66  Diabetes Mellitus

Published

October 23, 2025

66.1 Introduction

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycaemia resulting from defects in insulin secretion, insulin action, or both.
In children, diabetes is one of the most common endocrine and metabolic disorders encountered in clinical practice. The two main types seen are Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM), though other rare forms such as monogenic diabetes and secondary diabetes also occur.

In Ghana and many parts of sub-Saharan Africa, the incidence of Type 1 diabetes is increasing, with children presenting frequently in diabetic ketoacidosis (DKA). In recent years, Type 2 diabetes has emerged among adolescents due to rising rates of obesity and sedentary lifestyles.

This chapter provides a detailed overview of diabetes mellitus in children — covering definitions, classification, pathophysiology, clinical features, diagnosis, management, and complications — with special emphasis on practical approaches for medical students and paediatric residents.

66.2 Classification of Diabetes Mellitus

The American Diabetes Association (ADA) and World Health Organization (WHO) classify diabetes as follows:

Category Description Pathophysiology
Type 1 Diabetes Mellitus (T1DM) Autoimmune destruction of pancreatic β-cells leading to absolute insulin deficiency Immune-mediated; often associated with islet autoantibodies
Type 2 Diabetes Mellitus (T2DM) Combination of insulin resistance and relative insulin deficiency Associated with obesity, puberty, and family history
Monogenic Diabetes (MODY/Neonatal DM) Single-gene defects affecting β-cell function Often autosomal dominant inheritance
Secondary Diabetes Secondary to other conditions Pancreatitis, cystic fibrosis, steroid therapy, endocrine disorders

66.3 Epidemiology

  • Global trends: T1DM accounts for over 90% of diabetes in children globally. The incidence varies widely, from <1/100,000 in sub-Saharan Africa to >30/100,000 in Europe.
  • In Ghana: Studies in Kumasi, Accra, and Cape Coast indicate increasing T1DM cases among children aged 5–15 years, often presenting with DKA at diagnosis.
  • Type 2 diabetes: Previously rare, it is now reported among Ghanaian adolescents, especially those with obesity and a strong family history.

The rise in diabetes prevalence among children is attributed to improved awareness, urbanization, lifestyle changes, and possibly environmental triggers.

66.4 Physiology of Insulin and Glucose Homeostasis

The pancreas plays a central role in glucose metabolism.
The β-cells of the islets of Langerhans secrete insulin, a peptide hormone that facilitates glucose uptake by muscle and adipose tissue and suppresses hepatic glucose production.

66.4.1 Key Actions of Insulin

  • Increases glucose uptake via GLUT-4 transporters.
  • Promotes glycogen synthesis in liver and muscle.
  • Inhibits gluconeogenesis and glycogenolysis.
  • Enhances lipid and protein synthesis.

Deficiency or resistance to insulin leads to hyperglycaemia, lipolysis, ketogenesis, and protein catabolism, which underlie the metabolic disturbances seen in diabetes.

66.5 Pathophysiology

66.5.1 Type 1 Diabetes Mellitus (T1DM)

An autoimmune process targets pancreatic β-cells, resulting in progressive loss of insulin production.

66.5.1.1 Mechanism

  • Genetic predisposition (HLA-DR3, DR4, DQ2, DQ8).
  • Environmental triggers (viral infections—Coxsackie B, enterovirus, or toxins).
  • Presence of autoantibodies: GAD65, ICA, IA-2, or ZnT8.

Destruction of >80% of β-cells leads to insulin deficiency, hyperglycaemia, and ketone formation.

66.5.1.2 Natural History

  1. Genetic predisposition
  2. Autoimmunity initiation
  3. Progressive β-cell destruction
  4. Clinical diabetes (symptomatic hyperglycaemia or DKA)

66.5.2 Type 2 Diabetes Mellitus (T2DM)

Characterized by insulin resistance and relative insulin deficiency.

  • Strongly linked to obesity, acanthosis nigricans, and family history.
  • Insulin resistance is worsened by puberty hormones, sedentary lifestyle, and high-calorie diets.

66.5.3 Other Forms

  • Monogenic diabetes: Often presents in infancy or early childhood; may respond to sulfonylureas rather than insulin.
  • Secondary diabetes: Can follow steroid therapy, Cushing syndrome, or pancreatitis.

66.6 Clinical Features

The presentation of diabetes in children depends on its type and stage at diagnosis.

66.6.1 Classical Symptoms of Type 1 Diabetes

  1. Polyuria – due to osmotic diuresis.
  2. Polydipsia – compensatory thirst.
  3. Polyphagia – despite weight loss.
  4. Weight loss and fatigue – from catabolism.
  5. Enuresis or nocturia – previously toilet-trained child.
  6. Recurrent infections – especially skin and vulvovaginal candidiasis.

In many Ghanaian children, the disease is recognized late, often presenting as diabetic ketoacidosis (DKA) with vomiting, abdominal pain, and dehydration.

66.6.2 Features of Type 2 Diabetes

  • Often asymptomatic or mildly symptomatic.
  • Associated with obesity, acanthosis nigricans, hypertension, or dyslipidaemia.
  • May also present with ketosis (ketosis-prone T2DM).

66.7 Diabetic Ketoacidosis (DKA)

DKA is the most serious acute complication of diabetes in children and remains a major cause of morbidity and mortality in Ghana.

66.7.1 Pathophysiology

Absolute or relative insulin deficiency → increased lipolysis → free fatty acids converted to ketone bodies (acetoacetate, β-hydroxybutyrate) → metabolic acidosis.

66.7.2 Diagnostic Criteria (WHO/ISPAD)

  • Blood glucose >11 mmol/L
  • Venous pH <7.3 or bicarbonate <15 mmol/L
  • Presence of ketonaemia or ketonuria

66.7.3 Clinical Features

  • Dehydration
  • Kussmaul breathing (deep, laboured)
  • Fruity (acetone) breath
  • Abdominal pain, vomiting
  • Drowsiness or altered consciousness

66.7.4 Complications

  • Cerebral oedema (most feared, especially in children)
  • Shock and electrolyte imbalance

66.7.5 Management Principles

  1. Fluid resuscitation: 0.9% saline initially, then adjusted.
  2. Insulin therapy: IV infusion 0.05–0.1 U/kg/hr after initial fluid resuscitation.
  3. Electrolyte correction: especially potassium.
  4. Treatment of precipitating cause: infection, missed insulin dose, etc.
  5. Close monitoring: vital signs, glucose, electrolytes, and neurological status.

66.8 Diagnostic Evaluation

66.8.1 Diagnostic Criteria for Diabetes (WHO)

Test Diagnostic Value
Fasting plasma glucose ≥7.0 mmol/L (after ≥8 hours fasting)
Random plasma glucose ≥11.1 mmol/L with symptoms
2-hour OGTT plasma glucose ≥11.1 mmol/L
HbA1c ≥6.5% (in standardized lab)

In children, diagnosis is typically based on random glucose and clinical presentation, especially when symptomatic.

66.8.2 Additional Laboratory Tests

  • Urine dipstick for glucose and ketones
  • Serum electrolytes, urea, creatinine
  • Blood gas for acidosis (if DKA suspected)
  • HbA1c for baseline control
  • Autoantibody screening (GAD, ICA) when available
  • Lipid profile (for T2DM)

66.9 Differential Diagnosis of Polyuria and Polydipsia

Condition Key Features
Diabetes mellitus Hyperglycaemia, glucosuria, ketonuria
Diabetes insipidus Dilute urine, normal glucose
Psychogenic polydipsia Normal glucose, no ketones
Chronic renal disease Proteinuria, elevated creatinine

66.10 Management of Type 1 Diabetes Mellitus

The cornerstone of management is lifelong insulin therapy with education, diet regulation, and psychosocial support.

66.10.1 Insulin Therapy

66.10.1.1 Types of Insulin

Type Onset Peak Duration
Rapid-acting (Lispro, Aspart) 10–15 min 1–2 hr 3–5 hr
Short-acting (Regular) 30–60 min 2–4 hr 6–8 hr
Intermediate (NPH) 2–4 hr 6–10 hr 12–18 hr
Long-acting (Glargine, Detemir) 1–2 hr Minimal 24 hr

66.10.1.2 Insulin Regimens

  • Conventional: Two daily injections (mixed short- and intermediate-acting).
  • Basal–bolus: Long-acting basal + rapid-acting at meals.
  • Insulin pump therapy: Rarely available in Ghana but ideal for motivated families.

66.10.1.3 Dose

  • Starting total daily dose: 0.5–1.0 units/kg/day.
  • Adjust according to blood glucose trends.

66.10.1.4 Monitoring

  • Self-monitoring of blood glucose (SMBG): before meals and at bedtime.
  • HbA1c: every 3–6 months; target <7.5%.
  • Growth and pubertal assessment at each visit.

66.10.2 Nutritional Management

Dietary management aims at maintaining normoglycaemia while ensuring adequate growth.

66.10.2.1 Principles

  • Balanced diet with appropriate carbohydrate distribution (50–55% of calories).
  • Encourage high-fibre complex carbohydrates; limit refined sugars.
  • Consistent meal timing, coordinated with insulin action.
  • Carbohydrate counting for insulin adjustment.
  • Avoid fasting or skipping meals.

In Ghana, diets can incorporate local foods — e.g., whole grain banku, kontomire stew, beans, plantain — with attention to portion control and reduced oil.

66.10.3 Exercise

Regular physical activity improves insulin sensitivity and cardiovascular health.

Precautions: - Monitor glucose before and after exercise.
- Take extra carbohydrates if prolonged activity (>60 min).
- Avoid vigorous exercise if glucose >14 mmol/L with ketones.

66.10.4 Education and Psychosocial Support

Education is central to successful management. Children and caregivers must be taught:

  • Insulin injection technique and site rotation.
  • Glucose monitoring and record keeping.
  • Recognition and management of hypoglycaemia and DKA.
  • Importance of adherence, diet, and exercise.

Psychosocial counselling is essential to address school integration, stigma, and family stress. Peer support groups (e.g., Diabetes Youth Care Ghana) are beneficial.

66.11 Management of Type 2 Diabetes Mellitus

Management begins with lifestyle modification, followed by pharmacotherapy if control is inadequate.

66.11.1 Lifestyle Modification

  • Weight reduction through diet and exercise.
  • Reduction of sugary beverages and fried foods.
  • Screen family members for diabetes and obesity.

66.11.2 Pharmacological Treatment

  • Metformin is the first-line agent (500 mg once or twice daily, titrated as tolerated).
  • Insulin may be required temporarily if hyperglycaemia is severe or during intercurrent illness.
  • Blood pressure and lipid control are also essential.

66.12 Acute and Chronic Complications

66.12.1 Acute Complications

Complication Description Prevention
Hypoglycaemia Glucose <3.9 mmol/L due to excess insulin or missed meals Regular meals, dose adjustment, carry glucose snacks
Diabetic Ketoacidosis (DKA) Life-threatening metabolic acidosis Early recognition and adherence
Infections Urinary tract, skin, respiratory Good hygiene, immunizations

66.12.2 Chronic Complications

These are rare in well-controlled paediatric patients but may develop after years of poor control.

System Complication Screening
Eyes Retinopathy Fundoscopy from 11 years or 2 years post-diagnosis
Kidneys Microalbuminuria → nephropathy Annual urine albumin/creatinine ratio
Nerves Peripheral neuropathy Clinical exam annually
Cardiovascular Hypertension, dyslipidaemia BP check, lipid profile

Prevention lies in good glycaemic control (HbA1c <7.5%), healthy lifestyle, and regular follow-up.

66.13 Follow-Up and Long-Term Care

66.13.1 Key Components

  • Growth and pubertal monitoring.
  • Annual screening for complications.
  • Psychosocial evaluation.
  • Immunizations: influenza, pneumococcal, hepatitis B.
  • Transition planning from paediatric to adult diabetes care.

66.13.2 School Support

  • Teachers and school nurses should understand the child’s condition.
  • Allow glucose monitoring and snacks when needed.
  • Create an emergency plan for hypoglycaemia.

66.14 Special Considerations in Ghana

  • Late presentation due to limited awareness and poor access to diagnostic tools.
  • Insulin affordability remains a challenge; reliance on hospital pharmacies or NHIS coverage is common.
  • Refrigeration issues in rural areas affect insulin storage; traditional clay pot coolers may help.
  • Cultural beliefs sometimes lead to trial of herbal remedies, delaying therapy.
  • Education of healthcare workers at peripheral centres is vital to improve early diagnosis and management.

66.16 Summary Table

Type Mechanism Key Features Management
Type 1 Autoimmune β-cell destruction → insulin deficiency Polyuria, weight loss, DKA Insulin + diet + education
Type 2 Insulin resistance + relative deficiency Obesity, acanthosis nigricans Lifestyle + metformin ± insulin
Monogenic Single gene mutation Neonatal/childhood onset, family history May respond to sulfonylureas
Secondary Due to other diseases/drugs Variable Treat underlying cause

66.17 Key Takeaways

  • Diabetes mellitus is an increasingly common chronic condition in Ghanaian children.
  • Type 1 diabetes remains predominant, with DKA as the main presenting feature.
  • Insulin therapy, dietary regulation, and education are the cornerstones of management.
  • Early recognition, regular follow-up, and psychosocial support significantly reduce morbidity.
  • Improving awareness and healthcare access remain critical to improving outcomes.

66.18 Suggested Reading

  1. International Society for Pediatric and Adolescent Diabetes (ISPAD) Clinical Practice Guidelines, 2022.
  2. Nelson Textbook of Pediatrics, 22nd Edition.
  3. WHO Pocket Book of Hospital Care for Children, 3rd Edition.
  4. Ghana Health Service (GHS) Clinical Guidelines, 2024 Edition.
  5. Amissah-Arthur MB, et al. “Profile of childhood diabetes mellitus at Komfo Anokye Teaching Hospital, Kumasi.” Ghana Medical Journal 2020.