๐ Returning to practice โ diabetes general
The biggest change: NICE NG28 was updated in February 2026 โ first-line treatment has fundamentally shifted
Most people newly diagnosed with T2DM should now be offered modified-release metformin plus an SGLT2 inhibitor as first-line dual therapy. For those with ASCVD specifically, the recommendation is triple therapy: metformin + SGLT2i + subcutaneous semaglutide (Ozempic) up to 1mg. Oral semaglutide is included as a recommended GLP-1 RA at any licensed dose for other indications (early-onset T2DM, obesity, further treatment). If you have been away from diabetes medicine, this is the single most important change to know.
NG28 Feb 2026: metformin M/R + SGLT2i first-line for most T2DM
ASCVD specifically: metformin + SGLT2i + SC semaglutide up to 1mg
Oral semaglutide included for non-ASCVD GLP-1 RA indications
DKA guideline updated March 2023 โ FRIII 0.1u/kg/hr, reduce to 0.05u/kg/hr when BG <14
SGLT2i sick day rules: STOP if unwell, dehydrated, fasting, or pre-surgery
HbA1c unreliable on dialysis โ use CGM/SMBG for glycaemic assessment
๐ Guidelines
Diagnostic Criteria for Diabetes SCENICE NG12
WHO/NICE NG12 ยท UK standard
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Symptomatic + single testIf symptomatic (polyuria, polydipsia, unexplained weight loss, visual blurring): a single raised result is diagnostic. Fasting glucose โฅ7.0 mmol/L OR random glucose โฅ11.1 mmol/L OR HbA1c โฅ48 mmol/mol (6.5%). Source: WHO 2006; NICE NG12.
Asymptomatic โ two tests requiredIf asymptomatic: two separate abnormal results on different days are needed. Either two HbA1c โฅ48 mmol/mol, two fasting glucose โฅ7.0, or one of each. Source: WHO 2006; NICE NG12.
HbA1c limitationsHbA1c unreliable in: haemoglobinopathies, haemolytic anaemia, recent blood transfusion, iron deficiency (falsely elevates), renal anaemia (falsely lowers), pregnancy. Use glucose-based testing in these scenarios. Source: ABCD Glycaemic Assessment guidance.
Non-diabetic hyperglycaemia (IFG / IGT)Impaired fasting glucose (IFG): fasting glucose 6.1-6.9 mmol/L. Impaired glucose tolerance (IGT): 2h OGTT 7.8-11.0 mmol/L. HbA1c 42-47 mmol/mol (6.0-6.4%) = high risk. Source: NICE NG28; NICE PH38.
Diabetes can now be diagnosed by HbA1c alone in most cases. You do not need an OGTT or fasting glucose if HbA1c โฅ48 mmol/mol on two occasions (asymptomatic) or once if symptomatic. HbA1c is more reproducible, does not require fasting, and is less subject to acute stress responses. Use glucose-based tests when HbA1c is unreliable. Source: NICE NG12; WHO.
Investigating Diabetes Type โ Systematic Approach SCE
NICE NG17 ยท NICE NG28 ยท diabetesgenes.org
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Step-by-step diagnostic algorithm
1
Clinical features: Age at diagnosis, BMI, acanthosis, family history, autoimmune history, severity at onset, speed of progression
2
Islet autoantibodies: GAD-65 (most sensitive), IA-2, ZnT8, IAA (most useful in young children). Positive = T1DM. Negative does not exclude T1DM (absent in approximately 10%).
3
C-peptide: Measured at least 3 years after diagnosis (avoids honeymoon phase). Urine C-peptide:creatinine ratio (UCPCR) <0.2 nmol/mmol = severe insulin deficiency, suggesting T1DM. UCPCR โฅ0.6 = significant endogenous insulin, suggesting T2DM or MODY. Source: Diabetes Genes (Exeter); NICE NG17.
4
If antibody negative + preserved C-peptide: consider MODY if onset <35y, autosomal dominant family history (2-3 generations), lean/normal weight, C-peptide preserved. Use MODY probability calculator (Exeter).
5
If T3c suspected: History of pancreatic disease (pancreatitis, surgery, CF, haemochromatosis). Check exocrine markers (faecal elastase), imaging.
6
If LADA suspected: T2DM phenotype but progressive insulin requirement, antibody positive (especially GAD-65), age typically 25-50. See dedicated LADA tab.
Key biomarkers โ summary
| Test | T1DM | T2DM | LADA | HNF1A/4A MODY | GCK-MODY |
|---|---|---|---|---|---|
| GAD antibody | +ve ~80% | -ve | +ve (often low titre) | -ve | -ve |
| C-peptide | Low/absent | Normal/high | Initially preserved, declines | Preserved | Preserved |
| HbA1c progression | Progressive | Progressive | Gradual decline | Progressive | Stable, mild |
| Onset age | Any (peak childhood) | Usually >40 | 25-50 | <25-35 | Any age |
| SU response | None | Partial | Initially, then declines | Excellent | Not needed |
The UCPCR (urine C-peptide:creatinine ratio) is more practical than serum C-peptide in outpatients. No fasting required, first-morning void, send fresh to lab same day. A UCPCR โฅ0.6 nmol/mmol 5+ years after T1DM diagnosis strongly suggests the patient may have T2DM, MODY, or T3c. Reconsider the diagnosis. Source: Diabetes Genes (Exeter); NICE NG17.
MODY โ Types, Features & Management SCE
Diabetes Genes (Exeter) ยท NHS Genomics Education
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What is MODY?Maturity Onset Diabetes of the Young. The most common form of monogenic diabetes. Autosomal dominant single-gene mutations causing beta-cell dysfunction. Accounts for approximately 1-2% of people diagnosed with diabetes in the UK (approximately 20,000-40,000 people). Up to 90% are misdiagnosed as T1DM or T2DM. Source: Diabetes UK; NHS Genomics Education.
The MODY triad1. Diabetes diagnosed before age 35 (classical: under 25). 2. Autosomal dominant family history: diabetes in 2-3 consecutive generations. 3. Islet autoantibodies negative AND preserved C-peptide. If all three: MODY probability is high. Refer for genetic testing. Source: Diabetes Genes (Exeter).
MODY subtypes
| MODY type | Gene | Prevalence | Key features | Treatment |
|---|---|---|---|---|
| GCK-MODY (2) | Glucokinase | ~30% | Mild, stable fasting hyperglycaemia (6-8 mmol/L). HbA1c rarely exceeds ~58. Complications rare. | No treatment usually needed. |
| HNF1A-MODY (3) | HNF-1ฮฑ | ~30-60% | Progressive insulin secretory defect. Onset <25y. Low renal threshold for glucose (glycosuria at normal glucose). SU-sensitive. | Low-dose SU first-line. |
| HNF4A-MODY (1) | HNF-4ฮฑ | ~5% | Similar to HNF1A. Macrosomia. Transient neonatal hypoglycaemia. SU-sensitive. | Low-dose SU. |
| HNF1B-MODY (5) | HNF-1ฮฒ | ~5% | Renal developmental abnormalities (cysts, dysplasia). Pancreatic atrophy. Uterine malformations in females. Gout. | Usually requires insulin. |
| INS-MODY (10) | Insulin gene | Rare | Permanent neonatal diabetes / early-onset T1DM phenotype. | Insulin required. |
Management changes once MODY is confirmed
HNF1A/4A: switch to sulphonylurea, stop insulinMany HNF1A/4A-MODY patients are on insulin unnecessarily. Once genetically confirmed: transition to low-dose SU (e.g. gliclazide 40mg OD). This is one of the most impactful therapeutic changes in diabetes genetics. Source: Diabetes Genes (Exeter).
GCK-MODY: stop all treatmentMost patients can safely discontinue all glucose-lowering therapy. Stable mild hyperglycaemia that does not respond meaningfully to treatment and rarely causes complications. Exception: pregnancy. Source: Diabetes Genes (Exeter).
HNF1B-MODY: insulin usually neededCheck renal and pancreatic imaging. Pelvic ultrasound for uterine abnormalities in females (HNF1B associated with uterine malformations). Gout screen. Refer renal team. Source: Diabetes Genes (Exeter); NHS Genomics Education.
๐จ HNF1A/4A-MODY sensitivity to sulphonylureas: Patients with HNF1A/4A-MODY are exquisitely sensitive to sulphonylureas. Start at very low doses (e.g. gliclazide 40mg OD) and titrate slowly. Standard T2DM doses will cause hypoglycaemia. This is a patient safety point. Source: Diabetes Genes (Exeter).
GCK-MODY in pregnancy: if a pregnant woman has a GCK mutation and her baby also carries the mutation, the baby's glucose set-point is also elevated. Aggressive treatment of the mother may cause fetal growth restriction. If the baby does NOT carry the mutation, the baby will be larger. Fetal genotype guides treatment intensity. Refer to specialist obstetric diabetes. Source: Diabetes Genes (Exeter).
๐ Guidelines
LADA โ Latent Autoimmune Diabetes of Adults SCE
NICE NG17 ยท Immunology of Diabetes Society
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DefinitionLADA is slowly progressive autoimmune beta-cell destruction presenting in adulthood (typically age 25-50). Often initially misdiagnosed as T2DM because of the older age at onset, slower progression, and initial response to oral agents. Represents approximately 5-10% of people diagnosed with T2DM. Source: Immunology of Diabetes Society; Fourlanos et al, Diabetologia 2005.
Clinical clues suggesting LADA rather than T2DMAge 25-50 at diagnosis. Normal or low-normal BMI (but obesity does not exclude LADA). No features of metabolic syndrome. Progressive deterioration on oral agents within 1-5 years. Personal or family history of autoimmune disease. Insulin requirement developing earlier than expected for T2DM. Source: Leslie et al, Diabetes Care 2021.
InvestigationsGAD-65 antibody: positive (the defining feature). May also be IA-2 or ZnT8 positive. C-peptide: initially preserved but declines over months to years. Higher GAD titre correlates with faster progression to insulin dependence. Source: NICE NG17; Immunology of Diabetes Society.
ManagementOnce LADA is confirmed: prepare for eventual insulin requirement. Metformin is reasonable if insulin resistance coexists. Sulphonylureas are controversial (may accelerate beta-cell decline, though evidence is mixed). DPP-4 inhibitors may preserve C-peptide. Early insulin initiation is often appropriate, particularly if C-peptide is falling. Manage as T1DM once insulin-dependent. Source: NICE NG17; Leslie et al, Diabetes Care 2021.
๐จ When to suspect LADA: A patient labelled as T2DM whose response to oral agents suggests the diagnosis might not be correct. NICE NG28 (2026) specifically states: "If response to medicines suggests that type 2 diabetes might not be the correct diagnosis, see the recommendations on initial diagnosis in NICE's guideline on managing type 1 diabetes." Check GAD-65 and C-peptide. Source: NICE NG28 Feb 2026.
LADA is the diagnosis to consider when a slim 40-year-old with no family history of T2DM is started on metformin and gliclazide, does well for 18 months, then deteriorates. Checking GAD antibodies takes days, costs very little, and changes the entire management trajectory. If positive and C-peptide is falling, start planning insulin and educating the patient about T1DM self-management. Source: NICE NG17; Immunology of Diabetes Society.
๐ Guidelines
Type 3c Diabetes (Pancreatogenic) SCE
Oxford Handbook of Endocrinology and Diabetes ยท Hart et al, Lancet Gastro Hepatol 2016
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DefinitionType 3c (T3c) diabetes, also called pancreatogenic diabetes, results from exocrine pancreatic disease affecting the endocrine pancreas. Accounts for approximately 5-10% of all diabetes in adults and is significantly underdiagnosed. Source: Hart et al, Lancet Gastroenterology and Hepatology 2016; Oxford Handbook.
CausesChronic pancreatitis (most common), pancreatic surgery (pancreatectomy, Whipple's), pancreatic cancer, cystic fibrosis, haemochromatosis, trauma, hereditary pancreatitis.
How T3c differs from T2DMMalabsorption and exocrine insufficiency (diarrhoea, steatorrhoea, weight loss). Both insulin and glucagon secretion impaired, leading to brittle glucose control. Higher hypoglycaemia risk than T2DM on insulin because glucagon counterregulation is impaired. Metformin less effective (less insulin resistance). Source: Oxford Handbook; Hart et al 2016.
InvestigationsFaecal elastase (exocrine insufficiency), pancreatic imaging (CT/MRI/MRCP), HbA1c (may underestimate due to malabsorption/anaemia), C-peptide (reduced/absent depending on stage), autoantibodies (negative). Source: Oxford Handbook.
Management priorities1. Treat exocrine insufficiency: PERT (pancreatic enzyme replacement therapy, Creon). 2. Start insulin once oral agents fail. 3. Individualise HbA1c target (avoid over-tightening due to hypoglycaemia risk from loss of glucagon). 4. CF-related diabetes: insulin is the treatment of choice from diagnosis. Source: Oxford Handbook; NICE NG17 (CF diabetes).
T3c diabetes is commonly labelled as T2DM in clinic notes. Key clue: weight loss + steatorrhoea + new diabetes in a patient without obesity or classical T2DM risk factors. Treat the exocrine deficiency with PERT first. Unrecognised malabsorption will undermine glycaemic management. Source: Hart et al, Lancet Gastroenterology and Hepatology 2016.
Ketosis-Prone Type 2 Diabetes SCE
JBDS 02 DKA Guideline March 2023
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What is it?A distinct phenotype of T2DM where patients present with DKA (or severe ketosis) at diagnosis or during illness, despite having pathophysiology more typical of T2DM. Beta-cell function recovers after the acute episode. Source: JBDS 02 March 2023.
Demographics and characteristicsMost commonly affects adults of Afro-Caribbean or Hispanic descent. Typically obese or overweight. No or low islet autoantibodies. C-peptide recovers after DKA resolution. Note: HLA typing differs from T1DM but is a research tool, not routinely requested in UK clinical practice. Source: JBDS 02 March 2023.
Management of acute episodeTreat the same as any DKA with FRIII, fluids, potassium replacement. Do not assume T1DM. Source: JBDS 02 March 2023.
Post-DKA managementCheck GAD-65, IA-2 and C-peptide once clinically stable. If antibodies negative + C-peptide recovers: likely ketosis-prone T2DM. These patients often achieve insulin independence. Diabetes team review at 3-6 months with reassessment of insulin requirement. Source: JBDS 02 March 2023.
Ongoing riskHigh risk of recurrent DKA with intercurrent illness. Provide sick day rules. Advise ketone monitoring. Structured diabetes education essential. Source: JBDS 02 March 2023.
Ketosis-prone T2DM is the diagnosis to have at the front of your mind when an Afro-Caribbean or Hispanic adult presents in DKA but gives a history that does not fit T1DM: no previous insulin, overweight, family history of T2DM. Manage the acute episode identically to DKA. Review the diagnosis at 6 weeks. Many will come off insulin. Source: JBDS 02 March 2023.
๐ Guidelines
HbA1c Targets โ T2DM NICE NG28 2026
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| Treatment context | HbA1c target |
|---|---|
| Lifestyle/diet alone, or single non-hypoglycaemia-causing drug | 48 mmol/mol (6.5%) |
| On a drug associated with hypoglycaemia (SU, insulin) | 53 mmol/mol (7.0%) |
| HbA1c not controlled at target on single drug: intensify | Reinforce if โฅ58 mmol/mol (7.5%) |
| Older/frail adults | Individualise โ no fixed target |
| CKD / haemodialysis | 58-68 mmol/mol (7.5-8.4%) โ see dialysis tab |
Individualised targets โ 2026 emphasisThe 2026 NG28 update emphasises shared decision-making in HbA1c target-setting. NICE encourages agreeing targets collaboratively. Consider: personal preferences, comorbidities, polypharmacy risks, likelihood of benefiting from long-term interventions. Source: NICE NG28, February 2026.
Rapid HbA1c reduction โ retinal riskWhen starting treatment likely to cause rapid, substantial HbA1c reduction: notify ophthalmologist if patient attends specialist eye service. Risk of non-arteritic anterior ischaemic optic neuropathy (NAION) with semaglutide (rare but documented). Urgent ophthalmology referral if sudden vision loss on semaglutide. Source: NICE NG28 Feb 2026; MHRA; NICE NG242.
HbA1c Targets โ T1DM NICE NG17
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| Context | HbA1c target |
|---|---|
| Standard T1DM in adults | 48 mmol/mol (6.5%) |
| If 48 not achievable without problematic hypoglycaemia | 53 mmol/mol (7.0%) |
| Pregnancy (T1DM) | <48 pre-conception; <53 in pregnancy |
CGM and TIR targetsTIR (3.9-10 mmol/L) โฅ70%. TBR2 (<3.0) <1%. TBR1 (3.0-3.9) <4%. HbA1c and TIR provide complementary information. Source: NICE NG17; International Consensus on TIR, Diabetes Care 2019.
If a T1DM patient has a well-controlled HbA1c (e.g. 48-52) but CGM shows TBR2 >1% or frequent nocturnal hypoglycaemia, the HbA1c is misleading: over-representation of hyperglycaemic and hypoglycaemic periods averaging out. CGM/TIR data tells you what HbA1c cannot. Source: NICE NG17; Consensus on TIR 2019.
When to Start Insulin in T2DM NICE NG28
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IndicationsHbA1c remains above individualised target on optimal oral/injectable therapy. Symptomatic hyperglycaemia despite dual/triple therapy. Unintentional weight loss + hyperglycaemia (may indicate T1DM/LADA). Acute metabolic decompensation. Peri-operative. Pregnancy. Source: NICE NG28 Feb 2026.
First insulin regimenOffer basal insulin intended for once-daily or twice-daily administration as initial insulin therapy. Biosimilar insulins are endorsed as cost-effective alternatives. Use the least expensive option where equally suitable. Source: NICE NG28 Feb 2026.
Titration principlesStart at 10 units or 0.1-0.2 units/kg (local protocols vary). Titrate by 2 units every 3 days to fasting glucose target (typically 5-7 mmol/L). Monitor for hypoglycaemia. Continue metformin and SGLT2i alongside insulin unless contraindicated. Source: NICE NG28 Feb 2026.
When a T2DM patient's response to insulin suggests the diagnosis might not be correct, consider LADA. Check GAD-65 and C-peptide. NICE NG28 explicitly directs clinicians to consider revisiting the diagnosis in this situation. Source: NICE NG28 Feb 2026; NICE NG17.
๐ฅ Major update โ NICE NG28 February 2026
First-line T2DM treatment has fundamentally changed
For most people newly diagnosed with T2DM: offer modified-release metformin AND an SGLT2 inhibitor as first-line dual therapy. For those with ASCVD: triple therapy with metformin + SGLT2i + subcutaneous semaglutide up to 1mg weekly. Generic dapagliflozin is now available (estimated NHS savings of ยฃ560 million). Currently recommended GLP-1 RAs: liraglutide, dulaglutide, oral semaglutide (at any licensed dose for T2DM), and subcutaneous semaglutide (up to 1mg). SC semaglutide up to 1mg is the specific recommendation for ASCVD triple therapy.
๐ Source
NG28 2026 โ First-Line Drug Algorithm New Feb 2026NICE
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| Patient group | First-line offer | If metformin CI/not tolerated |
|---|---|---|
| No relevant comorbidity | Metformin M/R + SGLT2i | SGLT2i monotherapy |
| ASCVD | Metformin M/R + SGLT2i + SC semaglutide โค1mg | SGLT2i + SC semaglutide โค1mg |
| Heart failure | Metformin M/R + SGLT2i | SGLT2i monotherapy |
| Early-onset T2DM (<40y) | Met M/R + SGLT2i + consider GLP-1RA or tirzepatide | SGLT2i + consider GLP-1RA or tirzepatide |
| Obesity | Metformin M/R + SGLT2i | SGLT2i monotherapy |
| CKD eGFR โฅ30 | Metformin M/R + SGLT2i | SGLT2i |
| CKD eGFR 20-30 | Dapagliflozin or empagliflozin + DPP-4i | DPP-4i |
| CKD eGFR <20 | Consider DPP-4i | - |
| Frailty | Metformin M/R monotherapy (caution with SGLT2i) | Individualise |
Key principles from the 2026 update
Introduce drugs sequentiallyStart with metformin, confirm tolerability, then add SGLT2i. For triple therapy (ASCVD), add semaglutide after SGLT2i is tolerated. Do not start all three simultaneously. Source: NICE NG28 Feb 2026.
Modified-release metformin is now standardOffer metformin M/R to most new patients. Similar effectiveness, lower GI side effects, better adherence. Those already tolerating standard metformin do not need to switch. Source: NICE NG28 Feb 2026.
Cardiorenal, not just glucoseSGLT2i and GLP-1RA should be used for their cardiovascular and renal benefits independently of HbA1c. Continue SGLT2i for cardiorenal benefits even if glycaemic targets are met. Source: NICE NG28 Feb 2026.
GLP-1RA scope and specificsRecommended GLP-1 RAs: liraglutide, dulaglutide, oral semaglutide (at any licensed dose for T2DM), and SC semaglutide (up to 1mg). SC semaglutide โค1mg is specifically recommended for ASCVD triple therapy (based on CVOT certainty). Oral semaglutide is recommended for other indications including early-onset T2DM and obesity pathway. Tirzepatide is included for early-onset T2DM. Do NOT combine GLP-1RA or tirzepatide with DPP-4i. Source: NICE NG28 Feb 2026.
DPP-4 inhibitors moved downDPP-4i (sitagliptin, alogliptin etc.) no longer preferred second-line for most patients. No cardiorenal benefit, less cost-effective than generic SGLT2i. Offer only when SGLT2i/GLP-1RA not suitable. Source: NICE NG28 Feb 2026.
โ ๏ธ Equity concern highlighted in NG28 2026: Analysis of approximately 590,000 patients showed SGLT2i are underprescribed in women, older people, Black patients, and socioeconomically deprived groups. NICE explicitly asks clinicians to monitor and address these disparities. Source: NICE NG28 Feb 2026.
SGLT2i & GLP-1RA โ Dose & Renal Thresholds NICE NG28
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SGLT2i โ eGFR thresholds (glycaemic indication)
| Drug | Dose | Glycaemic initiation eGFR | CKD/cardiorenal |
|---|---|---|---|
| Dapagliflozin | 10mg OD | eGFR โฅ45 | CKD: eGFR โฅ15; HF: no lower limit (check SPC) |
| Empagliflozin | 10mg OD (up to 25mg) | eGFR โฅ45 | CKD: eGFR โฅ20; HF: no lower limit (check SPC) |
| Canagliflozin | 100mg OD (up to 300mg) | eGFR โฅ30 (check current SPC/BNF) | CKD: eGFR โฅ30 (check SPC) |
| Ertugliflozin | 5mg OD (up to 15mg) | eGFR โฅ45 | Limited cardiorenal outcome data |
GLP-1 RA โ renal use
| Drug | Renal use |
|---|---|
| Semaglutide (SC and oral) | No renal dose adjustment. No contraindication in CKD. |
| Dulaglutide | No renal dose adjustment. No contraindication at any eGFR. |
| Liraglutide | No renal dose adjustment. No contraindication at any eGFR. |
| Exenatide (Byetta/Bydureon) | Stop if eGFR <30. Renal clearance dependent. |
Dapagliflozin is now the first generic SGLT2i in the UK (from 2025). Generic dapagliflozin should be the default choice for most SGLT2i prescriptions unless there is a specific clinical reason to prefer another agent. Estimated NHS savings: ยฃ560 million over 2025-2027. Source: NICE NG28 Feb 2026.
๐ Guideline
DKA โ Diagnosis & Management EmergencySCEJBDS 02
JBDS 02 revised March 2023
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Diagnostic criteria (all three must be present)
DKA diagnostic triad1. Blood glucose >11 mmol/L (or known diabetes). 2. Venous pH <7.3 OR bicarbonate <15 mmol/L. 3. Blood ketones โฅ3.0 mmol/L OR urine ketones 2+ or more. Source: JBDS 02 March 2023.
Euglycaemic DKA (euDKA)Blood glucose may be <11 mmol/L in: SGLT2i-associated DKA, pregnancy, starvation ketosis. DO NOT use glucose alone to rule out DKA. Source: JBDS 02 March 2023.
Immediate management โ time 0 to 60 minutes
IV fluids: 0.9% sodium chlorideIf systolic BP <90 mmHg: 500ml boluses over 10-15 minutes until BP โฅ90. Then 1L over 60 minutes. Source: JBDS 02 March 2023.
FRIII (Fixed Rate IV Insulin Infusion)50 units human soluble insulin (Actrapid or Humulin S) in 50ml 0.9% NaCl. Rate: 0.1 units/kg/hr. Continue long-acting insulin analogue at usual dose alongside FRIII. Source: JBDS 02 March 2023.
Potassium replacementK+ <3.5: 40 mmol/L per litre bag. K+ 3.5-5.5: 20 mmol/L per litre. K+ >5.5: no potassium. Monitor K+ at 60 min, 2h, then 2-hourly. Source: JBDS 02 March 2023.
Targets while on FRIII
Biochemical targetsKetone fall โฅ0.5 mmol/L/hr. Bicarbonate rise โฅ3 mmol/L/hr. Blood glucose fall โฅ3 mmol/L/hr. Maintain K+ in normal range. Source: JBDS 02 March 2023.
When glucose falls to <14 mmol/LReduce FRIII from 0.1 to 0.05 units/kg/hr. Add 10% glucose alongside saline. Do NOT stop insulin. Stopping insulin will not clear the ketones. Source: JBDS 02 March 2023.
Resolution and transition
DKA resolution criteriaBlood ketones <0.6 mmol/L AND venous pH >7.3. Do not use bicarbonate as a resolution marker (hyperchloraemic acidosis from 0.9% NaCl lowers bicarbonate independently). Source: JBDS 02 March 2023.
Transition to SC insulinOnce resolved AND patient eating and drinking: give SC rapid-acting insulin with a meal. Overlap FRIII for approximately 30-60 minutes after SC dose before stopping IV insulin. This pragmatic overlap period (commonly 30 minutes) prevents rebound ketosis; the exact duration is not rigidly specified by JBDS but reflects standard UK practice. Source: JBDS 02 March 2023.
๐จ Never stop long-acting insulin in DKA. Continue the patient's usual long-acting insulin analogue (Glargine/Detemir/Degludec) at their usual dose alongside the FRIII. Stopping it increases the risk of rebound ketosis when the FRIII is discontinued. Source: JBDS 02 March 2023.
The 2023 JBDS 02 update introduced a key safety change: reduce the FRIII from 0.1 to 0.05 units/kg/hr when glucose falls below 14 mmol/L. The previous practice of maintaining 0.1u/kg/hr throughout was associated with increased rates of hypoglycaemia and hypokalaemia. Source: JBDS 02 March 2023.
๐ Guideline
HHS โ Diagnosis & Management EmergencySCEJBDS 06
JBDS 06 revised February 2022
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Diagnostic criteria (all four features)
HHS criteria1. Serum osmolality โฅ320 mOsm/kg. 2. Marked hyperglycaemia โฅ30 mmol/L. 3. No significant ketonaemia (blood ketones โค3.0). 4. No significant acidosis (pH โฅ7.3 AND bicarb โฅ15). Source: JBDS 06 Feb 2022.
Osmolality calculationCalculated = (2 x Na+) + glucose + urea (all mmol/L). Until urea available: (2 x Na+) + glucose. Source: JBDS 06 Feb 2022.
Mixed DKA/HHSMarked hypovolaemia + hyperosmolality + pH <7.3 + ketones >3.0. Treat with FRIII at 0.1 units/kg/hr as per DKA pathway. Source: JBDS 06 Feb 2022.
Management
Fluid: 0.9% NaClEstimated fluid loss 100-220 ml/kg. Caution in elderly (risk of pulmonary oedema with rapid rehydration). Source: JBDS 06 Feb 2022.
Osmolality fall target3.0-8.0 mOsm/kg/hour. Faster reduction risks cerebral oedema and osmotic demyelination. Source: JBDS 06 Feb 2022.
Insulin: use cautiouslyInsulin is NOT first-line in pure HHS. Fluids alone will lower glucose initially. Source: JBDS 06 Feb 2022.
๐จ HHS mortality is often >15%. Predominantly affects older adults. VTE prophylaxis is essential (highly thrombotic state). Major vascular events (MI, stroke, peripheral arterial thrombosis) are major complications. Source: JBDS 06 Feb 2022.
The sodium paradox in HHS: as insulin lowers glucose, water shifts back into cells and sodium rises. A rising sodium during treatment is expected and does NOT indicate worsening dehydration. Do not add hypotonic fluids in response. Source: JBDS 06 Feb 2022.
๐ Guideline
Inpatient Hypoglycaemia โ JBDS 01 EmergencyJBDS 01
JBDS 01 revised September 2022
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Definition and classification
Hypoglycaemia = CBG <4.0 mmol/LThis is the universal treatment threshold. Mild: CBG 3.0-3.9, patient alert and able to swallow. Severe: CBG <3.0 or patient unable to treat themselves (altered consciousness, seizure, requiring third-party assistance). Source: JBDS 01 Sept 2022.
Treatment algorithm
1
Mild (3.0-3.9, alert, able to swallow): 15-20g rapid-acting glucose (e.g. 150-200ml fruit juice, 4-5 Dextrosol tablets, Glucogel). Recheck in 15 minutes. If still <4.0, repeat up to 3 times. Follow with long-acting carbohydrate if meal not due.
2
Severe (<3.0 or unable to swallow): If IV access: 75-100ml of 20% glucose OR 150-200ml of 10% glucose. If no IV access: IM glucagon 1mg. Recheck in 10-15 minutes. Once CBG >4.0 and patient can swallow: give oral carbohydrate.
3
If on VRIII/FRIII: Stop the insulin infusion. Give IV glucose. Recheck. Restart infusion at reduced rate once CBG >4.0. Source: JBDS 01 Sept 2022.
Glucagon may be ineffective inSulphonylurea-induced hypoglycaemia (stimulates further insulin release), liver disease (depleted glycogen stores), alcohol-related hypoglycaemia, adrenal insufficiency. Use IV glucose in these situations. Source: JBDS 01 Sept 2022.
SU-induced hypoglycaemiaProlonged and recurrent. Long half-life drugs (glibenclamide, glimepiride) are worst. Gliclazide is preferred in the UK due to shorter-acting metabolites. Admit for observation (at least 24h for long-acting SU). Consider IV glucose infusion. Source: JBDS 01 Sept 2022.
๐จ Never give IV glucose as a bolus of 50% dextrose through a peripheral cannula. 50% dextrose is a vesicant and causes tissue necrosis if it extravasates. Use 20% glucose (75-100ml) or 10% glucose (150-200ml) peripherally. 50% glucose via central line only. Source: JBDS 01 Sept 2022.
Every episode of inpatient hypoglycaemia should trigger a medication review. The most common cause is a mismatch between insulin/SU dose and oral intake: patient is NBM, dose has not been adjusted, or meal was missed. Review, document, and amend the insulin prescription. Source: JBDS 01 Sept 2022.
๐ Guidelines
SGLT2i โ Sick Day Rules & euDKA Risk SCENG28 2026
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Why SGLT2i cause euDKASGLT2i shift fuel metabolism towards fat oxidation. In susceptible situations (starvation, illness, dehydration, reduced insulin): ketone production exceeds clearance, causing euglycaemic DKA. Glucose may be only modestly elevated or normal (<11 mmol/L). Source: JBDS 02 March 2023; MHRA.
When to STOP SGLT2i โ SADMAN rulesSurgery, Anaesthesia, Dehydration, Major illness, Abstaining from food/drink, No carbohydrates (ketogenic diet). Stop before elective surgery (many centres: 3 days before). Stop immediately if DKA suspected. Source: NICE NG28 Feb 2026; MHRA.
When to RESTARTOnly when: clinically recovered, eating and drinking normally, not dehydrated, intercurrent illness resolved. Do not restart automatically on discharge. Source: NICE NG28 Feb 2026.
Educate at every prescribing encounterNICE NG28 Feb 2026 explicitly states: "Give clear sick day rules in each person's individualised treatment plan." This is now a named guideline requirement. Source: NICE NG28 Feb 2026.
SGLT2i in T1DM โ UK contextSGLT2i use in T1DM in the UK is largely off-label and is not recommended by NICE. The EMA approved dapagliflozin for T1DM (Forxiga) but uptake in the UK has been very limited due to euDKA risk. If used off-label, patients must have blood ketone monitoring and robust sick day education. Source: MHRA; NICE.
๐จ euDKA is missed because clinicians check glucose and it is "normal". In any patient on an SGLT2i who presents unwell with nausea, vomiting, or abdominal pain: check a blood gas AND blood ketones, regardless of the blood glucose. Source: JBDS 02 March 2023; MHRA.
๐ Guideline
Steroid-Induced Hyperglycaemia & Diabetes SCEJBDS 08
JBDS 08 revised 2021
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DefinitionSteroid-induced hyperglycaemia: CBG >12 mmol/L on two or more occasions during steroid treatment. New steroid-induced diabetes: meets diagnostic criteria for diabetes that was not present before steroids were started. Prevalence: affects approximately 30-50% of patients receiving systemic corticosteroids. Source: JBDS 08 2021.
Timing patternOnce-daily morning prednisolone causes predominantly afternoon and evening hyperglycaemia (peak 8-12 hours post-dose). Fasting morning glucose may be normal. This pattern means HbA1c and fasting glucose can miss it entirely. Check CBG pre-lunch and pre-tea when screening. Source: JBDS 08 2021.
MonitoringAll patients started on systemic steroids should have CBG monitoring. Known diabetes: QDS before meals. No known diabetes: once daily pre-lunch for at least 48 hours. Source: JBDS 08 2021.
Management by severity
CBG 12-20, known T2DM, once-daily steroidFirst line: gliclazide 40-80mg with breakfast (matches the afternoon hyperglycaemia profile of prednisolone). Titrate up to 160mg BD. If already on gliclazide, increase dose. Source: JBDS 08 2021.
CBG persistently >20, or symptomaticStart or increase insulin. For once-daily prednisolone: intermediate-acting insulin (isophane/NPH) given with breakfast provides best profile match. Starting dose: 0.1-0.3 units/kg. Titrate by 10-20% every 24-48 hours. Source: JBDS 08 2021.
Twice-daily or dexamethasone steroidsThese cause 24-hour hyperglycaemia. Basal-bolus insulin or basal insulin (long-acting analogue) more appropriate than isophane alone. Source: JBDS 08 2021.
Steroid dose reductionWhen steroids are tapered: insulin/SU doses must be reduced proportionally to avoid hypoglycaemia. General rule: reduce insulin dose by 10-20% for each halving of steroid dose. Monitor closely. Source: JBDS 08 2021.
The most common inpatient scenario: a patient with COPD is started on prednisolone 40mg OD, nobody checks CBG, and the patient develops symptomatic hyperglycaemia 2-3 days later. The JBDS 08 guideline makes monitoring a requirement, not an optional extra. Gliclazide with breakfast is the pragmatic first-line for most ward patients with mild-moderate steroid hyperglycaemia. Source: JBDS 08 2021.
๐ Guideline
Peri-Operative Diabetes Management SCEJBDS 03
JBDS 03 2015/2016 (check local protocols for newer agents)
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BG target: 6-10 mmol/L (up to 12 acceptable)Avoid hypoglycaemia (<4) in anaesthetised patients. More dangerous than mild hyperglycaemia in the operative setting. Source: JBDS 03 2015.
Book diabetic patients first on the morning listMinimises fasting time. Day of surgery admission is the default. Source: JBDS 03 2015.
Never stop insulin in T1DMBasal insulin continues at usual dose even if fasting. If missing >1 meal: VRIII required. Source: JBDS 03 2015.
VRIII fluid5% dextrose in 0.45% NaCl with KCl. Not 5% dextrose alone. Not 0.9% saline alone. Source: JBDS 03 2015.
Drug management on day of surgery
| Drug | AM surgery (NBM) | PM surgery |
|---|---|---|
| Metformin | Continue normally | Continue normally |
| Sulphonylurea | Omit morning dose if NBM | Omit morning dose |
| SGLT2i | STOP 3 days before surgery (euDKA risk) | STOP 3 days before surgery |
| DPP-4i | Omit morning dose if NBM | Take with light meal |
| GLP-1RA | Omit on day of surgery | Omit on day of surgery |
| Pioglitazone | Continue | Continue |
โ ๏ธ SGLT2i and surgery: JBDS 03 (2015) predates current euDKA awareness. MHRA guidance and most UK centres now recommend stopping SGLT2i 3 days (72 hours) before elective surgery to reduce euDKA risk. Always check your local protocol. Source: MHRA SGLT2i safety communication.
๐ Guideline
Diabetes on Enteral (NG) Feeding SCEJBDS 05
JBDS 05 April 2024
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BG target: 6-12 mmol/L during enteral feedingAim lower end if feasible without hypoglycaemia. Source: JBDS 05 April 2024.
MonitoringPre-feed, then 4-6 hourly when feed running, when feed stopped, at least 2-hourly during feed breaks, hourly if feed unexpectedly off or glucose below range. Source: JBDS 05 April 2024.
Never omit basal insulin in T1DMContinue SC basal insulin at all times, even with additional IV/SC insulin. Source: JBDS 05 April 2024.
Match insulin to feed profileContinuous feed: background coverage. Bolus feed: rapid-acting insulin with each bolus. Source: JBDS 05 April 2024.
If feed stops unexpectedly >30 min after insulin givenHigh hypoglycaemia risk. Monitor CBG hourly. Treat <4.0 immediately. Source: JBDS 05 April 2024.
The most common cause of hypoglycaemia on NG feeds is the feed being interrupted (pump blockage, investigation, suctioning) after insulin has been given. The nursing handover must include: "if the feed stops for more than 30 minutes after insulin was given, check glucose immediately and call the diabetes team." Source: JBDS 05 April 2024.
๐ Guidelines
Diabetes on Haemodialysis SCE
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HbA1c is unreliable on HDRenal anaemia (shorter red cell survival) falsely lowers HbA1c. Iron deficiency falsely elevates. EPO therapy affects turnover. Do not rely on HbA1c alone. Source: ABCD Glycaemic Assessment in HD.
Preferred: direct glucose assessmentSMBG: offer to all people with diabetes on HD. CGM: consider for those on insulin/SU; periodic "diagnostic" CGM 1-2x per year. Source: ABCD guidance.
HbA1c target: 58-68 mmol/mol (7.5-8.4%)Based on U-shaped survival curves. Use as a guide alongside CBG/CGM. Source: ABCD/Renal 2021.
Drug management in CKD/dialysis
| Drug | CKD 3a-4 (eGFR 15-45) | CKD 5 / Dialysis |
|---|---|---|
| Metformin | Reduce dose; stop eGFR <30 | STOP. Lactic acidosis risk. |
| SU (gliclazide) | Use with caution; gliclazide preferred | Lowest doses. High hypo risk. |
| SGLT2i (glycaemic) | Reduced efficacy below eGFR 45 | No glycaemic role on dialysis. |
| DPP-4i | Dose adjust (linagliptin: no adjustment) | Linagliptin: no adjustment. Others: dose adjust/avoid. |
| GLP-1 RA (sema, dula, lira) | No dose adjustment. | No dose adjustment. Source: ABCD/Renal 2021. |
| Exenatide | Caution eGFR <45 | STOP eGFR <30. |
| Insulin | Safe. Reduce doses. | Doses need reduction. Prolonged action. |
Insulin requirements paradoxically decrease as CKD worsens. The kidney metabolises approximately 25-30% of circulating insulin. As eGFR falls, insulin clearance is reduced and the same dose has greater effect. Warn patients their doses may need to reduce and monitor for hypoglycaemia. Source: ABCD/Renal 2021.
๐ Guideline
Diabetic Foot โ Risk Stratification & Management SCENICE NG19
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Annual foot screening for all people with diabetesCheck: neuropathy (10g monofilament, vibration, ankle reflexes), circulation (peripheral pulses, ABPI if vascular disease suspected), skin integrity (callus, deformity, fissures, nail changes). Classify risk after examination. Source: NICE NG19.
Risk stratification โ NICE NG19
| Risk category | Criteria | Surveillance |
|---|---|---|
| Low risk | No risk factors present except callus alone | Annual โ primary care |
| Moderate risk | Deformity OR neuropathy OR non-critical limb ischaemia (single risk factor) | Every 3-6 months โ foot protection service |
| High risk | Previous ulceration OR previous amputation OR on renal replacement therapy OR neuropathy + non-critical ischaemia together OR neuropathy + callus and/or deformity OR non-critical ischaemia + callus and/or deformity | Every 1-2 months โ specialist MDT foot team |
| Active problem | Ulceration, spreading infection, critical ischaemia, gangrene, suspected acute Charcot | Same-day referral to MDT foot team |
Same-day referral criteria
Refer same dayNew ulceration. Spreading cellulitis. Suspected osteomyelitis. Critical ischaemia (absent pulses, rest pain, pallor, gangrene). Suspected Charcot arthropathy (hot, swollen foot with intact skin). Source: NICE NG19.
Charcot arthropathy: do not missHot, swollen, erythematous foot with intact skin. Temperature difference >2 degrees C between feet is a key sign. Easily mistaken for gout, cellulitis, or DVT. Treatment: total contact casting. Source: NICE NG19.
Osteomyelitis
Probe-to-bone testIf a sterile metal probe reaches bone through an ulcer: osteomyelitis probability is high. MRI is the gold standard (sensitivity ~89%, specificity ~93%). Plain X-ray is often normal in early osteomyelitis and cannot exclude it. Source: NICE NG19.
The hot swollen foot in a diabetic patient is Charcot arthropathy until proven otherwise. The three diagnoses to consider: gout, DVT, and Charcot. Charcot is the one you cannot afford to miss: delay in offloading leads to catastrophic midfoot collapse and rocker-bottom deformity. When in doubt: refer same day and offload the foot. Source: NICE NG19.
๐ Guidelines
BP Targets in Diabetes NICE NG136
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T2DM without albuminuria (NICE NG136)Clinic target: <140/90 mmHg. ABPM/HBPM target: <135/85 mmHg. Source: NICE NG136.
T2DM WITH albuminuria or high CVD risk (>20%)Tighter target: <130/80 mmHg. This applies to the significant proportion of diabetes patients with any grade of albuminuria. Source: NICE NG136; NICE NG28.
T1DMTarget: <135/85 mmHg. If microalbuminuria or macroalbuminuria: <130/80 mmHg. Source: NICE NG17.
First-line antihypertensiveACEi or ARB first-line if: diabetic nephropathy (any stage) or any diabetes + microalbuminuria. Do NOT combine ACEi + ARB (increased renal failure/hyperkalaemia risk). Source: NICE NG136.
BP management has been moved out of NICE NG28 and now sits in NICE NG136 (Hypertension in Adults). Always check for albuminuria when deciding the BP target in a diabetes patient: if present, the target drops to <130/80. Source: NICE NG136; NICE NG28 Feb 2026.
Lipids in Diabetes โ Corrected Doses SCENICE NG238
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Statin for primary prevention in T2DMOffer atorvastatin 20mg to all adults with T2DM where 10-year CVD risk โฅ10% (QRISK3). Also offer atorvastatin 20mg to adults with T1DM meeting criteria (age >40, diabetes >10 years, nephropathy). Source: NICE NG238 (formerly CG181), recommendation 1.3.26.
Statin for secondary prevention (established CVD)Offer atorvastatin 80mg. Use a lower dose if: potential for drug interactions, high risk of adverse effects, or patient preference. Source: NICE NG238.
Lipid targetsPrimary prevention: >40% reduction in non-HDL cholesterol from baseline (NICE approach). Secondary prevention: LDL-C โค2.0 mmol/L or non-HDL-C โค2.6 mmol/L. ABCD/UKKA 2024 align with ESC/EAS: LDL-C <1.8 mmol/L for established CVD or high-risk diabetes. Source: NICE NG238; ABCD/UKKA 2024.
If statin alone insufficientAdd ezetimibe 10mg if target not met on maximum tolerated statin. Consider PCSK9 inhibitor (evolocumab, alirocumab) for very high-risk patients: NICE TA394/TA733 criteria apply. Icosapent ethyl: NICE TA805 for raised triglycerides with established CVD. Source: NICE NG238; NICE TA805.
MonitoringCheck full lipid profile at 3 months after starting/changing statin. Non-HDL cholesterol is preferred to LDL-C in diabetes with hypertriglyceridaemia. Source: NICE NG238.
In a patient with T2DM and significantly elevated triglycerides (>10 mmol/L): risk of acute pancreatitis takes priority over LDL-C reduction. Fenofibrate, omega-3 fatty acids (icosapent ethyl, NICE TA805), and dietary fat restriction become the immediate focus. Source: ABCD/UKKA 2024; NICE TA805.
๐ Source
Diabetes and Driving โ DVLA Requirements SCE
DVLA guidance โ Diabetes and Driving (current)
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Group 1 (car/motorcycle) โ insulin-treatedMust notify DVLA. Licence normally issued/renewed for 1, 2, or 3 years. Must demonstrate adequate awareness of hypoglycaemia. Must monitor blood glucose at least twice daily, including before driving. Must not drive if blood glucose is below 5.0 mmol/L. Must keep rapid-acting carbohydrate within reach. Must have no more than 1 episode of severe hypoglycaemia requiring third-party assistance in the preceding 12 months. Source: DVLA Diabetes and Driving guidance.
Group 2 (bus/lorry, C1/D1) โ insulin-treatedStricter criteria. Must demonstrate: no severe hypoglycaemia in the preceding 12 months, full awareness of hypoglycaemia, regular blood glucose monitoring (at least twice daily and at times relevant to driving), understanding of the risks of hypoglycaemia. Must have annual consultant review confirming fitness. Three-yearly medical reviews. Source: DVLA guidance.
Diet/tablet-controlled (no hypo risk)If on diet alone, metformin, DPP-4i, SGLT2i, GLP-1RA, pioglitazone, or acarbose: no requirement to notify DVLA. These agents do not cause hypoglycaemia when used as monotherapy. Source: DVLA guidance.
Sulphonylurea or glinideMust notify DVLA only if hypoglycaemia occurs requiring third-party assistance, or if hypoglycaemia unawareness develops. Otherwise, no requirement to notify but should self-monitor. Source: DVLA guidance.
๐จ The "5 to drive" rule: Blood glucose must be at least 5.0 mmol/L before driving. If it is 5.0 or below, the patient should eat a snack and wait until glucose is above 5.0 before starting. If hypoglycaemia occurs while driving: stop the vehicle safely, switch off the engine, leave the driving seat, and do not restart driving until 45 minutes after blood glucose has returned to normal. Source: DVLA guidance.
Advising patients about driving is a frequently overlooked part of the diabetes consultation. When starting insulin or switching to a sulphonylurea, always discuss: the legal obligation to notify DVLA (if insulin), the need to check glucose before driving, and the "5 to drive" rule. Document the conversation. Source: DVLA Diabetes and Driving guidance.