Hypoglycaemia — Assessment & Management

Safety

Red Flags — Severe Hypoglycaemia, Prolonged Neuroglycopenia & Sinister Causes

Done

Unconscious or seizuring + blood glucose <3.0 mmol/L + unable to swallow Severe hypoglycaemia — requires parenteral treatment. → 999. IM glucagon 1 mg (GlucaGen — thigh or arm). IV glucose 75-100 mL 20% dextrose if IV access available. Place in recovery position. Continuous monitoring.

Prolonged unconsciousness (>30 min) after glucagon + glucose treated + persistent neurological deficit (aphasia, hemiplegia, confusion) Hypoglycaemic brain injury — prolonged neuroglycopenia causes irreversible neurological damage. → 999. CT head. Neurology. ICU.

Hypoglycaemia in a non-diabetic adult + no obvious cause (fasting, alcohol) + insulin level inappropriately elevated + C-peptide elevated Insulinoma (insulin-secreting pancreatic tumour). → 999/urgent endocrinology. CT pancreas + 72-hour supervised fast. Calcium stimulation test.

Hypoglycaemia + deliberately administered insulin/sulfonylurea by a carer or partner + unexplained recurrent episodes in a non-diabetic Factitious hypoglycaemia (Munchausen / induced illness). → 999. C-peptide (exogenous insulin = C-peptide suppressed; endogenous insulinoma = C-peptide elevated). Safeguarding referral if victim is a child or vulnerable adult.

Hypoglycaemia + Addisonian features (hyperpigmentation, postural hypotension, hyponatraemia, hyperkalaemia) Adrenal insufficiency causing hypoglycaemia (counter-regulatory cortisol deficiency). → 999. IM hydrocortisone 100 mg + IV glucose. Serum cortisol + ACTH urgently.

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. Target HbA1c relaxed (<64 mmol/mol acceptable — avoid over-tightening in elderly).

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. 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 (1938): for hypoglycaemia to be clinically diagnosed as the cause of symptoms, three criteria must be met: (1) symptoms consistent with hypoglycaemia; (2) low plasma glucose (<3.0 mmol/L) at time of symptoms; (3) relief of symptoms with glucose correction. 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.

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. The clinical management of sulfonylurea-induced hypoglycaemia: after initial glucose correction, the patient must be observed in hospital for 24-48 hours with frequent glucose monitoring because of the high risk of recurrence from the residual drug effect. GPs must not send home a hypoglycaemic patient on a long-acting sulfonylurea after a single glucose tablet and a blood glucose of 5 mmol/L.

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) · Insulin + C-peptide + proinsulin (during confirmed hypoglycaemic episode — distinguishes endogenous from exogenous) · Cortisol + ACTH (adrenal insufficiency screen) · LFTs + GGT (alcoholic hepatic failure) · Sulfonylurea screen (blood + urine in factitious/non-diabetic hypoglycaemia) · 72-hour supervised fast (inpatient, insulinoma diagnosis — specialist endocrinology)

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 (blood glucose <2.2 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 injection (factitious hypoglycaemia, 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. After positive 72-hour fast: CT pancreas (identifies approximately 70-80% of insulinomas), EUS-guided biopsy (endoscopic ultrasound — identifies small insulinomas), and calcium stimulation angiography (identifies region of overproduction). 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: strict hypoglycaemia avoidance for 3-6 weeks → restores IAH in many patients; real-time CGM with alarms at 4.5 mmol/L threshold; insulin pump; structured education (DAFNE).

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. Conduct at every T1DM or insulin-treated T2DM review. Any Gold score ≥4: refer to diabetes technology and education service (DAFNE, DESMOND, or specialist T1DM service).

High-risk groups for severe hypoglycaemia

Elderly on insulin or sulfonylurea (blunted counter-regulation). Very low HbA1c (<42 mmol/mol in T2DM = over-treated). 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 (UK Prospective Diabetes Study group, 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) · Prolonged neuroglycopenic symptoms after treatment · Suspected adrenal crisis with hypoglycaemia

Same-day medical assessment

Sulfonylurea-induced hypoglycaemia (observe 24-48h for recurrence) · Recurrent unexplained hypoglycaemia in non-diabetic patient · Any hypoglycaemia with focal neurological deficit (stroke mimicry)

Endocrinology (urgent)

Spontaneous hypoglycaemia in non-diabetic (insulinoma workup — 72h supervised fast) · Adrenal insufficiency-related hypoglycaemia (cortisol deficiency)

Diabetes team / DSN

IAH (Gold score ≥4) — CGM + technology escalation + DAFNE referral. 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 and stop/switch sulfonylurea in elderly (gliclazide MR safer than glibenclamide — shorter acting).

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. The target: HbA1c 53-64 mmol/mol (7-8%) is appropriate for most elderly frail patients; in very frail patients or those with limited life expectancy, even higher targets (up to 75 mmol/mol) may be appropriate 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 (too low) 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 re-target HbA1c 53-64 mmol/mol.

Treat

Hypoglycaemia Treatment — Level 1, 2 & 3

Done

Level 1 (BG 3.0-3.9 mmol/L — alert value, able to swallow)15g fast-acting carbohydrate: 4-5 Glucotabs (3.75g each), or 150-200 mL fruit juice, or 150 mL Lucozade Energy Original (original formulation), or 4 glucose sweets. Recheck BG after 15 minutes (15-15 rule). Repeat if BG still <4.0 mmol/L. 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). 200 mL Lucozade or 5 Glucotabs or equivalent. Recheck at 15 min. If unable to eat solid food: Glucojuice (concentrated glucose gel — buccal). Dextrogel (40% glucose) squeezed into cheek pouch. Follow with slow-acting carbohydrate. If on acarbose (alpha-glucosidase inhibitor): use glucose only (NOT sucrose/fructose drinks — acarbose inhibits disaccharide breakdown, making them ineffective).

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. Ineffective in: severe hepatic disease, prolonged fasting, alcohol-induced hypoglycaemia (glycogen depleted), starvation. IV 20% Dextrose 75-100 mL over 15 min (if IV access): faster + more reliable than glucagon. When conscious: give oral glucose + carbohydrate. If no response to glucagon at 15 min: IV glucose. 999 regardless. Observe for minimum 30 min after recovery.

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 (approximately £80 vs £15) 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. Reduce offending insulin dose by 10-20% (cautious reduction — avoid large dose reductions). Reassess within 1 week. 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

Gliclazide MR 30-60 mg OD: lower hypoglycaemia risk than glibenclamide (modified-release, shorter effective duration, less active metabolite). Glibenclamide: avoid in elderly and in renal impairment (CKD ≥3a) — accumulates, prolonged hypoglycaemia. Renal dosing: gliclazide MR 30 mg OD in eGFR 30-60; avoid if eGFR <30. 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). Stop sulfonylurea if: frail elderly, eGFR <30, HbA1c too low (<48 mmol/mol on sulfonylurea alone or with insulin).

Technology for hypoglycaemia prevention

Real-time CGM with predictive low glucose alarm (Dexcom G7, Libre 3 with alarm): alerts patient at BG of 4.0-4.5 mmol/L (before reaching hypoglycaemia threshold). Prescribable on NHS for all T1DM and for T2DM on insulin with ≥2 hypoglycaemic episodes per year (NICE). 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.

The CGM prescribing rights for T2DM on insulin is an important update in NICE NG17 (2023) — CGM is now available on NHS prescription not just for T1DM but also for T2DM patients on insulin who experience: (1) recurrent hypoglycaemia, especially severe episodes; (2) hypoglycaemia unawareness; or (3) significant anxiety about hypoglycaemia that limits self-management. The practical GP pathway: any T2DM patient on insulin with ≥2 hypoglycaemic episodes (Level 2 or Level 3) in the preceding 12 months should be referred to the diabetes team for CGM initiation. 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 (CONCEPTT trial and DIAMOND trial) 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. Glucojuice glucose gel. Lucozade Original 150 mL. Haribo jelly babies (10g carbohydrate per 2 bears). Patients on acarbose: must carry glucose tablets ONLY (not fruit juice or sweets containing sucrose/fructose). 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: one Baqsimi nasal glucagon (3 mg) per quarter + one GlucaGen HypoKit (1 mg) per quarter. 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 DVLA regulations (Group 1 licence): test blood glucose within 2 hours of starting to drive; test every 2 hours during journey; do not drive if BG <5 mmol/L; keep rapid-acting glucose in car; if hypo occurs while driving: pull over safely, turn engine off, remove keys, treat hypo, wait 45 min after BG returns to ≥5 mmol/L before driving again. Group 2 (HGV/PCV): BG must be ≥5 mmol/L for 45 consecutive CGM minutes before driving; no severe hypo in preceding 12 months. Notify DVLA of insulin treatment. 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 if nocturnal hypo: reduce long-acting insulin by 10-20%.

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. Strategies: reduce bolus insulin with the meal before exercise by 50%; eat 15-30g carbohydrate before exercise if BG <7 mmol/L; check BG before, during (every 45 min), and 90 min + 3h after exercise; raise CGM alarm threshold to 5.5 mmol/L for 8-12h post-exercise. 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. Do not reduce insulin before drinking to "prevent hypo." CGM overnight. NEVER advise a patient to reduce their basal insulin when drinking alcohol (this approach, while counterintuitive, prevents the glucose-lowering effect of alcohol from being compounded by insulin excess). Blood glucose on waking after heavy alcohol: check before injecting morning insulin.

Sick-day rules for hypoglycaemia prevention in T2DM T2DM patients on insulin or sulfonylurea: reduce or hold sulfonylurea dose when: not eating normally (illness, nausea, vomiting, surgical procedure). Reduce rapid-acting insulin dose by 25-50% if eating significantly less than usual. Increase glucose monitoring during illness. Seek medical advice if: unable to eat for >24h on insulin. SGLT2 inhibitor sick-day rules: STOP empagliflozin/dapagliflozin/canagliflozin when unwell, fasting, or peri-surgery.

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)

DSN contact or GP appointment. Identify cause. 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 <48 mmol/mol on sulfonylurea alone, reduce or stop. Frailty assessment: if frail (falls, CFS ≥5), consider stopping sulfonylurea or switching to DPP4 inhibitor. Stop glibenclamide in all elderly patients.

Post-hypoglycaemia DVLA guidance

If driving licence must be declared to DVLA: provide written advice + document in notes. Group 1 licence: advise BG >5 mmol/L before driving and 2-hourly checks. Group 2: recommend cessation of driving until specialist assessment if IAH or recurrent Level 3 events.

999

Level 3 (unconscious + seizing + unable to swallow) · Prolonged recovery or neurological deficit after treatment · Suspected adrenal insufficiency (Addisonian features + hypoglycaemia)

Same-day medical review

Sulfonylurea-induced hypoglycaemia (24-48h observation required) · Recurrent unexplained hypoglycaemia in non-diabetic · Level 2 not responding to repeated glucose administration

The sulfonylurea-induced hypoglycaemia hospitalisation standard represents an important safety requirement — the British National Formulary and JBDS guidelines specify that any patient with sulfonylurea-induced hypoglycaemia who has had a Level 2 or Level 3 episode should be admitted to hospital for a minimum of 24-48 hours of glucose monitoring. 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. This is a medicolegal risk and a patient safety risk — sulfonylurea hypoglycaemia requires hospital-level observation.