Diabetes mellitus management - regular screening for complications
When screening starts
- When screening starts differs by type
- T1DM - 5 years after diagnosis (T1DM has a defined onset)
- T2DM - at diagnosis (years of undiagnosed hyperglycaemia already elapsed; ~20% have retinopathy at diagnosis)
- Screening is for asymptomatic end-organ damage - symptoms mean assessment, not screening
The organs to screen
- Eye, kidney, foot/nerve, heart, liver, vascular tree
- Liver and heart-failure screening are the recent additions - MASLD and HFpEF were previously found late or not at all
Prevalence
- ~1.3 million Australians with diabetes; ~85-90% type 2
- Retinopathy present in ~20% of T2DM at diagnosis
- Diabetic kidney disease in ~30-40%; leading cause of ESKD in Australia
- Diabetes-related foot disease: ~4,400 amputations/year in Australia, >85% preceded by an ulcer
- Aboriginal and Torres Strait Islander peoples: earlier onset, higher complication rates, ~4x ESKD rate
Microvascular - glycaemia-driven
- Chronic hyperglycaemia -> polyol pathway flux, advanced glycation end-products, PKC activation, hexosamine pathway
- -> endothelial dysfunction, basement membrane thickening, pericyte loss, capillary occlusion
- Duration x glycaemia is the dominant determinant
- Metabolic memory / legacy effect - early tight control confers benefit persisting decades later (DCCT/EDIC, UKPDS)
Macrovascular - multifactorial
- Accelerated atherosclerosis; glycaemic control has modest effect
- BP, lipids and smoking matter more here than HbA1c
Lens
- Non-enzymatic glycosylation of lens proteins + sorbitol accumulation -> premature cataract
- Also increased incidence of open-angle glaucoma
Retina
- Dilated fundus examination or retinal photography
- Australian intervals:
- Every 2 years if no retinopathy and good control
- Annually for Aboriginal and Torres Strait Islander peoples, any retinopathy, poor control, pregnancy, long duration
- More often if proliferative/severe NPDR or maculopathy
- Pregnancy - screen pre-conception and each trimester (rapid progression; rapid glycaemic normalisation transiently worsens retinopathy)
Kidney
- Urine ACR + eGFR annually (T2DM from diagnosis; T1DM from 5 years)
- Albuminuria confirmed on 2 of 3 samples over 3-6 months - exercise, fever, UTI, menstruation, HF all raise it
- Refer nephrology: eGFR <30, ACR >30 mg/mmol, rapid decline, haematuria/atypical features
- Atypical features (no retinopathy, active sediment, rapid decline) -> consider non-diabetic renal disease
Foot and nerve - annually, more often by risk
- Inspect skin, deformity, footwear
- 10 g monofilament + one of vibration (128 Hz tuning fork), pinprick, ankle reflex
- Pedal pulses +/- ABI or toe pressures
- Risk stratification drives interval: low risk annually; moderate 3-6 monthly; high risk (previous ulcer/amputation) 1-3 monthly with a multidisciplinary foot service
Cardiovascular
- BP every visit; lipids at diagnosis then 1-5 yearly
- Absolute CVD risk calculation (Australian CVD risk calculator) - diabetes is not automatically high-risk in the current Australian calculator
- Natriuretic peptide (BNP/NT-proBNP) annually in T2DM to detect stage B / undiagnosed heart failure - newly recommended
- Resting ECG; routine ischaemia testing in asymptomatic patients is NOT recommended
Liver - MASLD
- FIB-4 from age, AST, ALT, platelets in all adults with T2DM or prediabetes + obesity
- FIB-4 >=1.3 -> transient elastography (FibroScan) or ELF as step 2
- ALT can be normal with advanced fibrosis - do not use it as the screen
Other checks
Other
- Vitamin B12 annually if on long-term metformin
- TSH at diagnosis and periodically in T1DM; coeliac serology in T1DM
- Hypoglycaemia awareness (Gold/Clarke score) and sick-day plan reviewed at every visit
- Depression, distress, cognition, OSA screening
- Dental review
Glycaemic monitoring
- HbA1c 3-monthly if not at target or therapy changed; 6-monthly if stable and at target
- CGM (time-in-range >70%, time-below-range <4%) increasingly replaces SMBG in insulin-treated diabetes
- HbA1c unreliable in haemoglobinopathy, haemolysis, recent transfusion, iron deficiency, CKD, pregnancy - use CGM/fructosamine or OGTT instead
What screening triggers
| Finding | Action |
|---|---|
| Any albuminuria | ACEi or ARB + SGLT2i; finerenone if albuminuria persists |
| eGFR <60 or ACR raised | SGLT2i regardless of HbA1c |
| Proliferative retinopathy / DMO | Urgent ophthalmology - panretinal photocoagulation, anti-VEGF |
| High-risk foot | Multidisciplinary foot service, offloading, podiatry |
| Raised NT-proBNP | Echocardiography; SGLT2i |
| FIB-4 >=1.3 with fibrosis on elastography | Hepatology; GLP-1/GIP-GLP-1 RA, weight loss |
| Established ASCVD | GLP-1 RA and/or SGLT2i with proven benefit, high-intensity statin |
Blood pressure target
- *<130/80 mmHg where tolerated* - the older 140/80-140/90 targets are superseded
Structural care
Structural
- Annual comprehensive review (cycle of care), structured diabetes education, smoking cessation
- Vaccination: influenza annually, pneumococcal, COVID-19
- Pre-conception counselling in all women of reproductive age
Microvascular complications
Microvascular
- Retinopathy, maculopathy, cataract, open-angle glaucoma
- Nephropathy -> CKD, ESKD
- Peripheral sensorimotor neuropathy, mononeuropathy, autonomic neuropathy (gastroparesis, postural hypotension, silent ischaemia, erectile dysfunction)
Macrovascular complications
Macrovascular
- IHD (often silent), stroke, peripheral arterial disease
Acute complications
Acute
- Hypoglycaemia, DKA, hyperosmolar hyperglycaemic state
Other complications
Other
- Foot ulceration and Charcot neuroarthropathy
- MASLD/MASH, cirrhosis, HCC
- Infection - skin, urinary, periodontal, mucormycosis
- Depression, cognitive impairment, dementia
- Limited joint mobility, frozen shoulder, Dupuytren, carpal tunnel
Natural history of complications
- Complications accrue with duration x glycaemic exposure, modified by BP, lipids, smoking and genotype
- Legacy effect - early good control protects decades later; late intensification does far less
- Retinopathy sequence: background -> pre-proliferative -> proliferative -> vitreous haemorrhage/tractional detachment
- Maculopathy is the commonest cause of visual loss in T2DM; proliferative disease in T1DM
- Nephropathy sequence: hyperfiltration -> microalbuminuria -> macroalbuminuria -> falling eGFR -> ESKD
- Albuminuria may regress with modern therapy - it is no longer a one-way street
- Neuropathy: length-dependent, glove-and-stocking, largely irreversible once established
- CVD remains the commonest cause of death
- Screening only changes outcomes if the abnormal result changes treatment - close the loop
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