MANAGEMENT

in children with DKA (n=50) found

that a lower rate of insulin infusion
(0.05 units/kg/hour compared with
0.1 units/kg/hour) did not significantly
increase the time to resolution of
acidosis but fewer children on the

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
85
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
lower dose developed hypokalaemia
(20% vs. 48%) or hypoglycemia (4%
vs. 20%).[133] [134]
• A subsequent RCT also in children
(n=60) had similar results.[135]
• UK paediatric guidelines on the
management of DKA recommend a
starting dose of 0.05 units/kg/hour
to reduce the risk of hypoglycaemia,
although they note that management
in children with severe DKA and
adolescents may be more similar to
that in adults, starting at a higher rate
and reducing if required.[2] [3]

Based on the other guidelines, and the

indirect evidence from children, the JBDS-IP
panel recommended that in adults with DKA
the insulin infusion rate should be reduced to
0.05 units/kg/hour when blood glucose falls
below 14 mmol/L.[2]

» Assess for resolution of DKA. This is defined

as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies

for Inpatient Care guideline advises
that the fixed-rate intravenous
insulin infusion (FRIII) should be
continued until bicarbonate is >18
mmol/L.[2]

plus monitor and treat complications

Treatment recommended for ALL patients in
selected patient group
» Monitor for complications regularly throughout
treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to

monitor for cerebral oedema.[2]

• If you suspect cerebral oedema,

seek immediate senior and critical
MANAGEMENT

care support.

• Give mannitol.[61]
• Consider ordering a CT
head if the Glasgow Coma
Scale score is deteriorating

86 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
or the patient has a new or
worsening headache.[136]

• Monitor vital signs closely according to

local protocols.

• Request a chest x-ray if oxygen

saturations fall as this may be
a sign of pulmonary oedema.
Consider performing an arterial
blood gas.

consider sodium bicarbonate

Treatment recommended for SOME patients in
selected patient group
» Only consider giving bicarbonate if venous
pH <6.9 and after discussion with a senior
consultant. Monitor the patient in a critical care
environment.[130]
consider thromboprophylaxis
Treatment recommended for SOME patients in
selected patient group
» Consider thromboprophylaxis in patients
with impaired consciousness, unless it is
contraindicated.[2] [43] See our topic VTE
prophylaxis.
serum potassium 3.5 to 5.5 1st intravenous fluids and potassium
mmol/L replacement

» Start intravenous fluids as soon as DKA is

confirmed.[2] [17] [43]

» Give 1 L of normal saline (0.9% sodium

chloride) over 1 hour. [2]

• Give more cautious intravenous fluids

and consider monitoring central venous
pressure in patients who:[2]

• Are young (aged 18-25 years)

as rapid fluid replacement may
increase the risk of cerebral
MANAGEMENT

oedema in these patients

• Are elderly or pregnant

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
87
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
• Have heart or kidney failure or other
serious comorbidities.

» Add 40 mmol/L potassium to the second

litre of intravenous fluids using pre-mixed
normal saline with potassium chloride.[2] [43]

• A typical fluid regimen for a 70 kg, well

adult is:[2] [17] [43]

Volume of normal saline (with potassium

chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litreover next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

» Give 10% glucose in addition to normal

saline if the glucose level falls below 14.0
mmol/L. [2] [47]

• Continue this until the patient is eating and

drinking normally.

consider supportive care and referral to critical care

Treatment recommended for SOME patients in
selected patient group
» Protect the airway.

• Insert a nasogastric tube and aspirate if

the patient is unresponsive to commands
or is persistently vomiting.[2] [43]

» Ensure continuous cardiac monitoring and

involve senior or critical care support if:[2] [17]

• There is persistent hypotension (systolic

MANAGEMENT

blood pressure <90 mmHg) or oliguria

(urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L

88 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart
or kidney failure or other serious
comorbidities.

» Insert a urinary catheter if there is incontinence

or no urine is passed after 1 hour of starting
treatment.[2] [43]
plus insulin
Treatment recommended for ALL patients in
selected patient group
Primary options

» insulin neutral: consult local protocols for

dosing guidelines

» Start a fixed-rate intravenous insulin

infusion (FRIII) at a dose of 0.1 units/kg/
hour or according to local protocols; continue
FRIII until DKA has resolved.[2] [17] [43] [47]
Continue long-acting basal insulin if the
patient is already taking this.[2]

• Ensure intravenous fluids have been

started before giving a FRIII.
• Seek advice from the diabetes
specialist team if >15 units/hour of
insulin are required.[2] [53]
• Use the following table as a guide:

Insulin dose per

Weight in kg hour (units)

60-69 6

70-79 7

80-89 8

90-99 9
MANAGEMENT

100-109 10

110-119 11

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
89
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
Insulin dose per
Weight in kg hour (units)

120-129 12

130-139 13

140-149 14

>150 15

» If the blood glucose falls below 14.0 mmol/

L, consider reducing insulin dose rate.[2] See
monitor biochemical markers below for more
information.

» Start regular subcutaneous insulin

when DKA is resolved and the patient is
eating and drinking. This should normally be
done by the diabetes specialist team and given
with a meal.[2] [60]

• Continue intravenous insulin for 30 to 60

minutes after administering subcutaneous
insulin to prevent relapse of DKA.[2]

» Continue intravenous fluids if the patient is not

eating and drinking.[2] [17]

• Start a variable rate intravenous insulin

infusion (VRIII) for these patients if DKA
has resolved.
• Measure blood glucose regularly.

plus identify and treat any precipitating acute

illness
Treatment recommended for ALL patients in
selected patient group
» Common causes of DKA are myocardial
infarction, sepsis, and pancreatitis.[30] [47]
plus monitor biochemical markers
Treatment recommended for ALL patients in
selected patient group
» Monitor biochemical markers as follows:[2] [43]
MANAGEMENT

KetonesGlucoseB icarbonate
Potassium
pH

0 # # # # #
hours

90 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
KetonesGlucoseB icarbonate
Potassium
pH

1 # # # # #
hour

2 # # # # #
hours

3 # #
hours

4 # # # # #
hours

5 # #
hours

6 # # # # #
hours

12 # # # # #
hours

» Aim for a reduction in blood ketones of 0.5

mmol/L/hour if blood ketone measurement is
available.

• Use venous bicarbonate or blood

glucose measurement if blood ketone
measurement is not available.

• Aim for an increase in venous

bicarbonate of 3.0 mmol/L/hour or
a reduction in blood glucose of 3.0
mmol/L/hour.

• If the target rates for blood ketones, blood

glucose, and venous bicarbonate are not
achieved:[2]

• Check the insulin infusion pump

is working and connected and
that the correct insulin residual
volume is present (to check for
pump malfunction)
• Increase the insulin infusion by 1
unit/hour (if there is no insulin pump
malfunction) until the target rates for
MANAGEMENT

ketones, glucose, and bicarbonate

are achieved.

» If the blood glucose falls to <14.0 mmol/L:[2]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
91
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
• Add 10% glucose. Give this concurrently
with normal saline to correct the
dehydration[47]
• Consider reducing the rate of
intravenous insulin infusion to 0.05 units/
kg/hour to avoid the risk of developing
hypoglycaemia and hypokalaemia.

Evidence: Reduction of insulin rate

when glucose concentrations drop to
<14.0 mmol/L

In people with DKA, reducing the insulin

rate once blood glucose <14 mmol/L may
help reduce the risk of hypoglycaemia and
hyperkalaemia.

In the Joint British Diabetes Societies for

Inpatient Care (JBDS-IP) guideline the panel
considered the issue of hypoglycaemia
and hypokalaemia, which a UK national
survey had identified as a significant
outcome in the management of DKA despite
widespread adoption of previous JBDS-IP
recommendations.[2] [132]

• The main cause was the use of insulin.

• Although there was an absence of
trial evidence in adults with DKA
the panel noted that other adult
guidelines, including the American
Diabetes Association 2009 consensus
statement, recommend considering
reducing the rate of intravenous insulin
infusion when the glucose level falls.[1]
[2]
• One randomised controlled trial (RCT)
in children with DKA (n=50) found
that a lower rate of insulin infusion
(0.05 units/kg/hour compared with
0.1 units/kg/hour) did not significantly
increase the time to resolution of
acidosis but fewer children on the
lower dose developed hypokalaemia
(20% vs. 48%) or hypoglycemia (4%
vs. 20%).[133] [134]
• A subsequent RCT also in children
(n=60) had similar results.[135]
• UK paediatric guidelines on the
management of DKA recommend a
MANAGEMENT

starting dose of 0.05 units/kg/hour

to reduce the risk of hypoglycaemia,
although they note that management
in children with severe DKA and
adolescents may be more similar to

92 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
that in adults, starting at a higher rate
and reducing if required.[2] [3]

Based on the other guidelines, and the

indirect evidence from children, the JBDS-IP
panel recommended that in adults with DKA
the insulin infusion rate should be reduced to
0.05 units/kg/hour when blood glucose falls
below 14 mmol/L.[2]

» Assess for resolution of DKA. This is defined

as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies

for Inpatient Care guideline advises
that the fixed-rate intravenous
insulin infusion (FRIII) should be
continued until bicarbonate is >18
mmol/L.[2]

plus monitor and treat complications

Treatment recommended for ALL patients in
selected patient group
» Monitor for complications regularly throughout
treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to

monitor for cerebral oedema.[2]

• If you suspect cerebral oedema,

seek immediate senior and critical
care support.

• Give mannitol.[61]
• Consider ordering a CT
head if the Glasgow Coma
Scale score is deteriorating
or the patient has a new or
worsening headache.[136]

• Monitor vital signs closely according to

MANAGEMENT

local protocols.

• Request a chest x-ray if oxygen

saturations fall as this may be
a sign of pulmonary oedema.

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
93
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
Consider performing an arterial
blood gas.

consider sodium bicarbonate

Treatment recommended for SOME patients in
selected patient group
» Only consider giving bicarbonate if venous
pH <6.9 and after discussion with a senior
consultant. Monitor the patient in a critical care
environment.[130]
consider thromboprophylaxis
Treatment recommended for SOME patients in
selected patient group
» Consider thromboprophylaxis in patients
with impaired consciousness, unless it is
contraindicated.[2] [43] See our topic VTE
prophylaxis.
serum potassium >5.5 1st intravenous fluids
mmol/L
» Start intravenous fluids as soon as DKA is
confirmed.[2] [17] [43]

» Give 1 L of normal saline (0.9% sodium

chloride) over 1 hour. [2]

• Give more cautious intravenous fluids

and consider monitoring central venous
pressure in patients who:[2]

• Are young (aged 18-25 years)

as rapid fluid replacement may
increase the risk of cerebral
oedema in these patients
• Are elderly or pregnant
• Have heart or kidney failure or other
serious comorbidities.

» Give ongoing fluid replacement after the

first litre of fluid has been given. Do not add
potassium chloride until potassium is ≤5.5
mmol/L. [2] [43]

• A typical fluid regimen for a 70 kg, well

MANAGEMENT

adult is:[2] [17] [43]

94 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
Volume of normal saline (with potassium
chloride as needed)

1 litre over 2 hours

1 litre over next 2 hours

1 litre over next 4 hours

1 litre over next 4 hours

1 litre over next 6 hours

» Give 10% glucose in addition to normal

saline if the glucose level falls below 14.0
mmol/L. [2] [47]

• Continue this until the patient is eating and

drinking normally.

consider supportive care and referral to critical care

Treatment recommended for SOME patients in
selected patient group
» Protect the airway.

• Insert a nasogastric tube and aspirate if

the patient is unresponsive to commands
or is persistently vomiting.[2] [43]

» Ensure continuous cardiac monitoring and

involve senior or critical care support if:[2]

• There is persistent hypotension (systolic

blood pressure <90 mmHg) or oliguria
(urine output <0.5 mL/kg/hour) despite
intravenous fluids
• Glasgow Coma Scale <12
• Blood ketones >6 mmol/L
• Venous bicarbonate <5 mmol/L
• Venous pH <7.0
• Oxygen saturations <92% on air
• Pulse >100 bpm or <60 bpm
• Anion gap >16
• The patient is pregnant or has heart
MANAGEMENT

or kidney failure or other serious

comorbidities.

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
95
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
» Insert a urinary catheter if there is incontinence
or no urine is passed after 1 hour of starting
treatment.[2] [43]
plus insulin
Treatment recommended for ALL patients in
selected patient group
Primary options

» insulin neutral: consult local protocols for

dosing guidelines

» Start a fixed-rate intravenous insulin

infusion (FRIII) at a dose of 0.1 units/kg/
hour or according to local protocols; continue
FRIII until DKA has resolved.[2] [17] [43] [47]
Continue long-acting basal insulin if the
patient is already taking this.[2]

• Ensure intravenous fluids have been

started before giving a FRIII.
• Seek advice from the diabetes
specialist team if >15 units/hour of
insulin are required.[2] [53]
• Use the following table as a guide:

Insulin dose per

Weight in kg hour (units)

60-69 6

70-79 7

80-89 8

90-99 9

100-109 10

110-119 11

120-129 12

130-139 13

140-149 14
MANAGEMENT

>150 15

» If the blood glucose falls below 14.0 mmol/

L, consider reducing insulin dose rate.[2] See

96 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
monitor biochemical markers below for more
information.

» Start regular subcutaneous insulin

when DKA is resolved and the patient is
eating and drinking. This should normally be
done by the diabetes specialist team and given
with a meal.[2] [60]

• Continue intravenous insulin for 30 to 60

minutes after administering subcutaneous
insulin to prevent relapse of DKA.[2]

» Continue intravenous fluids if the patient is not

eating and drinking.[2] [17]

• Start a variable rate intravenous insulin

infusion (VRIII) for these patients if DKA
has resolved.
• Measure blood glucose regularly.

plus identify and treat any precipitating acute

illness
Treatment recommended for ALL patients in
selected patient group
» Common causes of DKA are myocardial
infarction, sepsis, and pancreatitis.[30] [47]
plus monitor biochemical markers
Treatment recommended for ALL patients in
selected patient group
» Monitor biochemical markers as follows:[2] [43]

KetonesGlucoseB icarbonate
Potassium
pH

0 # # # # #
hours

1 # # # # #
hour

2 # # # # #
hours

3 # #
hours

4 # # # # #
MANAGEMENT

hours

5 # #
hours

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
97
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
 Diabetic ketoacidosis Management

Acute
KetonesGlucoseB icarbonate
Potassium
pH

6 # # # # #
hours

12 # # # # #
hours

» Aim for a reduction in blood ketones of 0.5

mmol/L/hour if blood ketone measurement is
available.

• Use venous bicarbonate or blood

glucose measurement if blood ketone
measurement is not available.

• Aim for an increase in venous

bicarbonate of 3.0 mmol/L/hour or
a reduction in blood glucose of 3.0
mmol/L/hour.

• If the target rates for blood ketones, blood

glucose, and venous bicarbonate are not
achieved:[2]

• Check the insulin infusion pump

is working and connected and
that the correct insulin residual
volume is present (to check for
pump malfunction)
• Increase the insulin infusion by 1
unit/hour (if there is no insulin pump
malfunction) until the target rates for
ketones, glucose, and bicarbonate
are achieved.

» If the blood glucose falls to <14.0 mmol/L:[2]

• Add 10% glucose. Give this concurrently

with normal saline to correct the
dehydration[47]
• Consider reducing the rate of
intravenous insulin infusion to 0.05 units/
kg/hour to avoid the risk of developing
hypoglycaemia and hypokalaemia.
MANAGEMENT

Evidence: Reduction of insulin rate

when glucose concentrations drop to
<14.0 mmol/L

98 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2024.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2024. All rights reserved.
Diabetic ketoacidosis Management

Acute
In people with DKA, reducing the insulin
rate once blood glucose <14 mmol/L may
help reduce the risk of hypoglycaemia and
hyperkalaemia.

In the Joint British Diabetes Societies for

Inpatient Care (JBDS-IP) guideline the panel
considered the issue of hypoglycaemia
and hypokalaemia, which a UK national
survey had identified as a significant
outcome in the management of DKA despite
widespread adoption of previous JBDS-IP
recommendations.[2] [132]

• The main cause was the use of insulin.

• Although there was an absence of
trial evidence in adults with DKA
the panel noted that other adult
guidelines, including the American
Diabetes Association 2009 consensus
statement, recommend considering
reducing the rate of intravenous insulin
infusion when the glucose level falls.[1]
[2]
• One randomised controlled trial (RCT)
in children with DKA (n=50) found
that a lower rate of insulin infusion
(0.05 units/kg/hour compared with
0.1 units/kg/hour) did not significantly
increase the time to resolution of
acidosis but fewer children on the
lower dose developed hypokalaemia
(20% vs. 48%) or hypoglycemia (4%
vs. 20%).[133] [134]
• A subsequent RCT also in children
(n=60) had similar results.[135]
• UK paediatric guidelines on the
management of DKA recommend a
starting dose of 0.05 units/kg/hour
to reduce the risk of hypoglycaemia,
although they note that management
in children with severe DKA and
adolescents may be more similar to
that in adults, starting at a higher rate
and reducing if required.[2] [3]

Based on the other guidelines, and the

indirect evidence from children, the JBDS-IP
panel recommended that in adults with DKA
the insulin infusion rate should be reduced to
0.05 units/kg/hour when blood glucose falls
MANAGEMENT

below 14 mmol/L.[2]

» Assess for resolution of DKA. This is defined

as:[2]

• Venous pH >7.3 AND

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 Diabetic ketoacidosis Management

Acute
• Blood ketone level <0.6 mmol/L AND
• Bicarbonate >15 mmol/L

• The Joint British Diabetes Societies

for Inpatient Care guideline advises
that the fixed-rate intravenous
insulin infusion should be continued
until bicarbonate is >18 mmol/L.[2]

plus potassium replacement (once serum

potassium is ≤5.5 mmol/L)
Treatment recommended for ALL patients in
selected patient group
» Add potassium to intravenous fluids once
serum potassium is ≤5.5 mmol/L using pre-
mixed normal saline with potassium chloride.[2]
plus monitor and treat complications
Treatment recommended for ALL patients in
selected patient group
» Monitor for complications regularly throughout
treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to

monitor for cerebral oedema.[2]

• If you suspect cerebral oedema,

seek immediate senior and critical
care support.

• Give mannitol.[61]
• Consider ordering a CT
head if the Glasgow Coma
Scale score is deteriorating
or the patient has a new or
worsening headache.[136]

• Monitor vital signs closely according to

local protocols.

• Request a chest x-ray if oxygen

saturations fall as this may be
a sign of pulmonary oedema.
Consider performing an arterial
MANAGEMENT

blood gas.

consider sodium bicarbonate

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Diabetic ketoacidosis Management

Acute
Treatment recommended for SOME patients in
selected patient group
» Only consider giving bicarbonate if venous
pH <6.9 and after discussion with a senior
consultant. Monitor the patient in a critical care
environment.[130]
consider thromboprophylaxis
Treatment recommended for SOME patients in
selected patient group
» Consider thromboprophylaxis in patients
with impaired consciousness, unless it is
contraindicated.[2] [43] See our topic VTE
prophylaxis.

Primary prevention
Patient education about management of their diabetes during periods of mild illness (sick-day management)
is vital for preventing DKA. Counsel patients about the precipitating cause and early warning symptoms of
DKA. Consider:[2] [17]

• Review of their usual glycaemic control

• Review of their injection technique, blood glucose monitoring, equipment, and injection sites
• Prevention of recurrence (e.g., provide written ‘sick day rules’)
• Checking the patient’s insulin prior to reuse (this may be expired or denatured)
• Assessing the need for provision of handheld ketone meters for use at home
• Provision of a contact number on how to contact the diabetes specialist team out of hours
• Provision of a written care plan which allows the patient to have an active role in their diabetes
management, with a copy of this sent to their GP.

Be aware that in the UK, all patients with type 1 diabetes mellitus should be offered real-time continuous
glucose monitoring (rtCGM) or intermittently scanned continuous glucose monitoring (isCGM, or ‘flash’
glucose monitoring), based on discussion of a range of factors including whether erratic blood glucose is
affecting their quality of life.[43]

Sodium-glucose co-transporter 2 (SGLT2) inhibitor-associated DKA in patients with type 2 diabetes is

typically precipitated by insulin omission or significant dose reduction, severe acute illness, dehydration,
extensive exercise, surgery, low-carbohydrate diets, or excessive alcohol intake. DKA prevention strategies
should include withholding SGLT2 inhibitors when precipitants are present, and avoiding insulin omission or
large insulin dose reduction.[44] [45]

Many cases can be prevented by better access to medical care, proper education, and effective
communication with a healthcare provider during an intercurrent illness. Adequate supervision by family and
healthcare provider may decrease the rates of hospitalisation and mortality.[1] [46]

Patient discussions
MANAGEMENT

Management should be reviewed periodically with all patients. This should include:

• When to contact the healthcare provider

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 Diabetic ketoacidosis Management
• Blood glucose goals and the use of supplemental short- or rapid-acting insulin during illness
• Means to suppress fever and treat infection
• Initiation of an easily digestible fluid diet containing electrolytes and glucose during illness.

Patients should be advised to always continue insulin during illness and to seek professional advice early.
Sodium-glucose co-transporter 2 (SGLT2) inhibitor-associated DKA in patients with type 2 diabetes is
typically precipitated by insulin omission or significant dose reduction, severe acute illness, dehydration,
extensive exercise, surgery, low-carbohydrate diets, or excessive alcohol intake. DKA prevention
strategies should include withholding SGLT2 inhibitors when precipitants are present, and avoiding insulin
omission or large insulin dose reduction.[44] [45]

The patient (or family member or carer) must be able to accurately measure and record blood glucose,
insulin administration, temperature, respiratory rate, and pulse. Blood ketone (BOHB) should be checked
when blood glucose is more than 16.7 mmol/L (300 mg/dL), and if it is high the patient should present to
hospital for further evaluation. The frequency of blood glucose monitoring depends on the patient's clinical
condition: in uncontrolled diabetes (HbA1c >53 mmol/mol [>7.0%]) it is recommended to check blood
glucose before each meal, plus at bedtime.[1] [141] In the UK, all patients with type 1 diabetes mellitus
should be offered real-time continuous glucose monitoring (rtCGM) or intermittently scanned continuous
glucose monitoring (isCGM, or ‘flash’ glucose monitoring).[43]
MANAGEMENT

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Diabetic ketoacidosis Follow up

Monitoring
Monitoring

FOLLOW UP
DKA is complicated to manage and needs close monitoring and treatment modifications.[17]

It is possible to manage mild DKA without admission to the intensive care unit (ICU); however, many
cases will require ICU care.

After admission to ICU, central venous and arterial lines are usually required. Swan-Ganz catheterisation
and continuous percutaneous oximetry are needed in patients with haemodynamic instability. Monitoring
of respiratory parameters is also required to ensure adequate oxygenation and airway protection.

1 to 6 hours
Review the patient hourly to ensure clinical and biochemical improvement and continue the fixed-rate
intravenous insulin infusion (FRIII).[2] [43]

• Order hourly blood glucose and hourly blood ketones.

• Perform a venous blood gas for pH, bicarbonate, and potassium at 60 minutes, 2 hours, and 2
hourly thereafter.

• Aim for a reduction in blood ketones of 0.5 mmol/L/hour if blood ketone measurement is
available.
• Use venous bicarbonate or blood glucose measurement if blood ketone measurement is not
available.

• Aim for an increase in venous bicarbonate of 3.0 mmol/L/hour or a reduction in blood

glucose of 3.0 mmol/L/hour.

• If the target rates for blood ketones, blood glucose, and venous bicarbonate are not
achieved:[2]

• Check the insulin infusion pump is working and connected and that the correct insulin
residual volume is present (to check for pump malfunction)
• Increase the insulin infusion according to local protocols (if there is no insulin pump
malfunction) until the target rates for ketones, glucose, and bicarbonate are achieved.

• Maintain the potassium level between 4.0 and 5.0 mmol/L.

• Maintain an accurate fluid balance chart.[2]

• Aim for a minimum urine output of 0.5 ml/kg/hour.

Monitor for complications regularly throughout treatment of DKA.[2] [43]

• Assess Glasgow Coma Scale hourly to monitor for cerebral oedema.[2]

• Monitor vital signs closely according to local protocols.

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 Diabetic ketoacidosis Follow up
• Request a chest x ray if oxygen saturations fall as this may be a sign of pulmonary oedema.
Consider performing an arterial blood gas.
FOLLOW UP

6 to 12 hours
Seek senior advice if clinical and biochemical markers are not improving.

• Check ketones, blood glucose, venous pH, bicarbonate, and potassium at 6 hours.

Assess for resolution of DKA. This is defined as:[2]

• Venous pH >7.3 AND

• Blood ketone level <0.6 mmol/L

12 to 24 hours
Check venous pH, bicarbonate, potassium, ketones, and glucose at 12 hours. Ensure DKA has resolved
within 24 hours.[2] [43]

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Diabetic ketoacidosis Follow up

Complications

Complications Timeframe Likelihood

FOLLOW UP
hypokalaemia short term high

This iatrogenic complication can occur with excessive high-dose insulin therapy and bicarbonate therapy. It
can be prevented by following current treatment protocols with frequent monitoring of potassium levels and
appropriate replacement.[1] [138] [139]

hypoglycaemia short term medium

This iatrogenic complication can occur with excessive high-dose insulin therapy. It can be prevented by
following current treatment protocols with frequent monitoring of plasma glucose and use of glucose-
containing intravenous fluids.[1]

arterial or venous thromboembolic events short term medium

Standard prophylactic low-dose heparin is certainly reasonable in these patients.[1] [46] [140] Applying
prophylactic treatment is based on clinical evaluation by the physician of risk factors for thromboembolic
events. Currently no evidence exists for full anticoagulation.

cerebral oedema/brain injury short term low

Assess Glasgow Coma Scale hourly to monitor for cerebral oedema.[2]

• Other features of cerebral oedema are recurrent vomiting, incontinence, irritability, abnormal
respirations, and cranial nerve dysfunction. These usually occur several hours after starting
treatment.[2] [60]
• If you suspect cerebral oedema, seek immediate senior and critical care support.

• Give mannitol.[61]
• Consider ordering a CT head if the Glasgow Coma Scale score is deteriorating or the patient
has a new or worsening headache.[136]

The exact cause of cerebral oedema is unknown. It occurs most commonly in children and adolescents,
and is rare over the age of 28. It is the most common cause of mortality in DKA.[2] [4] [60]

pulmonary oedema/acute respiratory distress short term low

syndrome (ARDS)

Pulmonary oedema and ARDS are rare but significant complications of treatment for DKA and present
with fluid overload and low oxygen saturations.[137]

• They occur when excess fluid is given, even in patients with normal cardiac function.
• They are more common in patients who are severely dehydrated or with higher glucose levels on
arrival.
• Look for an increased alveolar to oxygen gradient (AaO 2 ) and auscultate for lung crepitations.
• Request a chest x-ray if oxygen saturations fall. Consider performing an arterial blood gas.

Pulmonary oedema typically occurs several hours after treatment is started and can occur even in patients
with normal cardiac function.[2] [17]

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 Diabetic ketoacidosis Follow up

Complications Timeframe Likelihood

non-anion gap hyperchloraemic acidosis short term low
FOLLOW UP

This occurs due to urinary loss of ketoanions needed for bicarbonate regeneration, and also increased
reabsorption of chloride secondary to intensive administration of chloride-containing fluids. This acidosis
usually resolves and should not affect the treatment. It is more likely in pregnant women.[1] [139]

Prognosis

An improved understanding of the pathophysiology of DKA, together with close monitoring and correction
of electrolytes, has resulted in a significant reduction in the overall mortality rate from this life-threatening
condition. Mortality rates have fallen significantly in the last 20 years from 7.96% to 0.67%.[2]

Death is rarely caused by the metabolic complications of hyperglycaemia or ketoacidosis but rather relates to
the underlying illness. The prognosis is substantially worsened at the extremes of age and in the presence of
coma and hypotension.[1]

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Diabetic ketoacidosis Guidelines

Diagnostic guidelines

United Kingdom

The management of diabetic ketoacidosis in adults

Published by: Joint British Diabetes Societies for Inpatient Care Last published: 2023

Diabetes at the front door: a guideline for dealing with glucose related
emergencies at the time of acute hospital admission
Published by: Joint British Diabetes Societies for Inpatient Care Last published: 2021

Type 1 diabetes in adults: diagnosis and management

Published by: National Institute for Health and Care Excellence Last published: 2022

Diabetes in pregnancy: management from preconception to the postnatal

GUIDELINES
period
Published by: National Institute for Health and Care Excellence Last published: 2020

Management of diabetes: a national clinical guideline

Published by: Scottish Intercollegiate Guidelines Network Last published: 2017

North America

Standards of care in diabetes - 2023

Published by: American Diabetes Association Last published: 2022

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 Diabetic ketoacidosis Guidelines

Treatment guidelines

United Kingdom

The management of diabetic ketoacidosis in adults

Published by: Joint British Diabetes Societies for Inpatient Care Last published: 2023

Managing diabetes and hyperglycaemia during labour and birth

Published by: Joint British Diabetes Societies for Inpatient Care Last published: 2023

Type 1 diabetes in adults: diagnosis and management

Published by: National Institute for Health and Care Excellence Last published: 2022

Diabetes in pregnancy: management from preconception to the postnatal

period
GUIDELINES

Published by: National Institute for Health and Care Excellence Last published: 2020

Management of diabetes: a national clinical guideline

Published by: Scottish Intercollegiate Guidelines Network Last published: 2017

Management of children and young people under the age of 18 years with
diabetic ketoacidosis
Published by: British Society of Paediatric Endocrinology and Diabetes Last published: 2020

North America

Standards of care in diabetes - 2023

Published by: American Diabetes Association Last published: 2023

Oceania

National evidence-based clinical care guidelines for type 1 diabetes for

children, adolescents and adults
Published by: National Health and Medical Research Council Last published: 2011
(Australia)

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Diabetic ketoacidosis References

Key articles
• Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult patients with

REFERENCES
diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2009
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• Joint British Diabetes Societies for Inpatient Care. The management of diabetic ketoacidosis in adults.
Mar 2023 [internet publication]. Full text

• National Institute for Health and Care Excellence. Type 1 diabetes in adults: diagnosis and
management. Aug 2022 [internet publication]. Full text

References
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2. Joint British Diabetes Societies for Inpatient Care. The management of diabetic ketoacidosis in adults.
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3. British Society for Paediatric Endocrinology and Diabetes. BSPED interim guideline for the
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14. Centers for Disease Control and Prevention. National diabetes statistics report, 2017. February 2018
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Diabetic ketoacidosis Images

Images

IMAGES
Figure 1: Triad of DKA
Adapted with permission from Kitabchi AE, Wall BM. Diabetic ketoacidosis. Med Clin North Am.
1995;79:9-37.

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IMAGES Diabetic ketoacidosis Images

Figure 2: Pathogenesis of DKA and HHS; triggers include stress, infection, and insufficient insulin. FFA: free
fatty acid; HHS: hyperosmolar hyperglycaemic state
From: Kitabchi AE, Umpierrez GE, Miles JM, et al. Diabetes Care. 2009,32:1335-43; used with permission

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Diabetic ketoacidosis Images

IMAGES
Figure 3: Management of diabetic ketoacidosis 1. Intravenous fluid
by BMJ Knowledge Centre

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 Diabetic ketoacidosis Images

Figure 4: Management of diabetic ketoacidosis 2. Potassium

IMAGES

By BMJ Knowledge Centre

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Diabetic ketoacidosis Images

IMAGES
Figure 5: Management of diabetic ketoacidosis 3. Insulin
By BMJ Knowledge Centre

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IMAGES Diabetic ketoacidosis Images

Figure 6: Management of diabetic ketoacidosis 4. Resolution

By BMJ Knowledge Centre

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Diabetic ketoacidosis Disclaimer

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Contributors:

// Expert Advisers:

Edward Jude, MD, MRCP

Consultant Diabetologist and Endocrinologist
Tameside and Glossop Integrated Care NHS Foundation Trust, Honorary Professor, University of
Manchester, Honorary Professor, Manchester Metropolitan University Manchester, Manchester, UK
DISCLOSURES: EJ declares that he has no competing interests.

Acknowledgements,
BMJ Best Practice would like to gratefully acknowledge the previous team of expert contributors, whose
work has been retained in parts of the content:
Aidar R. Gosmanov, MD, PhD, FACE, Associate Professor of Medicine, Division of Endocrinology, Albany
Medical College, Chief, Endocrinology Section, Albany VAMC, Albany, NY, Laleh Razavi Nematollahi, MD,
Assistant Professor of Medicine, Case Western Reserve University, Cleveland, OH
DISCLOSURES: ARG and LRN declare that they have no competing interests.

// Peer Reviewers:

Gerry Rayman, MD, FRCP

Consultant Physician and Head of Service
Diabetes and Endocrine Centre and the Diabetes Research Unit, Ipswich Hospitals NHS Trust, Ipswich, UK
DISCLOSURES: GR has been paid for advisory board meetings with the following companies: Sanofi
Aventis, Abbott Diabetes UK, Lilly Diabetes, and Bayer. GR has received lecture fees from Sanofi Aventis,
Abbott Diabetes UK, Lilly Diabetes, Novo Nordisk, and Napp Pharmaceuticals Ltd.

Ketan Dhatariya, MBBS, MSc, MD, MS, FRCP, PhD

Honorary Professor of Medicine
Norwich Medical School, University of East Anglia, Consultant Diabetes & Endocrinology, Norfolk and
Norwich University Hospitals NHS Foundation Trust, Norwich, UK
DISCLOSURES: KD is the chair of the Joint British Diabetes Societies for Inpatient Care. KD has received
honoraria from Diabetes Professional Care to speak at its annual meeting about these guidelines. No other
reimbursement has been received from commercial organisations with respect to these guidelines. KD
has helped to develop educational materials on this subject for the European Association for the Study of
Diabetes, but did not receive any reimbursement. For other work as the chair of JBDS, KD has received
honoraria from Lilly for developing educational material.

// Editors:

Annabel Sidwell,
Section Editor, BMJ Best Practice
DISCLOSURES: AS declares that she has no competing interests.

Luisa Dillner,
Head of Research and Development, BMJ
DISCLOSURES: LD declares that she has no competing interests.
Anna Ellis,
Head of Editorial, BMJ Best Practice
DISCLOSURES: AE declares that she has no competing interests.

Rachel Wheeler,
Lead Section Editor, BMJ Best Practice
DISCLOSURES: RW declares that she has no competing interests.

Julie Costello,
Comorbidities Editor, BMJ Best Practice
DISCLOSURES: JC declares that she has no competing interests.

Adam Mitchell,
Drug Editor, BMJ Best Practice
DISCLOSURES: AM declares that he has no competing interests.