QuestionSBA
QuestionChoice
Hypercalcaemia has a broad range of features, including renal stones, bone pain, constipation, nausea, abdominal pain, confusion, polydipsia, polyuria, depression and psychosis. Over 90% of cases of hypercalcaemia are due to either primary hyperparathyroidism or malignancy, with other causes including sarcoidosis and Paget's disease of the bone. Although hypercalcaemia can cause polyuria and polydipsia (due to nephrogenic diabetes insipidus), diffuse abdominal pain and nausea, this does not explain the presence of Kussmaul breathing or hyperglycaemia. Therefore diabetic ketoacidosis is the most likely diagnosis
33612
e
Hypercalcemia
QuestionChoice
Diabetes insipidus is a rare condition affecting either the production of antidiuretic hormone (cranial) or the kidney's sensitivity to antidiuretic hormone (nephrogenic). These patients present with very severe dehydration, polydipsia and polyuria. However, they would not present with Kussmaul breathing or hyperglycaemia, making diabetic ketoacidosis the more likely diagnosis
33611
d
Diabetes insipidus
QuestionChoice
Hyperglycaemic hyperosmolar state (HHS) is a rare condition associated with type 2 diabetes. As a 19-year-old patient, in the absence of obesity, this patient is very unlikely to have type 2 diabetes. In addition, they have Kussmaul breathing suggesting metabolic acidosis. Metabolic acidosis is not a feature of HHS
33609
b
Hyperglycaemic hyperosmolar state
QuestionChoice
Appendicitis will typically have a shorter history over a few hours. They will typically have more localised abdominal pain, with nausea and low-grade fever. Kussmaul breathing, polydipsia, dehydration and hyperglycaemia are not typical features of appendicitis
33610
c
Appendicitis
QuestionChoice
This is a typical presentation of diabetic ketoacidosis (DKA). This patient presents with a prodrome of type 1 diabetes symptoms (including polydipsia and weight loss) which have now worsened. They have deep, laboured breathing in keeping with Kussmaul breathing, a sign of metabolic acidosis. They are also dehydrated, which is common in DKA. Their capillary glucose is 26, which is >11 mmol/L (part of the diagnostic criteria for DKA). Other diagnostic criteria include blood ketones ≥3 mmol/L and metabolic acidosis (pH <7.3 or bicarbonate <15). Management of this patient would include IV 0.9% NaCl (initially 1L over 1 hour), a fixed rate insulin infusion (0.1 units/kg/hour). Potassium is added to further bags of 0.9% NaCl (as insulin can cause hypokalaemia), and the underlying cause of their DKA should be considered (e.g. sepsis, non-compliance, myocardial infarction)
33608
a
Diabetic ketoacidosis
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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A 19-year-old man presents to the emergency department with diffuse abdominal pain and nausea. He has been feeling very thirsty for the past two weeks and lost some weight over that time period. On examination, he has dry mucous membranes, is tachypnoeic and breathing deeply. His capillary blood glucose level is 26.

What is the most likely diagnosis?
a