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Insulin therapy in type 1 diabetes

SNOMED: 28032008800 wordsUpdated 03/03/2026
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Exam Tips

  • In OSCEs, explain insulin replacement as physiological basal plus prandial bolus therapy, not just 'give insulin'.
  • Know UK examples by action profile: rapid (lispro/aspart), short-acting human (Actrapid), isophane (Humulin I), long-acting analogues (glargine/detemir/degludec).
  • State safety-critical prescribing: always prescribe by brand and concentration, and document dose in units.
  • Remember pump failure is a DKA emergency risk because there is no background long-acting insulin depot.
  • Use sick-day rules: never stop insulin completely, increase monitoring, and check ketones when unwell or hyperglycaemic.

Definition

Insulin therapy in type 1 diabetes is lifelong hormone replacement for absolute endogenous insulin deficiency caused by autoimmune beta-cell destruction. In UK practice, treatment aims to replicate physiological basal and meal-related insulin secretion to prevent acute metabolic decompensation (especially diabetic ketoacidosis) and reduce long-term microvascular and macrovascular complications.

Pathophysiology

In type 1 diabetes, immune-mediated loss of pancreatic beta cells causes near-complete insulin deficiency, so hepatic glucose output is unchecked and peripheral glucose uptake falls. Effective therapy replaces two physiological components: basal insulin (continuous background suppression of hepatic glucose release) and bolus insulin (prandial control of post-meal glucose excursions). Without adequate insulin, lipolysis and ketogenesis increase, creating risk of ketosis and DKA; with excess or mistimed insulin, hypoglycaemia occurs. See Figure: physiological basal-bolus insulin profile in a core endocrinology textbook insulin chapter.

Risk Factors

  • Missed insulin doses or pump delivery interruption (rapid progression to ketosis/DKA)
  • Intercurrent illness, infection, or surgery increasing insulin requirements
  • Puberty, psychological distress, and erratic meal patterns causing glycaemic variability
  • Alcohol intake, delayed meals, or unplanned exercise increasing hypoglycaemia risk
  • Renal impairment reducing insulin clearance and increasing hypoglycaemia risk
  • Medication errors from wrong insulin brand, formulation, or concentration (e. g, 100 vs 200 vs 300 units/mL)

Clinical Features

Symptoms

  • Polyuria, polydipsia, weight loss, fatigue, and blurred vision with under-replacement
  • Nausea, abdominal pain, vomiting, and drowsiness if evolving DKA
  • Sweating, tremor, palpitations, hunger, confusion, or nocturnal symptoms with hypoglycaemia

Signs

  • Dehydration, tachycardia, and possible Kussmaul breathing in severe insulin deficiency
  • Capillary glucose outside individual target range on SMBG/CGM
  • Injection-site lipohypertrophy or bruising from poor site rotation
  • Reduced awareness of hypoglycaemia in recurrent episodes

Investigations

Capillary blood glucose / CGM metrics:Hyperglycaemic excursions when insulin is inadequate; time-in-range reduced; hypoglycaemic episodes may be documented
HbA1c:Above individualized target if chronic under-replacement; may be deceptively near-target if frequent hypoglycaemia
Blood ketones (beta-hydroxybutyrate) or urine ketones during illness/hyperglycaemia:Raised ketones suggest insulin deficiency and risk of DKA
DKA work-up when unwell (venous blood gas, bicarbonate, electrolytes, renal function):Metabolic acidosis, low bicarbonate, and electrolyte disturbance if DKA develops
Injection/pump technique review:May identify dosing, timing, or device errors causing unstable glucose control

Management

Lifestyle Modifications

  • Structured diabetes education (e. g, carbohydrate counting, insulin dose adjustment, hypoglycaemia prevention, sick-day rules)
  • Frequent glucose monitoring with SMBG or CGM and clear action thresholds for ketone testing
  • Meal planning, exercise planning, and alcohol harm-reduction with proactive insulin adjustment
  • Injection-site rotation and device competency checks to reduce lipohypertrophy and dosing errors
  • Carry fast-acting carbohydrate and ensure family/carers know hypoglycaemia treatment

Pharmacological Treatment

Basal-bolus insulin replacement (first-line regimen in most people with type 1 diabetes)

  • Insulin glargine (e. g, Lantus 100 units/mL or Abasaglar 100 units/mL) once daily; basal component individualized within total daily dose
  • Insulin detemir (Levemir 100 units/mL) once or twice daily; basal component individualized
  • Insulin degludec (Tresiba 100 or 200 units/mL) once daily; basal component individualized
  • Rapid-acting mealtime insulin aspart (NovoRapid 100 units/mL), lispro (Humalog 100 or 200 units/mL), or glulisine (Apidra 100 units/mL) before meals

Typical total daily insulin requirement in adults is around 0.4-1.0 units/kg/day (often starting near 0.5 units/kg/day), then titrated to glucose trends; commonly ~30-50% as basal and remainder as prandial/correction doses. Prescribe insulin by brand and exact strength (units/mL). Do not switch concentrations or delivery devices without retraining, as MHRA-highlighted errors can cause severe hypo- or hyperglycaemia.

Alternative human insulin options

  • Short-acting human insulin: Actrapid 100 units/mL, Humulin S 100 units/mL (generally 20-30 minutes before meals)
  • Intermediate-acting isophane insulin: Humulin I 100 units/mL, Insulatard 100 units/mL

Can be used where clinically appropriate, but analogue-based basal-bolus regimens are commonly preferred for flexibility and hypoglycaemia reduction. Timing is crucial for short-acting human insulin due to slower onset.

Continuous subcutaneous insulin infusion (CSII, insulin pump)

  • Pump-delivered rapid-acting insulin analogue (commonly insulin aspart, lispro, or glulisine) as continuous basal infusion plus bolus doses

Initiate and supervise in specialist diabetes services. Pump interruption can rapidly precipitate ketosis/DKA because no long-acting depot insulin is present; patients need emergency backup injected insulin plans.

Hypoglycaemia rescue

  • Oral quick-acting glucose 15-20 g for conscious patient
  • Glucagon 1 mg IM (adult) for severe hypoglycaemia when oral treatment is not possible

Recheck glucose after treatment and follow with longer-acting carbohydrate when recovered. Review precipitating factors and insulin doses after any severe episode.

Complications

  • Severe hypoglycaemia, seizures, or hypoglycaemia unawareness
  • Diabetic ketoacidosis from insulin omission or delivery failure
  • Weight gain and glycaemic variability from overcorrection cycles
  • Injection-site lipohypertrophy causing erratic insulin absorption
  • Long-term microvascular disease (retinopathy, nephropathy, neuropathy) with chronic hyperglycaemia
  • Increased cardiovascular and cerebrovascular risk over time with poor control

Prognosis

With consistent basal-bolus replacement, education, and glucose monitoring, most people achieve good functional outcomes and major risk reduction for acute and chronic complications. Prognosis worsens with recurrent severe hypoglycaemia, frequent DKA, poor treatment adherence, or persistent hyperglycaemia.

Sources & References

🏥BMJ Best Practice(1)

NICE Guidelines(1)

📖Textbook References(14)

  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 921)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 972)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 921)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 973)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 973)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 972)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 873)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 12)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 11, 12)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 872, 873)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 11)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 251)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 250, 251)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 251)[context]

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