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Published on: June 11, 2012
Hyperglycemic crises and their complications in children
1Division of Endocrinology, Department of Pediatrics, University of Florida College of Medicine, Children's Medical Services Center, 1701 SW 16th Avenue, Gainesville 32608, USA. rosenal@peds.ufl.edu
Insights
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are serious diabetes complications. Cerebral edema is a key mortality cause, with early detection and careful treatment crucial for better outcomes.
Area of Science:
- Endocrinology and Metabolism
- Diabetology
- Critical Care Medicine
Background:
- Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute, life-threatening complications of diabetes mellitus.
- These conditions present significant challenges in diagnosis, management, and prevention of long-term disability or mortality.
- Cerebral edema is a particularly dangerous complication, accounting for a substantial portion of DKA-related deaths.
Purpose of the Study:
- To define criteria for DKA and HHS.
- To review current knowledge on causes of mortality and disability from DKA/HHS complications.
- To identify risk factors, early indicators, and contemporary treatment strategies for DKA/HHS, focusing on cerebral edema.
Main Methods:
- Comprehensive literature review of definitions, risk factors, and complications of DKA and HHS.
- Analysis of studies on the incidence, risk factors, and treatment of cerebral edema in DKA.
- Evaluation of proposed monitoring methods and treatment interventions for cerebral edema.
Main Results:
- DKA occurs at onset in 10-70% of type 1 DM and 5-52% of type 2 DM; HHS occurs in ~4% of new type 2 DM patients.
- Recurrent DKA rates are high, influenced by healthcare access and socioeconomic factors.
- Cerebral edema is a major cause of DKA mortality (2/3+), with incidence of 0.5-2.0%; risk factors include younger age, severe acidosis, hypocapnia, and dehydration. Vasogenic edema is the likely mechanism.
- Aggressive hyperventilation may adversely affect outcomes in cerebral edema treatment.
Conclusions:
- Preventing DKA/HHS at diabetes onset requires high provider awareness.
- Preventing recurrent DKA necessitates a diligent, team-based approach.
- Early detection and cautious management of cerebral edema are critical for improving patient outcomes.
Abstract:
The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
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