Acute neck infections in children: who is likely to undergo surgical drainage?

BACKGROUND: Superficial neck infections including lymphadenitis and abscesses are commonly encountered in pediatric emergency departments (PEDs). It is often unclear which patients are likely to develop an abscess that necessitates surgical drainage. In evaluating these patients, computed tomography (CT) and ultrasound are often used to identify/confirm abscess formation. The criteria for determining the need for imaging studies are not well defined. DESIGN/METHODS: All visits to the study PED were examined in 2009 to 2010. Visits with the diagnosis of cervical lymphadenitis or abscess were identified. Records were retrospectively reviewed to determine the duration of symptoms, fever, previous antibiotic therapy, prior PED visit, size of neck swelling, fluctuance on physical examination, white blood cell count, and results of CT and/or ultrasound obtained in the PED. Data were analyzed to determine which of these characteristics were more likely to be associated with an abscess that was operatively drained. RESULTS: A total of 768 patients were evaluated for neck infections. One hundred twelve (14%) of these pediatric patients underwent abscess drainage in the operating room. Two hundred eighty-nine patients underwent a neck CT and/or ultrasound, of which 119 were positive for abscess. Factors associated with surgical drainage included fluctuance (odds ratio [OR], 18.92; 95% confidence interval [CI], 3.66-31.37), previous emergency department visit (OR, 2.79; 95% CI, 1.34-5.84), and age less than 4 years (OR, 3.01; 95% CI, 1.15-9.87). A recursive partitioning model stratified patients' risk for going to the operating room. Patients without fluctuance and with no prior emergency department visit, along with no prior antibiotic use, have less than 4% chance of having an abscess that necessitates surgical drainage. CONCLUSIONS: Pediatric patients who are more likely to have a neck infection that necessitates surgical drainage can be stratified based on clinical characteristics. This knowledge may allow physicians to better predict the resource needs including hospital admission and emergent imaging for neck infection.

Effects of a system-wide fracture care program to enhance access and follow-up for orthopedics.

OBJECTIVES: Fractures of the extremities are commonly encountered in pediatric emergency departments (PEDs) nationwide. These fractures can lead to bone malformation and deformities if not managed properly. There are multiple barriers to obtaining necessary outpatient follow-up for fracture care, which leads to increased return to the PED for management. Because of these barriers, a "Fracture Care Program" was implemented at the study hospital's network. This study aimed to determine implementation of a Fracture Care Program would lead to reduced PED utilization. METHODS: All visits to the study PEDs were examined from January 1 to August 30, 2010. At PED discharge, patients were given a Fracture Care Program handout, which outlined step-by-step instructions for identifying and scheduling an appointment with a local orthopedic surgeon as an outpatient. A telephone hotline number was also provided where they could speak with a representative of the orthopedics department for assistance in obtaining follow-up. Detailed records were reviewed to determine whether these instructions were associated with lower rates of return. RESULTS: A total of 2120 patients met inclusion criteria. Of these, 1233 (58%) received the Fracture Care discharge instructions. After controlling for differences in payor status and demographic differences, patients who received instructions were less likely to return to the PED (odds ratio, 0.616; 95% confidence interval, 0.40-0.95) within 30 days for orthopedic care than patients who did not receive the instructions. CONCLUSIONS: This systematic coordination of services of a large tertiary care pediatric health care system, local pediatric orthopedic surgery private practices, academic practices, and hospital-affiliated practices improved overall access for families related to orthopedic follow-up care. This model may also aid in helping to improve follow-up in other pediatric subspecialties.

Pediatric abscess characteristics associated with hospital admission from the ED.

OBJECTIVE: To determine the characteristics of pediatric soft tissue abscesses that result in hospital admission. METHODS: All visits for soft tissue abscesses to the study emergency department (ED) were examined during 2008. Detailed records were reviewed to determine ED disposition, abscess size, location, presence of fever, duration of symptoms, previous antibiotic therapy, prior ED visit(s), and wound and blood culture results. Data were analyzed to determine which of these characteristics were associated with hospital admission from the ED. RESULTS: Six hundred twenty-two patients met the inclusion criteria. One hundred thirteen (18%) patients were admitted to the hospital and 509 (82%) were discharged home. Compared to those sent home, abscesses resulting in admission were more likely to be located in the genital area (odds ratio [OR], 3.08; 95% confidence interval [CI], 1.37-6.90), breast (OR, 4.8; 95% CI, 1.08-21.4), or face (OR, 4.39; 95% CI, 1.86-10.3), and were more likely to be larger than 3 cm (OR, 3.66, 95% CI, 2.10-6.36). Patients who were admitted to the hospital were also more likely to have fever (OR, 5.93; 95% CI, 3.4-10.3) and have had a prior ED visit with the same complaint (OR, 3.81; 95% CI, 1.77-8.2). Seventy-seven percent of abscesses that were cultured were positive for methicillin-resistant Staphylococcus aureus. CONCLUSIONS: Size and location (especially those in the genital region, breast, and face), appear to be associated with admission for pediatric abscesses. History of fever and previous ED visit also appear to be associated with hospital admission. Obtaining blood cultures for pediatric abscesses is likely of little clinical benefit.

Cultured retinal neuronal cells and Müller cells both show net production of lactate.

Glucose has long been considered the substrate for energy metabolism in the retina. Recently, an alternative hypothesis (metabolic coupling) suggested that mitochondria in retinal neurons utilize preferentially the lactate produced specifically by Müller cells, the principal glial cell in the retina. These two views of retinal metabolism were examined using confluent cultures of photoreceptor cells, Müller cells, ganglion cells, and retinal pigment epithelial cells incubated in modified Dulbecco's minimal essential medium containing glucose or glucose and lactate. The photoreceptor and ganglion cells represented neural elements, and the Müller and pigment epithelial cells represented non-neural cells. The purpose of the present experiments was two-fold: (1) to determine whether lactate is a metabolic product or substrate in retinal cells, and (2) to examine the evidence that supports the two views of retinal energy metabolism. Measurements were made of lactic acid production, cellular ATP levels, and cellular morphology over 4 h. Results showed that all cell types incubated with 5 mM glucose produced lactate aerobically and anaerobically at linear rates, the anaerobic rate being 2-3-fold higher (Pasteur effect). Cells incubated with both 5 mM glucose and 10 mM lactate produced lactate aerobically and anaerobically at rates similar to those found when cells were incubated with glucose alone. Anaerobic ATP content in the cells was maintained at greater than 50% of the control, aerobic value, and cellular morphology was well preserved under all conditions. The results show that the cultured retinal cells produce lactate, even in the presence of a high starting ambient concentration of lactate. Thus, the net direction of the lactic dehydrogenase reaction is toward lactate formation rather than lactate utilization. It is concluded that retinal cells use glucose, and not glial derived lactate, as their major substrate.

Effects of L-glutamate/D-aspartate and monensin on lactic acid production in retina and cultured retinal Müller cells.

We have investigated the dependence of the rate of lactic acid production on the rate of Na(+) entry in cultured transformed rat Müller cells and in normal and dystrophic (RCS) rat retinas that lack photoreceptors. To modulate the rate of Na(+) entry, two approaches were employed: (i) the addition of L-glutamate (D-aspartate) to stimulate coupled uptake of Na(+) and the amino acid; and (ii) the addition of monensin to enhance Na(+) exchange. Müller cells produced lactate aerobically and anaerobically at high rates. Incubation of the cells for 2-4 h with 0.1-1 mM L-glutamate or D-aspartate did not alter the rate of production of lactate. ATP content in the cells at the end of the incubation period was unchanged by addition of L-glutamate or D-aspartate to the incubation media. Na(+)-dependent L-glutamate uptake was observed in the Müller cells, but the rate of uptake was very low relative to the rate of lactic acid production. Ouabain (1 mM) decreased the rate of lactic acid production by 30-35% in Müller cells, indicating that energy demand is enhanced by the activity of the Na(+)-K(+) pump or depressed by its inhibition. Incubation of Müller cells with 0.01 mM monensin, a Na(+) ionophore, caused a twofold increase in aerobic lactic acid production, but monensin did not alter the rate of anaerobic lactic acid production. Aerobic ATP content in cells incubated with monensin was not different from that found in control cells, but anaerobic ATP content decreased by 40%. These results show that Na(+)-dependent L-glutamate/D-aspartate uptake by cultured retinal Müller cells causes negligible changes in lactic acid production, apparently because the rates of uptake are low relative to the basal rates of lactic acid production. In contrast, the marked stimulation of aerobic lactic acid production caused by monensin opening Na(+) channels shows that glycolysis is an effective source of ATP production for the Na(+)-K(+) ATPase. A previous report suggests that coupled Na(+)-L-glutamate transport stimulates glycolysis in freshly dissociated salamander Müller cells by activation of glutamine synthetase. The Müller cell line used in this study does not express glutamine synthetase; consequently these cells could only be used to examine the linkage between Na(+) entry and the Na(+) pump. As normal and RCS retinas express glutamine synthetase, the role of this enzyme was examined by coapplication of L-glutamate and NH(4) (+) in the presence and absence of methionine sulfoximine, an inhibitor of glutamine synthetase. In normal retinas, neither the addition of L-glutamate alone or together with NH(4) (+) caused a significant change in the glycolytic rate, an effect linked to the low rate of uptake of this amino acid relative to the basal rate of retinal glycolysis. However, incubation of the RCS retinas in media containing L-glutamate and NH(4)(+) did produce a small (15%) increase in the rate of glycolysis above the rate found with L-glutamate alone and controls. It is unlikely that this increase was the result of conversion of L-glutamate to L-glutamine, as it was not suppressed by inhibition of glutamine synthetase with 5 mm methionine sulfoximine. It appears that the magnitude of Müller cell glycolysis required to sustain the coupled transport of Na(+) and L-glutamate and synthesis of L-glutamine is small relative to the basal glycolytic activity in a rat retina.

Modulation of the Pasteur effect in retinal cells: implications for understanding compensatory metabolic mechanisms.

The purpose of the present experiments was to enhance understanding of the factors that are critical for the survival of retinal cells exposed to mitochondrial inhibition. Confluent cultures of Müller cells (rMC-1) and human retinal pigment epithelial cells (hRPE) were incubated in Dulbecco's minimal essential medium in the presence and absence of 1x10(-5)M Antimycin A, an inhibitor of mitochondrial electron transport. To modulate the rates of aerobic and anaerobic glycolysis, cells were incubated in media containing varying concentrations of glucose and 1-100 micro M of iodoacetic acid (IAA), an inhibitor of glyceraldehdye-3-phosphate dehydrogenase (G3PDH). Measurements were made of G3PDH, lactic acid production, and cellular ATP levels, along with an examination of cellular morphology, the latter providing an index of cellular viability. Control rMC-1 and hRPE produced lactate aerobically, respectively, at 0.48 and 1.50 micro molhr(-1)/10(6) cells. Anaerobically, lactate production increased 2-fold in rMC-1 and 3-fold in hRPE. Anaerobic ATP levels in both types of cells were maintained at control levels over 8hr. Experimental conditions were sought that would modulate only the capacity of rMC-1 and hRPE to increase glycolysis following mitochondrial inhibition, i.e. alter their Pasteur effect. We used low concentrations of IAA to partially inhibit G3PDH. Incubation of rMC-1 with IAA for 6hr caused a graded inhibition of G3PDH: 70% inhibition with 1 micro M, 90% with 5 micro M, 97% with 10 micro M, and 100% with 100 micro M. While the aerobic and anaerobic rates of lactic acid production were not altered by 1 micro M IAA, both were suppressed completely by 100 micro M IAA. However, incubation of rMC-1 with 5 micro M IAA caused a decrease of 30% in the rate of anaerobic lactic acid production but no change in the rate of aerobic glycolysis. Moreover, with 5 micro M IAA, rMC-1 incubated aerobically maintained ATP levels, but anaerobic ATP content decreased to a low level and cell morphology and viability were compromised. Essentially similar results were observed with hRPE. Both rMC-1 and hRPE are remarkably resistant to mitochondrial inhibition. This resistance is linked directly to the magnitude of the increase in the Pasteur effect. When the capacity of rMC-1 and hRPE to generate a Pasteur effect is selectively curtailed, these cells no longer are resistant to mitochondrial inhibition. It is suggested that in an intact tissue the ability of a cell to withstand a metabolic challenge will depend very much on the adequacy of the supply of glucose. Even a small limitation in the availability of this utilizable substrate and in the rate of the compensatory increase in the rate of anaerobic glycolysis could put the cell at greater risk during the challenge.