Cerebral Edema in Childhood Diabetic Ketoacidosis

Abstract

OBJECTIVE -Children who develop cerebral edema (CE) during diabetic ketoacidosis (DKA) exhibit definable signs and symptoms of neurological collapse early enough to allow intervention to prevent brain damage. Our objective was to develop a model for early detection of CE in children with DKA. RESEARCH DESIGN AND METHODS-A training sample of 26 occurrences of DKA complicated by severe CE and 69 episodes of uncomplicated DKA was reviewed. Signs of neurological disease were incorporated into a bedside evaluation protocol that was applied to an independent test sample of 17 patients previously reported to have developed symptomatic CE during treatment for DKA. Head computed tomograms and their reports were reviewed.RESULTS -The protocol allowed 92% sensitivity and 96% specificity for the recognition of CE sufficiently early for intervention. The diagnostic criteria were fulfilled in two temporal patterns, defining early-and late-onset CE. Although initial computed tomograms were often normal, the findings also included diffuse CE and focal brain injury, the latter only in patients with an early onset of abnormal neurological signs.CONCLUSIONS -CE may occur in the absence of acute changes on head computed tomograms. Early detection of CE at the bedside using an evidence-based protocol permits intervention in time to prevent permanent brain damage. Diabetes Care 27:1541-1546, 2004M ost children with diabetic ketoacidosis (DKA) exhibit abnormal neurological function. Therefore, evidence-based guidance for discerning the patients who require lifesaving intervention is needed. Cerebral dysfunction in DKA is usually a manifestation of metabolic derangement, but cerebral edema (CE) arises in ϳ1% of episodes and is a complication that frequently causes irreversible brain damage and death (1-7). Neurological collapse from CE is typically described as having sudden onset and progressing rapidly, with recovery depending on prompt reduction of intracranial pressure (4,8 -10). The object of this study was to delineate the signs and symptoms of neurological compromise that predict progression to severe CE in children with DKA.CE occurs rarely in patients older than age 20 years (8,11,12), despite the presence of asymptomatic CE in most adults and children with DKA (13-16). This age dependence may point to developmental changes in cerebral metabolism as critical elements in the pathogenesis of CE. For example, children's brains are reported to have higher fuel and oxygen requirements than those of adults (17,18). Hypoxia is further implicated because the brains of patients with DKA may extract blood oxygen less efficiently than healthy individuals (16) and the reported association of symptomatic CE with low partial pressures of carbon dioxide in arterial blood may reflect harmful cerebral vasoconstriction (5,6). Exuberant rehydration with hypotonic fluid and bicarbonate administration may aggravate the CE (5,6,9,11,12,19 -22); however, the evidence that CE is primarily iatrogenic is not compelling (6,8,(23)(24)(25)(26)(27)(28)(29)...

The UK case–control study of cerebral oedema complicating diabetic ketoacidosis in children

“…Thus children with these features at baseline should be considered at high risk of cerebral oedema and monitored closely. It has been suggested that, during treatment, it may be possible to identify impending cerebral oedema with careful monitoring, although this has not been proved prospectively [25].…”

Progressive Decrease inN-Acetylaspartate/Creatine Ratio in a Teenager with Type 1 Diabetes and Repeated Episodes of Ketoacidosis without Clinically Apparent Cerebral Edema: Evidence for Permanent Brain Injury: Fig 1.

“…5 The basal ganglia are a region thought to be particularly susceptible to injury caused by DKA-related cerebral edema. 6 The vulnerability of the basal ganglia has been hypothesized to be related to the high adenosine triphosphate demand of this region. 6 Some studies suggest that cerebral hypoperfusion may occur during DKA, resulting from dehydration and cerebral vasoconstriction related to hypocapnia.…”

Diabetic Ketoacidosis

“…Thus the etiology of DKA-related CE is multifactorial and results of an interplay of complex pathophysiological processes involving the brain [231][232][233][234][235]. The time of onset is not the same in all affected individuals; two-thirds of patients develops signs and symptoms in the first 6-7 hours and the rest from 10-24 hours after start of the treatment with the early-onset individuals tending to be younger [182,236,237].…”

“…The system allowed 92% sensitivity and 96% specificity for the recognition of CE early enough for intervention. One diagnostic criterion, two major criteria or one major plus two minor criteria is suitable to establish CE [236]. Diagnostic criteria, major criteria and minor criteria are shown in Table 6.…”

“…First of all the rate of fluid administration should be decreased and head of the bed lifted up [236]. Administration of IV mannitol in a dosage of 1.0 g/kg over 20 minutes when repeated as necessary in 1-2 hours shows an improvement in clinical outcome [224,227,228,239].…”