Tension Pneumoperitoneum: Management of a Surgical Emergency

Publication
Article
Surgical Rounds®March 2007
Volume 0
Issue 0

Siamak Milanchi, Resident of General Surgery, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA; Daniel R. Margulies, Director, Trauma Services, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA; Nicholas N. Nissen, Assistant Surgical Director, Center for Liver Disease and Transplantation, Cedars-Sinai Medical Center, Los Angeles, CA, Assistant Clinical Professor of Surgery, David Geffen

Siamak Milanchi, MD Resident of General Surgery

Department of Surgery

Cedars-Sinai Medical Center

Los Angeles, CA

Daniel R. Margulies, MD Director, Trauma Services

Department of Surgery

Cedars-Sinai Medical Center

Los Angeles, CA

Nicholas N. Nissen, MD Assistant Surgical Director

Center for Liver Disease and Transplantation

Cedars-Sinai Medical Center

Los Angeles, CA

Assistant Clinical Professor of Surgery

David Geffen School of Medicine

University of California Los Angeles

Los Angeles, CA

Tension pneumoperitoneum (TP) is the accumulation of free air under pressure in the peritoneal space. It rarely occurs and usually follows perforations or operations involving the gastrointestinal tract. This condition is a surgical emergency and may result in death if not addressed promptly. Needle decompression is the immediate treatment of choice, followed by surgery in most cases. The authors report a case of TP that was managed at their medical center. They also searched the Medline literature from 1949 to 2005 and provide a review of the published cases.

The accumulation of free intra-abdominal air under pressure is known as tension pneumoperitoneum (TP). Although this condition is rare, it usually occurs after gastrointestinal perforations or operations,1 and it is sometimes found in the presence of pneumothorax or during positive pressure ventilation.2 Patients present with a tense and distended abdomen and have hemodynamic collapse and respiratory failure. We report a case of TP in a patient who was treated at our institution and discuss the etiology, diagnosis, and management of this uncommon surgical emergency.

Case report

A 62-year-old woman with a history of upper abdominal pain of unknown etiology was admitted to our institution for diagnostic upper gastrointestinal endoscopy and endoscopic ultrasonography. She had previously undergone ultrasonography and computed tomography (CT) scanning of her abdomen, which showed a normal gallbladder, biliary tract, and pancreas. A hydroxy iminodiacetic acid scan revealed dyskinesia of the gallbladder with poor ejection. The purpose of endoscopic ultrasonography was to evaluate the gallbladder, bile ducts, and pancreas for possible pancreatitis or gallstones and to obtain a bile specimen to evaluate for microlithiasis.

The patient underwent intravenous sedation, and endoscopic ultrasonography was performed using a side-viewing, 11.3-mm endoscopic retrograde cholangiopancreatography (ERCP) duodenoscope. After the procedure, the patient suddenly developed respiratory distress and became hypoxic and hypotensive. Cardiopulmonary resuscitation (CPR) was started, and the patient was intubated.

Physical examination revealed a massively distended and tense abdomen, which was tympanic and hyper-resonant to percussion. Breath sounds were diminished at both sides on auscultation, and there was considerable resistance to ventilation and high peak inspiratory pressures. Subcutaneous air was noted in the anterior chest wall and neck. Radiographs of the chest and abdomen showed a large amount of air in the peritoneal cavity and under the diaphragm (Figure 1). The air displaced the intestines and pushed the diaphragm upward, causing low lung volumes with no pneumothorax.

Immediate decompression of the peritoneal cavity was undertaken using a paracentesis needle under ultrasound guidance. The patient’s clinical condition improved immediately. Her blood pressure, oxygenation, and bilateral breath sounds improved, and her peak inspiratory pressure decreased.

The patient was taken to the operating room for laparoscopy. Although no injury was initially identified and intraoperative upper gastrointestinal endoscopy showed a normal esophagus and stomach, insufflation of the duodenum revealed air emanating from the duodenum close to the porta hepatis. Laparotomy was performed, which revealed a 1-cm perforation in the lateral aspect of the second portion of the duodenum, 5 cm distal to the pylorus (Figure 2). The perforation was repaired primarily, and no other injuries were noted. Although the gallbladder appeared normal, cholecystectomy was performed because of the patient’s history of abdominal symptoms and gallbladder dyskinesia. After 2 days, chest radiographs showed average-sized bilateral pneumothoraces (20% right side and 15% left side), which were treated by placing chest tubes that were later removed.

We think our patient most likely had small or anterior pneumothoraces that initially were not obvious on chest radiographs and later became larger. The patient was discharged home in good condition on postoperative day 12. Histopathology of the gallbladder showed mild chronic cholecystitis with no gallstones.

Discussion

The first reported case of TP was by Conole and D’Angelo in 1952, in a patient who developed this condition after resection of a pharyngeal diverticulum.3 TP is characterized by rapidly increasing intra-abdominal pressure. This condition is rare, and its incidence is unknown. The difference between simple pneumoperitoneum and TP is the presence of tension in the peritoneal space, which can have fatal hemodynamic and respiratory consequences (Figure 3). One such consequence is decreased venous return to the heart due to compression of the inferior vena cava, which results in hypotension and can lead to shock in the elderly and those with cardiovascular diseases. Another possible consequence is respiratory insufficiency secondary to elevation of the diaphragm, which decreases lung volumes, diminishes ventilation, and can cause or worsen respiratory failure in patients with cardiovascular or respiratory diseases. TP can result in compression of the aorta, inferior vena cava, and mesenteric vessels, which can cause ischemia of the bowel or, very rarely, ischemia or venous congestion of the lower extremities.4 Massive TP can even result in aortic occlusion.5

As with tension pneumothorax, TP occurs when air enters but cannot escape from the peritoneal space, thereby increasing intraperitoneal pressure (valve mechanism). It is not known why the same situations that cause TP in some patients result in simple pneumoperitoneum in others.

Etiology TP has several etiologies (Table).

Gastrointestinal perforation

—Gastrointestinal perforation is the most common etiology of TP. Upper or lower gastrointestinal endoscopy, ERCP or any other instrumentation of the gastrointestinal tract, abdominal trauma, or peptic ulcer can lead to gastrointestinal perforation.1 Patients usually develop hemodynamic collapse or respiratory failure during or shortly after endoscopy. The air insufflated during endoscopy enters the peritoneal cavity through the stomach or bowel perforation that was caused by the endoscope. The air is trapped and accumulates in the peritoneal cavity, increasing intraperitoneal pressure.

Esophageal perforation after instrumentation of the esophagus for stricture,6 gastric perforation, and perforation of the duodenum (either iatrogenic or from duodenal ulcer), have all caused TP. The condition also has been reported after ERCP secondary to perforation of the duodenum or biliary ducts.4

Perforation of the colon and cecum secondary to colonoscopy has also led to TP. There was one report of this condition following abuse of an industrial high-pressure compressed air pump, which was inserted into the rectum and caused rupture of the sigmoid colon.7

TP may be observed following air reduction for treatment of intussusception. It may also appear after inadvertent gastrointestinal perforation from esophageal intubation during CPR, which can rupture the esophagus or stomach. A case of faulty nasal application of oxygen resulting in TP due to stomach rupture has been reported.8

Blunt abdominal trauma

—Perforation of hollow viscera due to trauma is a rare etiology of TP. In trauma patients, the condition can be secondary to pneumothorax, barotrauma, mechanical ventilation, or gastrointestinal perforations. Diaphragmatic hernias increase the risk of TP in patients with pneumothorax because they facilitate passage of air from the chest into the peritoneal cavity.

Operations of the gastrointestinal tract

—Operations of the gastrointestinal tract have been noted to cause TP, with the condition observed after laparotomy, colostomy closure,9 percutaneous endoscopic gastrojejunostomy,10 colonic anastomosis, and repair of a congenital diaphragmatic hernia.11

Pneumothorax and barotrauma

—TP is seen in patients who have sustained tracheal injury from trauma or laryngectomy. It can also be caused by barotrauma in ventilated patients, particularly those ventilated with high inflation pressures and positive end-expiratory pressures.2

TP is a rare but known complication of barotrauma secondary to pulmonary blast injuries incurred during explosions. TP attributed to barotrauma is usually accompanied by bilateral pneumothoraces, extensive subcutaneous air, and pneumomediastinum. TP is frequently associated with pneumothorax because it can cause or may be caused by this condition.

Laparoscopy

—In patients with severe cardiac or pulmonary failure, induced pneumoperitoneum for laparoscopy can have deleterious hemodynamic and respiratory consequences, even with intraperitoneal pressures as low as 15 mm Hg.

Gastrointestinal obstruction

—A few cases of TP caused by gastrointestinal obstruction have been reported.12 These cases involved perforation of the bowel proximal to the obstruction, resulting in expulsion of air into the peritoneal cavity. TP has been observed to occur with volvulus of the colon. Ischemic colitis and emphysematous gastritis13 have been reported to cause TP.

Other etiologies

—Several cases of spontaneous TP also have been reported; however, we think that most of these cases are secondary to gastrointestinal perforations or pneumothorax. Devine and colleagues reported a case of TP of unknown etiology following vomiting in a 69-year-old woman.14 This patient presented with hemodynamic and respiratory collapse and cyanotic, pulseless legs. Decompression of the peritoneal cavity with a 14-gauge catheter immediately reversed the hypotension and tachycardia and restored circulation to her legs.

Diagnosis Diagnosis of TP can present a dilemma. In typical cases, diagnosis can be made clinically based on the patient’s history and a physical examination. Chest or plain abdominal radiographs are diagnostic and should be done if the patient is stable enough. Radiographic studies show a large amount of air in the peritoneal cavity and under the diaphragm, displacing the intestines and pushing the diaphragm upward, causing low lung volumes. Pneumothorax may be observed, depending on the etiology of the TP. Ultrasonography can be diagnostic, although sometimes it does not differentiate intraluminal air (eg, megacolon) from free intraperitoneal air. Further diagnostic studies are not warranted because these patients are usually in critical condition and unnecessary testing delays treatment.

Treatment

Treatment of TP is decompression, which should be performed promptly. Decompression provides immediate relief of hemodynamic and respiratory signs and symptoms, improving the patient’s clinical condition. Needle decompression using a large bore angiocath or catheter can temporarily relieve the pressure. We used a paracentesis needle and decompressed our patient’s peritoneal cavity under ultrasonographic guidance; however, ultrasonographic guidance generally is not necessary. A large bore angiocath or catheter inserted into the anterior abdominal wall can be used safely, and treatment should not be delayed to obtain an ultrasound. Other ways of decompressing the abdomen include a minilaparotomy (eg, diagnostic peritoneal lavage) at the bedside or simply making an incision in the anterior abdominal wall and penetrating the parietal peritoneum. The advantage of a minilaparotomy is that it avoids injury to the bowel in cases where radiography or ultrasonography cannot be done and a definitive diagnosis of TP versus intraluminal air cannot be made.

Laparotomy for identification and repair of possible sites of perforation is usually advocated, depending on the etiology of TP. If the condition is caused by gastrointestinal endoscopy or abdominal trauma, laparotomy is warranted to repair the bowel perforation. In cases where the patient has pneumothorax, a chest tube should be placed. If the condition is caused by pneumothorax and the patient’s clinical condition improves after decompression of the peritoneal cavity and placement of a chest tube, laparotomy can be delayed. Patients should be observed and laparotomy undertaken if peritoneal signs develop. In cases of spontaneous TP, definitive treatment depends on the possible etiology and other associated findings. If there is any suspicion of bowel perforation, surgical intervention is mandated.

In experienced hands, laparoscopy instead of laparotomy can be used to repair a bowel perforation. Laparoscopy has the advantage of being less invasive and, in cases of suspicious bowel injury, it can confirm or rule out the injury.

Conclusion

TP is a rare event that has profound and deleterious hemodynamic and respiratory consequences. If the condition is not diagnosed and treated promptly, it can result in death. A high index of suspicion is required to diagnose TP, and the condition should be considered in any decompensating patient with massive abdominal distention. TP is the number one differential diagnosis in any patient who has cardiovascular or pulmonary collapse during or shortly after endoscopy.

Differentiating TP from megacolon (intraperitoneal air versus intraluminal air) can be difficult. Radiographic studies can differentiate these two conditions and should be performed if the patient is stable enough, because needle decompression can perforate the colon in a patient with megacolon who does not have TP.

Needle decompression is the initial treatment of choice for TP and should be followed by laparotomy or chest tube placement, depending on the case. Laparoscopy, in experienced hands, should be considered an option, as well as observing the patient. Diagnostic studies should not delay diagnosis and treatment, because immediate treatment can save a patient’s life.

Patients with TP are at higher risk of having pneumothorax. Small or anterior pneumothoraces may not be detected on chest radiographs; therefore, repeat radiographs or CT scans of the chest may be necessary to detect a pneumothorax.

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