Diferencia entre revisiones de «Cerebral edema in DKA»
(Text replacement - "==Diagnosis==" to "==Evaluation==") |
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*Almost all affected patients are <20yr <ref>Glaser NS, Wootton-Gorges SL, Buonocore MH, Marcin JP, Rewers A, Strain J, et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. Apr 2006;7(2):75-80.</ref> | *Almost all affected patients are <20yr <ref>Glaser NS, Wootton-Gorges SL, Buonocore MH, Marcin JP, Rewers A, Strain J, et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. Apr 2006;7(2):75-80.</ref> | ||
*Associated with initial bicarb level; not rate of glucose drop | *Associated with initial bicarb level; not rate of glucose drop | ||
===Pathophysiology=== | |||
Thought to be due to cerebral hypoperfusion and less likely osmotic shifts with rapid infusion of IVF's <ref> Kuppermann, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med 2018;378:2275-87</ref> | |||
===Risk Factors=== | ===Risk Factors=== | ||
Revisión del 03:14 11 ago 2018
Background
- 1% of patients with DKA[1]
- Almost all affected patients are <20yr [2]
- Associated with initial bicarb level; not rate of glucose drop
Pathophysiology
Thought to be due to cerebral hypoperfusion and less likely osmotic shifts with rapid infusion of IVF's [3]
Risk Factors
- Age <5yo
- Severe hyperosmolality
- Failure of Na to rise with therapy
- Severe acidosis
- Overaggressive fluid resuscitation is NOT a risk factor
Clinical Features
- Begins 6-12hr after onset of therapy or may begin before initiation of treatment or up to 48h afterward
- Many appear to be improving from their DKA before deteriorating from cerebral edema
- Premonitory symptoms:
- Headache
- Incontinence
- Seizure
- Acute Mental Status Change
- Signs of herniation
Differential Diagnosis
Hyperglycemia
Diabetic Emergencies
- Diabetic ketoacidosis (DKA)
- Diabetic ketoacidosis (peds)
- Hyperosmolar hyperglycemic state (HHS)
- Nonketotic hyperglycemia
- Euglycemic DKA (SGLT-2 inhibitors, pregnancy, fasting)
Diabetes Mellitus (New or Known)
- Type 1 diabetes mellitus (new-onset or uncontrolled)
- Type 2 diabetes mellitus (new-onset or uncontrolled)
- Medication noncompliance or insulin pump malfunction
- Gestational diabetes
- Latent autoimmune diabetes of adults (LADA)
Medication/Drug-Induced
- Corticosteroids (most common drug-induced cause)
- Thiazide diuretics
- Atypical antipsychotics (olanzapine, clozapine, quetiapine)
- Beta-blockers (especially non-selective)
- Phenytoin
- Tacrolimus, cyclosporine (transplant patients)
- Protease inhibitors (HIV antiretrovirals)
- Catecholamines (epinephrine, norepinephrine infusions)
- SGLT-2 inhibitors (paradoxical DKA with euglycemia)
- Total parenteral nutrition (TPN)
- Dextrose-containing IV fluids (iatrogenic)
- Niacin
- Pentamidine (initially hyperglycemia, then hypoglycemia from beta-cell destruction)
Physiologic Stress Response
- Sepsis / critical illness (stress hyperglycemia — very common in the ED)
- Trauma / major surgery / burns
- Acute coronary syndrome / myocardial infarction
- Stroke (especially hemorrhagic)
- Pancreatitis (both a cause and consequence)
- Shock (any etiology)
- Pain (catecholamine surge)
- Seizure (postictal)
- Physiologic stress alone rarely causes glucose >200 mg/dL in non-diabetics; glucose >200 in a "stress response" should prompt evaluation for undiagnosed diabetes or prediabetes
Endocrine
- Cushing syndrome / Cushing disease (cortisol excess)
- Pheochromocytoma (catecholamine excess)
- Hyperthyroidism / thyroid storm
- Acromegaly (growth hormone excess)
- Glucagonoma (rare)
- Somatostatinoma (rare)
Pancreatic
- Pancreatitis (acute or chronic — destruction of islet cells)
- Pancreatic malignancy (adenocarcinoma, neuroendocrine tumors)
- Post-pancreatectomy
- Cystic fibrosis-related diabetes
- Hemochromatosis (iron deposition in pancreas — "bronze diabetes")
Toxic/Overdose
- Iron toxicity (hepatic injury → impaired glucose regulation)
- Salicylate toxicity (can cause both hyper- and hypoglycemia)
- Sympathomimetic toxicity (cocaine, methamphetamine)
- Calcium channel blocker toxicity (impairs insulin secretion)
- Carbon monoxide toxicity (stress response)
Other
- Renal failure (chronic kidney disease, acute kidney injury — impaired insulin clearance AND insulin resistance)
- Cirrhosis / hepatic failure (impaired glycogenolysis regulation)
- Pregnancy (gestational diabetes, steroid administration for fetal lung maturity)
- Parenteral nutrition (TPN, dextrose-containing fluids)
- Post-transplant diabetes (immunosuppressants)
Complications of Diabetes (Not Causes of Hyperglycemia)
These are associated conditions that may be present alongside hyperglycemia but do not themselves cause elevated glucose:
- Diabetic foot infection
- Diabetic peripheral neuropathy
- Cerebral edema in DKA
- Diabetic retinopathy
- Diabetic nephropathy
Evaluation
- Stat head CT (non-contrast)
Management[4]
- Head of bed at 30 degrees
- Mannitol 0.5-1gm/kg IV bolus over 20 minutes
- Give a repeat does if there is an inadequate response
- If 2 doses of mannitol are ineffective, consider 3% saline 10mL/kg over 30min
- Fluid restriction - decrease the IVF infusion rate by 30%
- Treat noncardiogenic pulmonary edema, if present
- Consult PICU and neurosurgery
Disposition
Admit PICU/ICU
See Also
References
- ↑ Cooke & Plotnick. Management of diabetic ketoacidosis in children and adolescents. Pediatr Rev. 2008 Dec;29(12):431-5
- ↑ Glaser NS, Wootton-Gorges SL, Buonocore MH, Marcin JP, Rewers A, Strain J, et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. Apr 2006;7(2):75-80.
- ↑ Kuppermann, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med 2018;378:2275-87
- ↑ Cooke & Plotnick. Management of diabetic ketoacidosis in children and adolescents. Pediatr Rev. 2008 Dec;29(12):431-5