Last reviewed: 7 Nov 2021
Last updated: 23 Mar 2021



Common disorder characterised by insulin resistance and relative insulin deficiency. Most patients are asymptomatic and are diagnosed through screening (abnormal fasting plasma glucose, haemoglobin A1c, and/or oral glucose tolerance test).[1] Strong risk factors include older age, overweight/obesity, physical inactivity, prior gestational diabetes, pre-diabetes, non-white ancestry, family history of diabetes, or polycystic ovary syndrome. Modification of cardiovascular risk factors (e.g., hypertension, dyslipidaemia) are important treatment considerations, along with glycaemic control to prevent microvascular complications. Use of a sodium-glucose cotransporter 2 (SGLT-2) inhibitor or glucagon-like peptide-1 (GLP-1) receptor agonist is recommended in patients with established cardiovascular and/or renal disease.[2]

Characterised by absolute insulin deficiency. Most cases result from autoimmune pancreatic beta-cell destruction in genetically susceptible individuals.[1] Usually presents with acute symptoms or ketoacidosis in childhood or adolescence. Lifelong insulin therapy is required.

Obesity, leading to insulin resistance, is the primary cause of type 2 diabetes in children. The incidence of type 2 diabetes in youths (age 10 to 19 years) is increasing.[3] Commonly accompanied by acanthosis nigricans (90% to 95% of patients).[4]

GDM is diagnosed in the second or third trimester of pregnancy (usually between 24 to 28 weeks of gestation) on the basis of abnormal glucose tolerance testing.[1] Women at high risk of type 2 diabetes are tested at their first antenatal visit to detect pre-existing (overt) diabetes.[1]Risk factors include advanced maternal age (>40 years), obesity, personal history of gestational diabetes or macrosomia of previous child, polycystic ovary syndrome, non-white ancestry, and family history of diabetes mellitus.[1][5] Medical nutrition therapy is central to control of GDM and most women are adequately treated with diet alone.

DKA and hyperosmolar hyperglycaemic states are acute metabolic emergencies. DKA is characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complication of type 1 diabetes.[6] Successful treatment includes correction of volume depletion, hyperglycaemia and ketosis/acidosis, electrolyte imbalances, and comorbid precipitating events (e.g., infection), along with frequent monitoring.

Severe hyperglycaemia, hyperosmolality, and volume depletion, in the absence of severe ketoacidosis.[6] Occurs most commonly in older patients with type 2 diabetes, with high mortality. Treatment includes correction of fluid deficit and electrolyte abnormalities, and intravenous insulin.

Coronary artery disease and stroke are the most common manifestations, and account for most deaths in people with diabetes. Modification of cardiovascular risk factors (e.g., hypertension, dyslipidaemia) are important long-term treatment issues. Metformin and other glucose-lowering medications with demonstrated cardiovascular disease benefit, such as SGLT-2 inhibitors and GLP-1 receptor agonists should be used.[2]

Defined by albuminuria (increased urinary albumin excretion is defined as ≥3.4 mg/mmol [30 mg/g]) and progressive reduction in glomerular filtration rate (GFR) in the setting of a long duration of diabetes (>10 years' duration of type 1 diabetes; may be present at diagnosis in type 2 diabetes), and is typically associated with retinopathy.[1] Symptoms may be absent until the disease is advanced. Treatment includes intensive control of hyperglycaemia and hypertension.[7] Lipid reduction, low-protein diet, and smoking cessation may also be beneficial. The use of glucose-lowering medications, such as SGLT-2 inhibitors and GLP-1 receptor agonists, which reduce major adverse cardiovascular and renal outcomes should be considered.[2]

The most common chronic complication in diabetes affecting different parts of the nervous system and presenting with diverse clinical manifestations.[8] Peripheral neuropathy may present as loss of sensation, painless ulcers on pressure points, or pain, although many patients are asymptomatic. Treatment has traditionally focused on control of hyperglycaemia as a means of slowing progression or delaying onset, on targeting potential pathogenetic mechanisms, and on pain reduction; drug therapy may be used depending on variant of neuropathy.

Encompasses the conditions of diabetic foot ulcer (i.e., a full-thickness epithelial defect below/distal to the ankle) and diabetic foot infections (i.e., any soft-tissue or bone infection occurring in the diabetic foot). Prevention and/or healing of diabetic foot ulcers helps to prevent infections and minimizes the risk of limb loss.[9][10]

Consequence of chronic progressive diabetic microvascular leakage and occlusion.[11] Sight-threatening signs include macular oedema, ischaemia, or traction; vitreous haemorrhage; or retinal detachment. Main goals of therapy are to improve glycaemic, lipid, and blood pressure control and to ensure that disease is arrested before visual loss occurs.

Refers to identification and treatment of hyperglycaemia in hospital, in patients with either pre-existing diabetes or new-onset hyperglycaemia. The development of hyperglycaemia during acute medical or surgical illness may not be a physiological or benign condition but rather a marker of poor clinical outcomes and increased mortality. Effective management of hyperglycaemia often includes basal-bolus insulin protocols.

Cluster of common abnormalities, including insulin resistance, impaired glucose tolerance, abdominal obesity, reduced high-density lipoprotein-cholesterol levels, elevated triglycerides, and hypertension. However, this syndrome is not universally accepted as more clinically useful than assessment of individual cardiovascular risk factors.[12][13]

Characterised by polydipsia, polyuria, increased thirst, and hypotonic urine. Central DI is due to defective synthesis or release of arginine vasopressin (AVP).[14] Nephrogenic DI is due to renal insensitivity to AVP.[15] Treatment goals are correction of water deficits and reduction in ongoing excessive urinary losses.



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