QuestionSBA
QuestionChoice
HHS leads to a significantly elevated glucose and not such a significant acidosis
31874
b
Hyperosmolar hyperglycaemic state (HHS)
QuestionChoice
This is likely euglycaemic DKA. Although this is a rare phenomenon, one of the most known causes is SGLT2 inhibitors. These are typical symptoms associated with DKA, and her blood tests are all typical of DKA, with the exception of the normal glucose. Therefore, this is euglycaemic DKA. She should be treated with the local DKA protocol
31873
a
Diabetic ketoacidosis (DKA)
QuestionChoice
Gastroenteritis is unlikely to cause polyuria and acidosis such as this
31875
c
Gastroenteritis
QuestionChoice
Pyelonephritis is associated with dysuria and urinary frequency, not polyuria. It may cause nausea and vomiting. It would not normally cause an acidosis such as this
31877
e
Pyelonephritis
QuestionChoice
This is unlikely if her abdomen is soft and non-tender. Metabolic acidosis may occur in patients with peritonitis secondary to a perforated appendix, but they would almost certainly have a tender and rigid abdomen if this was the case
31876
d
Appendicitis
QuestionComment
Hiiiiiigh yield fam
9295
User
subscriber
Gas Womb
QuestionComment
such a great question but. like so many things it tests. impressed I am. 
12507
User
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DNA Tachycardia
QuestionComment
wouldnt you expect hyperglycaemia in this case?
22340
QuestionComment
SGLT2 inhibitors (-flozin) can cause euglycaemic DKA where they are in diabetic ketoacidosis but with normal range serum glucose
23345
User
subscriber
Yellow Nightshift
QuestionComment
SGLT2 inhibitors (-flozin) are known to cause ketoacidosis that is euglycaemic, so the serum glucose is normal
23394
User
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Yellow Nightshift
User
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Serotonin Suture
QuestionComment
why would you get DKA though with T2DM? Thought it was typically T1DM that you get DKA?
58921
User
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Loose Lung
QuestionComment
DKA and euglycemic DKA are not the same bloody thing
61679
QuestionComment
feel like it would have been easier if they put euglycaemic DKA as an answer option yea
62092
User
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Vaccine Complement
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TheRealMorgs
Concept
Chapter
# Summary
 
Diabetic ketoacidosis (DKA) is a life-threatening medical emergency characterised by hyperglycemia, acidosis and ketosis. DKA may be triggered by infection, dehydration or fasting, or may be the initial presentation of Type 1 diabetes. Symptoms include a 'fruity' breath odour, vomiting, dehydration, abdominal pain and altered mental state. Key investigations include blood glucose and ketones, urea and electrolytes and a venous blood gas to check pH. Management involves IV fluids and a fixed rate insulin infusion, with close monitoring both clinically and biochemically. Important complications that should be monitored for include cerebral oedema, hypoglycaemia and hypokalaemia. 

# Definition
 
Diabetic ketoacidosis (DKA) is a medical emergency characterised by the triad of:
 
 - Hyperglycemia (blood glucose >11 mmol/L)
 - Ketosis (blood ketones >3 mmol/L or urinary ketones ++ or higher)
 - Acidosis (pH <7.3 or bicarbonate <15 mmol/L)
  - Note: patients on SGLT-2 inhibitors may present with euglycemic DKA (where glucose is normal)
 

# Epidemiology
 
DKA is most common in individuals with Type 1 diabetes (T1DM) but around a third of cases occur in patients with Type 2 diabetes. The incidence of DKA is highest in young people aged 18-24. 

DKA is the leading cause of death in people aged under 58 years old with T1DM, with cerebral oedema the most common cause of mortality. However, mortality in the UK is still <1%.
 

# Aetiology 

- DKA occurs due to insulin deficiency (absolute or relative) leading to hyperglycaemia
- Ketones, including acetone, 3-beta-hydroxybutyrate, and acetoacetate, are produced from ketogenesis, whereby fatty acids are metabolised as an alternative energy source
- These ketones are responsible for the acidosis seen
- Hyperglycaemia causes an osmotic diuresis that contributes to severe dehydration as well as electrolyte imbalance
- Vomiting and decreased fluid intake secondary to altered mental state also exacerbate dehydration

**10-20% of presentations of DKA represent a first presentation of Type 1 Diabetes**

**Common triggers for DKA include:**

- Infections
- Dehydration and fasting
- Missing doses of insulin
- Medications e.g. steroid treatment or diuretics
- Surgery
- Stroke or myocardial infarction
- Alcohol excess or illicit drug use
- Pancreatitis

# Classification

Patients with at least one of the following may be classified as having **severe DKA**, which should prompt consideration of referral for higher dependency care:

- Blood ketones > 6mmol/L
- Bicarbonate < 5mmol/L
- Blood pH < 7
- Anion gap above 16
- Hypokalaemia on admission
- GCS less than 12
- Oxygen saturations < 92% in air
- Systolic BP < 90mmHg
- Brady or tachycardia (heart rate < 60 or > 100bpm)


# Signs and Symptoms
 
**Symptoms:**

- Nausea and vomiting
- Abdominal pain
- Polyuria
- Polydipsia
- Weakness

**Signs:**

- Dry mucous membranes
- Hypotension
- Tachycardia
- Altered mental state (drowsiness, confusion, coma)
- Kussmaul's breathing (deep, sighing breathing to compensate for metabolic acidosis by blowing off carbon dioxide)
- Fruit-like smelling breath (due to ketosis)

# Investigations
 
**Bedside tests:**
 
 - Capillary blood glucose
 - Blood or urinary ketones
 - Urine dip +/- MSU (looking for evidence of a urinary tract infection which may precipitate DKA)
 - ECG (for ischaemic changes which may precipitate DKA, or changes secondary to electrolyte imbalance e.g. hypokalaemia)

**Blood tests:**

- Venous blood gas (for acid-base balance)
- Urea and electrolytes (for electrolyte imbalance and AKI)
- Full blood count and CRP (for infection markers) 
- Blood cultures (if infection is suspected)
- HbA1c (to assess diabetic control over recent months)

**Imaging:**

- Consider chest X-ray as part of septic screen (if signs of infection as a trigger for DKA)

# Management

**Initial management:** 

- Initial **A to E assessment**
   - Drowsy patients may require airway protection and an **NG tube** to prevent aspiration
   - Ensure adequate IV access
   - If hypotensive give up to 1L in **fluid boluses** then seek urgent senior input if not resolved
   - Consider urinary catheterisation and monitor fluid balance
- **IV fluid replacement with normal saline**
   - A regimen of large volumes of IV fluid replacement given relatively quickly initially then over longer durations should be followed
   - Slower infusion rates should be considered in young adults, the elderly, those with heart or kidney failure or other serious comorbidities
   - An example in a healthy adult would be 1L over 1 hour, then 2x 1L over 2 hours, then 2x 1L over 4 hours, then 1L over 6 hours
   - **Potassium replacement** should be added after the first bag, depending on serum potassium levels, bearing in mind potassium can be infused at a maximum of 10mmol/h:

|  Potassium level (mmol/L)    | Potassium replacement mmol/L of next infusion |   
| :---------------: | :----------------: 
|       > 5.5          |       Nil            |         
|       3.5 - 5.5          |     40 mmol/L              |         
|        < 3.5         |      senior review – additional potassium required             |         
  
   
- After IV fluids have started, a **fixed rate insulin infusion** should be set up 
- This is provided as an infusion of 50 units of Actrapid in 50ml of 0.9% NaCl, at a rate of 0.1 units/kg/hour
- Continue long-acting insulin if the patient is already on this 
- Investigation and management of any underlying triggers (e.g. septic screen and start antibiotics if evidence of infection)
- Ensure **VTE prophylaxis** with low molecular weight heparin is prescribed as patients are at high risk of developing clots due to dehydration

**Ongoing emergency management:**

- Patients should be closely monitored with hourly blood glucose and ketones
   - The aim is for ketones to fall by > 0.5mmol/L/hour
   - Blood glucose should fall by 3 mmol/L/hour
   - If these targets are not met, the rate of insulin infusion should be continued
- Once blood glucose is below 14, a **10% glucose infusion** should be started alongside ongoing saline and insulin
- Regular venous blood gases should also be done to monitor potassium, bicarbonate and pH
- DKA is considered resolved once ketones are less than 0.6 mmol/L and pH is over 7.3 
   - If at this point they are able to eat and drink, a subcutaneous regimen of insulin should be started (usually with the input of a specialist diabetes team)
   - The insulin infusion should be stopped half an hour after the first dose of subcutaneous short acting insulin has been given 

# References
 
[ABCD Guidelines: The Management of Diabetic
Ketoacidosis in Adults](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_02_DKA_Guideline_with_QR_code_March_2023.pdf)

[RCEM - Diabetic Ketoacidosis](https://www.rcemlearning.co.uk/reference/diabetic-ketoacidosis/#1635853037528-05d8fa0f-621f)

[Patient UK - Diabetic ketoacidosis](https://patient.info/doctor/diabetic-ketoacidosis#presentation)
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Raised anion gap metabolic acidosis 2
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Quesmed Tutorial: Medical Emergencies
6375
Euglycaemic diabetic ketoacidosis can occur in patients on SGLT2 inhibitors, presenting with typical DKA symptoms despite normal glucose levels.
A 30-year-old female presents to the Emergency Department with a one-week history of polyuria, reduced appetite, nausea and vomiting. On examination, her abdomen is soft and non-tender. She has the following blood tests:

||||
|---------------------------|:-------:|------------------------------|
|Non-fasting Glucose|5.8 mmol/L|< 6.1|
|Bicarbonate|17.5 mmol/L|22 - 29|
|pH|7.26|7.35 - 7.45|
|Anion gap|20 mEq/L|6 - 12|


She has a background of type 2 diabetes, for which she takes dapagliflozin and metformin.


Which of the following is the most likely diagnosis in this patient?
a