CT for pediatric, acute, minor head trauma: clinician conformity to published guidelines.

BACKGROUND AND PURPOSE: In 2001, pediatric radiologists participating in a panel discussion on CT dose reduction suggested that approximately 30% of head CT examinations were performed unnecessarily. With increasing concern regarding radiation exposure to children and imaging costs, this claim warrants objective study. The purpose of this study was to test the null hypothesis that 30% of head CT studies for clinical evaluation of children with acute, minor head trauma do not follow established clinical guidelines. MATERIALS AND METHODS: Retrospective review of 182 consecutive patients with acute, minor head trauma from February 2009 to January 2010 at a tertiary care children's hospital emergency department was performed, and clinician adherence to published clinical guidelines for children younger than 2 years and children 2-20 years of age was determined. The binomial test was used for a null hypothesis of 30% unnecessary examinations against the actual percentage of head CTs deemed unnecessary on the basis of established guidelines. Statistical testing was performed for children younger than 2 years and 2-20 years of age. RESULTS: For children younger than 2 years of age, 2 of 78 (2.6%; 95% CI, 0.5%-8.3%) and, for children 2-20 years of age, 12 of 104 (11.5%; CI, 6.4%-18.7%) did not conform to established guidelines. These percentages were significantly less than the hypothesized value of 30% (P < .001). CONCLUSIONS: Clinician conformity to published guidelines for use of head CT in acute, minor head trauma is better than suggested by a 2001 informal poll of pediatric radiologists.

Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics.

BACKGROUND: Cerebral edema is an uncommon but devastating complication of diabetic ketoacidosis in children. Risk factors for this complication have not been clearly defined. METHODS: In this multicenter study, we identified 61 children who had been hospitalized for diabetic ketoacidosis within a 15-year period and in whom cerebral edema had developed. Two additional groups of children with diabetic ketoacidosis but without cerebral edema were also identified: 181 randomly selected children and 174 children matched to those in the cerebral-edema group with respect to age at presentation, onset of diabetes (established vs. newly diagnosed disease), initial serum glucose concentration, and initial venous pH. Using logistic regression we compared the three groups with respect to demographic characteristics and biochemical variables at presentation and compared the matched groups with respect to therapeutic interventions and changes in biochemical values during treatment. RESULTS: A comparison of the children in the cerebral-edema group with those in the random control group showed that cerebral edema was significantly associated with lower initial partial pressures of arterial carbon dioxide (relative risk of cerebral edema for each decrease of 7.8 mm Hg [representing 1 SD], 3.4; 95 percent confidence interval, 1.9 to 6.3; P<0.001) and higher initial serum urea nitrogen concentrations (relative risk of cerebral edema for each increase of 9 mg per deciliter [3.2 mmol per liter] [representing 1 SD], 1.7; 95 percent confidence interval, 1.2 to 2.5; P=0.003). A comparison of the children with cerebral edema with those in the matched control group also showed that cerebral edema was associated with lower partial pressures of arterial carbon dioxide and higher serum urea nitrogen concentrations. Of the therapeutic variables, only treatment with bicarbonate was associated with cerebral edema, after adjustment for other covariates (relative risk, 4.2; 95 percent confidence interval, 1.5 to 12.1; P=0.008). CONCLUSIONS: Children with diabetic ketoacidosis who have low partial pressures of arterial carbon dioxide and high serum urea nitrogen concentrations at presentation and who are treated with bicarbonate are at increased risk for cerebral edema.

Description of Missouri children who suffer burn injuries.

OBJECTIVE: This study uses Missouri's inpatient and outpatient E code data system to describe the demographic characteristics of Missouri children who suffered burn injuries during 1994 and 1995. METHODS: Retrospective review of Missouri E code data. RESULTS: Altogether 8,404 children aged 0-14 years were treated for burn injuries in Missouri hospitals during 1994 and 1995. The rate of burn injury in Missouri children was 339 per 100,000/year. African-American boys 0-4 years living in urban counties were at increased risk. In addition, African-American girls ages 0-4 years living in counties with a high poverty rate had raised burn injury rates. Burns from hot objects and scalds from hot liquids caused more than half of the burns. CONCLUSIONS: Hospital based E coding has proven an invaluable tool for the study of burns and will, no doubt, prove equally useful for other injuries.

Minor head injury in the pediatric patient.

Minor head injury is a common occurrence in children of all ages; however, controversy exists regarding the management of these children. Reports of neurologically intact children with intracranial injuries have caused many to recommend cautious management, while the infrequency of serious intracranial injuries after minor head trauma have prompted others to be less conservative. Based on recent literature reports, strategies for the management of children with minor head trauma are presented.

Diagnostic testing for acute head injury in children: when are head computed tomography and skull radiographs indicated?

OBJECTIVE: Despite the frequent occurrence of head injury in children, there is no agreement about clinical screening criteria that indicate the need for imaging studies. This study was undertaken to provide information relevant to the choice of imaging modalities in children with acute head trauma. METHODOLOGY: A prospective cohort of 322 children seeking care consecutively in an urban pediatric emergency department for nontrivial head injury was assembled. Skull radiographs, head computed tomography, and data forms including mechanism of injury, symptoms, and physical findings were completed for each child. RESULTS: Intracranial injury occurred in 27 children (8%), whereas 50 (16%) had skull fractures. Of those with intracranial injury, 16 (59%) had normal mental status and no focal abnormalities, and 1 of those 16 required surgery for evacuation of an epidural hematoma. Six (38%) of the 16 were younger than 1 year, 5 of whom had scalp contusion or hematoma without other symptoms. Findings not significantly associated with intracranial injury were scalp contusion, laceration, hematoma, abrasion, headache, vomiting, seizure, drowsiness, amnesia, and loss of consciousness for less than 5 minutes. Findings associated with intracranial injury were skull fracture, signs of a basilar skull fracture, loss of consciousness for more than 5 minutes, altered mental status, and focal neurologic abnormality. CONCLUSIONS: Intracranial injury may occur with few or subtle signs and symptoms, especially in infants younger than 1 year. The relative risk for intracranial injury is increased almost fourfold in the presence of a skull fracture, although the absence of a skull fracture does not rule out intracranial injury. The significance of nonsurgical intracranial injury in neurologically normal children needs further study.

A rapid method for the analysis of influenza virus genes: application to the reassortment of equine influenza virus genes.

We describe a rapid method for genetic characterisation of influenza virus genes using reverse transcription and amplification by polymerase chain reaction (RT/PCR) of all virus segments simultaneously (multiplex RT/PCR) using primers based on the conserved terminal sequences. The product has been shown to be suitable for determination of partial nucleotide sequences which can be used to search nucleotide sequence databases and rapidly map the genetic origin of each segment. We illustrate the use of the method by analysing genetic reassortment in H7N7 equine influenza viruses.

Evidence for a protein regulator from rat liver which activates acetyl-CoA carboxylase.

1. A regulator of acetyl-CoA carboxylase has been identified in high-speed supernatant fractions from rat liver. The regulator was found to activate highly purified acetyl-CoA carboxylase 2-3-fold at physiological citrate concentrations (0.1-0.5 mM). The effects of the regulator on acetyl-CoA carboxylase activity were dose-dependent, and half-maximal activation occurred in 7-8 min at 30 degrees C. 2. The acetyl-CoA carboxylase regulator was non-dialysable and was inactivated by heating or by exposure to carboxypeptidase. The regulator was enriched from rat liver cytosol by first removing the endogenous acetyl-CoA carboxylase and then using a combination of purification steps, including (NH4)2SO4 precipitation, ion-exchange chromatography and size-exclusion chromatography. The regulator activity appeared to be a protein with a molecular mass of approx. 75 kDa, which could be eluted from mono-Q with approx. 0.35 M KCl as a single peak of activity. 3. Studies of the effects of the regulator on phosphorylation or subunit size of acetyl-CoA carboxylase indicated that the changes in enzyme activity are most unlikely to be explained by dephosphorylation or by proteolytic cleavage. 4. The regulator co-migrates with acetyl-CoA carboxylase through several purification steps, including ion-exchange chromatography and precipitation with (NH4)2SO4; however, the proteins may be separated by Sepharose-avidin chromatography, and the association between the proteins is also disrupted by addition of avidin in solution. Furthermore, the binding of the regulator itself to DEAE-cellulose is altered by the presence of acetyl-CoA carboxylase. Taken together, these observations suggest that the effects of the regulator on acetyl-CoA carboxylase may be explained by direct protein-protein interaction in vitro.

Identification of a major maturation-activated acetyl-CoA carboxylase kinase in sea star oocytes as p44mpk.

Maturation-activated protein-serine/threonine kinases were investigated in the high-speed supernatant fractions from sea-star oocytes harvested at the time of germinal vesicle breakdown. One of the major stimulated protein kinases able to phosphorylate acetyl-CoA carboxylase in these extracts was found to co-purify with a 44 kDa myelin basic protein kinase (p44mpk) that is activated with a similar time course during oocyte maturation. Purified sea-star oocyte p44mpk phosphorylated acetyl-CoA carboxylase (purified from rat liver) predominantly on serine and to a small extent on threonine. Furthermore, the phosphorylation of acetyl-CoA carboxylase occurred principally on a tryptic phosphopeptide which displayed electrophoretic and chromatographic properties very similar to those of the peptide that has previously been shown to undergo increased phosphorylation in response to insulin in rat adipocytes [Brownsey & Denton (1982) Biochem. J. 202, 77-86]. The acetyl-CoA carboxylase was phosphorylated at a similar rate and to a similar extent by casein kinase II, which was also purified from maturing sea-star oocytes. Although casein kinase II was also activated approximately 3-fold near the time of nuclear envelope breakdown, it was responsible for only a minor component of the total enhanced acetyl-CoA carboxylase kinase activity measured in the soluble extracts from maturing oocytes. Acetyl-CoA carboxylase was a relatively poor substrate for the major S6 peptide kinase activity that was also stimulated during resumption of meiosis in the oocytes. The properties of the p44mpk are reminiscent of those of a microtubule-associated protein 2 (MAP-2) kinase that is activated in response to insulin and other mitogens in mammalian cells [Ray & Sturgill (1988) Proc. Natl. Acad. Sci. U.S.A. 85, 3753-3757; Hoshi, Nishida & Sakai (1988) J. Biol. Chem. 263, 5396-5401]. It is intriguing that several of the mammalian protein kinases that are acutely activated after mitogenic prompting of quiescent mouse fibroblasts (i.e. G0 to G1 transition), such as MAP-2 kinase, casein kinase II and S6 kinase II, have counterparts that are activated during M-phase in maturing sea star oocytes.