Diabetic Emergencies: DKA, HHS & Hypoglycaemia

Diabetic Emergencies in Pre-Hospital Care

Diabetes affects over 4.3 million people in the UK, making diabetic emergencies one of the most frequently encountered conditions in pre-hospital practice. As a student paramedic, you need to confidently differentiate between hypoglycaemia, diabetic ketoacidosis (DKA), and hyperosmolar hyperglycaemic state (HHS) — conditions that can look superficially similar but demand very different management approaches.

Hypoglycaemia: The Rapid Deterioration

Hypoglycaemia is defined as a blood glucose level below 4.0 mmol/L in the context of symptoms. It is by far the most common diabetic emergency you will encounter on the road, and it is potentially the most immediately life-threatening if missed.

Common Causes

• Excess insulin administration (including insulin pump errors)
• Missed or delayed meals after insulin or sulphonylurea medication
• Unplanned exercise without carbohydrate adjustment
• Alcohol consumption masking warning symptoms

Clinical Features

Symptoms result from both autonomic activation (sweating, tremor, tachycardia, pallor) and neuroglycopenia (confusion, aggression, slurred speech, reduced GCS, and in severe cases, seizures or unconsciousness). It is worth noting that patients on beta-blockers may have blunted autonomic symptoms, making clinical recognition harder.

JRCALC Management

Your approach depends on the patient's level of consciousness and ability to swallow safely:

1. If conscious and able to swallow — give 15–20g of fast-acting oral glucose (e.g., Glucogel, glucose tablets, or Lucozade Original).
2. If conscious but unable to swallow safely — administer buccal glucose gel with caution.
3. If unconscious or unable to protect the airway — IV access is first choice. Administer glucose 10% IV (typically 100–250ml) per your trust protocol. Glucagon 1mg IM is an alternative if IV access cannot be obtained, though it is less effective in alcohol-related hypoglycaemia or glycogen-depleted patients.

Following treatment, always recheck blood glucose after 10–15 minutes. Ensure the patient eats a complex carbohydrate meal before considering non-conveyance. Document carefully and follow your trust's 'treat and refer' or 'hear and treat' pathways where applicable.

Diabetic Ketoacidosis (DKA)

DKA is a life-threatening emergency predominantly seen in Type 1 diabetes, though it can occur in Type 2. It results from absolute or relative insulin deficiency, leading to uncontrolled lipolysis and the accumulation of ketone bodies, causing metabolic acidosis.

The DKA Triad

• Hyperglycaemia — blood glucose typically >11 mmol/L (though 'euglycaemic DKA' is possible, particularly with SGLT-2 inhibitors)
• Ketonaemia/ketonuria — blood ketones >3 mmol/L or urine ketones 2+ or more
• Metabolic acidosis — pH less than 7.3 (not measurable in most pre-hospital settings, but implied by clinical picture)

Clinical Features

DKA typically develops over hours to days. Look for polyuria, polydipsia, nausea and vomiting, abdominal pain, and progressive lethargy. On examination, you may find dehydration (dry mucous membranes, poor skin turgor), tachycardia, hypotension, and the characteristic Kussmaul breathing — deep, laboured respirations as the body attempts to compensate for acidosis by blowing off CO₂. A sweet or 'pear-drop' smell of acetone on the breath is a classic feature.

Pre-Hospital Management

DKA cannot be definitively managed in the pre-hospital environment — these patients need hospital admission for IV insulin infusion, careful fluid resuscitation, and electrolyte monitoring (particularly potassium). Your priorities are:

• Airway management and supplemental oxygen if SpO₂ is below 94%
• IV access and cautious fluid resuscitation with 0.9% sodium chloride — consult your trust guidelines for volume
• Continuous monitoring: ECG, SpO₂, blood glucose, GCS
• Pre-alert the receiving emergency department
• Do NOT give insulin in the pre-hospital setting unless operating under a specific critical care protocol

Hyperosmolar Hyperglycaemic State (HHS)

HHS is less common than DKA but carries a higher mortality — estimated at 10–20%. It occurs almost exclusively in Type 2 diabetes and is characterised by extreme hyperglycaemia, severe dehydration, and hyperosmolality without significant ketoacidosis.

How HHS Differs from DKA

The key distinction is that in HHS, residual insulin secretion is sufficient to suppress ketogenesis but not to control blood glucose. As a result, blood glucose levels are typically much higher than in DKA — often exceeding 30–40 mmol/L — and the clinical onset is far more gradual, developing over days to weeks. Patients are profoundly dehydrated (fluid deficits of 8–10 litres are not uncommon) and frequently present with neurological features including confusion, focal deficits, or seizures due to the hyperosmolar state.

Pre-Hospital Management

As with DKA, definitive care is in hospital. Pre-hospital priorities include:

• Airway protection — neurological compromise is common
• IV access and careful, slow fluid resuscitation; aggressive rehydration risks cerebral oedema
• Blood glucose measurement and documentation
• 12-lead ECG — hypokalaemia and hyperosmolality increase arrhythmia risk
• Urgent pre-alert to the emergency department, flagging likely HHS

Comparing the Three Conditions at a Glance

• Hypoglycaemia: Low BGL (<4 mmol/L), rapid onset, autonomic and neuroglycopenic symptoms, treat pre-hospitally
• DKA: High BGL, ketones, acidosis, Kussmaul breathing, hours–days onset, convey urgently
• HHS: Very high BGL, no significant ketosis, severe dehydration, days–weeks onset, high mortality, convey urgently

Key Pitfalls to Avoid

Mistaking hypoglycaemia for intoxication or a psychiatric episode is a classic and dangerous error — always check blood glucose in any patient with altered behaviour or reduced consciousness. Equally, do not assume a known diabetic presenting with vomiting is simply hypoglycaemic without measuring a blood glucose. In DKA and HHS, monitor for hypokalaemia, as both the underlying condition and treatment can dangerously lower potassium levels.