Cerebral Edema In Dka Risk Factors

Epidemiologic studies have identified several risk factors for cerebral edema in DKA. Younger age (31) and newly diagnosed diabetes both potentially increase risk of cerebral edema in DKA (6, 31, 35). Additionally, patients presenting with longer duration of symptoms are at increased risk (26), which may be related to severity of DKA (28). Other risk factors have been identified in retrospective case-controlled studies. A complete list of risk factors associated with cerebral edema in DKA is shown in Table 1.

Table 1

Risk factors associated with cerebral edema in diabetic ketoacidosis

DKA-related cerebral edema Riskfactors

Longer duration of symptoms (26) Acidosis (36, 37) Low PaCO2 (27, 28, 36-38) Hyperkalemia (37) Uremia (28, 37, 38) Bicarbonate therapy (28) Increased insulin dose (37) High i.v. fluid volumes (36, 37)

Low partial pressure of arterial carbon dioxide (pCO2) levels may be a marker of cerebral edema. A large multicenter study by Glaser et al. reported 61 cases of cerebral edema among 6,977 children with DKA (28). Cerebral edema was associated with lower pCO2 prior to treatment (for every decrease in 7.8mmHg, RR 3.4, 95% CI: 1.9-6.3). In a second study, hyper-capnia and low pCO2 levels were risk factors for the development of cerebral edema in 9 of 153 children admitted for one or more episodes of DKA (36). In patients with asymptomatic cerebral edema, low initial pCO2 and bicarbonate levels have also been associated with asymptomatic cerebral edema (27).

Hyponatremia, hyperkalemia, and uremia have also been associated with cerebral edema in DKA (37). Uremia and hyperkalemia may be reflective of longer illness duration, severity of insulin deficiency, and pre-renal failure states. Glaser et al. found an association with higher initial serum urea nitrogen levels (for each increase of 9 mg/dl, RR 1.7, 95% CI: 1.2-2.5) and cerebral edema (28). There was no association with the degree of hyperglycemia.

Mahoney et al. and Edge et al. also found no association with degree of hyperglycemia (36, 37). In a recently published study, MR diffusion-weight imaging was used to quantify cerebral edema (38). The apparent diffusion coefficients (ADCs) of brain water during and after DKA treatment were compared in 26 children and correlated with clinical and biochemical variables. Serum urea nitrogen levels and initial respiratory rates were elevated. ADC was not correlated with initial serum glucose or sodium abnormalities. Although initial reports suggested that changes in effective osmolality increased cerebral edema risk (39, 40), ADC did not correlate with initial osmolality (38).

It is unknown if certain therapies increase the risk for DKA-related cerebral edema. Edge and colleagues found cerebral edema associated with early insulin administration (37). Patients treated with insulin in the first hours were at higher risk for cerebral edema (OR 12.7, p = 0.02). Higher volumes of fluid administered over the first 4 h (OR 6.55, p = 0.01) (37)also increased the risk for cerebral edema. A second study also found higher initial intravenous fluid volumes (>50 ml/kg in the first 2-4 h) to be a risk factor (36). Although there is no definitive mechanism that characterizes cerebral edema, insulin activates the sodium/proton pump and allows for influx of sodium into brain cells (41). Insulin may also be involved in cerebral volume regulation via potassium and chloride influx (42). Therefore, early administration of both insulin and fluids may cause an influx of various electrolytes within the cell and increase cellular brain volumes (37). Dilute fluids have also been associated with higher odds ratios for cerebral edema, but the study by Edge et al. was not properly powered for significance (37). Although bicarbonate administration was not associated with an increased rate in cerebral edema in the study by Edge (37), Glaser et al. found an increased risk of cerebral edema with bicarbonate therapy (28).

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  • Leena
    Why DKA patient has low PaCO2 ?
    7 years ago

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