Книги по МРТ КТ на английском языке / Advanced Imaging of the Abdomen - Jovitas Skucas

Table 2.5. Causes of abnormal gastric communications

To peritoneal cavity:

Acute trauma

Peptic ulcer disease

Neoplasm

Ischemia

To bowel:

Surgical anastomosis

Peptic ulcer disease

Neoplasm

Primary gastric

Primary colonic

Crohn’s disease

To biliary tree:

Gallstone disease

Peptic ulcer disease

Neoplasm

To urinary tract:

Staghorn calculus

Perforation/Fistula

A gastric fistula with communication to another organ is less common than in the small bowel or colon. Part of the reason is the relatively thick gastric wall and its relatively rich blood supply, making gastric ischemia uncommon. Nevertheless, numerous abnormal communications involving the stomach have been reported (Table 2.5).

Vascular Lesions (Bleeding)

Clinical

Prophylactic aspirin use is recommended for a number of medical conditions, yet at times even low doses result in gastrointestinal bleeding.

Hematemesis implies bleeding proximal to the ligament of Treitz. Melena, or black tarry stool, usually is from an upper gastrointestinal site but occasionally is secondary to small bowel or even right colonic bleeding (incidentally, black tarry stool is melenic stool; melanotic stool implies the presence of melanin pigment). Common causes of hematochezia and melena in adults include a duodenal or gastric ulcer. Common etiologies of upper gastrointestinal bleeding in pediatrics range from gastritis and

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esophagitis to peptic ulcers and varices in older children.

An occasional patient with diabetic ketoacidosis develops upper gastrointestinal hemorrhage; bleeding generally is not severe and is self-limited. The most common cause of such bleeding is erosive esophagitis, less often gastritis and duodenitis.

Although ascariasis is usually associated with small bowel and biliary disorders, upper gastrointestinal ascariasis is a rare cause of gastric bleeding.

Diffuse gastric angiomatosis manifests with bleeding, at times life-threatening. Angiography should be diagnostic. Some of these patients require a total gastrectomy.

Imaging

Several available scintigraphic techniques identify gastrointestinal bleeding. Provided active bleeding occurs at time of scanning, Tc- 99m–sulfur colloid detects bleeding rates as low as 0.1mL/min. Intermittent bleeding tends to be missed because of rapid clearance of the sulfur colloid from circulation.

Tc-99m–red blood cell scintigraphy provides a prolonged blood pool and is more useful with intermittent bleeding. Only several milliliters of extravasated blood is needed for detection. Serial images up to 24 hours are obtained. One cause of false-positive results is secretion of free Tc-99m-pertechnetate into the gastrointestinal tract.

Angiographic detection of bleeding has been largely replaced by contrast-enhanced CT, except when performed as part of therapeutic embolization.

Tumors

Chronic bleeding and resultant iron-deficiency anemia are one of the clinical presentations of gastric carcinomas. Mesenchymal tumors and lymphoma also tend to ulcerate and bleed.

Some hemangiomas also bleed. Multiple gastric hemangiomas are occasionally found in Osler-Weber-Rendu syndrome.

Dieulafoy Lesions

Over a century ago a Parisian surgeon, G. Dieulafoy, described massive gastric bleeding

from an artery close to the mucosa and the term gastric Dieulafoy’s erosion entered the French medical literature. Over the years this condition has acquired a myriad of names (Table 2.6),with current usage mostly settled on Dieulafoy lesion. Although some authors refer to these lesions as gastric vascular malformation, this terminology is sufficiently similar to arteriovenous malformation to create confusion; Dieulafoy lesions are not related to arteriovenous malformations. Little evidence suggests that these lesions represent a separate disease or syndrome.

Initially these bleeding submucosal arteries were believed to be limited to the stomach, but over the last several decades similar lesions have also been described in the small bowel and colon. It usually consists of a wide-caliber submucosal artery without histologic evidence of a true aneurysm. Etiology and pathogenesis are unknown. A vascular dysplasia, or thrombosis and necrosis of an abnormal submucosal artery are considerations, but the lack of an inflammatory reaction around many of these lesions is puzzling. Bleeding is usually through a small overlying mucosal defect. The surrounding mucosa is normal.

These lesions are found throughout the stomach, although the posterior wall lesser curvature near the cardia is a common site. They are more prevalent in elderly men. Although previously believed to be rare, these lesions come to medical attention mostly when investigating massive, often life-threatening upper gastrointestinal bleeding.

The diagnosis is made from a resected specimen. Lately, however, endoscopists have become enamored with this entity, often making the diagnosis on visual inspection only and then initiating endoscopic therapy. Typical diagnostic criteria used by endoscopists are presence of

arterial bleeding or a visible nonbleeding superficial vessel without surrounding ulceration or erosion.

Endoscopic US aids in detecting subtle Dieulafoy lesions; a vessel several millimeters in diameter is detected penetrating through the muscularis propria and extending into submucosa. Partly filling the stomach with water helps identify these vessels.

Arteriography, if performed while the lesion is bleeding, should identify a feeding vessel and site of bleeding. The appearance is different from that seen with angiodysplasia or arteriovenous malformations; neither a tuft of abnormal vessels nor an early draining vein is seen with a Dieulafoy lesion.

Initially these lesions were managed by wedge resection or oversewing, although currently many are managed by endoscopic hemostasis. Focal acute ischemia is a potential complication after sclerotherapy agent injection. Endoscopic lesion localization followed by laparoscopic gastric wedge resection is an option in some patients.

Ectasia

Gastric vascular ectasia is found in two conditions: so-called watermelon stomach and portal hypertensive gastropathy. Both are rare causes of chronic gastric bleeding and iron-deficiency anemia. Whether the underlying pathogenesis differs in a watermelon stomach from portal hypertensive gastropathy is conjecture.

Watermelon Stomach

Gastric vascular ectasia, also called watermelon stomach, is a gastropathy of uncertain pathogenesis, often associated with autoimmune gastritis and connective tissue disorders. An

association appears to exist between watermelon stomach and scleroderma-like diseases (77). Many of these patients also have cirrhosis, portal hypertension, and hypergastrinemia. Antral vascular ectasia is associated with cirrhosis and bone marrow transplantation. Of interest is that histology reveals thicker than normal gastric mucosal capillary walls in these patients (78); gastric mucosal capillary dilation is not a reliable criterion. These capillaries often contain fibrin thrombi. Presence of neuroendocrine cells showing immunoreactivity for serotonin suggest a role for neuroendocrine mediators in this condition.

Clinically these often elderly patients present with anemia and unrelenting chronic blood loss. An occasional one develops a massive bleed.

The diagnosis cannot be made with barium studies. A characteristic endoscopic appearance consists of diffuse erythema and ectatic, tortuous capillaries. Endoscopic US reveals preservation of muscularis propria; these changes regress after laser ablation.

Tc-99m–labeled red cell imaging is useful to localize any bleeding site.

Endoscopic electrocoagulation or laser photocoagulation are often therapeutic; at times antrectomy is necessary. A-interferon therapy may have a role.

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pattern and hemorrhagic spots. Varices may or may not be present, although portal hypertensive gastropathy is more severe in those with prominent esophageal varices. Endoscopists classify the condition as mild when either a mosaic pattern or superficial reddening is seen and severe when diffuse cherry red spots are identified. These changes are flat and not detected with imaging, although some patients have thickened and nodular gastric fundal folds (79), a nonspecific finding.

Chronic blood loss is more common than acute massive bleeding. Gastric acid output is decreased and the mucosal barrier becomes impaired.

Endoscopic esophageal variceal sclerotherapy accentuates portal hypertensive gastropathy and gastric varices, and in some patients becomes evident only after sclerotherapy. Some patients bleed from portal hypertensive gastropathy and gastric varices after sclerotherapy.

In patients with portal hypertension and hypersplenism, portal hypertensive gastropathy tends to improve after splenic arterial embolization. Portal hypertensive gastropathy is reversed in most by portosystemic shunting, such as a central splenorenal decompressive shunt and presumably in this subgroup of patients venous congestion is the cause of gastropathy.

Portal Hypertensive Gastropathy

Portal hypertensive gastropathy and gastric vascular ectasia appear similar but probably are separate conditions, although little clear-cut pathologic differentiation exists between these two conditions. Usually ectasia in a watermelon stomach is limited to the antrum, whereas in portal hypertensive gastropathy the proximal stomach is more often involved.

Portal hypertensive gastropathy describes a spectrum of gross findings developing in gastric mucosa in patients with portal hypertension. Cirrhosis is not a prerequisite because noncirrhotic patients with portal hypertension also develop this condition. Gastric intramural vessels dilate, presumably secondary to both portal venous congestion and increased gastric blood flow. Arterial intimal hyperplasia is evident in some patients. Endogenous vasodilator overproduction and decreased vascular sensitivity to vasoconstrictors appear to play a role. The mucosa is atrophied and contains a mosaic

Varices

Detection

Isolated splenic vein thrombosis, regardless of etiology, leads to gastric varices without concomitant esophageal varices. Endoscopic US appears superior to endoscopy in detecting gastric varices. Endoscopic Doppler US also quantitates these varices; color Doppler US detects slow, steady flow in gastric varices located in a thickened gastric wall.

A double-contrast upper gastrointestinal tract examination readily detects gastric varices (Fig. 2.31). Most are located close to the gastric cardia and most have a typical verrucoid appearance. A minority of these varices, however, have a conglomerate mass-like appearance (80); in profile, these varices appear as smooth intramural masses having distinct borders, whereas en face they appear as thick, tortuous folds.

Contrast-enhanced CT also detects gastric varices. In particular, 3D CT portography

readily identifies gastric fundic varices. Portography is the gold standard (Fig. 2.32).

Therapy

In distinction to esophageal varices, gastric varices tend to have an extensive network of feeding vessels. Thus control of gastric variceal bleeding by endoscopic sclerotherapy is considerably more difficult. A combination of

Figure 2.32. Fundal varices (arrows). The study was performed via percutaneous portal vein puncture. (Courtesy of David Waldman, M.D., University of Rochester.)

decreasing the blood flow with band ligation followed by injection of a sclerosing agent is successful in some. At times a combination of sclerotherapy with percutaneous transhepatic variceal obliteration in patients with large gastric varices results in gastric variceal eradication. Transjugular intrahepatic portosystemic shunting (TIPS) does control bleeding from gastric varices but in some patients sclerotherapy achieves better long-term results. In one study the cumulative survival rates at 1 and 5 years were 81% and 40%, respectively, in the TIPS group and 96% and 76% in the sclerotherapy group (p < 0.01) (81); subdividing these patients, survival was higher for those in ChildPugh class A undergoing sclerotherapy rather than TIPS (p < 0.01), but no significant differences were found for those in Child-Pugh classes B and C.

Emergency TIPS in patients with variceal bleeding is equally effective in controlling gastric fundal variceal bleeding and esophageal variceal bleeding (82). In some patients splenic artery embolization reduces blood flow sufficiently to stop bleeding. An occasional patient requires a splenectomy to control bleeding.

Retrograde transvenous obliteration of gastric varices is feasible in presence of gastrorenal or gastrocaval collaterals. Using a balloon occlusion catheter, sclerosing agents injected into gastric varices led to variceal obliterated (83); gastric varices recur in a minority

of these patients and can be treated with repeat transvenous variceal obliteration. Esophageal varices also developed in some patients treated with endoscopic injection sclerotherapy.

In patients with hepatic schistosomiasis and bleeding gastric varices, emergency endoscopic sclerotherapy achieved hemostasis in 85% (84); patients who did not respond to sclerotherapy underwent emergency surgery.

Immunosuppression/AIDS

Unusual gastric infections develop in AIDS patients, and, in fact, occasionally an initial manifestation of AIDS is a cytomegaloviral or other rare gastric infection. Gastroduodenal involvement with Mycobacterium avium is a cause for hemorrhage (85).

Gastric toxoplasmosis is rare even in AIDS, presenting with gastric wall thickening; thickened rugae, and at times even an ulcer.

A barium study in AIDS patients with cryptosporidium gastropathy reveals antral narrowing resembling a carcinoma or Crohn’s gastritis; these patients tend to develop varying degrees of gastric obstruction, with the narrowing presumably related to underlying cryptosporidiosis; obstruction clears following therapy.

Emphysematous gastritis, gastric wall necrosis, and gastric perforation are rare conditions reported in HIV-infected patients. Gastric necrosis in one HIV-positive patient was believed to be secondary to a vasculitis (86).

Human herpesvirus type 8 (HHV-8 virus), belonging to the lymphotropic herpes family, is associated with lymphoid neoplasms in immunodeficient patients and with Kaposi’s sarcomas (87). This unusual virus contains genes encoding oncoproteins and is believed to also have a role in multiple myeloma, Waldenström’s macroglobulinemia and possibly in sarcoidosis.

Non-Hodgkin’s lymphoma is considerably more prevalent in AIDS patients than in the general population. Lymphoma tends to be generalized, often involving the gastrointestinal tract. Most are B-cell lymphomas.

AIDS-related Kaposi’s sarcomas occur primarily in homosexual patients. Endoscopic US identifies a hypoechoic and nonhomogeneous lesion involving either the submucosa or both the mucosa and submucosa (88).

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Postoperative Stomach

Cancer

After a hemigastrectomy, such as for peptic ulcer disease, mucosal dysplasia develops and these patients are at increased risk of developing a carcinoma, often called gastric stump or remnant cancer. These cancers start developing more than 10 years after hemigastrectomy. Biopsy detection of severe dysplasia is a worrisome sign and in this subgroup about half eventually develop an adenocarcinoma, at times at multiple sites. These gastric remnant cancers behave similarly to other gastric cancers.

After Fundoplication

Lumen obstruction after a fundoplication is due to either surrounding edema or too tight of a wrap. The former clears as edema subsides.

Rarely, the stomach herniates proximally through a fundoplication wrap. A gastric perforation can develop within the thoracic cavity, presumably on an ischemic basis.

Afferent Loop Syndrome

Afferent loop obstruction (syndrome) is a complication of a hemigastrectomy and gastrojejunostomy (Billroth II operation) (Fig. 2.33). Most of these obstructions manifest early after surgery, but an occasional stricture develops years later. Obstructive jaundice is a common presentation in these patients, although some have sudden onset of abdominal pain. Afferent loop obstruction is also a cause of recurrent acute pancreatitis.

Adhesions, kinking, internal herniation, or intussusception are causes of early obstruction, whereas stenosis and neoplasm lead to obstruction years later. Some patients do not have actual mechanical obstruction but preferential gastric emptying into the afferent loop leads to chronic distension, a condition more common in a left-to-right rather than a right-to-left gastrojejunostomy. In these latter patients an efferent loop obstruction is also in the differential diagnosis.

Computed tomography reveals a dilated, fluid-filled afferent loop. High-quality conventional radiographs also identify a fluid-filled

afferent loop, suggesting the diagnosis. An occasional afferent loop syndrome is detected on a postoperative cholangiogram. A barium study should be diagnostic.

A patient developed a large duodenal enterolith in a dilated afferent loop 24 years after a Billroth II anastomosis (89).

Intussusception

An infrequent complication after a Billroth II anastomosis is jejunogastric intussusception (Fig. 2.34). Most often the intussusceptum consists of the efferent loop; less often the afferent loop is involved. Some of these intussusceptions are associated with gastric outlet obstruction, whereas with others the patients are relatively asymptomatic due to partial obstruction. Occasionally this complication develops late after surgery.

Postpancreaticoenteric Anastomosis

A pancreaticoduodenectomy as therapy for carcinoma of the ampulla of Vater, first described by Whipple, currently consists of a hepaticojejunostomy, a gastroor duodenojejunostomy and a pancreaticoenteric anastomosis (usually a pancreaticojejunostomy). One complication of

this operation is breakdown of the pancreaticojejunostomy anastomosis, a region not directly accessible to imaging. Occasionally, a resultant fistula is first detected by contrast injected into

Figure 2.34. Jejunogastric intussusception in a patient with a Billroth II anastomosis. The intragastric valvulae conniventes have a coil spring appearance (arrows). A jejunal feeding tube is in place.

adjacently placed drains. Surgeons attempt to decrease breakdown of the pancreaticoenteric anastomosis by modifying the above technique and performing a pancreaticogastrostomy, where the residual portion of the pancreas drains into the stomach. Radiographically, the anastomosis presents as a broad-based intraluminal mass that should not be confused with a neoplasm.

Morbid Obesity Surgery

Over the years a number of surgical procedures have been designed to control morbid obesity. Because of complications, often metabolic in nature, a jejunoileal bypass is no longer performed. A number of patients with a jejunoileal bypass have had reversal of their bypass, at times with weight gain to previous levels.

A common indication for a barium study is failure to lose weight postoperatively. Not uncommonly these postoperative patients complain of nausea, vomiting, and an inability to eat. A barium study reveals typical postoperative findings with no complications, yet the patients are gradually losing weight and cannot understand why they are unable to eat almost constantly.

Helical CT not only identifies normal postoperative anatomy but is also very useful in detecting complications in these patients (90). Some loculated fluid collections are unrelated to a leak. One should also keep in mind that the residual fundus tends to mimic a loculated fluid collection.

Gastric Bypass

Gastric bypass results in a small proximal gastric pouch that drains via a gastrojejunostomy. The jejunostomy portion consists of a jejunal loop, a more distant jejunojejunostomy, or a Roux-en-Y (Fig. 2.35). The latter two are designed to prevent bile reflux into the gastric pouch. In most patients a gastric bypass leads to significantly more weight loss than with gastroplasty, and currently many surgeons favor gastric bypass. These patients have a high prevalence of gallstones, and some surgeons perform a cholecystectomy at the time of initial surgery.

The major early complication is a leak resulting in an abscess or even peritonitis. A contrast

Figure 2.35. Appearance of a side-to-side gastric bypass combined with a Roux-en-Y. A double row of staples divides the stomach into a smaller proximal pouch and a larger excluded segment.

study should be diagnostic. A temptation to simply instill contrast via a nasogastric tube and obtain one or two radiographs without fluoroscopic guidance should be avoided; invariably such an approach leads to a suboptimal and a missed diagnosis in these obese, often criticallyill patients.

Radiographic study of afferent limb obstruction (the bypassed segment) shows a dilated distal gastric segment and a dilated duodenojejunal loop. The proximal jejunal limb tends to be narrowed as it passes through the transverse mesocolon (91), but actual obstruction at this site is not common.

Late complications encountered with a gastric bypass include anastomotic stenosis and marginal ulcer.

Gastroplasty

Gastroplasty consists of gastric stapling to produce a small pouch at the gastric cardia, with a small opening left into the distal gastric segment. Initially transverse gastric stapling (partitioning) was in vogue, but subsequently

STOMACH

vertical stapling (Mason’s vertical banded gastroplasty) became more popular. A silicone ring or polypropylene mesh surrounds the gastric opening.

Laparoscopic gastroplasty leads to about 4% of patients developing early complications (perforation, early slippage, and respiratory problems) and 6% late complications (late slippage, incisional hernia, and port problems) (92). Other complications include gastroesophageal reflux, mesh erosion into the stomach lumen, and staple-line disruption with resultant weight gain.

Reflux esophagitis tends to be more severe with a gastroplasty, although some surgeons believe that gastric restriction operations do not increase the risk of reflux if a functioning antireflux barrier is also performed.

An upper gastrointestinal examination with barium detects both early and late postoperative complications.

laparoscopic gastric banding around the fundus with an inflatable band connected by a thin tube to an access port permits port puncture and stomal adjustment between the pouch and the stomach for optimal weight loss. Postoperative fluoroscopy confirms the band position and is used for stomal adjustment.

Unsatisfactory weight loss occurred in 20% of 98 consecutive postbanding patients (93); late complications, developing in about one third of patients, consist of pouch dilation, herniation, intragastric band penetration (94), disconnection or leaking port (95), and port infection. An unusual complication is a decrease in stoma caliber due to gastritis, found in 3% of patients in one study (96). Marked gastric pouch dilation is a less common complication.

Most complications are readily detected with a contrast study. Computed tomography detects port infection.

Gastric Banding

Gastric banding is an alternative procedure to gastric bypass and gastroplasty (Fig. 2.36). Initially more popular in Europe, it is gaining acceptance in the United States. Adjustable

Figure 2.36. Vertical banded gastroplasty. A mesh is wrapped around the stoma located close to the lesser curvature.

Biliopancreatic Diversion

Currently biliopancreatic diversion is gaining in popularity and preliminary results are promising. It consists of a distal gastrectomy and formation of a long Roux-en-Y loop. The biliopancreatic loop from the duodenum inserts at an enteroenterostomy about 200cm distal to the gastroenterostomy and about 50cm proximal to the ileocecal valve. Because the biliopancreatic loop is not in direct continuity with the stomach, it does not contain gas. Obstruction of this loop thus leads to CT and US simply showing a markedly dilated, fluid-filled loop of bowel. Obstruction of the gastroenterostomy loop, on the other hand, has the typical radiologic findings of obstruction.

Retained Gastric Antrum

One of the indications for a Billroth II gastrojejunostomy is intractable peptic ulcer disease. If antral mucosa is left behind or if ectopic gastrin-producing cells are present in the retained duodenum,the resultant gastrin output tends to reactivate the patient’s peptic ulcer symptoms. The blind afferent loop tip cannot be studied because it is not accessible either to a barium study or endoscopy.

A Tc-99m-pertechnetate scan (Meckel’s scan) is worthwhile in this setting. Tracer uptake is

Figure 2.37. A stomal ulcer (arrow) has developed after a previous gastroduodenostomy.

evident both in the residual gastric pouch and in any retained antral remnant. The latter is identified as a focus of radioactivity in the region of the duodenal stump. The reason for such antral uptake, which normally does not contain hydrochloric acid secreting parietal cells, is that pertechnetate uptake is primarily by mucin-secreting cells, which are located throughout the stomach.

After a simple gastrojejunostomy, ulcers tend to occur in the jejunum, opposite the anastomosis (Fig. 2.37).

Gastrostomy

A basic question concerning percutaneous gastrostomies is whether the initial decision to insert a gastrostomy is appropriate. Some of these patients have a poor subsequent clinical course. In a retrospective review, 33% of the surrogates interviewed were uncertain whether a decision to proceed to gastrostomy feedings was correct (97).

Whether a gastrojejunostomy feeding tube with its reduced risk of gastroesophageal reflux is preferred over a gastrostomy should be individualized. Most gastrostomies are permanent, although indications exist for a temporary one: during recovery of swallowing, preparation for surgery with a more proximal obstruction, and

ADVANCED IMAGING OF THE ABDOMEN

for drainage of some fistulas. Gastrostomies are performed surgically, endoscopically assisted, or by using a percutaneous approach with imaging guidance. Among surgeons, a laparoscopicassisted gastrostomy is becoming popular. A higher tube placement success rate is achieved when using an imaging technique rather than endoscopy (98); at times a hybrid percutaneousoral approach is easiest. Procedure related mortality rates are highest for surgically placed gastrostomies and lowest with an imaging approach.

Instead of fluoroscopy, at times US is used to guide gastric puncture. Computed tomogra- phy–guided gastrostomy or gastroenterostomy is also feasible and often is technically successful when an endoscopic approach is not possible or had failed. Some believe that gastropexy is not necessary, but gastropexy does prevent tube displacement resulting in leakage.

Percutaneous retrograde insertion of gastrostomy or gastrojejunostomy tubes can be performed safely in children. Similar to adults, complications include an extragastric tube location and small bowel or colon transgression. Marked hepatosplenomegaly in children occasionally denies adequate access.

Percutaneous gastrostomy tubes are readily inserted under fluoroscopic guidance using a modified Seldinger technique and without general sedation. Initially this technique was used mostly for patients with an obstructed esophagus where percutaneous endoscopic gastrostomy was not feasible, yet the ease of fluoroscopic gastrostomy tube insertion has led to its wider acceptance. Few contraindications exist for this technique; it has a high success rate and is associated with few serious complications (99).

One option is a pull-type gastrostomy tube, consisting of retrograde esophageal catheterization through the stomach and a gastrostomy tube then pulled through from the mouth into the stomach. This technique, performed either by endoscopists or interventionalists, has a high success rate and few complications.

Ascites is often considered a relative contraindication to a percutaneous gastrostomy, although gastropexy overcomes some of the problems encountered in this subset of patients. Initial paracentesis and prevention of fluid reaccumulation, together with gastropexy, aid in preventing pericatheter leakage. A gastrostomy

STOMACH

or gastrojejunostomy with gastropexy in 45 consecutive patients with ascites was associated with a 7% rate of major complications and one procedure-related death (100); of note is that half of the complications occurred in a setting of peritoneal spread by ovarian carcinoma.

Out of 643 patients referred for fluoroscopically assisted percutaneous gastrostomy or gastrojejunostomy, a catheter could not be placed in 4% of patients due to overlying viscera or prior gastric surgery (101); catheter revision was necessary in 14%, mostly due to tube dislodgment.

Complications associated with percutaneous gastrostomy insertion include bleeding, obstruction, gastric perforation, and peritonitis. Minor leaks and a postinsertion pneumoperitoneum are not uncommon. Catheter dislodgment occurred in 68% of 25 balloon-retained catheters (102), 11% of 75 pigtail-retained catheters (103), and in none of 55 mushroomretained gastrostomy catheters, and the authors concluded that mushroom catheters are more durable and preferred whenever possible.

Gastrostomy tube insertion through the transverse colon results in a cologastrocutaneous fistula or a colocutaneous fistula. Necrotizing fasciitis is a rare complication. Inserted through the gastrocolic ligament, a gastrostomy tube can end up in the lesser sac, superficially mimicking a correctly inserted tube. Occasional gastric pneumatosis develops after tube gastrostomy. Gastric wall dissection occurred during percutaneous gastrostomy, believed to be due to a tangential puncture of the stomach wall (104).

Several perforations have been associated with a Wills-Oglesby-type gastrostomy tube. Perforations in five patients were related to the distal catheter limb (105); these perforations occurred several months after tube placement, did not lead to peritonitis, and were managed medically.

A gastrostomy catheter can migrate distally, with the catheter tip lodging in the ileum. Occasionally a gastrostomy tube is cut and the inner tube button allowed to pass through the gastrointestinal tract. This procedure has been questioned, as the button has led to bowel obstruction.

In a setting of a malignancy, tumor seeding can occur after insertion of a percutaneous gastrostomy. This complication is more often

encountered after endoscopic rather than imaging percutaneous tube insertion (106), probably due to direct tumor implantation during the endoscopic procedure. CT identifies a stomal implant as a lobulated soft tissue tumor in the abdominal wall, less so at the entry or exit sites.

Examination Complications

Rather than use the term complications to describe misadventures during endoscopy, the term negative outcomes has been proposed (107); this latter system defines, classifies, and grades negative outcomes using a scoring system based on several measures:

Immediate negative outcome (O): effect of complication on completion of endoscopy, change in level of care, change in length of hospitalization, necessity for new invasive procedures

Disability (D): a residual or chronic negative outcome caused by a complication

Death (D): a value varying with circumstances

A quantitative measure is obtained by using an overall ODD score.

Positive blood cultures were detected in 25% of patients undergoing gastroscopy (108);

Staphylococcus species and Streptococcus species were most common.

References

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