Type 1 diabetes mellitus

Diagnosis

Diagnosis is made by either:

• Random blood glucose >11 mmol/L, or
  
• Fasting blood glucose >7 mmol/L.

Note: There is no need for oral glucose tolerance testing.

Clinical features

• Typical symptoms are polyuria, polydipsia or weight loss. Glycosuria and ketonuria are often present.
  
• Children presenting with diabetes may range from being mildly unwell to severely unwell in diabetic ketoacidosis. Management varies according to presentation.

Differential diagnosis

Transient hyperglycaemia

Transient elevation of blood glucose and glycosuria (and possibly ketonuria) may occur in children with an intercurrent illness or with therapy such as glucocorticoids. The risk of later developing diabetes mellitus is about 3%, but it is approximately 30% if these findings are picked up in an otherwise well child. Check HbA1c and diabetes-related autoimmune markers (antibodies against insulin, glutamic acid decarboxylase (GAD) and islet cells) and discuss with a specialist.

Type 2 diabetes mellitus

This form of diabetes was rare in children. It is being seen increasingly in children who are overweight, those with a family history of type 2 diabetes mellitus and in some specific ethnic groups.

New presentation, mildly unwell

Assessment

Less than 3% dehydration, no acidosis and not vomiting.

Management

Initial treatment

• 0.25 units/kg of quick-acting insulin s.c. stat. Halve dose if <4 years old.
  
• If within 2 h of a meal give mealtime dose only (see below). Halve dose if <4 years old.
  
• Before breakfast and lunch give 0.25 units/kg of rapid-acting insulin. Before the evening meal give 0.25 units/kg rapid-acting insulin and 0.25 units/kg of intermediate-acting insulin. If this is the first insulin dose give 0.25 units/kg rapid-acting insulin only, then a further 0.25 units/kg rapid-acting insulin at midnight followed by a snack. Continue until normoglycaemia and negative ketonuria are achieved.
  
• Encourage fluid intake with sugar-free fluid and a normal diet according to appetite, but exclude foods with quick-acting sugars.

Ongoing treatment

• Once normoglycaemia is achieved and ketonuria disappears, change insulin to twice-daily mixtures of short and intermediate insulins. Several regimes and insulin types with varying profiles are available.
  
• The usual initial total dose is 1 unit/kg/day. This is given as:

– 2/3 in morning and 1/3 at night.

– 2/3 of each dose intermediate-acting and 1/3 as rapid-acting.

• Older adolescents often go on to a basal bolus regimen: 30–40% intermediate acting insulin given at 2200 h, remainder given as quick-acting insulin in three equal doses before meals.
  
• Other treatment modalities now include insulin pump therapy; see p. 307.

Hyperglycaemia, mildly unwell (known diabetic)

Usually advised to take 10% of total daily dose as rapid acting insulin every 2 h until normoglycaemic (in addition to normal insulin). Consult with a specialist if uncertain.

Diabetic ketoacidosis

This is the mode of presentation in >30% of newly diagnosed diabetes in childhood and adolescence. Diabetic ketoacidosis (DKA) may occur in any child or adolescent with established type 1 diabetes. Rapid onset is more likely in patients with poor underlying control or in patients on an insulin pump.

Definition

• Hyperglycaemia >14 mmol/L.
  
• Metabolic acidosis (pH <7.3 or bicarbonate <15 mmol/L).
  
• Hyperketonaemia or moderate to severe ketonuria.

Causes

• Delayed diagnosis of insulin-dependent diabetes mellitus (IDDM).
  
• Omission of insulin (especially in adolescents with recurrent DKA).
  
• Acute stress (infection, trauma, psychological).
  
• Poor management of intercurrent illness.

History

• Polyuria, polydipsia, loss of weight and lethargy. These symptoms are usually of 1–3 weeks’ duration in newly diagnosed patients. Symptoms are either absent or of shorter duration in patients with established diabetes.
  
• There may be a family history of diabetes or other autoimmune disease.

Examination

• Degree of dehydration (often overestimated):

– Mild/nil (<4%): no clinical signs.

– Moderate (4–7%): easily detectable dehydration (e.g. tachycardia, reduced skin turgor, poor capillary return).

– Severe (>7%) poor perfusion, rapid pulse, reduced blood pressure, i.e. shock.

• Altered level of consciousness.
  
• Body temperature – hypothermia is common.
  
• Presence of a precipitating cause (e.g. infection).

Investigations

• Blood glucose, urea and electrolytes.
  
• Arterial or capillary acid/base.
  
• Urine – ketones, culture.
  
• Check for precipitating cause e.g. infection (urine, FBE, blood cultures; consider chest radiograph).
  
• In all newly diagnosed patients: islet cell antibodies, insulin antibodies, GAD antibodies, total IgA, antiendomyseal IgA gliadin and transglutaminase antibodies and thyroid function tests.
  
• Calculate:

– Serum osmolality = 2Na⁺ + glucose + urea.

– Adjusted Na⁺ = plasma Na⁺ + 0.3(plasma glucose – 5.5).

Management

Initial fluid requirements

• If hypoperfusion is present, give normal saline at 10 mL/kg stat.
  
• Repeat until perfusion is re-established (warm, pink extremities with rapid capillary refill).
  
• Commence rehydration with normal saline (see Table 25.1).
  
• Keep nil by mouth (except ice to suck) until alert and stable.
  
• Insert a nasogastric tube if patient is comatose or has recurrent vomiting; leave on free drainage.
  
• Rehydration may be completed orally after the first 24–36 h if the patient is metabolically stable.

Table 25.1 Diabetic ketoacidosis fluid rates (mL/h) including deficit and maintenance fluid requirements, to be given evenly over 48 h

Fluids once insulin is commenced

• Aim for maximum rate of fall of blood sugar of <5 mmol/L per hour. If the blood sugar falls more rapidly than this, very quickly, i.e. within the first few hours, change to normal saline (0.9%) with 5% dextrose.
  
• When the blood sugar reaches 12–15 mmol/L, use 0.45% NaCl with 5% dextrose. Aim to keep the blood sugar at 10–12 mmol/L.
  
• If the blood glucose falls below 10–12 mmol/L and the patient is still sick and acidotic, increase the dextrose in the infusate to 7.5–10%.
  
• Do not turn down insulin infusion.

Insulin

• Commence after treatment of shock.
  
• Add 50 units of clear/rapid-acting insulin (Actrapid or Humulin R) to 49.5 mL 0.9% NaCl (1 unit/mL solution).
  
• Ensure that the insulin is clearly labelled.
  
• Start at 0.1 unit/kg per hour in newly diagnosed children >2 years and those already on insulin who have glucose levels >15 mmol/L.
  
• Children who have had their usual insulin and whose blood sugars are <15 mmol/L and those <2 years of age should receive 0.05 units/kg per hour.
  
• Adjust the concentration of dextrose to keep blood glucose 10–12 mmol/L.
  
• Adequate insulin must be continued to clear acidosis (ketonaemia).
  
• Insulin infusion can be discontinued when the child is alert and metabolically stable (blood glucose <10–12 mmol/L, pH >7.30 and HCO₃ >15 mmol/L). The best time to change to s.c. insulin is just before meal time.
  
• The insulin infusion should only be stopped 30 min after the first s.c. injection of insulin.

Potassium

• Add potassium chloride (KCl) to the i.v. fluid at the time of starting the insulin infusion.
  
• Start KCl at a concentration of 40 mmol/L if body weight <30 kg, or 60 mmol/L if ≥30 kg.
  
• Measure levels 2 h after starting therapy and 2–4 hourly thereafter.
  
• Specimens should be arterial or venous. Do not give K⁺ if the serum level is >5.5 mmol/L or if the patient is anuric.

Bicarbonate

• This is usually not necessary if shock has been adequately corrected. Continuing acidosis usually means insufficient resuscitation.
  
• In extremely sick children (with pH <7.0 ± HCO₃ <5 mmol/L), small amounts may be given. Liaison with paediatric intensive care unit is advisable.
  
• The HCO₃ dose (mmol) = 0.3 × body weight (kg) × base deficit. Infuse half over 30 mins with cardiac monitoring. Reassess acid–base status. Remember risk of hypokalaemia.

Monitoring

Clinical

• Strict fluid balance.
  
• Check all urine for ketones.
  
• Hourly observations: pulse, BP, respiratory rate and neurological observations.
  
• Hourly glucose (glucometer) while on insulin infusion.
  
• 4 hourly temperature.

Note: Any headache or altered behaviour may indicate impending cerebral oedema.

Biochemical

• 2–4 hourly laboratory blood glucose levels (with hourly bedside glucometer readings).
  
• Serum sodium (adjusted for hyperglycaemia), potassium, chloride.
  
• pH.
  
• Serum osmolality: should not fall >0.5 mmol/kg per hour.

Note: Beware of falling adjusted sodium levels as glucose declines – hyponatraemia may herald cerebral oedema. If the sodium level falls, consider decreasing the rate of fluid administration to replace over 72–96 h; see Hypernatraemia section below.

Other instructions

• Intensive care is required if age <2 years, coma, cardiovascular compromise or seizures.
  
• Patient should remain nil orally until alert and stable.
  
• Nurse the patient in a head-up position and in good light.

Complications of diabetic ketosis

Hypernatraemia

Measured serum sodium is depressed by the dilutional effect of the hyperglycaemia. If Na is >160 mmol/L, discuss with a specialist. Sodium should rise as the glucose falls during treatment. If this does not happen or if hyponatraemia develops, it usually indicates overzealous volume correction and insufficient electrolyte replacement. This may place the patient at risk of cerebral oedema.

Hypoglycaemia

If blood glucose <2.2 mmol/L give i.v. 25% dextrose 2 mL/kg over 3 min or 10% dextrose 5 mL/kg. Do not discontinue the insulin infusion. Continue with a 10% dextrose infusion until stable. Where hypoglycaemia is recurrent, increase concentration of dextrose in i.v. fluids (e.g. to 12.5% or 15%).

Note: 15% infusions require central access.

Hypokalaemia

Monitor frequently and adjust potassium concentration in the infusate. Children at particular risk of this complication are those who are very acidotic or have low potassium levels at presentation.

Cerebral oedema

This is an uncommon (0.5–3.0%) but extremely serious complication of diabetic ketoacidosis in children, usually occurring 6–12 h after commencement of therapy. This condition is often fatal. If the patient survives there may be profound neurological impairment.

Prevention

Slow correction of fluid and biochemical abnormalities. Optimally, the rate of fall of blood glucose and serum osmolality should not exceed 5 mmol/L per hour, but in children there is often a quicker initial fall in glucose. Patients should be nursed head up.

Risk factors

• Newly diagnosed diabetes, young age, poorly controlled diabetes.
  
• Excessive fluid rehydration, particularly with hypotonic fluids.
  
• Severe initial acidosis.
  
• Hyponatraemia or hypernatraemia and negative sodium trend during the therapy.

Note: With appropriate therapy the serum sodium should remain stable or rise slightly as blood glucose falls. If the adjusted serum sodium falls during resuscitation, this may be a sign of excess fluid administration and may be associated with the development of cerebral oedema. If this occurs, decrease the rate of fluid administration to replace over 72–96 h.

Signs

• Early: negative sodium trend, headache, behaviour change (sudden irritability, depression of conscious state) and incontinence.
  
• Late: bradycardia, elevated blood pressure and depressed respiration.

Treatment

Cerebral oedema is a medical emergency.

• Administer 20% mannitol i.v. as a bolus dose at 0.25–0.5 g/kg (1.25–2.5 mL/kg of 20%). This can be repeated if the response is inadequate.
  
• Nurse the patient in a head-up position, maintain the airway.
  
• Severely restrict fluids.
  
• Transfer to an intensive care unit for intubation, intermittent positive pressure ventilation and further management.
  
• Do not delay treatment for radiological confirmation – diagnosis is clinical.

Hypoglycaemia in children with diabetes Common causes

• Missed meal/snack.
  
• Vigorous exercise (can be during exercise or hours afterwards).
  
• Alcohol.
  
• Too much insulin.

Management

See Table 25.2

Sick day management during intercurrent illness in the child with diabetes

Principles

• Frequent testing of blood sugar and urine ketones (Table 25.3).
  
• The meal plan may temporarily be dropped – replace with fluids and easily digested carbohydrates.
  
• Ensure good fluid intake – alternate sugar and non-sugar-containing fluids depending on blood sugar levels (water is best if high).
  
• Insulin doses usually need to be increased; never omit insulin.
  
• Keep in touch with medical staff.

Management of children with diabetes undergoing surgery

The main aims are to prevent hypoglycaemia before, during and after surgery and to provide sufficient insulin to prevent the development of ketoacidosis. Factors that must be considered are:

• Time of surgery.
  
• Duration of surgery.
  
• Urgency of surgery.

Minor elective morning surgery

• Admit the child on the evening before surgery.
  
• Aim for the patient to be first on the operating list.
  
• Administer normal food and insulin until midnight on the night before surgery.
  
• At 0600 h check blood glucose. If blood glucose is <10 mmol/L give lemonade or sugar
  containing clear fluid at 5–10 mL/kg (max = 200 mL) and inform the anaesthetist.
  
• Monitor blood glucose every 2 h and immediately before surgery. If blood glucose is <6 mmol/L insert i.v. line and give i.v. glucose.
  
• Give rapid-acting insulin equal to 1/10 of the total daily insulin dose (rapid- and intermediate-acting) at the usual time.
  
• An i.v. line with glucose will be inserted in the operating theatre (if not required preoperatively).
  
• Perform regular blood glucose every 2–4 h postoperatively, and adjust the i.v. glucose infusion as necessary. Give extra insulin 0.25 units/kg every 4–6 h to keep glucose between 5 and 10 mmol/L.
  
• When the patient can tolerate oral fluids stop the i.v. infusion and resume the normal insulin regimen.

Table 25.2 Management of hypoglycaemia in children with diabetes

* Note: As glucagon can cause headache/vomiting, mini-glucagon rescue is preferred. It is used when vomiting is associated with hypoglycaemia or for persistently low blood glucose levels resistant to oral therapy. The doses vary with age: ≤2 years 0.02 mg; 2–15 years 0.01 mg/year of age; >15 years 0.15 mg.

Table 25.3 Sick day management

Minor elective afternoon surgery

• Continue normal food and insulin until midnight on the night before surgery.
  
• Provide a light breakfast at the usual time.
  
• Give rapid-acting insulin equal to 1/10 of the total daily insulin dose, half an hour before breakfast.
  
• Monitor blood glucose every 2 h (commence i.v. glucose if BSL is <6 mmol/L, otherwise i.v. glucose can be commenced in theatre).
  
• Give additional insulin at the same dose at 1200 h.
  
• Adopt same regimen as above postoperatively.

Minor surgery/short anaesthetic

I.v. glucose may not be necessary, provided that the oral intake can be resumed soon after surgery and that the pre-operative blood glucose concentration does not fall below 6 mmol/L. If in doubt, it is safer to follow the routines outlined above.

Emergency and major surgery

• Urgent clinical and biochemical assessment as for diabetic ketoacidosis.
  
• Rehydrate and start i.v. insulin as required.
  
• Maintain i.v. 0.45% saline with 5% dextrose and insulin infusion at 0.05–0.1 units/kg per hour pre- and postoperatively until the patient is able to resume oral feeding.

Continuous subcutaneous insulin infusion use in children and adolescents

Continuous subcutaneous insulin infusion (CSII), or insulin pump therapy, is gaining increasing use in the treatment of type 1 diabetes in children and adolescents. It relies on the continuous delivery of rapid-acting insulin into the subcutaneous tissues by an insulin pump, which is worn on the belt or in a bra, or carried in a pocket. The insulin pump is connected to a subcutaneous cannula by a dual-lumen flexible catheter. The subcutaneous cannula is re-sited and the pump reloaded with insulin every 3 days. Insulin pumps can be disconnected for 1– 2 h at a time for bathing, swimming or contact sports.

Indications

• CSII can be used at any age but is currently most common in adolescent patients.
  
• Although it offers benefits in terms of reduction of hypoglycaemia, improved glycaemic stability and improved quality of life, it is not suitable for all patients.
  
• At a minimum, patients must do 4–6 finger-prick blood glucose measures per day, be able to carbohydrate count accurately and be cognitively able to cope with the challenges of operating the insulin pump.

Calculating dose

Insulin is delivered in two ways:

• A continuous background delivery (basal delivery). Basal delivery is pre-programmed and automatic.
  
• An intermittent meal or correction-based insulin delivery (bolus delivery). Bolus delivery is manually undertaken by the patient at the time of meals or when blood glucose levels are to be corrected.

Total daily insulin dose (TDD) on CSII is derived from pre-existing insulin requirements or based on weight.

• 40–50% of the TDD is given as basal insulin and the remainder given as bolus insulin.
  
• Patients may have multiple basal rates at varying times of the day and according to the varying levels of activity.
  
• Bolus insulin doses are calculated using the ‘500’ rule (500 ÷ TDD = the number of grams of carbohydrate covered by 1 unit of bolus insulin). Correct calculation of the amount of bolus insulin requires that the patient is able to accurately ‘carb count’ their meals.
  
• The amount of insulin given to correct a high blood glucose level (correction factor) is calculated using the ‘100’ rule (100 ÷ TDD = the number of mmols drop in blood glucose that will result from a correction bolus of 1 unit of insulin).
  
• Most modern insulin pumps will automatically calculate bolus doses after they have been confi gured and a blood glucose level has been entered into the pump software.

Note: Infants and toddlers will usually require lower insulin bolus doses than are indicated by the ‘500’ and ‘100’ rules.

Complications

Diabetic ketoacidosis is the most concerning acute complication of CSII use (Table 25.4). These patients are at higher risk of DKA because they do not use any long- or intermediate-acting insulin.

If CSII therapy is discontinued it is critical that these patients have ongoing, regular and frequent review due to the risk of rapid onset of ketosis.

Short stature

Table 25.4 Complications of CSII use

Questions to consider:

• Is the child short in relation to other children the same age (i.e. below the third percentile)?
  
• Is the child unexpectedly short for the family?

Growth rate

Ask for any previous height measurements and plot them on the percentile chart. If no previous measurements are available, review at 3 month intervals; after 6 months, calculate the height velocity and check this against a growth velocity (GV) chart. Growth velocity can only be reliably calculated from measurements taken over 6–12 months. In most children, GV tends to fluctuate and only a consistently low GV will lead to a falling-off in height percentile. The criterion for further investigation in a short child is a GV below the 25th percentile.

Questions to consider:

• Is the child growing slowly?
  
• If the child’s growth really is slow, what is the reason?
  
• Is the child growing at the rate expected for pubertal status? A growth spurt should always accompany puberty.

Causes

Physiological

Constitutional delay in maturation

This is a common (and often familial) normal variant. Characteristically, growth slows at about 2 years of age, producing a fall in the height percentile. Thereafter, growth is parallel to the 3rd percentile, but the prepubertal decline in growth is exaggerated and the onset of the growth spurt is later than average. Bone age is delayed. The final height is likely to be in keeping with that of other family members.

Familial short stature

• Several adult family members are short. Skeletal proportions and GV are normal. Bone age is equivalent to the chronological age.
  
• Some children from short families also have constitutional delay in maturation. Parents who have suffered protein–calorie malnutrition as children may not have achieved their own genetic potential and may be on a lower percentile than their children.

Organic

Organic causes of short stature are classified in Table 25.5. Clues to the diagnosis may emerge from the history and the child’s general appearance. Some serious medical conditions (e.g. chronic renal failure, coeliac disease, inflammatory bowel disease, craniopharyngioma) may present with slow growth as the only abnormal sign. Important clues include:

• Dysmorphic features (e.g. Turner syndrome).
  
• Cutaneous changes (e.g. café au lait markings).
  
• Hand changes (e.g. short 4th/5th metacarpals, narrow deep-set nails).
  
• Fundal changes (e.g. optic atrophy).

Measure the skeletal proportions (arm span/height and upper/lower segment ratios).

• The lower segment should be >1/2 the height beyond the age of 8 years.
  
• The arm span should be within a few centimetres of height at all ages.

Investigations

Check the bone age initially. If the GV is <25th percentile for bone age then tests are indicated.

• Thyroid function tests – thyroid stimulating hormone (TSH) is the usual screening test, check free T₄ (FT₄) if central dysfunction is considered.
  
• Haemoglobin and erythrocyte sedimentation rate (ESR) (inflammatory bowel disease).
  
• Renal function and urine MC&S.
  
• Serum calcium, phosphate and alkaline phosphatase.
  
• Consider testing for coeliac disease.
  
• Chromosomes (all short girls; lack of dysmorphism does not exclude Turner syndrome).
  
• Skeletal survey (if disproportionate).
  
• Consider growth hormone (GH) studies as a second step (always done fasting):

Table 25.5 Organic causes of short stature

AHO, Albright hereditary osteodystrophy; MMA, methylmalonic aciduria; MPS, mucopolysaccharidosis; MSUD, maple syrup urine disease.

– Exercise.

– Glucagon stimulation (the current defi nitive test for GH deficiency).

Note: Basal GH is a useless test and does not defi ne GH deficiency.

Interventions

Growth hormone therapy

Recombinant human GH is government-controlled in Australia; it costs an average of $20 000–$30 000 per year per child. To qualify, children must meet certain criteria:

• Height is below the 1st percentile.
  
• GV is below the 25th percentile for bone age.
  
• Bone age is <13.5 years for girls, or <15.5 years for boys.
  
• Must be free of any condition known not to respond to GH (e.g. high-dose steroid therapy or thalassaemia) or that could be worsened by GH therapy (e.g. insulin-dependent diabetes mellitus (IDDM), Fanconi anaemia or active malignancy).

Children with GH deficiency or Turner syndrome respond to growth hormone with an increase in final height. Use of growth hormone for other conditions without biochemical GH deficiency will increase growth velocity in the short term but usually does not result in significant increase in final height.

Note: These criteria differ if a child has GH deficiency following intracranial pathology or treatment including cranial radiation. Specialist assessment is required.

The dose of growth hormone is 14–22 units/m² per week divided into 6–7 doses/ week.

Tall stature

Hypothyroidism

Hyperthyroidism

Delayed puberty

Precocious puberty

Pubertal gynaecomastia

Table 25.6 Endocrine causes of obesity

Obesity

See chapter 8, Obesity, and Table 25.6.

Nutritional obesity is associated with growth acceleration and advancement of bone age. Endocrine obesity is associated with growth retardation and a delay in bone age.

Ambiguous genitalia

Adrenal hypofunction

Adrenal hyperfunction

Disorders of calcium metabolism

For causes, see Table 25.7.

Clinical features

• Rachitic changes in long bones (swollen wrists, etc.), rachitic rosary.
  
• Tetany (may be demonstrated using sphygmomanometer cuff above systolic pressure for up to 2 min).
  
• Laryngeal stridor.
  
• Fitting.
  
• Weakness, tiredness, irritability.
  
• Even extreme hypocalcaemia may be asymptomatic in an infant.

Investigations

• 25-OH vitamin D.
  
• Renal function, lipase, albumin.
  
• Magnesium, phosphate.
  
• Alkaline phosphatase.
  
• Parathyroid hormone (PTH).
  
• Total and ionised calcium.
  
• 1,25-diOH-vitamin D if hypophosphataemic rickets is suspected.
  
• Radiographs of wrist, knee (metaphyseal splaying).
  
• Malabsorption studies.
  
• ECG (prolonged QT interval).

Treatment

Emergency

• I.v. calcium chloride 10% (infusion 1 mmol/kg per 24 h in 5% dextrose), monitor calcium levels 6 hourly.
  
• Occasionally i.v. calcium chloride 10%, 0.2 mL/kg stat may be required for severe tetany.

Table 25.7 Causes of hypocalcaemia

• Correct magnesium if low.
  
• ECG monitor.
  
• 25-OH-vitamin D if nutritional rickets is suspected: 4000 IU/day for 2 weeks then maintenance (see below).
  
• 1,25-diOH-vitamin D if parathyroid disorders suspected: 0.01–0.02 mcg/kg per day starting dose may need to be increased.
  
• Treatment of underlying condition.

Note: In the first days to weeks after treatment is begun for rickets, bones are ‘hungry’ – large doses of calcium supplement may be required to maintain normocalcaemia and prevent carpopedal spasm once vitamin D is started.

Maintenance

• Adequate calcium intake, preferably as dairy products, 600–1500 mg/day depending on age.
  
• 500 IU/day 25-OH-vitamin D for months–years depending on cause (for infant rickets, usually treat to age 4).
  
• Stoss therapy is alternative method, using 100 000–150 000 units 25-OH-vitamin D every 3–6 months as required. Monitoring is required.
  
• 1,25-diOH-vitamin D (Rocaltrol) for vitamin D resistant rickets, hypoparathyroidism, patients on anticonvulsants.
  
• 1,25-diOH-vitamin D and phosphate for hypophosphataemic rickets (high dose).

Hypercalcaemia

For causes, see Table 25.8.

Clinical features

• Polyuria, polydipsia.
  
• Vomiting, dehydration.
  
• Failure to thrive.
  
• Abdominal pain (constipation, renal stones, pancreatitis).
  
• Confusion, apathy (if severe).

Investigation

• Total and ionised calcium, phosphate.
  
• Magnesium, albumin.
  
• Alkaline phosphatase.
  
• 25-OH-vitamin D ± 1,25-diOH-vitamin D.
  
• Thyroid function.
  
• Chest radiograph ± skeletal survey.
  
• Parathyroid imaging.
  
• Renal ultrasound (nephrocalcinosis).
  
• ECG (short QT interval).

Table 25.8 Causes of hypercalcaemia

Management of severe hypercalcaemia

• Rehydration with 0.9% saline/5% dextrose. For infants <2 years use 0.45% saline/5% dextrose.
  
• Diuretics (thiazide) are used in two situations:

– Acute hypercalcaemia: frusemide is given to reduce fluid overload while the patient is aggressively rehydrated.

– Chronic hypercalcaemia with hypercalciuria (or normocalcaemia with hypercalciuria): thiazides are given to reduce oedema and prevent nephrocalcinosis (by decreasing urinary calcium excretion).

• Bisphosphonates, particularly for increased bone resorption (e.g. immobilisation).
  
• Steroids for vitamin D excess (prednisolone 2 mg/kg per day, reducing).
  
• Low-calcium diet.
  
• Surgery if indicated, treatment of underlying condition.

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