John Vlot

Thoracoscopic repair in congenital diaphragmatic hernia: patching is safe and reduces the recurrence rate

PURPOSE Congenital diaphragmatic hernia (CDH) has traditionally been repaired via a laparotomy. More and more reports on thoracoscopic repair are being published. The aim of this study was to evaluate our series of thoracoscopic CDH repair and compare this group to an open repair group treated during the same period in the same institute. PATIENTS AND METHODS Between June 2006 and December 2008, 49 children with posterolateral CDH were admitted, of whom 23 (47%) were operated thoracoscopically and 23 (47%) using an open repair, depending on the discretion of the attending surgeon and the clinical condition of the patient. Three patients (6%) with CDH were not treated because of associated anomalies (twice Cornelia de Lange syndrome and once hypoplastic left heart syndrome). Six thoracoscopic operations (26%) were converted to open surgery. Nine defects (39%) were closed thoracoscopically without a patch. In 8 (35%) patients, a patch was used. We used a patch in 20 open procedures (87%). RESULTS Three (33%) of the 9 thoracoscopic repairs without patch and 1 (12%) of the 8 with a patch developed a recurrence. All these recurrences were repaired thoracoscopically. The 3 recurrences from the thoracoscopic primary repair were repaired using a patch. In the open group, 3 patients (13%) developed a recurrence, of whom 2 were repaired thoracoscopically. Mean operative time was significantly longer in the thoracoscopic patch repair group (158 minutes), when compared to the open repair group (125 minutes). CONCLUSION As in open repair, it seems wise to use large patches liberally, not only to reconstruct the dome of the diaphragm but also to avoid undue tension on the repair and prevent recurrences. The thoracoscopic approach is also considered feasible in case of a recurrence from either a thoracoscopic or open repair.

Eosinophilic myenteric ganglionitis as a cause of chronic intestinal pseudo-obstruction

Chronic intestinal pseudo-obstruction (CIPO) represents a rare and severe condition characterized by failure of the intestinal tract to propel its contents normally [1, 2]. The condition presents with clinical features such as abdominal pain, vomiting, distended abdomen, constipation, and diarrhea [1, 2]. These symptoms resemble an intestinal mechanical obstruction in the absence of a demonstrable lesion occluding the gut. It is thought that this can result from disturbance of the intestinal motor function, supplied by the enteric nervous system (ENS). The neurons of the ENS are contained in two groups of ganglia: the myenteric (Auerbachs) and the submucosal (Meissners) plexuses. The ENS has the unique ability to control most gut functions, such as regulating vascular tone, secretion/absorption, and gut motility [3, 4]. Given these important functions of the ENS, it is not surprising that damage to the ENS results in digestive disorders and reduced quality of life. Human and experimental evidence indicates that inflammation can occur in the ENS, resulting in severe intestinal motor impairment. Inflammation of the ENS has indeed been observed in some cases of CIPO [3, 5, 6]. Many efforts have been made to classify CIPO. Based on histological examination, CIPO may be categorized as primary, secondary, or idiopathic in nature [1]. Primary CIPO can be classified into three major categories of gastrointestinal neuromuscular disorders (GINMD): mesenchymopathies, myopathies, and neuropathies, depending on the predominant involvement of interstitial cells, smooth muscle cells, or enteric neurons, respectively [1, 7]. The enteric neuropathies underlying CIPO can be subdivided into two major entities: (a) degenerative neuropathies, without any evident inflammatory response and (b) inflammatory neuropathies, referred to as myenteric ganglionitis [3, 8]. Inflammation within the myenteric ganglia is a recognized primary cause of CIPO, but the mechanisms through which the dysfunction occurs and the mechanisms leading to enteric neuropathies remain poorly understood [3, 4]. In this case report, we present the first male neonate with eosinophilic myenteric ganglionitis underlying CIPO and report his successful recovery following steroid treatment.

Optimizing working space in laparoscopy: CT measurement of the influence of small body size in a porcine model

INTRODUCTION In our continuing research into the determinants of laparoscopic working space, the influence of small body size was investigated. METHODS In eight 6-kg pigs, the effects of intraabdominal CO2 pneumoperitoneum pressure (IAP), prestretching of the abdominal wall, and neuromuscular blockade (NMB) on laparoscopic working space volume and distances were studied. Computed tomography was used to measure working space during two stepwise abdominal insufflation-runs up to an IAP of 15mm Hg. Results were compared with data from earlier experiments in 20-kg pigs. RESULTS Cardiorespiratory parameters were stable up to an IAP of 8-10mm Hg. In 6-kg pigs working-space dimensions were five times smaller than in 20-kg pigs. Working-space volume, anteroposterior (AP) diameter and symphysis-diaphragm distance increased linearly up to an IAP of 8mm Hg. Above 8mm Hg, compliance decreased. Eighty percent of the total volume (618ml) and of AP diameter (3cm) at 15mm Hg had been achieved at an IAP of 10mm Hg. Prestretching by a first insufflation resulted in a statistically significant increase in working space volume and in AP diameter during the second insufflation. This effect was significantly larger than in 20-kg pigs. Neuromuscular blockade did not have a significant effect on working-space. CONCLUSIONS Working space in growing individuals is very limited. Eighty percent of the working space created by an IAP of 15mm Hg was already achieved at 10mm Hg, while cardiorespiratory side effects at an IAP of 8-10mm Hg seem acceptable. Prestretching of the abdominal wall significantly increased working space, even more so than in 20-kg pigs. As in 20-kg pigs, NMB had no significant effect on laparoscopic working space. Prestretching of the abdominal wall is a promising cheap, safe and easy strategy to increase laparoscopic working space, lessening the need for prolonged high-pressure pneumoperitoneum.

Invited Brief Commentary on IUVS -2017-0216

There is an ever-increasing focus in modern-day surgery on minimization of invasiveness and scars. Technical developments in instruments and insufflation equipment, but also advances in anesthesia have made possible even the most complex operations through single-site or even natural orifice surgery. The easily quantifiable benefit for the patient is in his or her scar. The disturbance of body homeostasis by anesthesia and surgery is much less easily quantified.1,2 The authors of this article describe an animal model using cytokines to measure the body’s response to the trauma of surgery.3 Although the use of cytokines is a well-known method, the true implications of minimal access surgery cover a vastly broader spectrum.4 Pain, time-to-return-to-work and long-term effects on body-wall integrity cannot be measured in animals. However, the strength of an animal model lies in its reproducibility of conditions and surgical trauma, so comparisons between surgical techniques can actually be better assessed here than in the patient population. Using rats instead of larger animals greatly reduces the financial and logistic burden of experiments. There are however some caveats with the representability for laparoscopy of the proposed model. Although conditions are comparable between the different study groups of rats, there are a few distinct differences between this model and actual laparoscopy. For one thing, spontaneous breathing against an intraabdominal pressure of 10 mm Hg seems quite an effort for a 300 g rat. But more importantly, the effect of elevating the bowels outside the abdominal cavity and exposing them to a large volume of dry and cold CO2 for 30 min greatly enhances the surgical trauma

Risk factors for refractory anastomotic strictures after oesophageal atresia repair: a multicentre study

Objective To determine the incidence of refractory anastomotic strictures after oesophageal atresia (OA) repair and to identify risk factors associated with refractory strictures. Methods Retrospective national multicentre study in patients with OA born between 1999 and 2013. Exclusion criteria were isolated fistula, inability to obtain oesophageal continuity, death prior to discharge and follow-up <6 months. A refractory oesophageal stricture was defined as an anastomotic stricture requiring ≥5 dilations at maximally 4-week intervals. Risk factors for development of refractory anastomotic strictures after OA repair were identified with multivariable logistic regression analysis. Results We included 454 children (61% male, 7% isolated OA (Gross type A)). End-to-end anastomosis was performed in 436 (96%) children. Anastomotic leakage occurred in 13%. Fifty-eight per cent of children with an end-to-end anastomosis developed an anastomotic stricture, requiring a median of 3 (range 1–34) dilations. Refractory strictures were found in 32/436 (7%) children and required a median of 10 (range 5–34) dilations. Isolated OA (OR 5.7; p=0.012), anastomotic leakage (OR 5.0; p=0.001) and the need for oesophageal dilation ≤28 days after anastomosis (OR 15.9; p<0.001) were risk factors for development of a refractory stricture. Conclusions The incidence of refractory strictures of the end-to-end anastomosis in children treated for OA was 7%. Risk factors were isolated OA, anastomotic leakage and the need for oesophageal dilation less than 1 month after OA repair.

Effects of Neonatal Thoracoscopic Surgery on Tissue Oxygenation: A Pilot Study on (Neuro-) Monitoring and Outcomes

Introduction Multiple reports have questioned the feasibility of neonatal thoracoscopic repair of congenital diaphragmatic hernia (CDH) and esophageal atresia (EA). The aim of this study is to examine the effects of CO2 pneumothorax on cerebral and renal rSO2 and to assess the potential predictive value of these data on neurodevelopmental outcome after neonatal thoracoscopic surgery for CDH or EA. Materials and Methods A prospective observational pilot study. Cerebral and renal regional tissue oxyhemoglobine saturation (rSO2) rSO2 were assessed using near‐infrared spectroscopy (NIRS) during thoracoscopic surgery in neonates with CDH and with EA, in addition to routine anesthesia monitoring. Cerebral and renal rSO2, linked to repeated arterial blood gas analyses, heart rate, blood pressure, and to structured longitudinal neurodevelopmental follow‐up. Results Baseline estimated marginal means of cerebral rSO2 values (CDH: 82%, EA: 91%) did not change significantly during pneumothorax (CDH: 81%, EA 79% [n.s. versus baseline]) despite severe acidosis (lowest pH, CDH: 6.99, EA: 7.1). Neurodevelopmental outcomes at 24 months were normal in all 7 patients who were available for evaluation. Conclusion Neonatal thoracoscopic repair of CDH and EA using CO2 ‐pneumothorax leads to severe acidosis. Cerebral rSO2 remained within clinical acceptable limits during intraoperative periods of acidosis. Neurodevelopmental outcome was favorable within the first 24 months. The potential of NIRS to further improve perioperative care and long‐term outcome in this specific patient group deserves further investigation.