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DKA (Diabetic Ketoacidosis) — Assessment & ManagementKetones β‰₯3.0 + pH <7.3 = DKA β†’ 999 · potassium replace before insulin if K+ <3.5 · FRIII 0.1 unit/kg/h · never stop long-acting basal insulin · dextrose when glucose <14 (not stop insulin) · SGLT2 sick-day rules stop 3 days pre-surgery · cerebral oedema paediatric mannitol · euglycaemic DKA SGLT2
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The full reasoning pathway β€” in any unwell person with diabetes, check glucose AND ketones; the ketone/acidosis level (not the glucose) defines DKA. Resuscitate, never omit insulin, replace potassium, treat the precipitant. Remember euglycaemic DKA on SGLT2 inhibitors.StartDecisionInvestigateActionReferStop / Admit
PresentationUnwell person with diabetes
Polyuria, thirst, vomiting, abdominal pain, drowsiness, Kussmaul breathing, ketotic breath. Check capillary glucose AND blood ketones immediately β€” in anyone on insulin or an SGLT2 inhibitor who is unwell.
Step 1 Β· Safety β€” is this DKA?Ketones + acidosis = emergency
  • Blood ketones β‰₯3.0 mmol/L (or urine ketones β‰₯++)
  • Glucose >11 mmol/L OR known diabetes (glucose may be near-normal β€” euglycaemic DKA on SGLT2i)
  • Acidosis β€” venous pH <7.3 or bicarbonate <15 mmol/L
YES β€” DKA
Stop Β· admit999 β€” emergency admission
Blue-light to hospital. IV access, start 0.9% saline, fixed-rate IV insulin 0.1 units/kg/h, continue long-acting (basal) insulin, replace potassium. HDU/ICU if pH <7.1, K⁺ <3.5, GCS↓, SBP <90 or sats low.
NO β€” ketosis without acidosis
Step 2 Β· InvestigateFind & treat the cause
VBG, U&E, glucose, ketones, FBC/CRP, cultures, ECG. Identify the precipitant: infection, missed insulin, new diabetes, SGLT2i, MI, pancreatitis. Sick-day rules + correction insulin; recheck ketones.
Step 7 Β· hospital management
Step 7 Β· Action β€” JBDS protocol (hospital)Fluids Β· insulin Β· potassium
  • Fluids: 0.9% saline β€” 1 L stat then replace deficit; add glucose 10% when CBG <14 mmol/L.
  • Insulin: fixed-rate IV insulin 0.1 units/kg/h; continue basal insulin throughout.
  • Potassium: replace once K⁺ <5.5 and patient passing urine (insulin drives K⁺ intracellularly).
  • Monitor: hourly CBG + ketones; aim ketone fall β‰₯0.5 mmol/L/h, bicarbonate rise; VTE prophylaxis.
Step 6 Β· escalation
Step 6 Β· ReferEscalation thresholds
  • 999 / admit all DKA β€” DKA cannot be managed in primary care.
  • HDU/ICU severe markers: pH <7.1, ketones >6, bicarbonate <5, K⁺ <3.5 on admission, GCS↓, SBP <90, sats <92%.
  • Diabetes team review before discharge β€” cause, education, insulin adjustment, recurrent DKA support.
Step 8 Β· prevention
Step 8 Β· Lifestyle & preventionSick-day rules β€” prevent the next DKA
Never stop insulin when ill (even if not eating) Β· check ketones when unwell or glucose >15 Β· maintain hydration and carbohydrate Β· hold SGLT2 inhibitors when acutely unwell Β· ensure a working ketone meter and a clear sick-day plan.
Step 9 Β· safety-net
Step 9 Β· Safety-netCall 999 / recheck
999 for vomiting + ketones, drowsiness, rapid deep breathing or abdominal pain in a person with diabetes. Anyone on insulin/SGLT2i who is unwell should check ketones β€” a normal glucose does not exclude DKA.
⚠️ Euglycaemic DKA: SGLT2 inhibitors (‑gliflozins) cause DKA with normal or only mildly raised glucose β€” always check ketones, not just glucose, in any unwell patient on insulin or an SGLT2i. And never omit insulin during illness β€” missed insulin is the commonest preventable trigger.
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Safety

Red Flags β€” DKA Emergency Recognition & Cerebral Oedema Risk

Known or newly diagnosed diabetes + blood glucose >11 mmol/L + ketonuria (β‰₯2+) or blood ketones β‰₯3.0 mmol/L + bicarbonate <15 or venous pH <7.3 Diabetic ketoacidosis confirmed. β†’ 999. IV access. IV 0.9% NaCl. Fixed-rate insulin infusion (FRIII) 0.1 unit/kg/h. U&Es + VBG every hour initially. Never stop insulin until ketones <0.3 mmol/L.
DKA + headache + vomiting + confusion + drowsiness + bradycardia + fixed dilated pupil in a child Cerebral oedema β€” most feared DKA complication in children (mortality approximately 20-50%). β†’ 999. Stop current IV fluids. IV mannitol 0.5-1 g/kg (or hypertonic saline 3% 5 mL/kg over 30 min). Paediatric ICU immediately.
Glucose >30 mmol/L + serum osmolality >320 mOsm/kg + confusion + no/minimal ketosis + severe dehydration + elderly type 2 diabetes Hyperosmolar hyperglycaemic state (HHS) β€” not DKA. β†’ 999. Slower correction required (different from DKA protocol β€” max osmolality fall 3-8 mOsm/kg/h; no immediate insulin until sodium corrected). IV 0.9% NaCl.
DKA + chest pain + ECG changes + potassium >6.0 or <3.0 mmol/L on IV insulin Dangerous potassium abnormality in DKA. β†’ 999. Continuous cardiac monitoring. Potassium replacement (add KCl to IV fluids). Do NOT give insulin if K+ <3.5 mmol/L until corrected.
DKA in pregnancy (any trimester) Foetal mortality in maternal DKA approximately 9-35% even with apparently mild maternal symptoms. β†’ 999. Obstetric team + obstetric ICU. Foetal monitoring. Lower glucose threshold for DKA in pregnancy (euglycaemic DKA can occur at glucose 11-13 mmol/L β€” particularly on SGLT2 inhibitor or in fasting state).
Euglycaemic DKA: normal or mildly elevated glucose + ketonaemia β‰₯3.0 + acidosis + recent SGLT2 inhibitor use SGLT2 inhibitor-induced euglycaemic DKA. β†’ 999. Stop SGLT2 inhibitor. DKA protocol (insulin + dextrose to maintain glucose). SGLT2 inhibitors must be stopped 3 days before elective surgery (sick-day rules).
Cerebral oedema in paediatric DKA is the most feared complication of DKA treatment, responsible for approximately 70-80% of DKA-related deaths in children β€” the mechanism is not fully understood but is associated with: rapid fluid administration (>20 mL/kg in first hour), too-rapid fall in plasma osmolality (dropping more than 3-4 mOsm/kg/h), too-rapid fall in blood glucose (>5 mmol/L/h), or high blood urea on presentation. The ISPAD (International Society for Paediatric and Adolescent Diabetes) guidelines recommend: (1) initial fluid resuscitation of 10 mL/kg 0.9% NaCl over 30-60 min (maximum 20 mL/kg) for haemodynamic compromise β€” not the historical 20 mL/kg boluses; (2) maximum fluid replacement of 5% deficit over 48 hours; (3) maintaining blood glucose fall at 3-5 mmol/L/h; (4) never exceeding 5% dextrose in the replacement fluid. Any child in DKA who develops headache, agitation, or a change in conscious level during treatment must be assumed to have cerebral oedema until proved otherwise β€” stop fluids, give mannitol, and transfer to PICU.
2
Diagnose

DKA Diagnosis β€” Biochemical Criteria

JBDS DKA Diagnostic Criteria (UK)
All THREE required: (1) Ketonaemia β‰₯3.0 mmol/L blood ketones (or ketonuria β‰₯2+ on urine dipstick). (2) Hyperglycaemia blood glucose >11 mmol/L (or known diabetes regardless of glucose). (3) Acidosis bicarbonate <15 mmol/L OR venous pH <7.3 (VBG).
DKA severity classification
Mild DKA: pH 7.25-7.30, bicarbonate 15-18 mmol/L, Glasgow Coma Scale (GCS) 15 β€” may be managed on general medical ward. Moderate DKA: pH 7.00-7.24, bicarbonate 10-14 mmol/L, GCS 15 β€” medical ward or high-dependency. Severe DKA: pH <7.00, bicarbonate <10 mmol/L, GCS <15 β€” ICU/HDU.
Precipitating factors
New-onset T1DM (30-40% of DKA) β€” first presentation. Infection (most common precipitant β€” UTI, pneumonia, skin/soft tissue infection β€” always look for source). Insulin omission (disrupted routine, deliberate self-harm, eating disorder β€” approximately 20-30% of DKA). Myocardial infarction / acute coronary syndrome β€” always check ECG + troponin. Pregnancy. SGLT2 inhibitor (euglycaemic DKA). Cocaine / recreational drugs β€” sympathomimetic insulin resistance.
Insulin omission as a DKA precipitant is significantly underrecognised in clinical practice β€” approximately 20-30% of DKA admissions in the UK are caused by deliberate or inadvertent insulin omission, and a substantial proportion of these involve young women with type 1 diabetes and eating disorders (diabulimia β€” the intentional restriction of insulin to reduce weight, as glycosuria causes caloric loss). Diabulimia affects approximately 30-40% of young women with T1DM and carries a mortality risk approximately 3x higher than T1DM without eating disorder. Any young woman with T1DM and recurrent DKA should be screened for eating disorders (SCOFF questionnaire), and referral to a specialist eating disorder service with T1DM expertise should be offered. The psychological complexity of diabetes and eating disorder overlap requires integrated care from diabetes specialist nurse, dietitian, and psychologist.
3
Diagnose

Assessment β€” History, Examination & Investigations

History
Symptoms of DKA: polyuria + polydipsia (osmotic) + nausea + vomiting + abdominal pain (can mimic surgical abdomen β€” pseudo-peritoneum from ketonaemia) + blurred vision + weakness + confusion. Duration of symptoms. Precipitating event: fever/infection symptoms, chest pain, omission of insulin (ask directly and non-judgementally), new medication. Current insulin regimen: dose, type, timing, last dose. Blood glucose trends (if monitoring). Ketone monitoring (JBDS recommends blood ketone monitoring β€” more accurate than urine). Known trigger: surgery, trauma, stress. First presentation of diabetes.
Examination
Consciousness level (GCS). Hydration: dry mucous membranes, reduced skin turgor, sunken eyes. Kussmaul breathing (deep, sighing respirations β€” compensatory hyperventilation to blow off COβ‚‚, reducing acidosis). Smell of ketones (pear-drop/acetone breath β€” present in approximately 50%, absent in approximately 50% β€” cannot be relied on). Abdominal tenderness (pseudo-peritoneum from ketonaemia β€” may be severe but resolves with DKA treatment; if abdomen hard and peritonitic: consider true surgical emergency). Peripheral vascular access (IV). Signs of infection: focus examination (chest, urine, skin). Temperature (hypothermia is a poor prognostic sign in DKA).
Investigations
Blood ketones (capillary) (point-of-care; β‰₯3.0 = DKA) · VBG (venous blood gas) (pH + bicarbonate + potassium β€” critical; obtain simultaneously with blood tests) · FBC + U&Es + glucose + HbA1c · Blood cultures + urine culture + CXR (identify infection trigger) · ECG (hyperkalaemia/hypokalaemia changes + MI trigger) · Urinalysis + MSU (glucose + ketones; UTI screen) · Troponin (if chest pain or ECG changes) · Serum amylase/lipase (abdominal pain β€” pancreatitis trigger; amylase often mildly elevated in DKA without true pancreatitis)
The potassium management in DKA is one of the most critical and counterintuitive aspects of the treatment protocol β€” patients presenting with DKA are always total body potassium depleted (from osmotic diuresis, vomiting, and intracellular loss) even if their serum potassium appears normal or elevated on admission. The apparent hyperkalaemia (K+ 5-6 mmol/L on admission) occurs because severe acidosis drives potassium out of cells into the extracellular space (K+ shifts out in exchange for H+ entering cells to buffer the acidosis). As insulin is administered and the acidosis corrects: potassium rapidly moves back into cells, and the serum potassium can fall precipitously to dangerously hypokalaemic levels within 1-2 hours if potassium replacement is not started. The JBDS protocol rule: if K+ >5.5 mmol/L β€” do NOT add potassium to IV fluids yet; if K+ 3.5-5.5 mmol/L β€” add 40 mmol KCl to each litre of 0.9% NaCl; if K+ <3.5 mmol/L β€” DO NOT start insulin until potassium corrected (cardiac arrhythmia risk) β€” give IV KCl and recheck K+ before starting insulin.
4
Diagnose

DKA vs HHS Distinction & SGLT2-Related DKA

DKA vs HHS β€” key differences
DKA: predominantly type 1 diabetes. Glucose typically 14-40 mmol/L. Severe ketosis (blood ketones β‰₯3.0). pH <7.3. Osmolality moderately elevated (300-320 mOsm/kg). Onset over hours-days. Rapid correction (DKA resolution expected within 24h). HHS: predominantly type 2 diabetes. Glucose typically >30 mmol/L. No/minimal ketosis (blood ketones <3.0, bicarbonate >15). pH normal or mildly reduced. Osmolality markedly elevated (>320 mOsm/kg). Onset over days-weeks. Slow correction required (over 48-72h β€” cerebral oedema risk from overcorrection). Significantly higher mortality than DKA (15-20%).
Mixed DKA + HHS
Approximately 20-30% of hyperglycaemic emergencies have features of both β€” moderately elevated ketones (1.5-3.0) + glucose >25 mmol/L + bicarbonate 15-18 + osmolality >320 mOsm/kg. Management: JBDS HHS/DKA crossover protocol. Prioritise slow osmolality correction while managing ketosis. Specialist diabetes/endocrine input.
SGLT2 inhibitor euglycaemic DKA
Blood glucose normal or mildly elevated (typically 11-16 mmol/L) + ketones β‰₯3.0 + pH <7.3. Occurs with: fasting, alcohol excess, infection, surgery, low-carbohydrate diet β€” in patients on empagliflozin, dapagliflozin, or canagliflozin. Missed because glucose is not markedly elevated. KEY RULE: SGLT2 inhibitors must be stopped 3 days before ANY elective surgery (NHS England sick-day rules β€” TREND-UK).
The SGLT2 inhibitor sick-day rule is a critical prescribing safety point β€” sodium-glucose cotransporter-2 inhibitors (empagliflozin, dapagliflozin, canagliflozin, ertugliflozin) work by blocking renal glucose reabsorption, causing glycosuria and reducing blood glucose. However, by reducing glucose availability to cells, they promote fatty acid oxidation and ketone production. During periods of physiological stress (infection, surgery, fasting, alcohol excess), SGLT2 inhibitors can precipitate DKA even at normal glucose levels β€” called euglycaemic DKA. The NHS England/TREND-UK sick-day rules for SGLT2 inhibitors specify: stop empagliflozin/dapagliflozin/canagliflozin when: (1) clinically unwell (infection, fever, unable to eat or drink); (2) elective surgery (stop 3 days before); (3) fasting procedure. Resume only when: eating and drinking normally for 24-48 hours. Failure to follow these rules is associated with potentially life-threatening euglycaemic DKA. GPs prescribing SGLT2 inhibitors should ensure patients have received TREND-UK sick-day rule guidance (available at trend-uk.org) and that it is documented in the clinical record.
5
Refer

Referral Pathways

999
All DKA β€” confirmed or suspected (ketones β‰₯3.0 + glucose >11 + pH <7.3) Β· Altered consciousness Β· Suspected cerebral oedema in child Β· Potassium <3.5 or >6.5 Β· Pregnancy + DKA
Same-day endocrinology/diabetes team (hospital)
Mild DKA (pH 7.25-7.30) may be managed in a specialist diabetes/endocrinology unit if: fully conscious, able to tolerate fluids, no vomiting β€” but requires IV access + hourly monitoring. HHS (glucose >30 + minimal ketosis) β€” always hospital.
GP management (not DKA β€” sick day rules)
Pre-DKA (ketonuria 1+ or blood ketones 1.5-2.9 + glucose elevated): sick day rules, increase SABA, increase fluid, 4-hourly ketone checks. DO NOT manage confirmed DKA (ketones β‰₯3.0 or pH <7.3) in primary care β€” always 999.
After DKA discharge (shared care)
Follow-up within 24h of discharge (DSN β€” diabetes specialist nurse). GP appointment within 1 week. Identify and address precipitant. Review insulin regimen, sick-day rules, blood ketone monitoring. Psychological assessment if insulin omission. Annual HbA1c, renal function, retinopathy, neuropathy.
The pre-DKA prevention protocol with sick-day rules is the most important primary care intervention for T1DM management β€” patients who recognise early ketosis (blood ketones 1.5-2.9 mmol/L) and apply sick-day rules correctly can prevent progression to full DKA. The JBDS sick-day rules for T1DM: (1) Never stop insulin β€” even if not eating; reduce dose only if BG <6 mmol/L; (2) Test blood glucose every 2-4 hours; (3) Test blood ketones every 2-4 hours; (4) Increase rapid-acting insulin by 10-20% if ketones rising or BG >14 mmol/L; (5) Drink plenty of sugar-free fluids; (6) Seek medical help if: unable to keep fluids down, blood ketones β‰₯3.0 mmol/L, blood glucose >25 mmol/L, drowsy or confused. GPs should ensure every T1DM patient has: a blood ketone meter (available on NHS prescription β€” Freestyle Optium, Abbott Optium Neo), written sick-day rules (JBDS sick-day rule card β€” available at diabetes.org.uk), and a 24h contact number for the diabetes team.
6
Treat

DKA Treatment Protocol β€” JBDS 2023

Step 1 β€” Immediate resuscitation (first 30 minutes)IV 0.9% NaCl 500 mL over 10-15 min (resuscitation bolus if haemodynamically compromised β€” systolic BP <90). If haemodynamically stable: 1L over 1h. 2 x large-bore IV access. Continuous cardiac monitoring. Urinary catheter if unconscious. VBG + U&Es immediately. Blood ketones (capillary). ECG.
Step 2 β€” Fixed-rate intravenous insulin infusion (FRIII)Insulin 0.1 unit/kg/h (via IV infusion pump β€” use short-acting soluble insulin: Actrapid/Humulin S). Continue patient's long-acting basal insulin (if T1DM on basal-bolus regimen β€” do NOT stop Lantus/Levemir/Tresiba). Target: blood ketone fall of 0.5 mmol/L/h; glucose fall of 3-4 mmol/L/h; bicarbonate rise of 3 mmol/L/2h. When glucose falls to <14 mmol/L: add 10% dextrose 125 mL/h alongside 0.9% NaCl (do not reduce insulin β€” ketosis must clear first).
Step 3 β€” Fluid replacement (ongoing)After initial bolus: 0.9% NaCl + KCl (if K+ 3.5-5.5 mmol/L): 1L over 2h β†’ 1L over 2h β†’ 1L over 4h β†’ 1L over 4h β†’ 1L over 6h. Add KCl to each bag (40 mmol/L if K+ 3.5-5.5). Potassium monitoring every 1-2h initially. Do NOT add KCl if K+ >5.5. If K+ <3.5: hold insulin, give KCl IV, recheck before restarting insulin.
Step 4 β€” Resolution criteria and transition to SC insulinDKA resolved when: blood ketones <0.3 mmol/L AND bicarbonate >18 mmol/L AND pH >7.3. Do NOT stop IV insulin until patient has eaten a meal AND subcutaneous insulin has been given (overlap by 30-60 min for fast-acting SC insulin). Transition: give subcutaneous insulin at normal meal dose with the meal, continue IV insulin for 30 min after, then stop infusion. HbA1c at admission: guides subsequent diabetes management.
The 'never stop the long-acting insulin' principle in DKA management is a fundamental change from older protocols β€” historically, insulin infusion was the only insulin given during DKA and all insulin was stopped when transitioning to subcutaneous. The JBDS 2023 protocol now specifies that T1DM patients who take long-acting basal insulin (Lantus/insulin glargine, Levemir/insulin detemir, Tresiba/insulin degludec) should continue their usual dose of long-acting insulin throughout DKA treatment, even when receiving IV insulin. The reason: abrupt cessation of long-acting basal insulin during DKA and rebound after can cause rapid rebound hyperglycaemia and ketosis after the infusion is stopped. Maintaining basal insulin reduces DKA recurrence after discharge and makes the transition to subcutaneous insulin smoother. For newly diagnosed T1DM presenting with DKA: the diabetes team decides the starting basal insulin dose after ketosis resolves.
7
Treat

Post-DKA Management & Prevention

Post-DKA discharge protocol
HbA1c review (reflects glycaemic control over preceding 3 months β€” context for DKA). Identify precipitant and address (treat infection, counsel re: insulin omission, review sick-day rule knowledge). Insulin regime review: consider switching to basal-bolus (MDI) if not already, or pump (CSII) if recurrent DKA. Blood ketone meter: prescribe if not already owned. Sick-day rules: written + verbal. Urgent DSN follow-up within 24-48h. GP appointment within 1 week post-discharge. Psychological assessment if eating disorder, depression, or deliberate insulin omission suspected.
Prevention of DKA recurrence
Sick-day rules education at every T1DM review. Ketone monitoring: blood ketone meter prescribed on FP10 (Freestyle Optium Neo strips β€” available on NHS). Technology: flash glucose monitoring (Libre) or CGM (Dexadoc, Guardian) β€” trend arrows warn of rising glucose + ketones. Free on NHS for all T1DM patients (NICE NG17). Insulin pump (CSII): reduces DKA rates by approximately 30-40% vs MDI in high-risk patients. Closed-loop insulin delivery ("artificial pancreas" β€” hybrid NICE-approved systems: MiniMed 780G, iLet, Omnipod 5): significantly reduces time in hypoglycaemia and hyperglycaemia.
Type 2 DKA (rare but increasingly recognised)
T2DM DKA: most commonly precipitated by severe illness, particularly in Black/African Caribbean patients (ketosis-prone diabetes or Flatbush diabetes β€” fulminant beta-cell exhaustion from severe hyperglycaemia). After DKA resolution, approximately 30-40% can subsequently be managed without insulin. Identify: HbA1c at presentation, C-peptide (preserve beta-cell function), GAD antibody (if T1DM features). SGLT2 inhibitor DKA β€” see Step 4.
The hybrid closed-loop insulin delivery system (artificial pancreas) represents the most significant advancement in T1DM management since CGM β€” it combines a continuous glucose monitor (CGM) with an insulin pump that automatically adjusts insulin delivery based on real-time glucose readings and predictive algorithms. NICE approved NHS funding for hybrid closed-loop systems in T1DM (Technology Appraisal TA943, November 2023) for adults, children over 2 years, and pregnant women with T1DM. The clinical evidence: the CREATE trial and multiple other RCTs demonstrate that hybrid closed-loop systems increase time in target glucose range (3.9-10 mmol/L) from approximately 60% to approximately 70-75%, reduce time in hypoglycaemia from approximately 4% to approximately 2%, and significantly reduce HbA1c. GPs who have T1DM patients with recurrent DKA, recurrent hypoglycaemia, very high HbA1c (>75 mmol/mol) despite optimised MDI, or those with problematic hypoglycaemia, should refer to the diabetes team for hybrid closed-loop system assessment.
8
Lifestyle

T1DM Self-Management, Technology & Ketone Monitoring

Blood ketone monitoring β€” the primary prevention tool All T1DM patients should have a blood ketone meter β€” blood ketone measurement (beta-hydroxybutyrate β€” BHB) is more sensitive and more specific than urine ketones for early DKA detection. Urine ketones reflect ketones approximately 4-6h ago; blood ketones are real-time. Ketone action thresholds: <0.6 mmol/L = normal; 0.6-1.4 = monitor closely; 1.5-2.9 = sick-day rules, call diabetes team if not improving; β‰₯3.0 = DKA β€” call 999. Blood ketone meter (Freestyle Optium Neo β€” Optium Ξ²-ketone strips) prescribable on FP10.
Continuous glucose monitoring (CGM) β€” NHS provision All T1DM patients are entitled to NHS-funded flash glucose monitoring (Freestyle Libre 2 or 3) or real-time CGM (Dexcom G7, Medtronic Guardian 4). CGM trend arrows: a rising glucose with upward arrow is the first warning of developing DKA. CGM significantly reduces DKA admissions by approximately 30-40% in T1DM (by enabling earlier intervention). GPs should ensure all T1DM patients are on CGM β€” if not, refer to diabetes team for prescription/training.
Sick-day rules β€” the key preventive knowledge Every T1DM patient should know JBDS sick-day rules by heart: Never stop insulin. Test glucose + ketones every 2h when unwell. Increase rapid-acting insulin by 10-20% if ketones rising. Drink sugar-free fluids (100-200 mL/h). Ring diabetes team or go to A&E if: ketones β‰₯3.0 mmol/L, glucose >25, vomiting, drowsy. SGLT2 inhibitor sick-day rules: STOP empagliflozin/dapagliflozin if unwell, fasting, or pre-surgery.
Exercise and T1DM ketone management High-intensity or prolonged exercise can increase ketone production in T1DM (stress hormone-driven counter-regulatory response). Post-exercise ketone testing: if blood ketones rise above 1.5 mmol/L after exercise + glucose elevated: treat with insulin correction dose. Fasted exercise without adequate insulin: particular risk of exercise-related DKA. Exercise nutrition: consume 15-30g carbohydrate before and during prolonged exercise; reduce basal insulin before prolonged aerobic exercise (DAFNE programme guidance).
Alcohol and DKA prevention Alcohol + T1DM = hypoglycaemia risk (alcohol inhibits gluconeogenesis) AND ketosis risk (if eating is reduced while drinking). Key advice: always eat when drinking alcohol. Do not reduce insulin before drinking "to prevent hypo" β€” this risks DKA. Use CGM overnight to detect nocturnal hypoglycaemia post-alcohol. Blood ketone test the morning after heavy drinking (ketosis may develop overnight).
Psychological support for T1DM and DKA T1DM carries significant psychological burden β€” diabetes distress (worry about complications, guilt about HbA1c, burnout), depression (2-3x higher prevalence than general population), and eating disorders (diabulimia β€” insulin omission for weight loss). Screen at every T1DM review: PHQ-9 + PAID (Problem Areas in Diabetes) questionnaire. Recurrent DKA from insulin omission: specialist eating disorder service + diabetes psychology. IAPT: for depression and anxiety in T1DM. Diabetes UK Helpline (0345 123 2399). JDRF (jdrf.org.uk): T1DM peer support.
Driving and T1DM DVLA regulations for T1DM: notify DVLA if on insulin. Group 1 (car): annual DVLA declaration; must test glucose within 2h of driving and every 2h during journey; must not drive if BG <5 mmol/L; keep rapid-acting glucose in car. Group 2 (HGV/PCV): more stringent β€” stricter BG thresholds, CGM evidence required (sustained readings above 5 mmol/L for 45 min before driving), no severe hypoglycaemia in preceding 12 months. GPs must advise patients of DVLA obligations and document this advice.
Pre-conception care in T1DM DKA in pregnancy has foetal mortality of approximately 9-35% even at lower glucose thresholds. Preconception: target HbA1c <48 mmol/mol before conception. Folic acid 5 mg OD (high-dose β€” T1DM has elevated NTD risk). Retinopathy screening (pregnancy can worsen diabetic retinopathy). Refer to joint diabetes-obstetric antenatal clinic before conception. During pregnancy: glucose targets 3.5-5.9 mmol/L fasting, <7.8 mmol/L 1h post-meal. CGM mandatory in pregnancy (NICE NG17). DKA in pregnancy: lower glucose threshold, euglycaemic DKA more common.
The Libre 2 flash glucose monitoring system is now available on NHS prescription for all T1DM patients β€” the NICE guideline NG17 (updated 2023) confirms that all adults and children with T1DM should be offered either intermittently scanned CGM (isCGM β€” Libre 2 or Libre 3) or real-time CGM. The GPprescription pathway: the treating diabetes team initiates CGM prescription and training; GPs issue subsequent repeat prescriptions on FP10 (Libre 2 sensors: 2 sensors per 28 days, 14-day wear). GPs should not refuse to prescribe CGM sensors for T1DM patients already established on the system by their diabetes team. The prescribing code: Freestyle Libre 2 sensor 14-day wear, 2 sensors per 28-day pack. Annual cost to NHS approximately Β£1,200-1,500 per patient β€” cost-effective given DKA hospitalisation avoidance and improvement in HbA1c.
9
Safety

Post-DKA Monitoring & Annual T1DM Review

Post-DKA follow-up
Within 24-48h: DSN (diabetes specialist nurse) contact β€” ketone meter checked, sick-day rules reinforced, insulin regime reviewed. Within 1 week: GP appointment β€” precipitant addressed, HbA1c result reviewed, psychological assessment if insulin omission. At 3 months: HbA1c + diabetes team review. Escalation if: recurring DKA (second episode in 12 months) β€” closed-loop pump referral + psychology.
Annual T1DM review (NICE NG17)
HbA1c (target <48 mmol/mol for most adults; individualise for hypoglycaemia unawareness or young children). eGFR + albumin/creatinine ratio (nephropathy screen). Retinopathy screening (annual). Monofilament + vibration (neuropathy). Blood pressure + lipids (cardiovascular risk). Weight + BMI. CGM/flash monitoring review. Thyroid function (autoimmune thyroid disease β€” 5-10x more common in T1DM β€” annual TFTs). Coeliac screen (tTG-IgA) at diagnosis and every 5 years (T1DM + coeliac 5-10x more common).
DKA triggers safety-netting
At every T1DM review: confirm patient knows to ring 999 for ketones β‰₯3.0 or vomiting + inability to keep fluids down. Confirm blood ketone meter is working and strips are in date. Confirm sick-day rules understood.
999
Blood ketones β‰₯3.0 mmol/L Β· pH <7.3 Β· Altered consciousness Β· Unable to keep fluids down + unwell T1DM patient Β· Glucose >25 + ketones >1.5 + not responding to sick-day rules
Same-day diabetes team
Blood ketones 1.5-2.9 + vomiting Β· Recurrent mild DKA Β· Euglycaemic DKA (glucose normal/mildly elevated but ketones elevated in SGLT2 inhibitor patient)
The T1DM coeliac disease co-screening is an important and frequently missed annual review task β€” the prevalence of coeliac disease in T1DM is approximately 5-10% (vs approximately 1% in the general population), due to shared genetic susceptibility (HLA-DR3/DQ2 and HLA-DR4/DQ8 haplotypes are shared between T1DM and coeliac). Coeliac disease in T1DM causes: hypoglycaemia from malabsorption (reducing glucose absorption, making insulin dosing unpredictable), worsened glycaemic control despite good adherence, and increased DKA risk. NICE NG17 recommends: coeliac serology (anti-tTG IgA + total IgA) at T1DM diagnosis and repeated every 5 years (or earlier if symptoms develop). Positive serology: refer to gastroenterology for duodenal biopsy confirmation. Confirmed coeliac: strict gluten-free diet, which often dramatically improves glycaemic control in T1DM + coeliac.
Educational use only. Based on JBDS DKA Guidelines 2023, NICE NG17 T1DM 2015 updated 2023, TREND-UK Sick-Day Rules, ISPAD DKA Guidelines 2022, NICE NG17 CGM Provision, BNF insulin prescribing.