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Management of Diaphragmatic Hernia During Pregnancy

Fleyfel, Maher MD; Provost, Nathalie MD; Ferreira, Jorge F. MD; Porte, Henri MD; Bourzoufi, Karim MD

doi: 10.1213/00000539-199803000-00009
Case Report

Departments of (Fleyfel, Provost, Ferreira, Bourzoufi) Anesthesiology 2 and (Porte) General Surgery, Hopital Huriez, University of Lille, France.

Accepted for publication October 21, 1997.

Address correspondence and reprint requests to Maher Fleyfel, MD, Department of Anesthesiology 2, Hopital Huriez, 59037 Lille Cedex, France.

Diaphragmatic hernia, with the exception of hiatal hernia, is an uncommon condition during pregnancy. Although one third of the patients are symptom-free, it can lead to a high mortality rate, ranging from 22% to 80%, if strangulation occurs [1]. We describe the management of a pregnant woman with a left diaphragmatic hernia associated with a right pneumothorax; diaphragmatic rupture resulted from previous surgical trauma.

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Case Report

A 29-yr-old woman, secundigravida, primapara was admitted to our emergency department at 28 wk gestation for acute dyspnea. The patient had been suffering for 15 days from severe abdominal pain and intractable vomiting, unrelieved by metoclopramide. Her weight decreased from 45 kg to 43 kg. Vital signs showed moderate distress and shortness of breath, a respiratory rate of 25 bpm, a systolic blood pressure of 90 mm Hg and a diastolic blood pressure of 60 mm Hg, heart rate at 100 bpm, and body temperature at 37[degree sign]C. Physical examination revealed reduced breath sounds over the lungs and tympany to percussion on the left side. The abdomen was soft and the uterine fundal height was 28 cm. The remainder of the clinical examination was normal. A chest radiograph demonstrated a left diaphragmatic hernia with a herniation of the stomach into the chest and a right pneumothorax (Figure 1). The patient's medical history revealed temporal epilepsy, depression, two episodes of spontaneous right pneumothorax secondary to pulmonary blebs, and constipation associated with megacolon. The patient's first pregnancy, 10 yr previously, had been entirely uneventful. She denied any previous trauma but had undergone a laparotomy with left nephrectomy for left adrenal adenoma 3 yr previously. A splenectomy was performed for tumor infiltration and was complicated by hemorrhage from diaphragmatic vessels. Since that time, she had complained of postprandial abdominal pain radiating to the left shoulder. An ultrasound demonstrated a normal gallbladder, liver, and biliary ducts. Recurrence of adrenal tumor was ruled out, and a hiatal hernia was diagnosed. Antacid therapy was given. Pneumothorax was aspirated with a chest tube introduced via the right fifth intercostal space, and a nasogastric tube was inserted to decompress the stomach. The patient's general condition was improved initially by reducing this mediastinal compression. Fetal growth, as assessed by ultrasonography, was normal. The patient was then transferred to the surgical ward, and conservative management with nasogastric aspiration and IV fluid and total parenteral nutrition by a central venous line was started. The chest tube was removed 3 days later. Because the patient's condition showed no symptoms of infection, and in the absence of abdominal obstruction, conservative treatment was planned until fetal maturity was reached.

Figure 1

Figure 1

During the following days, nausea and vomiting recurred despite nasogastric aspiration. A barium meal showed partial volvulus of the stomach (Figure 2), and repair of the diaphragmatic hernia was believed to be necessary. The patient was premedicated with sublingual midazolam 5 mg and oral cimetidine 400 mg. In the operating room, the patient was placed in supine position, with a wedge for uterus displacement. Fetal cardiac rate was monitored with a stethoscope placed on the periumbilical area throughout the surgery. The arterial blood pressure was 120/70 mm Hg, heart rate was 85 bpm, and fetal heart rate was 140 bpm. Once the surgeon was ready to operate, 100% oxygen was given, and a rapid sequence induction with thiopentone 200 mg, sufentanyl 20 [micro sign]g, and vecuronium 6 mg was accomplished. Cricoid pressure was applied and the trachea was intubated with a double-lumen endotracheal tube. The lungs were ventilated with 50% oxygen in air with the peak airway pressure kept below 15 cm H2 O and minute ventilation adjusted to maintain carbon dioxide end-tidal pressure at 35-40 mm Hg. The patient was carefully positioned to lie with the left side placed uppermost by watching arterial blood pressure and fetal heart rate. No change in fetal cardiac rate was noted during the patient's positioning. A left thoracotomy was performed with findings of an 8-cm tear in the left hemidiaphragm with herniation of the dilated stomach. No evidence of ischemic damage was noted. The viscera was returned to the peritoneal cavity, and the defect in the diaphragm was closed. There were no major hemodynamic or fetal heart rate changes during surgery. The chest was closed with left pleural drainage, which was removed on Postoperative Day 5. Pain relief was achieved with a patient-controlled analgesia device with morphine chlorydrate (bolus of 1.5 mg, lockout 5 min). Prophylactic tocolysis with IV salbutamol infusion at a rate of 0.2 mg/h was instituted postoperatively and maintained for 36 h. The patient was discharged at 31 wk with normal fetal ultrasound. She remained well, and delivery was accomplished by cesarean section at 39 wk gestation under epidural anesthesia because of the risk of rupture of a pulmonary bleb and pneumothorax during labor. Postoperative pain was managed with morphine by the same protocol of patient-controlled analgesia.

Figure 2

Figure 2

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Diaphragmatic hernias during pregnancy are classified into three categories [2]: paraesophageal or hiatal, congenital, and traumatic hernia. Hiatal hernias are 6 times more common than the other two types, and occurs from increased intraabdominal pressure during the second and third trimesters of pregnancy (up to 18% of multipara and 5% of the primipara) [3]. Congenital hernias are caused by defects in the diaphragm arising from faulty embryologic development in the posterolateral (Bochdalek) or the substernal (Morgagni) portion of the diaphagm. Symptoms may occur during pregnancy [4]. Traumatic diaphragmatic hernia results from blunt trauma, which increases intraabdominal pressure and tears diaphragmatic fibers [5]. In the nonpregnant patient, 90% of these hernias occur on the left side, because the liver offers protection to the right side [6]. Thirty-two cases of traumatic and congenital hernia have been discovered in the second part of pregnancy [7]. In our case, the posterocentral location of the tear suggested a traumatic origin of the hernia. We believe that an unnoticed tear occurred during the previous splenectomy or that the left leaflet was weakened by the hemorrhagic surgical procedure [8,9]. Since this patient's surgery, repeated increases in intraabdominal pressure (caused by coughing, sitting positions, constipation, and straining) likely enlarged the unnoticed tear [1] or contributed to further stretching of the weakened diaphragm fibers, eventually resulting in a rent. Pregnancy provides additive factors of increased intraabdominal pressure: nausea and vomiting until the 16th week and the enlarged pregnant uterus in the second trimester. With advancing pregnancy, as the uterus enlarges, it forces an increasing amount of abdominal content into the chest. All these factors may convert an occult defect to one that is symptomatic and increase the risk of twisting and torsion of herniated viscera. Surgical closure is required before delivery, because spontaneous rupture of the diaphragm might occur during labor [10]. Cesarean section can be performed simultaneously once fetal maturity is documented [7].

Clinical findings vary. In our case, the stomach alone was involved; hence, the symptoms were suggestive of vague postprandial epigastric distress [11]. Radiographs provided the diagnosis and showed a high diaphragm, cardiac shift, or air bubble and fluid in the chest [11]. The main life-threatening complications are acute dyspnea caused by compression atelectasis, mediastinal shift, and strangulation and gangrene of the herniated viscera [6]. In these cases, the maternal mortality rate ranges between 42% and 58.3% [1,7,10,12]. Fetal mortality and morbidity result from premature labor and compomise maternal oxygen delivery [13].

Treatment of nausea and vomiting with drugs or by nasogastric suction is therapeutic [11] because it allows decreased intraabdominal pressure. During anesthesia, the fetal heart rate, blood pressure, and central venous pressure and maternal oxygenation during the patient's change of position must be watched. To avoid hypotension during induction, uterus displacement with a wedge is indicated [14]. If the hernia is approached through a thoracotomy incision [6], the affected side is placed uppermost. Mediastinal shift [15], which compromises venous return and collapse of the lower lung, may be worsened by positional compression from the herniated dilated viscera. A rapid-sequence induction is indicated because the patient is at risk of pulmonary aspiration.

Lung ventilation must be undertaken with low tidal volume or low airway pressure until the abdominal contents have been removed from the chest or until thoracotomy has been performed. Cardiovascular collapse might occur during positive pressure ventilation. The reexpanded lung previously compressed by herniated viscera may shift mediastinal structures, and venous return may be impeded [16,17]. Increased pleural pressure from mechanical ventilation is transmitted to the abdomen. It results in increased upward displacement of the viscera toward the diaphragm and may worsen cardiovascular collapse [17,18]. A surgeon must be ready to operate before ventilation is begun [16].

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