Cerebral oedema

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This is almost exclusively a condition of childhood; over 95 per cent of cases in the largest reported series occurred under the age of 20 years, with one-third under the age of 5 years. Mortality from cerebral oedema is around 25-30 per cent and around 30 per cent of survivors are left with major neurological morbidity. It is more common in children with newly diagnosed type 1 diabetes.

Table 2.5 Clinical features of cerebral oedema complicating diabetic ketoacidosis

• irritability

• reduced conscious level

• convulsions

• increasing blood pressure, slowing pulse

• papilloedema - not always present acutely

• possibly impaired respiratory drive

Subclinical brain swelling appears to be common during the treatment of diabetic ketoacidosis, and may be present even before intravenous rehydration is commenced. Whether severe, sudden clinical cerebral oedema is an extension of this process, or whether the two are distinct entities, remains to be determined. The clinical signs of cerebral oedema are variable. Most cases have occurred between 4 and 12 hours from the start of treatment. Signs and symptoms of cerebral oedema are presented in Table 2.5.

Cerebral oedema is a feared complication of diabetic ketoacidosis in children.

If warning features are not recognised, there is commonly a sudden deterioration, manifest as loss of consciousness, appearance of fixed dilated pupils or respiratory arrest. Possible contributing factors include

• cerebral anoxia from the reduced blood volume and haemo-concentration

• high initial plasma glucose concentration

• excessive rates of intravenous fluid administration

• a rapid fall in plasma sodium concentration.

Animal studies have suggested that insulin is required for cerebral oedema to occur, and hypoxia resulting from rapid bicarbonate infusion has also been implicated. However, none of these theories provides a complete explanation, and the fact that the incidence has remained the same over several decades, despite changes in fluid regimens, suggests that the fluid regimen may not be a crucial factor. More recent studies suggest that the most severely dehydrated children are at greatest risk.

The aetiology and optimal treatment of cerebral oedema complicating diabetic ketoacidosis remain uncertain.

Only half of patients have a period of neurological deterioration during which intervention might be effective before respiratory arrest. Therefore, prevention of this complication remains one of the most important goals of the management of diabetic ketoacidosis in children. If cerebral oedema is suspected

• exclude hypoglycaemia

• inform senior medical staff immediately

• give intravenous mannitol 0.5 g/kg stat (= 2.5 mL/kg mannitol 20 per cent over 15 min); administer as soon as possible

• restrict intravenous fluids to two-third maintenance requirements and replace deficit over 72 rather than 24 h

• transfer child to intensive care unit

• if necessary arrange for the child to be intubated and hyperventilated to reduce blood pCO2

• exclude other diagnoses by computed tomography - other intracerebral events may occur (thrombosis, haemorrhage or infarction) and present in the same way

• intracerebral pressure monitoring may be indicated

• repeated doses of mannitol (dose as above every 6 h) can be used to control intracranial pressure (recently it has been suggested that hypertonic saline may be a more effective osmotic agent, but insufficient studies have yet been performed).

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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