Hypoglycaemia — Assessment & Management

Safety

Red Flags — Severe Hypoglycaemia, Prolonged Neuroglycopenia & Sinister Causes

Done

Unconscious, seizuring or unable to swallow + low glucose Severe hypoglycaemia — requires parenteral treatment. → 999. Nothing by mouth. IM glucagon 1 mg (GlucaGen — thigh or arm) by a trained carer or clinician. IV glucose by a skilled professional if IV access (JBDS: 100 mL 20% or 200 mL 10% over 15 min — follow local protocol). Place in recovery position. Continuous monitoring.

Consciousness or focal neurological signs not improving promptly after confirmed glucose correction Treat as an emergency: ABCDE, repeat glucose (ongoing or recurrent hypoglycaemia), and consider stroke, seizure/post-ictal state, intracranial haemorrhage, sepsis, intoxication, electrolyte disturbance, hepatic or uraemic encephalopathy. → 999 / urgent hospital assessment. Do not assume irreversible hypoglycaemic brain injury.

Recurrent spontaneous hypoglycaemia in an adult without diabetes + no obvious cause (fasting, alcohol, drugs) Possible endogenous hyperinsulinaemic hypoglycaemia (e.g. insulinoma). → Urgent endocrinology referral (999 only if acutely unwell). Document Whipple's triad; if safe and before treatment, take laboratory glucose, insulin, C-peptide, proinsulin, β-hydroxybutyrate and sulfonylurea/meglitinide screen. Supervised 72-hour fast (fasting) or mixed-meal test (postprandial) and any imaging are specialist-led, only after biochemical confirmation.

Unexplained recurrent hypoglycaemia in a person without diabetes + possible access to insulin or sulfonylureas Suspected exogenous insulin or sulfonylurea exposure. Consider medication error, accidental exposure, deliberate self-administration or safeguarding concerns. Interpret insulin, C-peptide and drug-screen results together (exogenous insulin = C-peptide suppressed). Do not infer a psychiatric diagnosis from biochemistry alone. If a child or vulnerable adult may have been deliberately exposed by another person, follow safeguarding procedures.

Hypoglycaemia + Addisonian features (hyperpigmentation, postural hypotension, hyponatraemia, hyperkalaemia) Adrenal insufficiency causing hypoglycaemia (counter-regulatory cortisol deficiency). → 999. If adrenal crisis is suspected, give emergency hydrocortisone immediately according to the local adrenal-crisis protocol (plus glucose) and arrange hospital assessment. Take cortisol/ACTH before treatment only if this can be done without delaying hydrocortisone.

Recurrent hypoglycaemia in an elderly care home resident on insulin or sulfonylurea with no documented review in >6 months Potentially preventable iatrogenic hypoglycaemia from hypoglycaemic polypharmacy in a frail elderly patient. → Same-day clinical review. Stop/reduce sulfonylurea. Review insulin dose. Relax the HbA1c target on an individual basis (NICE NG28) — avoid over-tightening in older or frail people.

The prolonged hypoglycaemia-induced brain injury is a preventable catastrophe — neurons are exquisitely sensitive to glucose deprivation. At blood glucose below 2.0 mmol/L, neuronal function deteriorates within minutes. Prolonged hypoglycaemia (>20-30 minutes at <2 mmol/L) can cause permanent hippocampal damage, cortical injury, and in extreme cases, death. The critical prevention principle: treat hypoglycaemia immediately, aggressively, and to a confirmed blood glucose above 4.0 mmol/L. Do not wait to 'observe' a drowsy or unresponsive diabetic patient — treat first, investigate the cause after. If consciousness or focal signs do not improve promptly after confirmed correction, treat as an emergency and consider recurrent hypoglycaemia, stroke, seizure, intracranial haemorrhage, sepsis, intoxication or metabolic causes — do not assume irreversible hypoglycaemic brain injury. In primary care, the office response to a severely hypoglycaemic patient must be immediate: IM glucagon 1 mg, call 999, and monitor continuously. Every GP practice should have unexpired glucagon in the emergency kit — a glucagon kit that has expired or is unavailable when needed represents a clinical governance failure.

Diagnose

Hypoglycaemia Classification & Causes

Done

Whipple's Triad (diagnostic framework)

Whipple's triad confirms spontaneous hypoglycaemia in people without diabetes, or where the diagnosis is uncertain: (1) symptoms/signs compatible with hypoglycaemia; (2) low plasma glucose on a reliable laboratory sample at the time of symptoms; (3) resolution when glucose is corrected. Do not diagnose non-diabetic hypoglycaemia from a capillary meter alone, and do not apply <3.0 mmol/L as a universal diagnostic threshold. Whipple's triad is not required in insulin-treated diabetes — a low capillary glucose with compatible symptoms is enough to treat immediately and review medication; in diabetes, treat any glucose <4.0 mmol/L. This triad is essential for distinguishing hypoglycaemia from pseudohypoglycaemia (glucose measured by glucometer but not venous laboratory confirmation) and from non-hypoglycaemic causes of the same symptoms (anxiety, cardiac arrhythmia, transient ischaemic attack).

Hypoglycaemia severity classification

Level 1 (mild — alert value): BG 3.0-3.9 mmol/L. Symptomatic or asymptomatic. Self-treated. Level 2 (clinically significant): BG <3.0 mmol/L. Requires immediate action. May or may not self-treat. Level 3 (severe): Requires assistance from another person (regardless of glucose level). Unable to self-treat. Altered consciousness.

Common causes by clinical context

Insulin-treated T1DM + T2DM: most common — excess insulin dose, missed meal, increased exercise, alcohol. Sulfonylurea (gliclazide, glibenclamide): second most common cause in primary care — longer-acting agents (glibenclamide) cause prolonged hypoglycaemia. Reactive hypoglycaemia: 2-4h post-meal in patients with reactive hyperinsulinism (post-bariatric surgery, idiopathic). Alcohol-induced: alcohol inhibits hepatic gluconeogenesis — commonly 6-12h after heavy drinking. Sepsis/organ failure: critical illness causes hypoglycaemia via cortisol/glucagon deficiency + hepatic failure. Insulinoma: rare — spontaneous fasting hypoglycaemia, elevated insulin/C-peptide. Post-bariatric hypoglycaemia: postprandial — confirm Whipple's triad, establish timing after meals, review diet and medicines, and refer to endocrinology/metabolic service. Do not use a prolonged fast; a supervised mixed-meal test may be used in specialist care. CGM supports pattern recognition but should not be used alone to diagnose.

The sulfonylurea-induced hypoglycaemia is particularly dangerous in elderly patients because of two compounding factors: (1) longer duration of action — glibenclamide has an active metabolite with a half-life of 12-18 hours, meaning a sulfonylurea-induced hypoglycaemia can recur for 24-36 hours after the triggering dose even after initial glucose correction; and (2) hypoglycaemia unawareness — the autonomic warning symptoms (sweating, tremor, palpitations) are blunted in the elderly by reduced adrenergic responsiveness and by concurrent beta-blocker use, meaning the patient may have severe neuroglycopenic hypoglycaemia (confusion, drowsiness) without the usual alerting symptoms. Hospital observation is appropriate for severe hypoglycaemia, recurrent episodes, long-acting or modified-release sulfonylureas, renal impairment, older/frail people, intentional or uncertain overdose, and any episode needing IV glucose or glucagon — JBDS notes recurrence may persist for 24–36 hours after the last long-acting insulin or sulfonylurea dose, particularly with renal impairment. Persistent or recurrent sulfonylurea hypoglycaemia may need prolonged glucose monitoring and specialist toxicology/endocrine management, including octreotide (hospital treatment, not primary care).

Diagnose

Assessment — History, Examination & Investigations

Done

Hypoglycaemia history

Symptoms — adrenergic (counter-regulatory hormones activated at BG 3.5-3.8 mmol/L): sweating, tremor, palpitations, hunger, anxiety. Neuroglycopenic (at BG <3.0 mmol/L): confusion, slurred speech, difficulty concentrating, drowsiness, seizure, loss of consciousness. Time of onset: fasting (insulinoma, Addison's, alcohol) vs postprandial (reactive, post-bariatric) vs nocturnal (insulin-related — nocturnal hypoglycaemia unawareness). Duration and severity. How treated (self-managed vs required assistance). Current antidiabetic medications: insulin type + dose + timing; sulfonylurea (which one — long or short acting). Recent changes: dose change, new medication, new diet, exercise, alcohol. Preceding meal: missed, late, inadequate carbohydrate. Impaired awareness of hypoglycaemia (IAH): patient does not feel symptoms until BG very low — very high risk of severe hypoglycaemia.

Examination

Neurological: GCS (if acute presentation). Focal deficit (hypoglycaemia can mimic stroke). Vital signs: HR (tachycardia in acute hypo), BP (postural drop if Addisonian). Signs of Addison's disease (hyperpigmentation in skin creases, buccal mucosa, scars). Signs of liver disease (hypoglycaemia from hepatic failure). Tumour mass (insulinoma — rare, usually <2 cm, not palpable). Injection sites (insulin lipohypertrophy — altered absorption from lipohy sites).

Investigations

Capillary blood glucose (immediate — treat before investigating) · Laboratory venous glucose (confirm — glucometer ±20% accuracy at low values) · HbA1c (too-tight control = risk factor) · Renal function (reduced insulin/sulfonylurea clearance) · Cortisol ± ACTH (targeted — weight loss, hyperpigmentation, hypotension/postural symptoms, hyponatraemia, hyperkalaemia, recurrent fasting hypos, autoimmune disease or steroid withdrawal) · Without diabetes only — during spontaneous hypoglycaemia, if safe and before treatment: laboratory glucose, insulin, C-peptide, proinsulin, β-hydroxybutyrate, sulfonylurea/meglitinide screen ± insulin antibodies. Not routine in insulin-treated diabetes — the cause is usually clear from insulin type/dose/timing, food, exercise, alcohol, renal function, injection sites, medication changes and CGM/CBG pattern. Never delay treatment of severe hypoglycaemia to take samples. · LFTs + GGT (alcoholic hepatic failure) · Supervised 72-hour fast or mixed-meal test (specialist endocrinology only — fasting vs postprandial presentations; imaging only after biochemical confirmation)

The 72-hour supervised fasting test for insulinoma diagnosis is the gold-standard investigation for spontaneous hypoglycaemia in a non-diabetic patient — the diagnostic criteria: prolonged fasting induces hypoglycaemia (plasma glucose <3.0 mmol/L) with inappropriately elevated plasma insulin (>3 mIU/L or >18 pmol/L), elevated C-peptide (>0.6 ng/mL or >0.2 nmol/L), and elevated proinsulin (>5 pmol/L) at the time of hypoglycaemia. C-peptide elevation differentiates endogenous insulin overproduction (insulinoma) from exogenous insulin exposure (where C-peptide is suppressed because the exogenous insulin feedbacks to suppress endogenous insulin). In approximately 95% of insulinomas, the 72-hour fast produces diagnostic hypoglycaemia within 48 hours. Localisation (CT/MRI, endoscopic ultrasound and, rarely, calcium stimulation testing) is undertaken only after biochemical confirmation, usually through an endocrine/HPB MDT — these are not GP investigations. For postprandial presentations, a specialist-supervised mixed-meal test is used rather than a prolonged fast. Surgery (enucleation or distal pancreatectomy) is curative in approximately 90% of benign insulinomas.

Diagnose

Hypoglycaemia Unawareness & Risk Stratification

Done

Impaired awareness of hypoglycaemia (IAH)

IAH: loss of the normal adrenergic warning symptoms at BG 3.5-3.8 mmol/L — patient no longer sweats, trembles, or feels hungry when glucose falls. They present directly with neuroglycopenic symptoms (confusion, drowsiness) without warning. Causes: repeated hypoglycaemic episodes (counter-regulatory response is blunted by repeated low glucose exposure), autonomic neuropathy (reduced adrenergic signalling), beta-blocker use (masks adrenergic symptoms). Prevalence: approximately 25% of T1DM patients. Assessment: Gold score or Clarke score questionnaire. IAH significantly increases severe hypoglycaemia risk (approximately 6-fold). Management: structured education (e.g. DAFNE where available); insulin-regimen review; avoid recurrent hypoglycaemia — a period of avoiding hypoglycaemia may improve awareness in some people, but persistent impairment requires specialist assessment and technology/education review; CGM and pump therapy per NICE criteria (alarm thresholds individualised). In type 1 diabetes, do not relax individualised glucose targets as the primary response — optimise education, insulin therapy and technology.

Gold Score for IAH assessment

Clarke Score question (simplified): "Do you become aware of your low blood sugars usually, sometimes, or never?" — or Gold Score: single question "Please rate your overall awareness of hypoglycaemia: 1 (always aware) to 7 (never aware)." Gold score ≥4 = impaired awareness — HIGH RISK. Assess at least annually in adults with type 1 diabetes (NICE NG17) and at insulin-treated T2DM reviews. A Gold score ≥4 is a useful marker, not an automatic mandate for a particular device or course: plan structured education (e.g. DAFNE where available), avoidance of recurrent lows, insulin-regimen review, CGM per NICE NG17/NG28 criteria, and specialist diabetes review where severe events recur.

High-risk groups for severe hypoglycaemia

Elderly on insulin or sulfonylurea (blunted counter-regulation). HbA1c below the individually agreed target on insulin or a sulfonylurea (NG28: target 53 mmol/mol on drugs that cause hypoglycaemia; no national lower threshold). IAH. Chronic kidney disease (eGFR <30 — reduced insulin and sulfonylurea clearance). Liver disease. Alcohol use. Eating disorders (T1DM). Post-bariatric surgery. Dementia or cognitive impairment (unable to recognise or self-treat). Living alone (severe hypo may go untreated).

The DAFNE (Dose Adjustment for Normal Eating) programme for T1DM is one of the best-evidenced diabetes education interventions in the UK — it is a 5-day structured group education programme that teaches T1DM patients to carbohydrate-count accurately and match their quick-acting insulin dose precisely to the carbohydrate content of each meal. The DAFNE RCT (DAFNE Study Group, BMJ 2002) showed that DAFNE significantly reduced HbA1c, improved QoL, and reduced hypoglycaemia frequency. NICE NG17 recommends that all adults with T1DM should be offered DAFNE (or equivalent structured education). The waiting time for DAFNE on the NHS varies from weeks to months depending on the centre. GPs who diagnose T1DM or review T1DM patients who have not attended DAFNE should refer — eligibility criteria: T1DM diagnosis, age ≥18, willing and able to engage in group education. The DAFNE programme also teaches hypoglycaemia recognition and treatment, which directly reduces severe hypoglycaemia frequency.

Refer

Referral Pathways

Done

999

Unconscious or seizing hypoglycaemia (level 3) · Glucose still <4.0 mmol/L after 3 treatment cycles (give glucagon if available) · Consciousness or focal signs not improving promptly after confirmed glucose correction (consider stroke, seizure and other causes) · Suspected adrenal crisis with hypoglycaemia

Same-day medical assessment

Sulfonylurea hypoglycaemia that is severe or recurrent, needed glucagon/IV glucose, or involves a long-acting/MR agent, renal impairment, frailty or uncertain overdose (hospital observation — recurrence possible for 24–36 h) · Recurrent unexplained hypoglycaemia in non-diabetic patient if acutely unwell (if stable → urgent endocrinology referral) · Any hypoglycaemia with focal neurological deficit (stroke mimicry)

Endocrinology (urgent)

Spontaneous hypoglycaemia without diabetes once Whipple's triad documented (specialist biochemical testing — supervised 72-hour fast or mixed-meal test; imaging only after biochemical confirmation) · Post-bariatric hypoglycaemia · Adrenal insufficiency-related hypoglycaemia (cortisol deficiency)

Diabetes team / DSN

Any severe (level 3) episode. IAH (e.g. Gold score ≥4) — structured education, insulin-regimen review, CGM/pump per NICE criteria; specialist review if severe events recur. Recurrent hypoglycaemia in insulin-treated diabetes (insulin regime review, pump consideration). HbA1c too low in elderly T2DM (over-treatment with sulfonylurea or insulin).

GP management

Single mild-moderate hypoglycaemic episode with clear precipitating cause (missed meal, exercise, alcohol): education + review insulin/sulfonylurea dose + safety-net. Relax HbA1c target in elderly frail T2DM. Review sulfonylurea in older/frail people — use the lowest effective dose or stop (de-intensify rather than simply switching sulfonylurea); avoid glibenclamide; seek diabetes-team advice if eGFR <30, recurrent hypoglycaemia or frailty.

The HbA1c target individualisation in frail elderly patients with T2DM is a critical clinical governance issue — NICE NG28 specifies that for people with T2DM who are frail, elderly, or have multiple comorbidities and limited life expectancy, the HbA1c target should be relaxed to avoid hypoglycaemia. NICE does not set a number for the relaxed target — agree it with the person case by case, to avoid symptomatic hypoglycaemia. A common and dangerous prescribing pattern: an elderly care home resident with T2DM on insulin glargine 30 units + gliclazide 80 mg BD with an HbA1c of 45 mmol/mol (well below a relaxed individual target) represents potentially fatal over-treatment. The review action: reduce or stop gliclazide (sulfonylureas are the highest-risk hypoglycaemia agents in the elderly), reduce insulin dose, and agree a relaxed individual HbA1c target.

Treat

Hypoglycaemia Treatment — Level 1, 2 & 3

Done

Level 1 (BG 3.0-3.9 mmol/L — alert value, able to swallow)15–20 g fast-acting carbohydrate: glucose tablets (number depends on product glucose content — check product information/local formulary), or 150-200 mL fruit juice, or a glucose drink in the volume its label gives for 15–20 g of sugar (Lucozade Energy was reformulated in 2017 with about half the sugar — check the label), or 4 glucose sweets. Recheck BG after 10–15 minutes. Repeat if BG still <4.0 mmol/L, up to 3 cycles. Still <4.0 mmol/L after 3 cycles → give glucagon if available and call 999. When BG >4.0 mmol/L: follow with 15g slow-acting carbohydrate (one slice of bread, two biscuits, or next planned meal if within 1h) to prevent recurrence. Do NOT use chocolate (fat slows glucose absorption).

Level 2 (BG <3.0 mmol/L — symptomatic, still conscious and able to swallow)20g fast-acting carbohydrate (as above, slightly larger dose). Glucose tablets or a glucose drink to an equivalent glucose content (check the label). Recheck at 10–15 min; repeat up to 3 cycles as for level 1. If unable to eat solid food: a 60 mL glucose juice shot (formerly Glucojuice), or 40% glucose gel (e.g. GlucoGel, Dextrogel) squeezed into the cheek pouch. Follow with slow-acting carbohydrate. If on acarbose (alpha-glucosidase inhibitor): use glucose tablets, glucose gel or glucose solution — not sucrose-containing sweets or table sugar (acarbose delays breakdown of sucrose and starch).

Level 3 (severe — unable to swallow, unconscious, seizing)IM Glucagon 1 mg (GlucaGen HypoKit or Baqsimi nasal glucagon 3 mg): thigh or upper arm. Acts within 10-15 min by mobilising hepatic glycogen. Call 999; recovery position; no oral glucose or gel. Glucagon may be given by trained carers. Less reliable in: sulfonylurea-related hypoglycaemia, severe hepatic disease, prolonged fasting/malnutrition, alcohol excess (glycogen depleted). IV glucose by a skilled healthcare professional with IV access — JBDS inpatient regimen 100 mL 20% or 200 mL 10% over 15 min (harmonise with local protocol). Reassess at about 10 min and continue monitoring. When conscious and able to swallow: oral glucose then longer-acting carbohydrate.

The Baqsimi nasal glucagon (3 mg dry powder intranasal glucagon) is a significant practical advancement over traditional IM glucagon kits — traditional GlucaGen HypoKit requires reconstitution (mixing the lyophilised powder with the diluent) before IM injection, which is difficult and stressful for an untrained carer in an emergency. Baqsimi is a pre-filled single-use nasal applicator that requires no reconstitution, no injection, and no mixing — it is administered by inserting the tip into one nostril and pressing the plunger. Clinical trial data shows it is equivalent in efficacy to IM glucagon with onset of action approximately 10-15 minutes. It can be administered even if the patient is unconscious (does not require swallowing, does not require IV access). NHS prescribing: prescribe Baqsimi alongside the standard IM glucagon emergency kit to provide the carer with both options. Cost is higher than IM glucagon, but the improved usability in emergency situations justifies the cost for appropriate patients (particularly those living alone or with carers who are uncomfortable with injections).

Treat

Preventing Recurrence & Insulin/Sulfonylurea Optimisation

Done

Insulin dose review after hypoglycaemia

Identify timing of hypoglycaemia vs insulin dose: breakfast rapid-acting → late morning hypo = too much morning rapid-acting dose; bedtime long-acting → nocturnal hypo = too much basal insulin. Adjust the responsible dose according to the patient's diabetes-team plan (individualised — no universal percentage) and reassess promptly. Check CGM or glucose diary for pattern identification. Consider: DAFNE or structured carbohydrate counting education. Review injection sites: lipohypertrophy causes erratic absorption.

Sulfonylurea review — the frailty-sensitive drug

Sulfonylureas carry a hypoglycaemia risk that increases with CKD, poor intake, older age and frailty, and are not a good option in significant renal impairment. Avoid glibenclamide in older/frail people and significant renal impairment. Use the lowest effective dose or discontinue where appropriate — de-intensify rather than simply switching to another sulfonylurea. Seek diabetes-team advice if eGFR <30, recurrent hypoglycaemia or frailty. Consider switching from sulfonylurea to: sitagliptin (DPP4 inhibitor — hypoglycaemia-neutral), empagliflozin (SGLT2 inhibitor — but stop in sick days), or insulin (more controllable than long-acting sulfonylurea in some patients). Reduce or stop the sulfonylurea (with diabetes-team advice) if: frail elderly, eGFR <30, HbA1c below the individually agreed target (NG28: 53 mmol/mol on drugs that cause hypoglycaemia).

Technology for hypoglycaemia prevention

Real-time CGM with predictive low glucose alarm (Dexcom G7, Libre 3 with alarm): alarm thresholds individualised (for driving, set appropriately above 4.0 mmol/L; alarms do not replace active monitoring). Offered on the NHS to adults with T1DM (NICE NG17); intermittently scanned CGM to adults with T2DM on multiple daily insulin injections who have recurrent or severe hypoglycaemia, impaired hypoglycaemia awareness, cannot self-monitor with finger-prick testing, or would otherwise need to test 8 or more times a day (NICE NG28). Insulin pump (CSII) with automatic insulin suspension (e.g., MiniMed 780G suspend-before-low feature): stops insulin delivery when CGM predicts BG falling to 3.9 mmol/L. Hybrid closed-loop: automatically adjusts insulin to prevent both highs and lows.

Next steps: see Type 1 diabetes · Type 2 diabetes · Insulin in type 2 diabetes · Driving and the DVLA

CGM for T2DM on insulin comes from NICE NG28 (CGM recommendations added 2022; guideline updated February 2026), while NICE NG17 (2022) offers CGM to all adults with T1DM. NG28 offers intermittently scanned CGM to adults with T2DM on multiple daily insulin injections who have: (1) recurrent or severe hypoglycaemia; (2) impaired hypoglycaemia awareness; (3) a condition or disability that prevents finger-prick monitoring; or (4) would otherwise need to self-test at least 8 times a day. The practical GP pathway: identify eligible patients at review and refer or initiate per local arrangements. GPs can also prescribe CGM directly for patients already established on the technology by their diabetes team, issuing repeat prescriptions for sensors (Freestyle Libre 2 — 2 sensors per 28 days, or Dexcom G6 sensors). The clinical evidence: CGM in T2DM on insulin (DIAMOND type 2 and MOBILE trials; international) shows reduced HbA1c, reduced hypoglycaemia events, and improved patient confidence.

Lifestyle

Hypoglycaemia Preparedness & Patient Empowerment

Done

Always-carry glucose — the non-negotiable rule Every insulin-treated or sulfonylurea-treated diabetic patient must carry fast-acting glucose at all times. Recommended: Dextro Energy glucose tablets (2.5-4g each) — compact, non-melting, pre-measured dose. Glucose gel (e.g. GlucoGel) or a 60 mL glucose juice shot. A glucose drink — check the label, as Lucozade Energy now has about half its former sugar. Patients on acarbose: carry glucose tablets, gel or solution (not sucrose-containing sweets or table sugar). Keep glucose in: car glove compartment, workplace desk, bedside table. Annual review: confirm patient always carries glucose.

Glucagon kit at home — who should have one All T1DM patients should have a glucagon emergency kit (GlucaGen HypoKit IM or Baqsimi nasal) at home and at places where they spend significant time (school, workplace). Prescribe glucagon (GlucaGen HypoKit 1 mg IM — 0.5 mg if child under 25 kg or under 6–8 years; or Baqsimi 3 mg nasal, same dose in children — check the SPC for the licensed age) in a quantity that fits the person's needs and the local formulary. Train carers (partner, family, teachers, workplace first aiders) to administer — in-clinic demonstration essential. Glucagon kit: check expiry date at every diabetes review. Replace on prescription before expiry.

Driving and hypoglycaemia — DVLA rules Provide the patient with the current DVLA guidance and document advice. Drivers must not drive during or immediately after hypoglycaemia. Insulin-treated drivers must check glucose before driving and at least every 2 hours during a journey, and keep fast-acting glucose in the vehicle. If a hypo occurs while driving: stop safely, treat, and do not resume until recovered and the required DVLA waiting period has passed. CGM alarms should be set appropriately above 4.0 mmol/L but do not replace active monitoring and symptoms. Group 2 (HGV/PCV) on insulin: full hypoglycaemia awareness, no episode of severe hypoglycaemia in the preceding 12 months, and glucose checked at least twice daily and at times relevant to driving (within 2 hours before and every 2 hours while driving) on a meter with a memory, with 3 months of readings for the annual specialist review (DVLA Assessing fitness to drive). Group 1 and Group 2 criteria differ — refer to the current DVLA guidance for notification and licensing criteria. GPs must advise DVLA requirements and document.

Nocturnal hypoglycaemia prevention Nocturnal hypoglycaemia (BG <3.9 mmol/L between midnight and 6am) is particularly dangerous — most patients are unaware. CGM with overnight alarms: most effective intervention. Bedtime glucose target: BG 5.5-8.0 mmol/L before bed for insulin-treated patients (higher target than daytime to provide safety margin). Bedtime snack: only recommended if BG <6 mmol/L at bedtime (15g slow-acting carbohydrate — one slice bread, 2 digestives). Review basal insulin dose with the diabetes team if nocturnal hypos occur.

Exercise and hypoglycaemia prevention in T1DM Aerobic exercise causes late hypoglycaemia (3-12h post-exercise) from increased insulin sensitivity. Resistance/strength training is less hypoglycaemia-prone than aerobic. Use the patient's structured exercise plan and diabetes-team guidance. Consider reducing prandial insulin and/or taking carbohydrate according to the activity and insulin-on-board. Monitor before, during and after exercise, including delayed hypoglycaemia. Individualise to exercise intensity, duration and timing, starting glucose and trend arrows, recent hypoglycaemia, pump/closed-loop settings, and ketones or illness. JDRF and Diabetes UK: exercise guidance resources for T1DM.

Alcohol and hypoglycaemia prevention Alcohol inhibits hepatic gluconeogenesis for 8-12h after heavy drinking — hypoglycaemia risk peaks overnight (6-12h after alcohol intake) when food has been metabolised but gluconeogenesis is still inhibited. Key advice: eat before and with alcohol. Avoid binge drinking; eat carbohydrate-containing food; monitor glucose, including overnight; be aware of delayed and nocturnal hypoglycaemia; avoid drinking alone if recurrent severe hypoglycaemia or impaired awareness. Any insulin adjustment around alcohol is individualised — follow the person's diabetes-team alcohol plan. Blood glucose on waking after heavy alcohol: check before injecting morning insulin.

Sick-day rules for hypoglycaemia prevention Type 1 diabetes: never stop basal insulin; urgent diabetes advice if unable to eat, vomiting or ketones present. Type 2 diabetes on insulin: insulin adjustment is individualised — no universal percentage reductions. Sulfonylurea: withhold or seek advice when not eating, particularly in older/frail people. Insulin pumps: do not stop without an alternative basal-insulin plan and specialist guidance. SGLT2 inhibitor: interrupt during acute serious illness, dehydration, vomiting or major surgery; check blood ketones if DKA is suspected, even with normal glucose (MHRA). Increase glucose monitoring during illness.

Psychological impact of severe hypoglycaemia Severe hypoglycaemia (Level 3) causes significant psychological trauma for both the patient and carers/witnesses. Fear of hypoglycaemia (FOH): a significant driver of under-treatment, poor glycaemic control, and anxiety in T1DM and insulin-treated T2DM. FOH leads to deliberate glucose over-correction, keeping BG persistently above 10-12 mmol/L "to feel safe" — worsening long-term complications. PHQ-9 + PAID questionnaire at each review. Hypoglycaemia-focused CBT (specialist psychology) for persistent FOH. DAFNE education reduces FOH by increasing patient confidence in self-management.

The fear of hypoglycaemia (FOH) is a clinically underrecognised driver of sub-optimal glycaemic control in insulin-treated diabetes — FOH is a state of chronic anxiety about hypoglycaemia that causes patients to deliberately maintain elevated blood glucose (above the target range) to avoid the feared event. The consequences: a T1DM patient with FOH who keeps their BG between 9-15 mmol/L 'to feel safe' is accumulating vascular damage from chronic hyperglycaemia while avoiding the short-term discomfort of hypoglycaemia. FOH is measurable using validated questionnaires (Hypoglycaemia Fear Survey — HFS) and is treatable with cognitive-behavioural therapy combined with CGM education (demonstrating objectively how the alarm technology provides a safety net). GPs who see T1DM or insulin-treated T2DM patients with persistently elevated HbA1c (above 75 mmol/mol) should ask directly about FOH: 'Do you sometimes keep your blood glucose higher than the target because you're worried about going hypo?' An affirmative answer should trigger: CGM prescription, DAFNE/structured education referral, and diabetes psychology referral if available.

Safety

Follow-Up, Monitoring & Driving Safety

Done

Post-severe hypoglycaemia review (within 24h)

Diabetes-team/DSN review after any severe or recurrent episode. Identify cause (medication, food intake, exercise, alcohol, illness, renal function). Review insulin/sulfonylurea dose. Confirm carer/partner trained on glucagon. Confirm CGM in place or refer. DVLA driving review if applicable. HbA1c check (is it too low?). Psychological impact acknowledgement.

Annual diabetes review — hypoglycaemia assessment

Gold Score or IAH assessment at every T1DM review. Frequency of Level 1/2/3 events in past year (document). SMBG frequency / CGM adherence. Glucagon kit expiry. DVLA compliance.

Sulfonylurea annual safety review

Annual eGFR check: reduce/stop gliclazide if eGFR <30. HbA1c: if below the individually agreed target on a sulfonylurea (NG28: 53 mmol/mol on drugs that cause hypoglycaemia), reduce or stop. Frailty assessment: if frail (for example falls), consider stopping sulfonylurea or switching to DPP4 inhibitor. Avoid glibenclamide in older people and significant renal impairment.

Post-hypoglycaemia DVLA guidance

If driving licence must be declared to DVLA: provide written advice + document in notes. Group 1: check glucose before driving and at least every 2 hours during a journey; do not drive during or immediately after hypoglycaemia. Group 2 requirements are stricter. Refer to the current DVLA guidance for notification and licensing criteria — not every severe hypo requires Group 1 notification.

999

Level 3 (unconscious, seizing or unable to swallow) · Glucose still <4.0 mmol/L after 3 treatment cycles (give glucagon if available) · Consciousness or focal signs not improving promptly after confirmed glucose correction · Suspected adrenal insufficiency (Addisonian features + hypoglycaemia)

Same-day medical review

Sulfonylurea hypoglycaemia that is severe or recurrent, needed glucagon/IV glucose, or involves a long-acting/MR agent, renal impairment, frailty or uncertain overdose (hospital observation) · Recurrent unexplained hypoglycaemia in non-diabetic if acutely unwell (if stable → urgent endocrinology referral)

Sulfonylurea hypoglycaemia needs a low threshold for hospital observation, but a fixed rule to observe every episode for 24–48 hours is too broad. Hospital observation is appropriate for severe hypoglycaemia, recurrent episodes, long-acting or modified-release sulfonylureas, renal impairment, older/frail people, intentional or uncertain overdose, and any episode requiring IV glucose or glucagon; JBDS notes recurrence may persist for 24–36 hours after the last dose, particularly with renal impairment. The rationale: long-acting sulfonylureas (particularly glibenclamide) and their active metabolites continue to stimulate insulin secretion for many hours after the acute hypoglycaemic episode has been treated. Glucose correction with one or two glucose tablets will raise the blood glucose temporarily, but as the glucose is metabolised, the persistent sulfonylurea stimulus for insulin secretion will cause the blood glucose to fall again — sometimes more severely than the initial episode. A patient on glibenclamide who has been 'treated' with Lucozade and sent home from the GP surgery may re-enter hypoglycaemia in the middle of the night, potentially while living alone. Where any of the higher-risk features apply, arrange hospital-level observation; octreotide may be needed in sulfonylurea toxicity (hospital/specialist treatment).