Trocar site hernia after laparoscopic gynecologic surgery, complicated by parietal (Richter) strangulation

Catedra Chirurgie Generală, USMF „N.Testemițanu”, SCM nr.1, Chișinău, Moldova, Al XI-lea Congres al Asociației Chirurgilor „Nicolae Anestiadi” din Republica Moldova și cea de-a XXXIII-a Reuniune a Chirurgilor din Moldova „Iacomi-Răzeșu” 27-30 septembrie 2011Chirurgia laparoscopica este larg implementata în practica medicală, posedînd o siguranță demonstrată. Una din complicațiile sale specifice, deși rară, este hernia ”post- trocar” (HPT). Se disting 3 tipuri de HPT: (1) cu debut precoce – dehiscenta planurilor fasciale anterior și posterior și a peritoneului; (2) cu debut tardiv – doar dehiscenta planurilor fasciale și (3) tipul special – dehiscenta întregului perete abdominal și protruzia viscerelor. Noi prezentăm 2 cazuri de HPT după laparoscopii ginecologice, complicate cu strangularea parietală a intestinului subțire. Ambele paciente, în vîrstă de 53 si 49 de ani, au suportat chistectomie ovariană laparoscopică programată. Bolnavele au fost externate în stare satisfăcătoare, însă spre a 6-a și a 9-a zi, respectiv, a apărut durerea continuă în regiunea periombilicală pentru care au fost internate în Clinica chirurgie generală. Prezența tumefierii dolore periombilicale la examenul clinic s-a determinat doar într-un caz. Radiografia de ansamblu a abdomenului (n=2) și evaluarea pasajului baritat (n=1) au relevat semne de ocluzie intestinală. La revizia cavității peritoneale prin laparotomie medio-mediană s-a depistat strangularea parietală a ansei intestinului subtire, la cca 80 si, respectiv, 110 cm de la unghiul iliocecal. După eliberarea ansei, s-a observat defectul parietal subombilical, prin locul plasării trocarului de 10 mm (HPT tip I). Ansa intestinală a fost apreciată ca viabila în ambele cazuri. Defectul abdominal parietal a fost reparat prin suturi separate pe planurile aponeurotice și peritoneu. Operațiile au fost finisate cu drenarea cavității peritoneale. Perioada postoperatorie a decurs fără complicații. În diagnosticul diferențial al durerii abdominale în perioada precoce după operații laparoscopice trebuie să se țină cont de posibilitatea dezvoltării HPT. Defectul parietal în urma plasării trocarului de 10 mm necesită a fi suturat pe straturi în vederea prevenirii HPT cu ulterioara strangulare.Laparoscopic surgery is widely implemented in medical practice, possessing a proven safety. One of its specific complications, although rare, is trocar site hernia (TSH). There are three types of TSH: (1) early-onset type – dehiscence of the anterior and posterior fascial planes, and peritoneum; (2) late-onset type – dehiscence of fascial planes only and (3) special type – dehiscence of the whole abdominal wall with protrusion of viscera. We present two cases of TSH after gynecological laparoscopy, complicated by parietal strangulation of the small intestine. Both patients, aged 53 and 49 years, underwent elective laparoscopic ovarian cystectomy. Patients were discharged in satisfactory condition, but for the 6th and 9th days, respectively, were admitted to department of surgery due to continuous pain in the periumbilical region. Presence of swelling dolor periumbilicale mass was determined during physical examination in only one case. Abdominal x-ray (n=2) and evaluation of intestinal passage (n=1) revealed signs of intestinal obstruction. During the revision of peritoneal cavity through median laparotomy was found parietal strangulation of small intestine loop, localised at 80 cm and 110 cm, respectively, from the ileocecal angle. After releasing of the loop, subumbilical parietal defect was observed by 10-mm trocar site placement (TSH type I). Intestinal loop was assessed as viable in both cases. Parietal abdominal defect was repaired by separate sutures of the aponeurotic plan and peritoneum. The operations were finished with the peritoneal cavity drainage. Postoperative period were uneventful. In the differential diagnosis of abdominal pain after laparoscopic surgery it must be taken into account the possibility of developing of TSH. Parietal abdominal defect after placement of 10 mm trocar needs to be sutured in layers in order to prevent the further occurence of TSH and its strangulation

Vasodilators and vasoconstrictors (NO and Endothelin-1) in chronic heart failure in children

Department of Pediatrics, State University of Medicine and Pharmacy "Nicolae Testemitanu", Chisinau, Republic of MoldovaEndothelial dysfunction in chronic heart failure (CHF) secondary to congenital systemic-to-pulmonary shunts (CSPS) associated with Pulmonary Arterial Hypertension (PAH) conducts to chronically impaired production of vasodilator and antiproliferative agents,e.g. NO, further leading to the overexpression of vasoconstrictor and proliferative substances - endothelin-1 (ET-1). The aim: To accentuate the pathophysiological particularities of NO and ET-1 in CHF secondary to CSPS associated with PAH. Methods and materials:Seventy children with CHF secondary to CSPS associated with PAH (mean age 37,4±3,4 months) were involved in the study. The patients were separated into 3 groups: 1st – 16 pts with CHF and PAH moderate, and 2nd – 54 pts with CHF (the majority with RV’s dysfunction) and PAH severe, 3rd - 16 pts with CHF and without PAH. 15 health children with innocent cardiac murmur constituted the witness group. The groups were comparable w.r.t. the age and sex. Using ELISA method (DRG International Inc., SUA)NO and ET-1 were determined. Results: Patients with CHF and PAH moderate had a higher level of NO - 116,45±6,1 fl mol/l comparing to children with PAH severe - 93,06±3,34 (p<0,05) and to those with CHF but without PAH - 90,91±4,07 (p<0,05), and versus the healthy children - 77,32±5,1 (p<0,001). In PAH severe the pulmonary vasodilators’ mechanisms with the diminishing of NO got worse. ET-1 had higher values in children with PAH severe - 7,78±0,28 pg/ml with high statistical significance w.r.t. patients with PAH moderate - 3,88±0,21, vs those without PAH - 3,69±0,24 (p<0,001) and healthy - 2,9±0,27 (p<0,001). The hemodynamic stress within the CSPS associated with PAH is responsible for the endothelium’s lesion which leads to the stimulation of ET-1 production by the endothelium cells. Conclusions:The overall results reveal the major role ET-1 and NO in pathophysiology of PAH secondary to CSPS with CHF. At patients with CHF and PAH severe the endothelium’s lesion leads to a disequilibrium between the production of the mediators with vasodilators effects and those with vasoconstrictor properties; at patients with PAH moderate the NO level being significantly higher vs those with PAH severe, while the ET-1 values were higher at pts with PAH severe vs those with a moderate level and without PAH