The General Abdomen

Free Intraperitoneal Air

Free intraperitoneal air is expected in the immediate postoperative period. The frequency and duration of its detection may vary with the diagnostic modality utilized. The clinical importance of its detection may depend on whether the patient is receiving mechanical ventilation. Free intraperitoneal air may result from the dissection of air from a ruptured alveolus, back along the tracheobronchial tree, through the mediastinum, and either transdiaphragmatic^ or via the retro-and subperitoneum into the abdominal spaces [1]. This can lead to a false positive diagnosis with resultant unnecessary exploration of the patient [1].

Free air may also result from peritoneal dialysis. Faulty bag exchange or exterior line exchange may allow air entry into the abdomen. Chest x-rays may show free air in 4% of patients [2]. However, up to 11% of cases of free air in patients undergoing peritoneal dialysis may be secondary to gastrointestinal (GI) tract perforation. The amount of the air cannot be used to differentiate mechanical causes from pathological ones [2].

Conventional (plain film) radiographs of the abdomen may reveal free air in 30 to 77% of patients immediately after surgery [3-7]. This decreases to 38% on day 3 and 17% on day 17 [8]. The left lateral decubitus film, which allows air to rise and be highlighted between the liver and the parietal peritoneum, is positive in 53% of patients on postoperative day 3 and in 8% on day 6. As would be expected, these results compare unfavorably with the use of computerized tomography (CT) to detect free air. On postoperative day 3, 87% of CT images are positive for free air, and fully half are positive on day 6 [8]. Serial examinations in 10 patients showed a decrease in the amount of free air in six patients during the same examination period, and a complete disappearance in the other four [8].

An area of some controversy is whether body habitus affects the rate at which free air is absorbed. Two older studies, based on plain films, detected a higher rate of free air in asthenic individuals [3,5]. A more recent study utilizing both CT and plain films led to markedly different findings [8]. The plain film showed that obese individuals had a significantly lower rate of free air than others. Surprisingly, CT examinations showed no difference between asthenic and obese individuals in the detection of free air. The differences between these two techniques may be explained by the susceptibility of the plain film to degradation by increased scattered radiation and decreased penetration and density secondary to obesity.

The plain film findings of free air are numerous and are enumerated in Table 1.1 [9] (Fig. 1.1). The optimal film and phase of respiration for the detection of free air are the end inspiratory chest x-ray, and the end expiratory left lateral decubitus films of the abdomen [10]. Besides the usual findings on plain films, computed tomography has shown two new areas, both along the undersurface of the anterior abdominal wall, in which free air may be detected. Above the level of the umbilicus, air may collect in the recess between the two rectus abdominal muscles (along the linea alba). Similarly, below the umbilicus, air may collect along the lateral margins of the rectus sheath [8].

Barium or Water-Soluble Contrast Media

The question of which contrast medium to use in cases of suspected or known perforation is a difficult one to answer. The response depends on what level of the GI tract is involved, whether the patient is at risk of aspirating the contrast medium, and whether there is a risk of fecal contamination. Each of these possible scenarios is further complicated by personal preferences, demands of the referring physician, local practice, dogma, and somewhat contradictory and often outdated experimental evidence.

Based on experimental work done on cats, James and his colleagues published two often cited works on the effects of water-soluble contrast medium, barium sulfate, oral pharyngeal flora, and mixtures of flora and contrast media on the feline mediastinum [11,12]. Postmortem examinations were done over time intervals reaching 90 days.

Barium was initially evenly distributed in the mediastinum, but clumps were noted by 3 to 5 days postinstallation. Even after 90 days an estimated 50% of the barium remained but was not detected in the draining lymph nodes of the mediastinum. Histological sections revealed that the barium was incorporated into reactive surface mesothelial cells and large macrophages after 2 to 5 days. By one month, fibrous connective tissue surrounded nodules of barium-filled macrophages. Some inflammatory cells were present along with foreign body giant cells. The addition of esophageal flora comprising coliform, Proteus, Gram-positive aerobic spore-forming bacilli, micro-aerophilic and anaerobic streptococci, and lactobacilli did not significantly change these findings [11,12].

Pure Gastrografin injected into the cat mediastinum led to no gross pathologic changes. A few inflammatory cells were noted 7 days later. The addition of oral pharyngeal flora led to no significant change in

Table 1.1. Signs of pneumoperitoneum on a supine radiograph.

I. Upper abdomen

A. Right upper quadrant

1. Anterior to liver (subtle)

a. Anterior-superior bubble b. Ill-defined periduodenal lucency c. Right upper quadrant slit d. Lucent liver

2. Anterior to liver (gross)

a. Falciform ligament sign b. Ligamentum teres sign c. Diaphragm muscle slip sign

3. Within liver a. Ligamentum teres sign

4. Posterior to liver a. Morrison's pouch—doge's cap sign

5. Inferior to liver a. Hepatic edge sign b. Ligamentum teres notch sign c. Visible gallbladder

B. Paramedian

1. Lesser sac gas

2. Cupola sign

3. Visible lower cardiac border

C. Left upper quadrant—left-sided pneumoperitoneum

II. Midabdomen

A. Free gas

1. Rigler's sign

2. Triangle sign

3. Football sign

4. Visible transverse mesocolon

5. Visible small bowel mesentery

B. Air confined in intraperitoneal ligaments

1. Pneumo-omentum

2. Pneumomesocolon

III. Lower abdomen

A. Urachus

B. Medial umbilical folds

C. Later umbilical folds

D. Visible bladder roof

E. Pneumoscrotum

F. Isolated lower abdominal free air

IV. Extra-abdominal intraperitoneal free air

A. Free air in hiatal hernia sac

B. Free air in ventral hernia sac

V. Unrecognized plain film signs

A. Midrectus sign

B. Pararectus sign

Hernia With Visible BowelsFreie Luft Abdomen

Figure 1.1. Plain film findings of free air. (A) Massive free air. Supine film of the abdomen reveals a massive pneumoperitoneum following misplaced gastrostomy tube. (B) Falciform ligament sign. Coned-down view of the same patient shows the falciform ligament as a linear density obliquely oriented in the midabdomen. (C) Incomplete inverted V sign. Coned-down view of the pelvis in the same patient reveals the soft tissue densities of the medial collateral ligaments, as well as remnants of the umbilical arteries. When these converge upon the umbilicus they form the inverted V sign of pneumoperitoneum.

Figure 1.1. Plain film findings of free air. (A) Massive free air. Supine film of the abdomen reveals a massive pneumoperitoneum following misplaced gastrostomy tube. (B) Falciform ligament sign. Coned-down view of the same patient shows the falciform ligament as a linear density obliquely oriented in the midabdomen. (C) Incomplete inverted V sign. Coned-down view of the pelvis in the same patient reveals the soft tissue densities of the medial collateral ligaments, as well as remnants of the umbilical arteries. When these converge upon the umbilicus they form the inverted V sign of pneumoperitoneum.

histological appearance. Surprisingly, the injection of pharyngeal flora alone did not lead to significant mediastinitis. This may have been secondary to the use in the experiment of too dilute a concentration. Severe mediastinitis could be produced by using a more concentrated mixture, but this led to so many experimental deaths that the results were meaningless. Experience in humans with esophageal perforation leads us to conclude that oral pharyngeal flora leads to severe and potentially fatal mediastinal infections.

When contrast medium is aspirated into the tracheobronchial tree, or enters via an esophageal airway fistula, the lungs' reaction is very different from that seen in the mediastinum. Huston et al. instilled a commercial preparation into rat airways and defined four major patterns of histologic response [13].

The first was that of the initial inflammatory response. In this stage, the alveoli and smaller bronchioles are filled with the barium suspension and large numbers of polymorphonuclear leukocytes. Little fluid (exudate) was seen in the alveolus. These changes developed within 12 hours but by 24 hours the white blood cells had started to degenerate.

The next phase, mononuclear infiltration, developed within 48 hours and lasted up to 15 days. This stage was characterized by mononuclear cells containing phagocytosed barium suspension. Other mononuclear cells had replaced the lining epithelium of the smaller airways. Two weeks later, many of these mononuclear cells had fused together. Retractile masses filled with barium were noted, secondary to rupture of some of these mononuclear cells. This stage was entitled mononu-clear disintegration.

The last phase was that of tissue reaction. At 90 to 120 days after the administration of barium, installation the lung tissue looked grossly normal. A few small areas, related to the retractile masses noted earlier, showed early giant cell formation. No fibrosis was yet noted.

At no stage was barium noted in either draining lymph nodes or the liver or spleen. Most aspirated barium is cleared either by coughing or by mucociliary action [13].

In a more recent study, published in 1984, Ginai et al. [14] compared pure barium sulfate with Gastrografin, a commercial preparation of barium sulfate, and two nonionic water-soluble contrast agents. Both pure barium sulfate and the commercial preparation led to patchy bronchopneumonia by the eighth day, accompanied by epithelioid cell granulomas in the lung. By 6 weeks intramural granulomas were noted within the bronchial walls as well. Many of these changes seen by both Huston and Ginai may be secondary to mechanical plugging of the smaller airways by the ingested barium with subsequent atelectasis and inflammatory reaction [13,14].

In contrast to the barium preparations, and their long-lasting and long-standing mechanical effect, water-soluble contrast media are rapidly absorbed from the lungs as evidenced by their faint visualization just minutes after instillation and total disappearance by 24 hours. The severely hypertonic Gastrografin (its osmolality of 1900 is approximately six times that of plasma) causes a shift of fluid from the intravas-cular compartment to perivascular spaces and the lung parenchyma that may result in pulmonary edema or death [15,16]. Gastrografin also leads to the early development of perivascular infiltrates with mononuclear cells. Collapse and minimal alveolar infiltrates were also noted. By the fourth day, swelling and desquamation involving the alveolar lining was noted. The low osmolar contrast invoked very minimal changes in the perivascular spaces as well as within the alveolus.

Experimental evidence of the effects of barium sulfate or water-soluble contrast agents on the pleural surface is not available to the best of our knowledge. Given the similarity of the mesothelial lining of the chest and abdomen, it is reasonable to assume that these effects would mimic those discussed shortly [17].

Below the diaphragm, consideration of which contrast to use is complicated by the interaction of the contrast agent and enteric flora, especially fecal material. Cochran and colleagues examined the effects in dogs of pure barium sulfate [U.S. Pharmacopeia (USP) grade] and commercial barium preparations with and without the addition of fecal material [18]. When commercial barium sulfate was injected into the peritoneal cavity it almost immediately disbursed widely throughout over the next 2 to 5 days; clumping, most likely secondary to water resorption and the effect of fibrinous exudates, was noted. Extensive adhesions with severe hemorrhagic or purulent peritonitis developed, resulting in the death of most of the experimental animals. Sterilizing the barium did not significantly change these results.

When feces alone were injected into the peritoneal cavity, diffuse peritonitis ensued with multiple adhesions. When the fecal material was sterilized, no deleterious effects were noted. When barium and unsterile feces were mixed, a rapidly fatal hemorrhagic peritonitis resulted. Retroperitoneal infusion of barium led to granuloma formation [19]. However, in the absence of infection, extravasated barium led to no significant complications.

The conclusion the authors reached, which seems justifiable to this day, is that barium and feces are synergistic in their effects [18]. In addition, the additives to pure barium sulfate, used to stabilize the suspension and add to its properties (mucosal coating ability, palatability), adversely affect the peritoneal membranes. The negative effects of the fecal material are due to the accompanying infection, rather than the physical nature of the bacteria.

Ferrante and colleagues injected water-soluble contrast into rat abdomens [20]. They found no significant difference in the various ionic and nonionic contrast agents used. This was in marked distinction to barium injections, which resulted in adhesions and ascites.

Tubes and Lines

Nasogastric and nasoenteric tubes may be placed for a variety of diagnostic and therapeutic reasons. A whole host of mishaps and complications may be associated with their use, however, despite the usually benign nature of their insertion and usage.

Complications associated with insertion include perforation and malpositioning within the tracheobronchial tree. Complications arising from positioning in the GI tract include those related to obstruction, rupture of the mercury bag, perforation, and local irritating effects [21].

Perforation by a nasogastric or nasoenteric tube often occurs at the level of the pharynx, where the tip of the tube is often directed laterally into the piriform sinus. Exiting the piriform sinus, the tube may tract inferiorly, alongside the esophagus for a variable distance. Resistance may be encountered at multiple levels as it passes various medi-astinal components (Fig. 1.2). When contrast is injected, it outlines a

Piriform Sinus Injection
Figure 1.2. Misplaced NG tube. Chest film shows nasogastric tube misplaced in the mediastinum secondary to a perforation in the neck. No return was obtained from this tube. A CT image of the neck, not shown, demonstrated its path in the neck, lateral to the esophagus and trachea.

nonmotile tract that is slightly irregular and does not usually communicate with the GI tract. Multiple tracts may be seen in association with multiple attempts at tube placement (Fig. 1.3). The esophagus itself may be perforated with a greater potential for mediastinitis secondary to reflux and entrance of gastric secretions and flora into the mediastinum [22-24].

Feeding Tube Small Intestine
Figure 1.3. Unsuccessful attempts at feeding tube insertion. (A) False tracks of a feeding tube. Single-contrast esophagogram shows two thin, parallel tracks of barium in the chest, neither of which represents the esophagus. Both are false lumens secondary to unsuccessful attempts at

passing a metallic-tipped feeding tube. (B) Feeding tube within a false track. Another film from the subsequent study shows the feeding tube in one of the false lumens. (Courtesy of K. Cho, MD, Newark, NJ)

Patients with impaired neurological status are most at risk for inadvertent tube placement in the tracheobronchial tree. Depending on how far the tube is inserted, it may lie within a major bronchus (Figs. 1.4-1.6) or even be pushed through smaller and smaller airways, eventually perforating the visceral pleura to lie within the pleural space itself (Fig. 1.7A). Obviously, initiating feeding through such a malpositioned tube would have dire consequences. A pneumothorax may also be the sequela of such a malpositioned tube [25,26] (Fig. 1.7B). Some authors have advocated the use of a routine chest x-ray before any nasogastric (NG) tube is utilized [24]. They believe that clinical tests of tube placement are inadequate. The American College of Radiology, in its Appropriateness Criteria, also cites the value of obtaining a routine postprocedure film [27].

Feeding Tube Small Intestine

Figure 1.4. Feeding tube in a left-sided bron- Figure 1.5. Feeding tube in a right-sided chus. Chest film demonstrates a metallic-tipped bronchus. Chest film with a feeding tube in a feeding tube in the left lower lobe bronchus. Since right lower lobe bronchus. the right main stem bronchus has a more oblique takeoff at the carina, most tubes go there.

Figure 1.4. Feeding tube in a left-sided bron- Figure 1.5. Feeding tube in a right-sided chus. Chest film demonstrates a metallic-tipped bronchus. Chest film with a feeding tube in a feeding tube in the left lower lobe bronchus. Since right lower lobe bronchus. the right main stem bronchus has a more oblique takeoff at the carina, most tubes go there.

Pleural Cavity Chest Tube

Figure 1.7. Malpositioned feeding tube and tree and lies coiled in the pleural space. (B) Pneu-

sequela. (A) Feeding tube within the right pleural mothorax following chest tube removal. Another cavity. Chest film demonstrates a feeding tube that chest film taken of the same patient after removal has been advanced through the tracheobronchial of the feeding tube shows a pneumothorax.

Figure 1.7. Malpositioned feeding tube and tree and lies coiled in the pleural space. (B) Pneu-

sequela. (A) Feeding tube within the right pleural mothorax following chest tube removal. Another cavity. Chest film demonstrates a feeding tube that chest film taken of the same patient after removal has been advanced through the tracheobronchial of the feeding tube shows a pneumothorax.

Poly(vinyl chloride) tubes that are exposed to gastric acidity harden over time. This may lead to either perforation or difficulty in removal [21,28,29]. Thus long-term usage should be avoided. Other local complications of short- and long-term NG tube intubation include naso-pharyngeal irritation and ulceration, sinusitis, serous otitis, and pharyngitis [21]. The polyvinyl NG tube may also predispose a patient to gastroesophageal reflux and ulceration (Fig. 1.8). Rapid onset of a stricture may ensue (Fig. 1.9), although it is not clear whether this effect is due to reflux, the presence of the tube, or both [30].

Two of the more commonly used long intestinal decompression tubes are the Cantor and Miller-Abbott. Both utilize a mercury-filled bag at the proximal end to facilitate passage distally through the GI tract. A Miller-Abbott tube has a venting channel alongside the decompression lumen.

Figure 1.8. Ulcerations induced by an NG tube.

Single-contrast esophagogram shows multiple ulcerations secondary to the placement of an NG tube.

Figure 1.9. Stricture induced by an NG tube.

Esophagogram demonstrates a distal esopha-geal stricture, caused by previous NG tube placement.

Figure 1.8. Ulcerations induced by an NG tube.

Single-contrast esophagogram shows multiple ulcerations secondary to the placement of an NG tube.

Figure 1.9. Stricture induced by an NG tube.

Esophagogram demonstrates a distal esopha-geal stricture, caused by previous NG tube placement.

The latex balloon may act as a semipermeable membrane, allowing intestinal gaseous contents (predominantly carbon dioxide and hydrogen sulfide) [31] to enter the bag [32] (Fig. 1.10). This may occur in 0.3% of patients according to Cantor, as cited by others [32]. This gaseous accumulation may lead to increasing distention of the balloon until the partial pressures within it and the intestinal lumen equilibrate. At that point the balloon no longer distends [33]. Other factors affecting the gaseous distention include the surface area and thickness of the balloon wall and the length of time it is exposed to intestinal gases [34]. Ten days is often cited as the point in the time at which the distention reaches a critical diameter [34]. The dilated air- and mercury-filled balloon may cause considerable clinical problems.

Tube Accumulative Time
Figure 1.10. Air-distended mercury bag of a Cantor tube. Supine (A) and upright (B) films of the abdomen with a Cantor tube in place. Note the large amount of air in the mercury-filled bag.

First, it may cause obstruction of the lumen of the small bowel, thus creating or exacerbating the very condition it is intended to treat [21,33-35]. When this occurs, gentle retraction is usually tried. If this is not successful, decompression of the balloon may be attempted before laparotomy is necessitated [34]. Cutting of the tube hoping for its eventual expulsion is another but often unsuccessful therapeutic maneuver [32] (Fig. 1.11). Yet another possibility is placing another long intestinal tube, proximal to the offending tube, attempting to decompress the small-bowel lumen as an aid in the reverse flow of gas across the latex membrane [32].

Intestinal Insertion

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