Catherine Baujard

Human herpesvirus-6 infection: a prospective study evaluating HHV-6 DNA levels in liver from children with acute liver failure.

The aim of this prospective study was to investigate the role of HHV‐6 infection in children with acute onset of liver failure using real‐time quantitative PCR. Twenty‐three children (median age, 24 months) were included: 6 cases of fulminant hepatic failure of undetermined cause (group 1); 4 cases of fulminant hepatic failure of recognized cause (group 2); 3 cases of acute decompensation of chronic liver disease (group 3); and 10 cases of chronic liver disease (group 4). HHV‐6 genomic DNA was detected and quantified using real‐time PCR in plasma and livers obtained at the time of transplantation. HHV6‐DNA detection rate was significantly higher among groups 1, 2, and 3 compared to group 4 (76.9% vs. 20% P = 0.02). Viral loads ranged from 6 to 32,500 copies/106 cells. Significantly higher viral loads were found in 4 of 9 children with acute onset of liver failure of unknown origin (group 1, n = 3; group 3, n = 1) and 1 child with fulminant autoimmune hepatitis (group 2) (P = 0.03). These results strongly support the hypothesis that HHV‐6 may cause fulminant hepatic failure and acute decompensation of chronic liver disease in children. Nevertheless, a threshold viral load value still remains to be determined. J. Med. Virol. 80:1051–1057, 2008.

Experience With Endoscopic Management of High-Risk Gastroesophageal Varices, With and Without Bleeding, in Children With Biliary Atresia

BACKGROUND & AIMS Biliary atresia, the most common cause of childhood cirrhosis, increases the risks for portal hypertension and gastrointestinal bleeding. We report the results from a single-center study of primary and secondary prophylaxis of bleeding in children with portal hypertension and high-risk varices. METHODS We collected data from 66 children with major endoscopic signs of portal hypertension, including grade 3 esophageal varices or grade 2 varices with red wale markings and/or gastric varices, treated consecutively from February 2001 through May 2011. Thirty-six children (mean age, 22 mo) underwent primary prophylaxis (sclerotherapy and/or banding, depending on age and weight). Thirty children (mean age, 24 mo) who presented with gastrointestinal bleeding received endoscopic treatment to prevent a relapse of bleeding (secondary prophylaxis). RESULTS In the primary prophylaxis group, a mean number of 4.2 sessions were needed to eradicate varices; no bleeding from gastroesophageal varices was observed after eradication. Varices reappeared in 37% of children, and 97% survived for 3 years. In the secondary prophylaxis group, a mean number of 4.6 sessions was needed to eradicate varices. Varices reappeared in 45%, and 10% had breakthrough bleeding; 84% survived for 3 years. There were no or only minor complications of either form of prophylaxis. CONCLUSIONS Endoscopic therapy as primary or secondary prophylaxis of bleeding appears to be well tolerated and greatly reduces the risk of variceal bleeding in children with biliary atresia and high-risk gastroesophageal varices. However, there is a risk that varices will recur, therefore continued endoscopic surveillance is needed.

The transesophageal Doppler and hemodynamic effects of epidural anesthesia in infants anesthetized with sevoflurane and sufentanil.

BACKGROUND: It is thought that pediatric epidural anesthesia (EA) provides hemodynamic stability in children. However, when compared with information relating to adults, little is known about the hemodynamic effects of epidural EA on cardiac output (CO) in infants. METHODS: Using transesophageal Doppler to monitor CO, we prospectively studied 14 infants <10 kg who were scheduled for abdominal surgery. During sevoflurane general anesthesia, CO transesophageal Doppler monitoring was performed before and after lumbar EA with 0.75 mL/kg of 0.25% bupivacaine and 1:200,000 adrenaline. CO, arterial blood pressure, and heart rate were measured before and 5, 15, and 20 min after performance of EA. RESULTS: In patients anesthetized with sevoflurane and sufentanil, EA resulted in an increase in stroke volume by 29% (P < 0.0001) and a decrease in heart rate by 13% (P < 0.0001). EA also induced a significant decrease in systolic, diastolic, mean arterial blood pressure, and systemic vascular resistance by 11%, 18%, 15%, and 25%, respectively. Conversely, CO remained unchanged. CONCLUSIONS: The increase in stroke volume observed is probably explained by optimization of afterload because of the sympathetic blockade induced by EA. These results confirm that EA provides hemodynamic stability in infants weighing <10 kg and supports the use of EA in this pediatric population.

General anesthesia for intussusception reduction by enema

Intussusception is the most frequent cause of bowel obstruction in children. Although enema is usually used as the initial treatment, surgery may be required in more than 50% of patients. General anesthesia (GA) has been suggested to increase the rate of enema success. The purpose of this study was to evaluate whether GA increases the success rate of reduction by air enema.

Development and validation of a risk score to predict the probability of postoperative vomiting in pediatric patients: the VPOP score

Few data are available in the literature on risk factors for postoperative vomiting (POV) in children.

Isoflurane-induced Neuroapoptosis in the Neonatal Rhesus Macaque Brain: Isoflurane or Ischemia-Reperfusion?

1. Brambrink AM, Evers AS, Avidan MS, Farber NB, Smith DJ, Zhang X, Dissen GA, Creeley CE, Olney JW: Isofluraneinduced neuroapoptosis in the neonatal rhesus macaque brain. ANESTHESIOLOGY 2010; 112:834 – 41 2. Creeley CE, Olney JW: The young: Neuroapoptosis induced by anesthetics and what to do about it. Anesth Analg 2010; 110:442– 8 3. Hansen TG, Danish Registry Study Group, Flick R, Mayo Clinic Pediatric Anesthesia and Learning Disabilities Study Group: Anesthetic effects on the developing brain: Insights from epidemiology. ANESTHESIOLOGY 2009; 110:1–3

Pudendal nerve block by nerve stimulation in a child with Waardenburg disease.

patient was transferred to the ICU. Finally, the first site of insertion for central catheters in our department is right internal jugular vein. The reason for preferring the left subclavian vein in this case was because of an ongoing clinical research project. In conclusion, all medical professionals involved in the establishment of invasive central venous access or in the application of invasive cardiovascular procedures should be aware of the possibility of the presence of persistent LSVC and the potential risks related to it. Persistent LSVC should be considered especially when central venous catheterization via left subclavian or jugular veins become difficult in children with congenital heart disease. Its recognition will avoid medical errors, loss of time, and adverse results. Elif A. Akpek* Arash Pirat* Birgül Varan† S ükrü Mercan Departments of *Anesthesiology, †Pediatric Cardiology, Baskent University Faculty of Medicine, Ankara, Turkey and ‡Department of Cardiovascular Surgery, Saad Specialist Hospital, Khobar, Saudi Arabia (email: elifakpek@baskent-ank.edu.tr)

Péritonite et syndrome du compartiment abdominal chez l’enfant

Chez l’enfant comme l’adulte, la classification de Hambourg distingue les peritonites primitives (encore appelees bacteriennes spontanees) et les formes secondaires, qui sont communautaires (PC) ou nosocomiales (PN) mais le plus souvent postoperatoires. Les auteurs anglosaxons identifient par ailleurs les peritonites tertiaires (PT), qui correspondent a des peritonites persistantes ou recidivantes en depit d’un traitement chirurgical et d’une antibiotherapie initiale adequate. Leur evolution est volontiers emaillee d’abces ou de fistules digestives necessitant des reprises iteratives [1–2]. De facon pragmatique, ce sont les peritonites compliquees, communautaires ou nosocomiales, qui continuent de poser aux reanimateurs des problemes de prise en charge et conditionnent le pronostic dans une population d’enfants souvent indemnes de comorbidite.