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Pediatric diabetic ketoacidosis and cerebral oedema: a systematic review
Emad Uddin Siddiqui1, Ahmed Othman1, Abdul Hadi Tashkandi1
1Prince Mohammad bin Abdul Aziz Hospital, Madinah, KSA.
Insights
Diabetic ketoacidosis (DKA) in new-onset type 1 diabetes can cause cerebral edema, leading to permanent neurological deficits. This review discusses management options for DKA-related cerebral edema.
Area of Science:
- Pediatric Endocrinology
- Neurology
- Metabolic Disorders
Background:
- Diabetic ketoacidosis (DKA) is a common complication of new-onset type 1 diabetes in children.
- Cerebral edema is a rare but serious complication of DKA, potentially causing permanent neurological damage.
- The exact pathophysiology of DKA-related cerebral edema remains unclear.
Purpose of the Study:
- To review current management strategies for cerebral edema in pediatric DKA.
- To provide an overview of targeted treatment options for DKA-associated cerebral edema.
- To highlight the importance of prompt intervention for DKA-related cerebral edema.
Main Methods:
- Literature review of DKA management and cerebral edema treatment.
- Analysis of existing therapeutic modalities for cerebral edema.
- Synthesis of information on fluid restriction, neuroprotection, and osmotherapy.
Main Results:
- Hyperglycemia and ketosis are key indicators in DKA patients with cerebral edema.
- Standard treatment involves intravenous fluids and insulin.
- Management of cerebral edema may include fluid restriction, ABCs, neuroprotective agents, and osmotherapy (mannitol/hypertonic saline).
Conclusions:
- DKA-related cerebral edema requires prompt and targeted management.
- A combination of strategies, including osmotherapy, may be necessary.
- Further research into the pathophysiology and optimal treatment of DKA-related cerebral edema is warranted.
Abstract:
Diabetic ketoacidosis (DKA) is present in about 30% of pediatric patients diagnosed with new-onset type 1 diabetes. Among such patients, cerebral oedema is relatively uncommon (<1%), representing about 0.1%-0.3% of deaths. However, 25% of these survivors of cerebral oedema suffer permanent neurologic deficits. Clinical presentation may be nonspecific, but the laboratory parameters of hyperglycaemia and ketosis are present in almost all cases, and treatment mainstay depends on intravenous fluids and insulin. The pathophysiology of cerebral oedema and related injury to the brain cells is not fully understood. Different modalities have been used to manage cerebral oedema related to DKA. Here we will review such targeted management options to allow immediate treatment regardless of cause. Such techniques could include fluid restriction, ABC, neuroprotective measures, and osmotherapy with mannitol and/or hypertonic saline.
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