Non-resolution of acidosis and ketosis
| Acidosis not improving | Ketosis not improving |
| Underlying sepsis? | Underlying sepsis? |
| Insufficient insulin or drug error? | Insufficient insulin prescribed? |
| Inadequate resuscitation? | Incorrect preparation of insulin infusion? |
| Hyperchloraemic acidosis? (related to excessive use of chloride containing fluids) | Inadequate fluid input? |
| Recreational or prescription drugs? | Check infusion lines |
Cerebral oedema
Cerebral oedema has high mortality and morbidity. [9,10,48]
Late signs are associated with extremely poor prognosis.
Senior staff must be informed immediately if suspected.
Discuss with PICU consultant and arrange urgent transfer.
| Warning signs [19,22] | Risk factors [22] |
| Headache | Younger age |
| Change in neurological status (reduction in GCS, change in restlessness, irritability or incontinence) | Initial presentation of T1DM [7] |
| Focal neurological signs (i.e. cranial nerve palsies) | Longer duration of symptoms |
| Relative bradycardia & hypertension (Cushing’s reflex) | Greater volumes of fluid within the first 4 hours of treatment [50] |
| Reduced oxygen saturations | Insulin infusion started within the first hour of treatment [50] |
| Abnormal posturing | Use of bicarbonate during treatment [9] |
| Oculomotor palsies, pupillary inequality or dilatation | Greater hypocapnia at presentation [9,51] |
| Late signs: convulsions, coma, papilloedema, respiratory arrest | Increased serum nitrogen at presentation[9,51] |
| More severe acidosis at presentation [50] |
Immediate management of cerebral oedema involves the following [19]: