Unintended stray energy from monopolar instruments: beware the dispersive electrode cord.

BACKGROUND: The monopolar instrument emits stray radiofrequency energy from its cord when activated. This is a source of unintended thermal injury to patients. Stray energy emitted from the dispersive electrode cord has not been studied. The purpose of this study was to determine whether, and to what extent, the dispersive electrode cord contributes to unintentional energy transfer and describe practical steps to minimize risk. METHODS: In a laparoscopic simulator, a monopolar generator delivered radiofrequency energy to an L-hook. Thermal imaging quantified the change in tissue temperature nearest to the tip of a non-electrical instrument following activation. The orientation of the dispersive electrode cord was varied relative to other instruments. RESULTS: When the dispersive electrode cord is parallel to the camera cord, tissue temperature increased at the telescope tip by 46 ± 6 °C from baseline (p < 0.001). Similar heat was generated when the camera cord was oriented parallel to the active electrode cord (46 ± 6 vs. 48 ± 7 °C, respectively, p = 0.48). Adding a second dispersive electrode decreased the temperature change (46 ± 6 vs. 25 ± 9 °C, p < 0.001). Temperature increase was greater with coagulation versus cut mode (33 ± 7 vs. 22 ± 6 °C, p < 0.001). CONCLUSION: Stray energy emitted from the dispersive electrode cord heats tissue >40 °C via antenna coupling; the same magnitude as the active electrode cord. Practical steps to minimize stray energy transfer include avoiding orienting the dispersive electrode cord in parallel with other cords, adding a second dispersive electrode, and using low-voltage cut mode.

Aortic valve calcification is mediated by a differential response of aortic valve interstitial cells to inflammation.

BACKGROUND: Although calcific aortic stenosis is common, calcification of the other three heart valves is not. The aortic valve interstitial cell (VIC) has been implicated in the pathogenesis of aortic stenosis. Proinflammatory stimulation of aortic VICs induces an osteogenic and inflammatory phenotypic change. We hypothesized that the VICs of the other heart valves do not undergo these changes. Using isolated human VICs from normal aortic, mitral, pulmonary, and tricuspid valves, our purpose was to compare the osteogenic response to proinflammatory stimulation via toll-like receptor 4 (TLR-4). MATERIALS AND METHODS: Aortic, pulmonic, mitral, and tricuspid (n=4 for each valve type) VICs were isolated from hearts valves explanted from patients undergoing cardiac transplantation. Cells were cultured and grown to confluence in passage 2-6 before treatment with Lipopolysaccharide (LPS) (100-200 ng/mL) for 24 or 48 h. Cells were characterized by immunofluorescent staining. TLR-4 expression was analyzed (immunoblotting, flow cytometry). Bone morphogenetic protein 2 and intercellular adhesion molecule 1 production were determined (immunoblotting). Monocyte chemoattractant protein 1 levels were determined by enzyme-linked immunosorbent assay. Statistics were by Mann-Whitney U test. RESULTS: TLR-4 stimulation induced bone morphogenetic protein 2 production only in aortic VICs (P<0.05). Intra-cellular adhesion molecule 1 production and monocyte chemoattractant protein 1 secretion increased in a similar fashion among TLR-4-stimulated VICs from all four valves. CONCLUSIONS: Proinflammatory stimulation induces an osteogenic phenotype in aortic VICs but not mitral, pulmonic, or tricuspid VICs. We conclude that this differential osteogenic response of aortic VICs contributes to the pathogenesis of calcific aortic stenosis.

ox-LDL induces PiT-1 expression in human aortic valve interstitial cells.

BACKGROUND: The aortic valve interstitial cell (AVIC) has been implicated in the pathogenesis of calcific aortic stenosis. When appropriately stimulated, AVICs undergo a phenotypic change from that of a myofibroblast to that of a bone-forming-like cell. An elevated blood level of low-density lipoprotein (LDL) cholesterol is a clinical risk factor for aortic stenosis, and oxidized LDL (ox-LDL) cholesterol has been consistently found in calcified aortic valve leaflets. However, whether it plays a role in the pathogenesis of aortic stenosis is unknown. The process of aortic valve leaflet calcification has been associated with the deposition of calcium phosphate, mediated in part by the phosphate inorganic transporter 1 (PiT-1), a sodium-phosphate ion cotransporter. Therefore, we hypothesized that ox-LDL induces an osteogenic change in human AVICs marked by the induction of PiT-1. Using isolated human AVICs, the purpose of the present study was to examine the effect of ox-LDL on the expression of PiT-1 and the osteogenic factor bone morphogenetic protein 2 (BMP-2), which is a protein necessary for bone formation. METHODS: Human AVICs were isolated from nonstenotic aortic valves obtained from the explanted hearts of patients undergoing cardiac transplantation (n = 4) and grown in culture. The cells were treated with serum-free media, serum-free media with dimethyl sulfoxide (vehicle control), 40 µg/mL of ox-LDL, or 40 µg/mL of ox-LDL plus 2.5 mM phosphonoformate hexahydrate acid. Phosphonoformate hexahydrate acid is a competitive inhibitor of PiT-1 by mimicking inorganic phosphate. Cell lysis was performed at 24 h after treatment. Cell lysates were analyzed using immunoblot and densitometry for PiT-1 and BMP-2. Statistical analysis was performed using analysis of variance. P < 0.05 was significant. RESULTS: ox-LDL stimulation of AVICs induced an increase in PiT-1 and BMP-2. ox-LDL induced increased production of the phosphate transporter, PiT-1, and the osteogenic factor, BMP-2. Inhibition of PiT-1 with phosphonoformate hexahydrate acid prevented ox-LDL-induced BMP-2 expression. CONCLUSIONS: These data offer mechanistic insight into the pathogenesis of calcific aortic stenosis.

Early diffuse slowing on electroencephalogram in pediatric traumatic brain injury: Impact on management and prognosis.

INTRODUCTION: We hypothesized that the finding of diffuse slowing on bedside EEG in children with moderate to severe traumatic brain injury (TBI) is associated with prolonged hospital stay and worse functional outcomes. METHODS: We reviewed the medical records of all patients admitted to a single level I pediatric trauma center with moderate or severe TBI from 1/10-12/12 (defined by GCS<10 on admission). EEG monitoring results, patient demographics, clinical characteristics, length of stay and postinjury outcomes were recorded. We compared outcomes between patients with and without diffuse slowing on EEG. Data are presented as mean±SEM; p<0.05 was considered statistically significant. RESULTS: 219 children with TBI were identified; 81 had a bedside EEG performed within 48 hours of admission. Diffuse slowing was present in 50 (mean age 5.7+0.7 years) and absent in 31 (n=31, mean age 4.2+0.9 years). Patients with diffuse slowing had a significant increase in ventilator days, ICU LOS, need for rehabilitation, and rehabilitation length of stay. CONCLUSION: The presence of diffuse slowing on EEG in children with TBI is associated with prolonged patient recovery and poor functional outcomes. This finding should prompt early consideration for rehabilitation and the need for intensive therapy.

Intraoperative chest tube removal following thoracoscopic lung biopsy results in improved outcomes.

BACKGROUND: Traditionally, chest tubes are left following video assisted thoracoscopic surgery (VATS) to treat a potential air leak or significant drainage. Recognizing the potential complications, our aim was to determine if intraoperative chest tube removal in children undergoing VATS lung biopsy is safe and if outcomes differ from when a chest tube is left in place. METHODS: We identified all children who underwent VATS lung biopsies from 2009 to 2013 and performed a retrospective review of the medical records. Pulmonary resection patients were excluded as were those with an air leak present in the operating room. RESULTS: A total of 90 VATS lung biopsies were performed. 41 children had a postoperative chest tube left in place (Group A), and 49 children had it removed intraoperatively (Group B). Mean age was 9 ± 6.4 years. One child in Group A and 2 children in Group B required replacement of a chest tube (p=NS). Group B patients had a lower postoperative pain score on day one, fewer postoperative chest X-rays, and a shorter length of postoperative stay. CONCLUSIONS: These data suggest that intraoperative chest tube removal is safe and may be associated with improved outcomes following lung biopsy in children.

Head injury and unclear mechanism of injury: initial hematocrit less than 30 is predictive of abusive head trauma in young children.

PURPOSE: Head injury secondary to abusive head trauma (AHT) is a major cause of morbidity and mortality in susceptible young infants and children. Diagnosing AHT remains challenging and is often complicated by a questionable mechanism of injury. Concern of ionizing radiation risk to children undergoing head CT imaging warrants a selective approach. We aimed to evaluate initial findings that could direct further investigation of AHT. METHODS: A retrospective review of the trauma databases at a two level one pediatric trauma centers was performed. We reviewed all patients age five years and under with a diagnosis of traumatic brain injury (TBI) from 2002-2011. RESULTS: A total of 1129 patients (mean age 1.7 ± 1.7 years; 64% male) with TBI were identified, 429 (38%) of which were the result of AHT. Complete data was available for 921 patients (82%) and were included in statistical evaluation. Forty-eight percent of patients in the AHT group had a hematocrit ≤ 30% on presentation compared to 19% of patients in the non-AHT group. On univariate analysis, a hematocrit of ≤ 30% was predictive of AHT as the cause of injury (P<.0001), as was a platelet count of greater than 400,000 (P<.0001). After controlling for age, sex, ISS, GCS on presentation, need for CPR, and survival to hospital discharge, hematocrit of ≤ 30% and platelets of greater than 400,000 were predictive of AHT as the cause of TBI (P<.05). CONCLUSIONS: In the setting of head injury and unclear history of trauma, a hematocrit of ≤ 30% on presentation increases the likelihood of abusive head trauma in children up to the age of 5 years.

Blood component transfusion increases the risk of death in children with traumatic brain injury.

BACKGROUND: Blood transfusion has been associated with worse outcomes in adult trauma patients with traumatic brain injury (TBI). However, the effects in injured children have not been evaluated. We hypothesize that blood transfusion is also associated with worse outcomes in children with TBI. METHODS: A retrospective review of the trauma database at two Level I pediatric trauma centers was performed. We reviewed all patients 18 years and younger with TBI, who survived at least 24 hours, from 2002 to 2011. Exclusion criteria include those who underwent craniotomy, thoracotomy, exploratory laparotomy, and any orthopedic procedure. RESULTS: A total of 1,607 children with TBI were included in the study population (mean age, 6.4 [5.7] years; 65% male), 178 of whom received a blood transfusion. Mean Injury Severity Score (ISS) was 16.5 (9.1). Patients who received a transfusion had a higher ISS than those who did not (26.7 vs. 15.3). After controlling for age, sex, ISS, Glasgow Coma Scale (GCS) score on presentation, and mechanism of injury, patients who received a blood transfusion were more likely to be admitted to the intensive care unit (p < 0.0001), less likely to survive to hospital discharge (p = 0.02), more likely to be discharged to a rehabilitation facility (p = 0.01) and be dependent on caretakers at follow-up (p < 0.0001), as well as more likely to develop urinary tract infection (p = 0.02) and bacteremia (p = 0.02) during their hospital stay. These differences in outcomes among those who did and did not receive a blood transfusion began to disappear in patients with a nadir hemoglobin of less than 8.0 g/dL. CONCLUSION: Pediatric patients sustaining TBI who receive blood transfusion and do not require operative intervention have worse outcomes compared with patients who do not receive transfusion. This includes an increased risk of death. These data suggest that a transfusion trigger of hemoglobin level at 8.0 g/dL in injured children with TBI may be beneficial. LEVEL OF EVIDENCE: Epidemiologic study, level III. Therapeutic study, level IV.

Glasgow motor scale alone is equivalent to Glasgow Coma Scale at identifying children at risk for serious traumatic brain injury.

BACKGROUND: Glasgow Coma Scale (GCS) is a validated assessment of neurologic state. Assessment of the eye and verbal components is difficult to reliably obtain in children. We hypothesized that an abnormal Glasgow motor scale (GMS) score alone will reliably identify children with serious traumatic brain injury (TBI). METHODS: We reviewed all children with a diagnosis of TBI from 2002 to 2011 at two urban Level I pediatric trauma centers. We used logistic regression to model GCS, GMS, Glasgow verbal scale (GVS), and Glasgow eye scale (GES) for seven outcomes: need for craniotomy, intracranial pressure monitoring, admission to the intensive care unit, hospital stay of 5 days or longer, discharge to rehabilitation, dependence on caretakers at follow-up, and survival to hospital discharge. We then used three measures of fit analysis to determine which scale offered the best fit for each of the outcomes. RESULTS: A total of 2,341 patients (mean [SD] age, 6.9 [5.8] years; 64.7% male) with TBI and GCS data available were identified. The median GCS on presentation was 15 (interquartile range [IQR], 8-15); the median GMS on presentation was 6 (IQR, 4-6). The median GVS was 5 (IQR, 1-5), and the median GES was 4 (IQR, 2-4). GCS as a whole offered the best fit for the data in predicting need for intensive care unit admission, need for intracranial pressure monitoring, prolonged hospital length of stay, and discharge to rehabilitation but was equivalent to GMS in predicting need for craniotomy, survival to hospital discharge, or dependence on a caretaker at follow-up. Further analysis revealed that GMS was more predictive of these outcomes than GVS + GES, indicating that GMS provides the greatest contribution to the predictive ability of the GCS. CONCLUSION: GMS score alone and GCS do not differ in identifying children with serious TBI. Eliminating the eye and verbal components of GCS does not adversely affect the accuracy of this tool to identify children at risk for serious TBI. LEVEL OF EVIDENCE: Prognostic study, level III.

Radiation induces osteogenesis in human aortic valve interstitial cells.

OBJECTIVE: Irradiation of the chest or chest wall has been shown to cause calcific aortic stenosis. However, the mechanisms are unknown. Aortic valve interstitial cells have been implicated in the pathogenesis of aortic stenosis; they have been shown to change from the phenotype of a myofibroblast to an osteoblastlike cell. We therefore hypothesized that irradiation of human aortic valve interstitial cells induces an osteogenic phenotype. In isolated human aortic valve interstitial cells, our purpose was to determine the effect of irradiation on the production of osteogenic factors: (1) bone morphogenetic protein 2, (2) osteopontin, (3) alkaline phosphatase, and (4) the transcription factor Runx2. METHODS: Human aortic valve interstitial cells were isolated from normal aortic valves obtained from explanted hearts of patients undergoing cardiac transplantation (n = 4) and were grown in culture. The cells were grown to confluence, irradiated with 10 Gy using a cesium-137 irradiator, and then lysed 24 hours after irradiation. Cell lysates were analyzed via immunoblot and densitometry for bone morphogenetic protein 2, osteopontin, alkaline phosphatase, and Runx2. Statistical analysis was performed using analysis of variance, with P < .05 indicating significance. RESULTS: Irradiation induced an osteogenic phenotype in human aortic valve interstitial cells. Irradiation induced a 2-fold increase in bone morphogenetic protein 2, a 7-fold increase in osteopontin, a 3-fold increase in alkaline phosphatase, and a 2-fold increase in Runx2. CONCLUSIONS: Radiation induces an osteogenic phenotype in human aortic valve interstitial cells. The irradiated cells had a significantly increased expression of the osteogenic factors bone morphogenetic protein 2, osteopontin, alkaline phosphatase, and Runx2. These data offer mechanistic insight into the pathogenesis of radiation-induced valvular heart disease.