**7. Morbidity and mortality from DKA**

The mortality rate from DKA in children is 0.15% to 0.30% [11,12]. Cerebral edema accounts for 60% to 90% of all DKA deaths [13,14]. Ten % to 25% of survivors of cerebral edema have significant residual morbidity [29]

**Epidemiological factors •** Newly diagnosed cases

**•** Young age: < 5 years old

**•** Prolonged illness

**Features at presentation**

**•** High Blood urea nitrogen

**•** Abnormal mental status **Therapeutic interventions**

**•** Severe Hypernatremia

**•** Persistent hyponatremia

nence)

**•** Rising blood pressure

**•** Decreased oxygen saturation

**•** Non closure of the anion gap

**•** Headache & slowing of heart rate

**•** Severe dehydration

**•** Longer duration of symptoms

**•** Severe acidosis (initial pH < 7.1)

**•** Extended history of poor metabolic control

**•** Rapid rehydration (> 50cc/ kg in first 4 hrs)

**•** Bicarbonate therapy for correction of acidosis

**•** Insulin administration in the first hour of therapy **Changes in biochemical values during treatment**

**Warning signs and symptoms of cerebral edema include:**

**•** Specific neurological signs (e.g., cranial nerve palsies)

**•** An attenuated rise in measured serum sodium concentrations during therapy

**•** Change in neurological status (restlessness, irritability, increased drowsiness, inconti‐

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Clinically significant cerebral edema usually develops 4–12 hours after treatment has start‐ ed, but can occur before treatment has begun or, rarely, may develop as late as 24–48 hours

**•** Greater hypocapnia after adjusting for degree of acidosis

Other rare causes of morbidity and mortality include:


#### **7.1. Cerebral edema**

Cerebral edema is responsible for the majority of deaths related to DKA in children, and sig‐ nificant neurologic morbidity persists in many of the survivors. The incidence of cerebral edema in national population studies is 0.5–0.9% and the mortality rate is 21–24%.The pathogenesis of both its initiation and progression is unclear and incompletely understood, although a number of mechanisms have been proposed. These include cerebral ischemia and hypoxia, fluid shifts caused by inequalities in osmolarity between the extravascular and intravascular intracranial compartments, increased cerebral blood flow, and altered mem‐ brane ion transport. Demographic factors that have been associated with an increased risk of cerebral edema include [13,14,29]:
