Diaphragmatic Emergencies Ulrich Schoeffel · Moshe Schein

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Ulrich Schoeffel · Moshe Schein

The only diaphragmatic pathology of interest to the emergency abdominal surgeon is the diaphragmatic hernia through which a single or multiple abdominal structures may migrate into the thorax and become incarcerated or strangulated.

These may occur in three different settings, each of which however shares most of the same clinical features.

Diaphragmatic Hernia

Rupture of the Diaphragm due to Blunt or Penetrating Trauma

Here the hernia may become symptomatic acutely,immediately after the injury, or may present many years later – in a patient who has almost forgotten the trivial car accident 14 years ago.Read about the diagnosis and treatment of acute traumatic hernia in

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Chaps. 34 and 35. Late complications are diagnosed and managed along the lines described below for the non-traumatic diaphragmatic hernia.

Congenital Diaphragmatic Hernia

These very rare entities are either the Bochdalek hernia (posterolateral defect

in the trigonum lumbocostale) or Morgagni hernia (just posterior to the xyphoid at

the foramen Morgagni or the trigonum sternocostale), or a defect of the tendineous

center of the left diaphragm, or the paraesophageal hernia. Left-sided defects more

commonly become symptomatic because the liver seals those of the right side. Most

congenital hernias are symptomatic and require operative treatment during the

first hours of life due to compression of lungs and mediastinal structures. This can

easily be accomplished from an abdominal incision by manual reposition (there are

no adhesions between thoracic structures and abdominal viscera in these cases) and

direct closure of the defect. If several organs are transposed intra-thoracically, the

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reposition should follow the order stomach first, small bowel next, then large bowel, and finally parenchymal organs such as the spleen.

If there is no overt herniation during the fetus’s development, the newborn may appear normal but may develop an acute herniation anytime later during his life. It then would present like any acquired diaphragmatic hernia, with the final diagnosis established at operation when the exact localization of the defect is revealed.

Acquired Diaphragmatic Hernia

In clinical practice, only two different entities have to be considered in this context: the herniation through a traumatic or preformed defect of the tendinous part of the left diaphragm and the paraesophageal hernia.

 Left diaphragmatic hernia. It has been stated commonly that older post-

traumatic hernia should be approached via a thoracotomy and non-traumatic hernia by laparotomy. Indeed, the presence of a peritoneal envelope generally sim- plifies reposition by gentle traction from below, whereas perforation or rupture of the diaphragm often includes a tear in the peritoneal lining, thus leading to dense adhesions between thoracic and herniated abdominal structures. However, in the individual case, the etiology is often not clear and the presence or absence of a peritoneal hernia sac is difficult to predict preoperatively. Therefore the operative strategy often is influenced by probability and personal experience. It has to be stressed,however,that a posterolateral thoracotomy in the seventh intracostal space always allows for careful dissection of herniated organs and exploration of the sub- diaphragmatic space whereas the abdominal approach may prove more difficult and hazardous. If, irrespective of the approach, a small hernia ring has to be enlarged, the radial ramifications of the phrenic nerve have to be respected.

 Paraesophageal hernia. Here the gastroesophageal junction lies inside the

abdomen anchored by the phrenoesophageal membrane (non-sliding hernia!) and the herniation – most commonly of the stomach – develops through the enlarged esophageal hiatus and a defect in the phrenoesophageal membrane alongside the esophagus. The fundus of the stomach may role up and down intermittently, pro- ducing no or only “subacute” symptoms but occasionally a larger portion or even the whole of the stomach may herniate into the chest producing the so-called intra- thoracic gastric volvulus (the “upside-down stomach”,or giant type II hiatal hernia).

Common complications include gastric strangulation with infarction, necrosis and

perforation, mucosal bleeding, or acute intrathoracic dilatation causing compres-

sion of other intrathoracic structures.

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Gastric Volvulus

Gastric volvulus is defined as an abnormal rotation of the stomach of at least 180 degrees, creating a closed loop obstruction.According to the axis around which the stomach rotates,volvulus of the stomach may be organoaxial or mesenteroaxial, or a combination of both.

In organoaxial volvulus – which is the more common variant – the stomach rotates around an axis that connects the gastroesophageal junction and the pylorus.

In this situation the stomach flips up into the chest with the greater curvature – drag- ging with it the ometum – coming to lie at the top; this kinks the esophagogastric junction as well as the distal stomach – producing in between a “closed loop gastric obstruction”. A mesenteroaxial volvulus (the less common variant) occurs around the axis that runs from the center of the greater curvature of the stomach to the gastric angulus. Gastric volvulus can occur at any age and with equal frequency in both men and women and has been reported in neonates and infants.

Clinical features

Acute gastric volvulus may develop against a background of intermittent non- specific dyspepsia attributed to the known presence of a paraesophageal hernia but usually it presents acutely “out of the blue.”Precipitating events may be a heavy meal or any event that increases intra-abdominal pressure, such as postoperative ileus, pregnancy or parturition.

The abdomen is relatively innocent with little epigastric pain and no abdomi- nal findings on examination. There is more pain substernally or in the chest and the compression of the left lung by the herniated stomach (or other viscera) may result in acute respiratory distress. The shift of mediastinal structures to the right may result in cardiovascular instability while kinking of the gastroesophageal junction may produce retching. The diagnostic triad described by Moritz Borchardt (1868–1948) includes epigastric/substernal pain, retching without vomiting, and

the inability

to pass a nasogastric tube.

Traditionally acute gastric volvulus was diagnosed on a chest X-ray showing

a retrocardiac air bubble or a large fluid level in the chest (

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Fig. 15.1). A contrast

study, showing obstruction of the stomach at the site of the volvulus, would have

then confirmed the diagnosis. Currently, however, a CT scan can offer an immediate

diagnosis with all anatomical details (see

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Figs. 15.2 and 15.3).

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Fig. 15.1. “What is your stomach doing in the chest?”

Fig. 15.2. Scout film of the CT scan showing a distended stomach occupying the left hemithorax with gross shift of mediastinum to the right

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Fig. 15.3a, b. Axial CT scan through the lower thorax. a Air fluid level in a distended stomach with shift of the heart to the right. The “bubble” on the right represents the gastric antrum. Note the nasogastric tube in the distal esophagus to the right of aorta. b A lower cut with the spleen visible on the left. The left bubble represents the gastric fundus. Note the

“transition line” between the two “bubbles” representing the site of the volvulus

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Management

Although emergency room staff tend initially to eyeball these patients and label them as suffering from “respiratory failure”or myocardial infarction,a prompt chest X-ray will suggest the diagnosis and promote further aggressive imaging studies. The presence of the stomach (and/or other viscera) in the chest is a dire surgical emergency because of the unpredictability of the situation,the patient may appear well but the stomach may be rapidly becoming necrotic! On the other hand, of course, an asymptomatic upside-down stomach may coincide with other intra- thoracic emergencies.

The treatment of acute gastric volvulus is surgical, consisting of a laparotomy, reduction of the volvulus, and assessment of gastric viability. The vast majority of acute diaphragmatic hernias can be reduced through the abdomen and very rarely is there a need to add a thoracotomy. Reduction of the herniated viscera may be aided by two maneuvers. Inserting a wide tube through the diaphragmatic defect abolishes the negative,“sucking” thoracic pressure and the nasogastric tube may be manipulated into the distended stomach to reduce its size.When the latter is not suc- cessful a decompressive gastrotomy is necessary before the stomach can be reduced into the abdomen. This should be performed carefully in order not to contaminate the thoracic cavity – an event that often leads to postoperative empyema.

After the hernia is reduced the hernial sac is excised and the diaphragmatic defect is closed with interrupted sutures.A very large defect may need to be patched with a synthetic prosthesis although this is not advised in the presence of contami- nation. Finally, some experts would recommend a tube gastrostomy – well-sutured to the anterior abdominal wall – to decompress the stomach and prevent recurrence of the volvulus. Others have recommended gastropexy – suturing of the stomach to the abdominal wall. The addition of an anti-reflux procedure such as fundoplica- tion is controversial – and most probably inadvisable – in such emergency situations when it is unknown whether the patient has also a sliding hernia and gastroeso- phageal reflux.

When the stomach is found to be non-viable,gangrenous portions are resected by partial or total gastrectomy as required. In the moribund patient who needs total gastrectomy it may be safer to postpone the reconstruction, insert a tube into the distal esophagus, close the duodenal stump and place a tube jejunostomy distal to the level of the eventual planned entero-entero component of the Roux-en-Y loop jejunoesophagostomy which will be performed once the patient is stabilized and ready for such an intervention.