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Brain concussion produces transient hypokalemia in children
L Lazar1, I Erez, M Gutermacher
1Department of Pediatric Surgery, Meir General Hospital, Sapir Medical Center, Kfar Saba, Israel.
Insights
Transient hypokalemia (low potassium) and hyperglycemia (high blood sugar) can occur in children after minor head trauma, like a concussion. These metabolic changes resolve spontaneously within 24 hours without treatment.
Area of Science:
- Pediatric neurology
- Neurotraumatology
- Pediatric endocrinology
Background:
- Severe head trauma can trigger catecholamine release, leading to hyperglycemia and hypokalemia.
- The neuroendocrine and metabolic response to minor head trauma in children remains less understood.
Purpose of the Study:
- To investigate the occurrence of neuroendocrine and metabolic changes in children following minor head trauma (concussion).
- To compare these changes with those observed in children with long bone fractures and healthy controls.
Main Methods:
- Prospective study involving 150 children (ages 2-14) divided into three groups: concussion, long bone fracture, and hernia repair (control).
- Blood samples collected on admission and at 6, 12, and 24 hours for concussion group to measure electrolytes and glucose.
- Electrocardiograms and catecholamine levels were assessed in selected patients.
Main Results:
- Children with concussion exhibited significantly lower serum potassium (hypokalemia) and higher serum glucose levels compared to controls.
- No correlation was found between serum electrolytes and Glasgow Coma Scale (GCS) scores.
- No electrocardiogram abnormalities or elevated catecholamine levels were detected; hypokalemia resolved within 24 hours.
Conclusions:
- Minor head trauma, such as concussion, can transiently induce hypokalemia and hyperglycemia in children.
- These metabolic disturbances are self-limiting and resolve spontaneously within 24 hours.
- The findings suggest a distinct metabolic response to minor head trauma in pediatric patients.
Abstract:
Hyperglycemia and hypokalemia caused by catecholamine discharge have been reported to occur in patients after severe head trauma. The aim of this prospective study was to evaluate whether a similar neuroendocrine and metabolic response is found in children after minor head trauma such as brain concussion (Glasgow Coma Scale (GCS) > or = 13). One hundred fifty patients aged 2 to 14 years (average, 6 years) were divided into three groups (n = 50 in each group). Group 1 included patients admitted to the emergency department for brain concussion (Glasgow Coma Scale (GCS) > or = 13); group 2 included patients admitted for fractures of long bones without head injury; and group 3 were control patients electively admitted for hernia repair. All patients had complete physical and neurological examinations. Complete blood count and blood chemistry were obtained on admission. All blood tests were repeated at 6, 12, and 24 hours in patients belonging to group 1. An electrocardiogram was obtained in selected patients and catecholamine levels were measured in some patients. Statistical analysis was performed using analysis of variance (ANOVA). Serum potassium and sodium levels in patients with brain concussion (group 1) were 3.6 +/- 0.6 and 136 +/- 3 mEq/L, respectively and were significantly lower (P < 0.01) than those in patients belonging to group 2, 4 +/- 0.4 and 138 +/- 3, respectively, and the controls (group 3), 4.2 +/- 0.5 and 140 +/- 2, respectively. Serum glucose level was 124 +/- 34 and 118 +/- 32 mg% in groups 1 and 2 and was significantly higher than that of the controls (group 3), 90 +/- 23 mg%. There was no correlation between serum electrolytes and GCS. No electrocardiogram changes or elevation of serum catecholamines were found. Hypokalemia resolved spontaneously within 24 hours. All patients recovered without neurological sequalae. Transient hypokalemia frequently occurs in children even with minor head trauma. This hypokalemia resolves spontaneously, without treatment and within 24 hours.