Diabetes mellitus, Type 1
D E F I N I T I ON Metabolic hyperglycaemic condition caused by absolute insufficiency of
pancreatic insulin production.
AET IOLOGY Caused by destruction of the pancreatic insulin-producing b-cells, resulting in
absolute insulin deficiency. The b -cell destruction is caused by an autoimmune process in
90% of patients.
Likely to occur in genetically susceptible subjects and is probably triggered by environmental
agents. Polymorphisms of a number of genes may influence the risk of type 1 diabetes.
These include the gene encoding preproinsulin and a number of genes related to immune
system function such as HLA-DQb and HLA-DR, PTPN22 and CTLA-4.
Pancreatic b-cell autoantigens may play a role in the initiation or progression of autoimmune
islet injury. These include glutamic acid decarboxylase (GAD), insulin, insulinoma-associated
protein 2 (IA-2) and cation efflux zinc transporter (ZnT8).
E P IDEMI OLOGY One of the most common chronic diseases in childhood with a prevalence
of 0.25% in the UK. Considerable geographic variation in the incidence. The US and
Northern Europe have an incidence of 8–17/100 000 per year.
H I S T O RY AND EXAMI N AT ION Often of juvenile onset (<30 years). Polyuria/nocturia
(osmotic diuresis caused by glycosuria), polydipsia (thirst), tiredness, weight loss. Symptoms
of complications (see below) Diabetic ketoacidosis: Nausea, vomiting, abdominal
pain, polyuria, polydipsia, drowsiness, confusion, coma, Kussmaul breathing (deep and
rapid), ketotic breath, signs of dehydration (e.g. dry mucous membranes, # tissue turgor).
Signs of complications: Fundoscopy (to look for diabetic retinopathy). Examination of feet
(test for neuropathy: 10 g monofilament testing and vibration sensation; palpate dorsalis
pedis and posterior tibial pulses). Measure BP.
Signs of associated autoimmune conditions e.g. vitiligo, Addison’s disease, autoimmune
thyroid disease.
I N V E S T IGATIONS Blood glucose: Fasting blood glucose >7 mmol/L or random blood
glucose >11 mmol/L. Two positive results are needed before diagnosis.
HbA1C: Estimates overall blood glucose levels in past 2–3 months.
FBC: MCV, reticulocytes (" erythrocyte turnover causes misleading HbA1c levels).
U&E: Monitor for nephropathy and hyperkalaemia caused by ACE inhibitors.
Lipid profile.
Urine albumin creatinine ratio (to detect microalbuminuria).
Patients presenting with suspected DKA Blood: FBC (" WCC even without infection), U&E ("
urea and creatinine from dehydration), LFT, CRP, glucose, amylase (may "), blood
cultures, ABG (metabolic acidosis with high anion gap), blood/urinary ketones.
Urine: Glycosuria, " ketones, MSU (microscopy, culture).
CXR: To exclude any infection.
ECG: To look for acute ischaemic changes.
MANAGEMENT Diabetic ketoacidosis Consider HDU/ICU input, central line, arterial line
and urinary catheter if severe acidosis, hypotensive or oliguric.
Insulin: 50U of soluble insulin in 50 mL 0.9% saline—start at 0.1 U/kg/h (6–7 U/h) until
capillary ketones <0.3, venous pH >7.30, and venous bicarbonate >18 mmol/L. At this
point, if the patient is able to eat and drink, change to SC insulin regimen. If not, change to
IV insulin sliding scale. Do not stop insulin infusion until 1–2 h after regular SC insulin is
restarted.
Fluids: 500mL 0.9%saline over 15–30 min until systolic BP >100mmHg. Then 1 L 2-hourly3
and 1 L 3-hourly3. IV dextrose is started in conjunction with 0.9% saline when blood
glucose reaches 15mmol/L: 1 L 5% dextrose over 8 h when blood glucose is 7–15mmol/L
and 500mL 10% dextrose over 4 h when blood glucose is <7mmol/L
Potassium replacement (start in the second bag of fluid, if passing urine). Adjust amount of
potassium added to fluids according to plasma potassium (If >5.50 mmol/L: Nil. If
2.5–5.5 mmol/L: 40 mmol/L, If <2.5 mmol/L 60–80 mmol/L).
Monitor blood glucose, capillary ketones and urine output hourly, U&Es 4-hourly, and venous
blood gas at 0, 2, 4, 8, 12 h and before stopping fixed rate insulin regimen. Monitor
phosphate and magnesium daily.
Broad spectrum antibiotics if infection suspected.
Thromboprophylaxis.
NBM for at least 6 h (gastroparesis is common).
NG tube: If GCS is reduced (to prevent vomiting and aspiration).
There is no strong evidence for the use of IV bicarbonate.
Refer to diabetes team for patient education.
Glycaemic control
Advice and patient education: Diabetes nurse specialists and dietitians. SC insulin: Shortacting
insulin (e.g. Lispro, aspart, glulisine) three times daily before each meal and one
long-acting insulin (isophane, glargine, detemir) injection once daily. Injection sites should
be rotated.
Insulin pumps may give slightly better glycaemic control. However, they are costly and
cumbersome for some patients and ketoacidosis may occur if the pump malfunctions.
Motivated patients can attend DAFNE (dose adjustment for normal eating) courses to learn
how to calculate their carbohydrate intake and adjust their insulin doses accordingly.
Monitor: Control of symptoms (e.g. thirst, tiredness), regular finger prick tests by the patient,
monitoring HbA1c levels (target <7%) every 3–6 months.1
Screening and management of complications. See Diabetes mellitus, Type 2.
Treatment of hypoglycaemia: If # consciousness: 50 ml of 50% glucose IV or 1mg glucagon
IM. If conscious and cooperative: 50 g oral glucose (e.g. in the form of Lucozade, milk,
sugar or 3 dextrose tablets), followed with a starchy snack. Should not drive for 45 min.
Screening and management cardiovascular risk factors See Diabetes mellitus, Type 2.
COM P L IC A T I ONS Diabetic ketoacidosis: # Insulin and " counter-regulatory hormones
result in " hepatic gluconeogenesis and # peripheral glucose utilization. Renal reabsorptive
capacity of glucose is exceeded causing glycosuria, osmotic diuresis and dehydration.
" Lipolysis leads to ketogenesis and metabolic acidosis. Diabetic ketoacidosis may be
precipitated by infection (30%), errors in management (15%), newly diagnosed diabetes
(10%), other medical disease (5%), no cause identified (40%).
Microvascular: Retinopathy, nephropathy, neuropathy (see Diabetes mellitus, Type 2).
Macrovascular: Peripheral vascular disease, ischaemic heart disease, stroke/TIA. Susceptible
to infections (especially on feet).Complications of insulin treatment: Weight gain. Fat
hypertrophy at insulin injection sites. Hypoglycaemia caused my missing a meal or
overdosage of insulin (Patients present with neuroglycopenic and adrenergic signs:
personality change, fits, confusion, coma, pallor, sweating, tremor, tachycardia, palpitations,
dizziness, hunger and focal neurological symptoms). Hypoglycaemic symptoms
may be masked by autonomic neuropathy, b-blockers and brain adapting to recurrent
episodes.
PROGNOSIS Depends on early diagnosis, good glycaemic control and compliance with
screening and treatment. Vascular disease and renal failure are major causes of increased
morbidity and mortality.
1 Diabetes control and complications trial (DCCT) showed that strict glycaemic control in type 1 diabetes
mellitus # the risk of development and progression of diabetic microvascular complications
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