Esophageal atresia is a congenital malformation incompatible with life due to the inability to eat on the one hand but also to tracheobronchial flooding. Its morbidity and mortality has clearly improved in developed countries but still remains very high in Africa.

Our study reports the observations of the first two cases out of ten, having survived the surgical treatment of this pathology at the CHU Mère-enfant Fondation jeanne Ebori in Libreville over a period of 2 years, as well as the means highlighted to achieve this.

Observation 1

BB N. newborn born at the end of 40 weeks+2 days, vaginally, of a pregnancy having benefited from 5 antenatal consultations and weighing 3280g. The first minute apgar was 10/10. He was treated for a maternal-fetal infection with a birth fever of 39.8°C. He was then transferred to D7 of life in front of the diagnostic suspicion in our structure.

The Admission Exam Found

Dehydration, hypersialorrhea, jaundice and rales of bronchial congestion.

The thoraco-abdominal x-ray showed the nasogastric tube in the proximal esophageal cul-de-sac with digestive aeration in favor of an esophageal fistula.

The management consisted of hospitalization, conditioning, dorsal decubitus in the proclive position and continuous aspiration.

First-line antibiotic therapy (cefotaxime, Gentamycin, metronidazole), basic intakes with SG10% enriched in electrolytes. No associated malformation was found on ultrasounds.

He was operated on at day 8 of life. The treatment consisted of an end-to-end anastomosis with closure of the tracheal fistula and verification of the seal, after right anterolateral thoracotomy and an extra-pleural approach. A transanastomotic nasogastric tube and a chest tube were placed. 

The patient was extubated on an operating table with spontaneous breathing.

The diagnosis of type III esophageal atresia was confirmed intraoperatively. Immediately postoperatively, the patient was put on second-line antibiotic therapy (ceftazidine, vancomycin and metronidazole) with parenteral nutrition with Kabivein *, adjusting the intake to the child's weight.

The chest tube and nasogastric tube were removed on D6 postoperatively.

The postoperative follow-up was marked on D6 postoperatively by suppuration of the wall with CRP at 181ng / l treated with daily local care with Dakin and the replacement of ceftazidine by imipenem. The TOGD performed on D7 postoperatively confirmed esophageal continuity and allowed the start of enteral feeding.

On post-operative day 8, the onset of fever and abdominal distension with collateral venous circulation caused enteral feeding to be suspended until resumption of transit 48 hours later.

He also received a blood transfusion for anemia at 8.6g / dl.

On postoperative D10 the wound was clean and bacteriological examination of the pus had found Enterobacter sensitive to ciprofloxacin.

The patient was discharged on D29 postoperative and D30 of hospitalization.

The follow-up at 18 months was normal.

Observation 2

BB L. was born at 40 AG, with a weight of 3425 g. He was transferred from a Regional Hospital Center on suspicion of esophageal atresia at day 6 of life. He was born vaginally at the end of an unsuccessful pregnancy with a 7/10 Apgar and stained amniotic fluid.

The examination upon admission found: Respiratory distress with hypersialorrhea, bronchial congestion and crackling rales in both lung fields.

The thoraco-abdominal x-ray showed the nasogastric tube coiled in the proximal esophageal cul-de-sac with digestive aeration in favor of an esophageal fistula (Figure 1). 

Figure 1: Digestive Aeration in Favor of an Esophageal Fistula

No associated malformations were found on cardiac, abdominal and trans-frontanellar ultrasounds.

The management consisted of conditioning; dorsal decubitus, in a proclive position with continuous aspiration of the esophageal fornix.

First-line antibiotic therapy (cefotaxime, Gentamycin, metronidazole) and basic intakes with SG10% enriched with electrolytes.

He was operated on the day 8 of his life (ie 48 hours after his admission). The intraoperative diagnosis confirmed type III esophageal atresia. The treatment consisted of an end-to-end anastomosis with closure of the fistula after a right anterolateral and extra-pleural thoracic approach. The tracheal seal was checked, a transanastomotic nasogastric tube and a chest tube were placed. The patient was extubated on an operating table with spontaneous breathing.

Immediately postoperatively, the patient was placed on second-line antibiotic therapy (ceftazidine, vancomycin, metronidazole) and parenteral nutrition. The transanastomotic nasogastric tube was accidentally torn from H3 postoperatively). The biological assessment was normal on D2 postoperative.

On D3 the symptoms were marked by profuse hypersialorrhea and bronchial congestion. The chest x-ray performed showed right pulmonary atelectasis (Figure 2). 

Figure 2: Chest X-Ray Performed Showed Right Pulmonary Atelectasis

The treatment then consisted of a left lateral decubitus and physiotherapy with normal radiographic control after 48 hours.

A TOGD was done on D13 postoperatively showing esophageal stenosis (X-ray Figure 3).

Figure 3: D13 Postoperatively Showing Esophageal Stenosis

Twenty-two days after the first operation, the patient is returned to the operating room for a thoracotomy after an unsuccessful attempt at dilation. It was a complete esophageal stenosis.

Immediately postoperatively, he was placed on Imipenem and fed parenterally, then on D3 postoperatively with the transanastomotic probe.

The removal of the chest tube was done on D4 postoperatively.

The control TOGD performed on D7 postoperatively was normal (Figure 4). Three days after, i.e., D38 of hospitalization, the patient is authorized to go out. The follow-up at one year was normal.

Figure 4: Control TOGD Performed on D7 Postoperatively was Normal

Esophageal atresia is an emergency the prognosis of which depends on the earliness of the treatment and therefore the diagnosis. In developed countries, antenatal diagnosis is performed at least once in two [1]. In Africa, antenatal diagnosis is rarely made, this is the case for the studies by Tambo et al. [2] in Cameroon, Fall et al. [3] in Senegal, Mohamed Benkirane in Morocco and Bouguermouh in Algeria. A hydramnios is found in a few cases, but the ignorance of the malformative pathology in the ultrasound follow-up of parturients explains the fact that this does not lead to in-depth investigations for the diagnosis.

For our two patients the antenatal diagnosis was not made either.

This condition, being unknown, is therefore neither systematically sought in the antenatal period (hydramnios, pouch sign on ultrasound, etc.), nor in the delivery room where the systematization of the test of the nasogastric tube previously required seems to have been required. moved back. This explains the late diagnosis period of 6 days which is ours. It is also in Ehua et al. [4] or 6.6 days and in Tambo [2]. These deliveries took place in a hospital environment.

Neither of the 2 patients was born in our facility. In Benkirane [5] 74% of their patients were outborn. Type III esophageal atresia is the most common. Benkirane [5] and Bouguermouh  and Salem [6] found 67 and 74% of type III, respectively.

The malformative assessment did not show any anomalies.

Al-Salam et al. [7] in Saudi Arabia found 50% of associated malformations, 49% of which were of cardiac origin; Tandon et al. [8] in India also found these same comorbidities. Randriamizao et al. [9] in Madagascar did not perform a malformative assessment because of its unavailability.

We performed right extra pleural thoracotomies. Tandon et al. [8] also used this therapeutic approach for the majority of their patients. They also benefited from parenteral nutrition immediately after surgery.

The intervention time for our patients was 8 days. The intervention times in the studies by Fall et al. [3] and Ehua [4] were 4.8 and 5.7 days, respectively, these times are lengthened in most African studies. Ehua [4] found long intervention times of 11 and 15 days in her two survivors and also had recourse to unauthorized parenteral nutrition in the absence of neonatal parenteral nutrition available. Although the literature describes a short time to intervention as a factor of good prognosis, survivors in our study and even more in Ehua's study have a long time to intervention and generally in African studies are operated late (2, 3.6). If the absence of an antenatal diagnosis and the late diagnosis do not allow early surgical management, the extension of the intervention time has also made it possible to treat aspiration pneumonia by continuous aspiration and incisor antibiotic therapy and to restore the hydro-electrolyte balance. This preoperative resuscitation improves the prognostic classification of these patients, particularly in our study from class B to class A by Wastson.

It might be wise in our African context not to rush in front of these cases but to take the time to stabilize the vital functions of these patients to improve their chances of survival and proceed to their malformative assessment. This peri-operative resuscitation probably improved the survival of our patients, in particular the second despite a resumption of surgery 22 days after the first intervention. Our patients were extubated on an operating table with spontaneous breathing and immediately put on triple broad-spectrum antibiotic therapy. In fact, sepsis and mediastinitis, along with anastomotic fistulas and after associated cardiac malformations, constitute the mortality factors found in most studies.

The survival of 2 of our patients with a follow-up of a year and a half shows that it is possible to manage this condition successfully in our country.

Esophageal atresia is a condition with high mortality. It is an obsession for the pediatric surgeon in developing countries. However, the late treatment did not put a strain on the vital prognosis of our patients. A powerful and broad antibiotic therapy as well as an adapted parenteral diet (adult without inherent complications so far) were the strong points of the postoperative resuscitation of these patients.

1. Garabedian, C. et al. “Atrésie de l’œsophage: Prévalence, Diagnostic Anténatal et Pronostic.” Journal de Gynécologie Obstétrique et Biologie de la Reproduction, vol. 43, no. 6, 2014, pp. 424-430.

2. Tambo, F.F. et al. “Difficulties in the Management of Esophageal Atresia in Developing Countries.” Le Mali Medical, vol. 25, no. 4, 2010, pp. 36-38.

3. Fall, M. et al. “Oesophageal Atresia: Diagnosis and Prognosis in Dakar, Senegal.” African Journal of Paediatric Surgery (AJPS), vol. 12, no. 3, 2015, p. 187.

4. Ehua, A.M. et al. “Surgical and Anaesthesiology Management of Esophageal Atresia: What Are the Mortality Factors in a Developing Country?” Surgical Science, vol. 9, no. 12, 2018, p. 496.

5. Benkirane, Mohamed. Prise en Charge de l’Atrésie de l’Oesophage en Réanimation Pédiatrique au CHU de Marrakech. Thesis no. 184, 2020.

6. Bouguermouh, D. and A. Salem. “Esophageal Atresia: A Critical Review of Management at a Single Center in Algeria.” Diseases of the Esophagus, vol. 28, no. 3, 2015, pp. 205-210.

7. Al-Salem, A.H. et al. “Esophageal Atresia with or without Tracheoesophageal Fistula: Success and Failure in 94 Cases.” Annals of Saudi Medicine, vol. 26, no. 2, 2006, pp. 116-119.

8. Tandon, R.K. et al. “Esophageal Atresia: Factors Influencing Survival—Experience at an Indian Tertiary Centre.” Journal of Indian Association of Pediatric Surgeons, vol. 13, no. 1, 2008, p. 2.

9. Randriamizao, H.M.R. et al. “Prise en Charge Péri-Opératoire de l’Atrésie de l’Oesophage: Petits Pas Non Négligeables à Madagascar.” Pan African Medical Journal, vol. 27, no. 1, 2017.