Acute Gastritis and Enteritis

D. Regent, V. Croise-Laurent, J. Mathias, A. Fairise,H. Ropion-Michaux, and C. Proust

Contents

1 Acute Gastritis . . . . . . . . . . . . . . . . . . . . . . . .1.1 General Characteristics . . . . . . . . . . . . . . . . . . .1.2 The Main Aetiological Forms of Acute Gastritis (Levine

2008; Kim and Pickhardt 2007; Gelfand et al. 1999) . .1.3 Diagnosis of Acute Gastritis by CT Scan . . . . . . .

2 Acute Duodenitis and Enteritis . . . . . . . . . . . . .2.1 General Characteristics (Macari and Balthazar 2001;

Thoeni and Cello 2006; D’Almeida et al. 2008;Macari et al. 2007) . . . . . . . . . . . . . . . . . . . . . .

2.2 Acute Infectious Conditions of the Duodenumand Small Intestine (Mazzie et al. 2007) . . . . . . .

2.3 Vascular Acute Inflammatory Conditionsof the Duodenum and Small Intestine . . . . . . . . .

2.4 The Acute Appearance of Crohn’s Diseasein the Small Intestine (Madureira 2004;Gourtsoyianni et al. 2009) . . . . . . . . . . . . . . . . .

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

In acute gastric or small bowel conditions, whetherthey are infectious, inflammatory, or ischemic, theCT scan objectifies submucosal oedema with pari-etal stratification, producing ‘target’ or ‘doublehalo’ images that can be easily analysed in venousphasis. Precise analysis of proximal peritonealreactions and of endoluminal content are the firststeps of diagnostic approach In an acute clinicalcontext, a number of hypotheses must be discussed(perforation, infection, arterial ischaemia, capillaryhyperpermeability, congestion by portal venousstasis, etc.) certain of which may be supported byabdominal/pelvic exploration, as a general rulecomplemented by thoracic exploration if there areno contra-indications for the radiation risk (youngsubjects and women of childbearing potential).In all cases, the clinical context and laboratory testsare fundamental for orientating the diagnosis: ahistory of abdominal pain and diarrhoea, a state ofacquired immunosuppression, a recent stay in acountry where there are endemic parasites, apurpuric rash on the lower limbs, a marked inflam-matory syndrome seen in laboratory tests, etc., areall signs providing pointers for the right directionwhich one needs to know how to find out by precise,directed questioning and clinical examination

1 Acute Gastritis

There are many different causes of acute gastritis. Themost frequent complaints are due to limited histo-logical lesions of the mucosa. They are diagnosed

D. Régent (&), V. Croisé-Laurent, J. Mathias, A. Fairise,H. Ropion-Michaux, and C. ProustService de Radiologie Adultes, CHU Nancy-Brabois,Rue du Morvan, 54511 Vandoeuvre les Nancy Cedex,Francee-mail: d.regent@chu-nancy.fr

Medical Radiology. Diagnostic imaging, DOI: 10.1007/174_2010_84, � Springer-Verlag Berlin Heidelberg 2010

exclusively by endoscopy and histology after biopsy.Only deep acute gastric lesions extending into thesubmucosa, and the muscular layers can be seenduring a CT examination performed because of apainful set of hyperalgesic epigastric symptoms withvomiting which may be haemorrhagic.

1.1 General Characteristics

The term ‘acute gastritis’ covers a very wide spectrumof inflammatory damage to the gastric mucosa, dif-ferentiated by distinct characteristics which dependon the depth of the parietal damage and the physio-pathological mechanisms involved.

Two major groups can be differentiated:• erosive gastritis which includes the superficial

forms, deep lesions and haemorrhagic forms;• non-erosive gastritis, the main form of which is

gastritis caused by Helicobacter pylori.Most frequently, where involvement is limited to the

mucosa, there is little or no correlation between themicroscopic anatomopathological data, and the clinicalsymptoms which are often absent or non-specific(epigastric discomfort, nausea, vomiting). Diagnosis isessentially by endoscopy and biopsy, and there is noplace here for any radiological method. There are manypossible causes: alcohol, bile reflux, medicinal drugs, etc.

In severe erosive gastritis, in particular where thereare deep ulcerations, and where the acute clinicalpicture reveals painful epigastric seizures associatedwith vomiting or haematemesis, a CT scan can beperformed quite early and provides important semi-otic data for a positive and differential diagnosis.

1.2 The Main Aetiological Forms of AcuteGastritis (Levine 2008; Kim andPickhardt 2007; Gelfand et al. 1999)

1.2.1 Reactive Acute Gastritis or ReactiveGastropathy

There are many causes: non-steroidal anti-inflammatorydrugs (NSAIDs), platelet aggregation inhibitors of theaspirin type whether they are administered orally orsystemically, at therapeutic doses or in excessive doses,alcohol, stress, bile reflux and ischaemia. In NSAIDgastritis, secondary to oral ingestion, the lesions arepreferentially sited on the greater curvature due to theeffect of gravity (Table 1).

1.2.2 Bacterial GastritisPhlegmonous gastritis is severe acute damage ofbacterial origin, caused by various microorganismssuch as Escherichia coli, Pseudomonas aeruginosa,Clostridium perfringens, Enterobacter aerogenes,Proteus vulgaris, Staphylococcus aureus or non-haemolytic streptococci; more rarely, its origin maybe fungal (candidiasis, mucormycosis) (Jung et al.2003; Asrani et al. 2007).

In general, it occurs in subjects in a poor generalstate of health. It is often secondary to massiveingestion of alcohol and coexists with respiratoryinfections. It is also found in AIDS patients (Fig. 1).

The infection affects the deep layers, the submu-cosa, muscularis propria and serous, it may have agangrenous appearance and lead to peritonitis by per-foration. The prognosis is very unfavourable, with amortality rate in the order of 65%, even with treatment.

Table 1 Aetiology of acute gastritis and gastropathies

Drug-induced NSAIDs and aspirin

Cocaine

Colchicine

Antimitotic agents

Massive acute alcoholism withhighly alcoholic drinks: whisky,vodka, gin

Bacterial infections H. Pylori

H. Heilmani

Streptococci

Staphylococci

Enterobacteria of thegenus Proteus

Bacteria of the genusClostridium

E. coli

Tuberculosis

Syphilis

Viral infections CMV

Fungal infections C. albicans

Histoplasmosis

Parasitic infections Anisakiasis

Cardiogenic stress and shock

Irradiation

Allergies and food poisoning

Biliary reflux

Ischaemia

D. Regent et al.

An intramural gastric abscess is a localised formof suppurative bacterial gastritis. It is a conditionknown since the time of Galen; diagnosis can bemade with a CT scan when a liquid collectionis seen within a gastric wall thickened byinflammation.

Other infectious causes of severe acute gastritisinclude:• Viral infections, particularly cytomegalovirus infec-

tions, generally seen in immunosuppressed subjects,particularly in transplanted patients, those withcancer, and in AIDS. CMV gastritis may behaemorrhagic (Fig. 2). Acute gastritis caused byherpes simplex virus is exceptional.

• Acute fungal infections, in particular caused byCandida albicans, may be serious and even lethal.They occur above all in immunosuppressed sub-jects. This is also the case for the uncommon typeof gastritis due to mucormycosis (pre-disposingfactors: above all diabetes, but also leukaemia,lymphoma, chronic renal impairment, solid organtransplantation, septicaemia, severe burns, malnu-trition, corticosteroid treatment and long-termantibiotic therapy). Histoplasma capsulatum canalso be the cause of ulcerated gastritis which can be

erosive or with large rugae, but does not generallyoccur in an acute form.

• Acute gastric parasitic infections, including anisaki-asis caused by a nematode contaminating sushi orother dishes based on raw fish. The worm digs into thegastric mucosa along the greater curvature, leading tosymptoms of acute pain that can persist for severaldays, linked to erosive and/or ulcerative lesionsassociated with large oedematous folds (Fig. 3).

• Gastric tuberculosis is generally a subacute condi-tion most often found in the context of immuno-suppression (AIDS) or disseminated tuberculosis.Secondary syphilis has become a rare cause of

gastritis that is generally subacute or chronic.

1.2.3 Haemorrhagic and UlceronecroticAcute Gastritis

As a general rule, these are seen in patients who arecritically ill, particularly with shock, severe infections,respiratory insufficiency or acute renal impairment,head injuries, extensive burns, etc.). The mechanism isessentially ischaemia secondary to hypotension andhypovolaemic shock, to which are added the effects ofthe vasoconstrictor treatment administered, but theaetiology often remains unknown.

Fig. 1 Phlegmonous gastritisdue to Pseudomonasaeruginosa (obs. by C. Aubé,Angers). Very considerableoedematous thickening of thewhole of the gastric body andfundus, in places exceeding20 mm

Acute Gastritis and Enteritis

The lesions, essentially petechial or diffusehaemorrhages are similar to those seen in acutedrug-induced acute gastritis (aspirin, NSAID), exceptthat their distribution is different, occurring in thefundus and body of the stomach.

1.2.4 Acute Gastritis Caused by Physicalor Chemical Agents

Acute radiation gastritis is seen after exposure greaterthan 16 Gy and more frequently affects the antrum thanthe fundus; it can be complicated by pyloric stenosis.

Fig. 3 Anisakiasis (obs. byDr J. M. Hervochon, LaRochelle). Acute painfulepigastric symptoms in ayoung woman. Veryconsiderable diffuseoedematous thickening of thewhole gastric body and antralregion (white arrow) withoedematous infiltration of thelesser omentum. Aetiologicalquestioning revealed recentingestion of sushi andendoscopy confirmedanisakiasis

Fig. 2 Gastritis due to CMV. Irregular thickening of the antralwall with submucosal hypodensity. Presence of eroded parietalnodules on the double contrast image. Endoscopy confirmed the

presence of whitish ulcerations surrounded by hypervascular-ised folds of a nodular character

D. Regent et al.

Caustic gastritis is the consequence of accidentalor voluntary ingestion of corrosive substances, usu-ally acids (Fig. 4).

In both cases, a CT scan shows inflammatoryparietal thickening and contributes to revealing earlycomplications and associated lesions.

1.2.5 Idiopathic Inflammatory Gastritis MayQuite Rarely Present in an AcuteClinical Picture

• Crohn’s disease only affects the stomach in 2–7%of patients in whom the classic ileal and/or coliclocations coexist.

• Eosinophilic gastritis is often seen in the context ofeosinophilic gastroenteritis but it may be

encountered in association with many other condi-tions, such as food allergies (eggs, milk, soya pro-teins), collagenosis, digestive parasitosis, gastriccancer, lymphoma, Crohn’s disease, vasculitis, drugallergies or H. pylori infection. The eosinophilicinfiltrate can be limited to the mucosa or extend tothe whole intestinal wall.

1.3 Diagnosis of Acute Gastritis by CTScan

The semiotic data on which the positive diagnosis ofacute gastritis and possibly the orientation of theaetiological diagnosis may be based need to be

Fig. 4 Acute oesophagitis and gastritis after ingesting bleach. The CT scan confirmed diffuse circumferential thickening of thelower oesophagus and all gastric walls with marked submucosal oedema

Acute Gastritis and Enteritis

considered. Moreover, the direction taken by thedifferential diagnosis must take into considerationthe other possible causes of ‘acute’ thickening of thegastric wall.

1.3.1 Positive Diagnostic Data for AcuteGastritis on a CT Scan

• The main CT scan signs are seen in major trans-mural acute inflammatory conditions, in particularin bacterial phlegmonous gastritis, and combine:– localised or diffuse thickening of the gastric wall

with visible stratification indicating the oedemaof the muco–submucosa complex; enhancementof the mucosal and muscle capillary networks,seen better in venous phasis with the ‘target sign’appearance and best perceived if the stomach isdistended with liquid (Jung et al. 2007). In othercases, a ‘double halo’ appears, defined as thejuxtaposition of two concentric rings, the moreinternal, hypodense ring corresponding to theoedema of the submucosa, while the externalhyperdense ring corresponds to the thickening ofthe muscularis propria. This semiotic data arevaluable for differentiating inflammatory parietalthickening from tumoral thickening (speciallyfrom an adenocarcinoma in which the collagenfibrous reaction stroma can be objectified by lateenhancement in the post-equilibrium phase).

– Oedematous hypertrophy of regular or nodularrugae is easier to analyse in a stomach distendedwith liquid.

• Phlegmonous gastritis is a suppurative bacterialinfection of the gastric wall. It can present in adiffuse or localised form, generally antral. Clini-cally, it appears in the form of an acute abdomencombined with an infectious syndrome, epigastricpain, nausea, vomiting—sometimes haemorrhagicin heavy drinkers—often following a seriousrespiratory infection. The different imaging tech-niques show the presence of localised or morediffuse parietal thickening, specially concerning thesubmucosa, that can be difficult to differentiatefrom a gastric adenocarcinoma in a scan (and byendoscopy!). The acute clinical context of therevelation, a septic and inflammatory picture inlaboratory tests, an inflammatory reaction of theperitoneal serosa (thickened appearance with per-sistent enhancement, surrounding liquid reaction,

etc.) even, in certain cases, the appearance of apartially liquid parietal collection (gastric wallabscess) may orientate the diagnosis.

• The presence of gas in a thickened gastric wall is akey sign that can be observed in various circum-stances which must be clearly differentiated:– Emphysematous gastritis is either a form of

bacterial infectious gastritis caused by microor-ganisms producing large quantities of gas (by amechanism similar to that incriminated inemphysematous cholecystitis) or phlegmonousgastritis of bacterial or fungal origin which canform an abscess (Jung et al. 2007; Loi et al.2007). The appearance in the scan combinesmore or less extensive thickening of the gastricwall, generally in the fundus and the greatercurvature with irregular bubbles of gas in spotsor bunches; these gas bubbles remain in placewhatever the subject’s position or the degree ofaspiration by the naso-gastric tube naso-gastricaspiration.

– Gastric emphysema is usually a regular linearinfiltration of the gastric wall, which is not thick-ened or little thickened, by gas from the gastriclumen, the surface of the peritoneal serosa or fromthe connections of the stomach with the oesoph-agus or duodenum. Gastric emphysema usuallyresults from barotrauma without any infectiousbacterial involvement; it is particularly seen inchronic liquid and or gas distension of the stomachwhatever the mechanical (neoplastic antro-pyloricstenosis or stenosis of inflammatory origin by anulcerative disease) or functional nature (gastro-paresis) (Figs. 5 and 6) (Buyt et al. 2003). Thisgastric emphysema is usually asymptomatic and isgenerally reabsorbed without treatment. A casehas been reported in a 16-year-old adolescentboy, after ingestion of a large quantity of CocaCola. It was combined with hepatic portal venousgas and duodenal wall emphysema in a seriousclinical condition which resolved with treatment(Hadas-Halpren et al. 1993).

The prognosis for these various conditions istherefore very different, and the presence of gas in thegastric wall must be carefully correlated with theclinical situation and probabilistic physiopathologicalhypotheses to correctly orientate therapeuticmanagement.

D. Regent et al.

1.3.2 Differential Diagnosis of AcuteGastritis on a CT Scan

A not inconsiderable number of acute abdominalclinical pictures can be accompanied by markedthickening of the gastric wall with muco-submucosal

oedema, the origin of the ‘target’ signs on thescan section. Causes may be local or moreremote; they must be looked into systematicallyto avoid upsetting diagnostic or therapeuticorientations.

Fig. 5 Gastric emphysema ina patient with ankylosingspondylitis. The intraparietalgaseous images in a stomachdistended with liquid arealready clearly visible on theplain film pictures. The CTscan confirms the cysticgaseous dissection. Thegastric emphysema occurredwith gastroparesis. Clinicaland radiological resolutionafter aspiration of the gastriccontents

Fig. 6 Gastric emphysema ina 74-year-old patient withhepatic portal venous gas, onD3 after fitting a total hipprosthesis. The abdominalplain film showedconsiderable gaseousdistension of the stomach and,to a lesser degree, of the smallintestine and colon, the wholepicture corresponding topostoperative ileus. The CTscan confirmed the parietalgaseous dissection of thestomach (white arrow) andhepatic portal venous gas(point of black arrow). Thecondition evolved favourablyafter resumption of transit

Acute Gastritis and Enteritis

• Parietal pneumatosis of the stomach, seen in thecontext of a painful acute abdomen and usuallyaccompanied by intrahepatic portal venous gas, mustbe clearly differentiated from parietal emphysema.It is associated with the absence of parietalenhancement after injection of contrast medium andgenerally indicates transmural ischaemic necrosis ofthe stomach (Fig. 7). It can be observed after startingchemotherapy in carcinomas (Fig. 8).

• Portal hypertensive gastropathy is a rare cause ofdigestive haemorrhage, and is generally not verysevere in cirrhotic patients. Its probably multifac-torial physiopathological mechanism remains opento discussion, involving raising the pressure inthe portal system, increasing splanchnic bloodflow and local modifications to the regulation of

microcirculation. The prevalence of portal hyper-tensive gastropathy varies from 7 to 98% in theseries published, depending on the diagnostic cri-teria and methods chosen for selecting patients, etc.The circumferential thickening of the gastric wallwith an image of parietal stratification by submu-cosal oedema, seen in severe portal hypertensionwith ascitic decompensation, may suggest thediagnosis (Figs. 9 and 10) but it is known thatthere is no correlation between the portal pressurevalues measured, the severity of the cirrhosis, thedegree of cellular dysfunction and the severity ofthe gastropathy when viewed endoscopically(Curvelo et al. 2000). Multiphase explorationobjectifies defective segmental or subsegmentalperfusion of the mucosa of the gastric body or

Fig. 7 Gastric necrosis.Transmural gastric necrosis ina 24-year-old patient with anantiphospholipid antibodysyndrome and high-gradestenosis of the coeliac trunkby the arcuate ligament of thediaphragm. A CT scan wasperformed because ofhyperalgesic painfulepigastric symptoms. The CTscan confirmed the presenceof massive gaseous dissectionof the walls of the stomachwhich were not enhancedafter contrast mediuminjection. Presence of a largequantity of intraperitonealfluid but the patient has aventriculoperitoneal shunt fora cerebral expansive lesion.Hepatic portal venous gas ispresent. The surgicalprocedure confirmedtransmural necrosis of all thegastric walls

D. Regent et al.

fundus. This has been observed to disappear in theportal phase or during post-equilibrium in 75% ofcases of endoscopically controlled portal hyper-tensive gastropathy but in only 11% of cirrhoticpatients without endoscopically visible gastropathy.This method would therefore seem to provideuseful, more specific information for diagnosis(Kim et al. 2008).

• Inflammatory reactions of the gastric wall duringacute pancreatitis are frequent (1/3 of cases) andmust be clearly identified. They have been knownfor a long time (Balthazar 1979) and predominateon the posterior wall, resulting in generally exten-sive oedematous muco-submucosal thickening incontact with anterior peri-pancreatic infiltrationsand collections, whether recent or organised (true

pseudocysts) (Figs. 11, 12, and 13). Analogousimages can be seen on contact with infected col-lections (left subphrenic abscesses) complicatingulcerous or surgical perforations (Chen et al. 2007;Brown et al. 1982).

• Persistent pseudotumoral hypertrophy of the gastricwall, in a context of epigastralgia which may bemajor, which is resistant to anti-ulcer treatment, in ayoung subject (in his 20 or 30s), with heterogeneousdensity and above all progressive enhancementincreasing in the areas of tissue in the post-equilibrium phase, indicating the significant presenceof collagen, should bring to mind an inflammatorypseudotumour (Fig. 14). Only surgical ablation canconfirm the diagnosis as endoscopic biopsies cannotreach the significant areas.

Fig. 8 Tumoral necrosis ina 30-year-old patient with avery large anaplastic gastricadenocarcinoma. a, b Initialfindings: massive thickeningof the gastric wall with veryvoluminous hypodenseadenopathies of the lesseromentum, coeliacs andsplenic hilum. Presence ofhepatic metastasis (blackarrow). c-f A week afterthe start of chemotherapy:massive necrosis of the gastricwall tumour with lack ofparietal enhancement andgaseous dissection. Massivemetastatic and lymph nodedissemination

Acute Gastritis and Enteritis

• The presence of gastric trichophytobezoar, gener-ally seen in trichotillomaniac girls, is associatedwith diffuse regular thickening, with intense, per-sistent enhancement of the gastric wall and nohypertrophy of the rugae (Fig. 15). The trichophy-tobezoar may extend a long way into the lumen ofthe duodenum and small intestine, producing

Rapunzel’s syndrome, named after the Grimmbrothers’ story with this name.

• Other possible causes of inflammatory thickeningof the gastric wall which can be seen in the clinicalcontext of an acute abdomen include:– Lymphocytic varioliform gastritis, for which an

immunoallergic origin is plausible. It appears

Fig. 9 Portal hypertensivegastritis. A 72-year-oldcirrhotic patient with portalcavernoma and chroniccalcifying pancreatitis. Veryconsiderable submucosaloedema of the stomach wall(straight white arrow) andcolon (curved arrow) in acontext of extremegeneralised oedema due todecompensated cirrhosis. Theparietal submucosalthickening exceeds 15 mm inthe body of the stomach

Fig. 10 Portal hypertensivegastritis in a patient withascitic decompensatedcirrhosis. Very considerablesubmucosal oedema of thewhole stomach predominantlyin the fundic region (whitearrow)

D. Regent et al.

as parietal thickening and large rugae withumbilicated nodules viewed by endoscopy, anabundant liquid content in the stomach sometimes

accompanied by gastric loss of proteins withoedema and hypoalbuminaemia. Associationswith coeliac disease, collagenous colitis,

Fig. 11 Inflammatoryreaction of the posterior wallof the fundus during acutecaudal pancreatitis. The CTscan objectifies the parietalthickening limited to the floorand posterior wall of thefundus (white arrow) in directrelation with moderateinflammation of the caudalpancreas

Fig. 12 Acute caudalpancreatitis with pseudocystand peritoneal fluid effusion.The CT scan confirmsmassive gastric parietalthickening affecting the lessercurvature (point of blackarrow), the fundus and theantral region (curved whitearrow). The pseudocyst(white arrow) is the site ofbleeding responsible for thehyperdensity of the lowerpart. Gastric parietalthickening is massive,exceeding 20 mm

Acute Gastritis and Enteritis

lymphocytic colitis, Ménétrier’s disease andH. pylori gastritis have been described.

– Zollinger–Ellison syndrome with diffuse thick-ening of the gastric wall and rugae in the fundus

with spontaneous liquid distension of the lumenby hypersecretion linked with hypergastrinaemia(Fig. 16). The endocrine lesion must be sought inthe pancreatico-duodenal region; this may be

Fig. 13 Acute pancreatitiswith small caudal pancreaticpseudocyst. Presence of adiffuse oedematousinflammatory reaction of thewhole of the stomach wall

Fig. 14 Gastric inflammatory pseudotumour in a young(27-year-old) patient. Painful epigastric symptoms, ulcerouspain developing over the past 4 months resistant to PPI.Presence of parietal pseudotumoral thickening of the antral

region with massive persistent enhancement accentuated on lateimages. Surgical procedures confirmed the diagnosis of aninflammatory pseudotumour complicating an intramural antralectopic pancreas.

D. Regent et al.

small in size and hypervascularised or morevoluminous and metastatic (Fig. 17).

– Ménétrier’s disease, which can be revealed bypseudo-ulcerous pain.

– The parietal thickening is related to considerablehypertrophy of the muscularis propria and tocystic dilatation of mucosal glands, at the originof a cerebriform hypertrophy of the fundic rugae(Fig. 18). The disease essentially affects middle-aged men, usually alcohol and tobacco users; it isaccompanied by leakage of gastric protein,causing oedema and microcytic anaemia.

– Submucosal fatty metaplasia or submucosalpseudolipomatosis, thickening of the submucosawith a regular homogeneous fatty density. Initiallydescribed in chronic inflammatory conditions ofthe small intestine and colon after corticosteroidtherapy, then in patients treated by chemotherapyin which it can appear within a few weeks(Muldoney et al. 1995), it is, in fact, not unex-ceptional to see it in routine examinations,generally in overweight adults, more often males.It is easily identified because of its typical

Fig. 15 Gastric and jejunal bezoar in a young (16-year-old)female trichotillomaniac patient. The heterogeneous sphericalcontent of the gastric fundus (white asterisk) is accompanied bythickening of the gastric wall with significant persistentenhancement (a). Identical images are seen in the proximaljejunum (b) which confirmed a heterogeneous compact

endoluminal foreign body (curved white arrow). Surgicalexploration showed very considerable transparietal inflamma-tory reaction of the proximal jejunum affecting the serous side(c). The surgical procedure extracted the jejunal bezoar (d) andthe gastric trichophytobezoar (e)

Fig. 16 Gastrinoma in a 50-year-old patient. The CT scanobjectifies considerable hypertrophy of the gastric mucosalrugae with major enhancement (point of white arrow) andthe presence of a hypervascularised lesion of the head of thepancreas corresponding to the gastrinoma (black arrow). Thereis a hepatic angioma (curved black arrow)

Acute Gastritis and Enteritis

appearance (fat halo sign) (Fig. 19). It is much lessfrequent in the stomach than in the small intestineand colon where it has been observed in more than20% of adult patients in a North American study.Obviously, it must not be confused with an acuteinflammatory condition (Harisinghani et al. 2003).

2 Acute Duodenitis and Enteritis

2.1 General Characteristics (Macariand Balthazar 2001; Thoeniand Cello 2006; D’Almeida et al.2008; Macari et al. 2007)

Acute inflammatory and infectious conditions of thesmall intestine may benefit from an emergency scanproviding useful diagnostic data depending on thelocation and size of the anomalies objectified. Evidently,only severe infectious conditions that are resistant totreatment or which occur with major repercussions onthe general condition of the patient necessitating hospi-talisation will result in a scan being performed.

In general, these are above all localised transmurallesions which can be identified better, with Crohn’sdisease and its complications in the lead.

In acute diffuse conditions, whether they areinfectious or inflammatory, the scan objectifies sub-mucosal oedema with parietal stratification of theloops, producing ‘target’ or ‘double halo’ imagesthat can be easily analysed in venous time (70 s afterinjection at 3 ml/s) Gore et al. 2000. In the face ofthis, in an acute clinical context, a number ofhypotheses must be discussed (arterial ischaemia,capillary hyperpermeability, congestion by portalvenous stasis, etc.), certain of which may be sup-ported by abdominal/pelvic exploration, as a generalrule complemented by thoracic exploration if thereare no contra-indications for the radiation risk(young subjects and women of childbearingpotential).

In all cases, the clinical context and laboratorytests are fundamental for orientating the diagnosis: ahistory of abdominal pain and diarrhoea, a state ofacquired immunosuppression, a recent stay in acountry where there are endemic parasites, a pur-puric rash on the lower limbs, a marked inflamma-tory syndrome seen in laboratory tests, etc., are allsigns providing pointers for the right direction whichone needs to know how to find out by precise,directed questioning and clinical examination(Fig. 20).

Fig. 17 Gastrinoma. Veryconsiderable hypertrophy ofthe mucosal rugae over thewhole stomach with majorpersistent enhancement. Nosign of liquid hypersecretion.Presence of a smallhypervascularised nodule atthe isthmus of the pancreascorresponding to thegastrinoma

D. Regent et al.

2.2 Acute Infectious Conditionsof the Duodenum and SmallIntestine (Mazzie et al. 2007)

The aetiology of acute infections of the small intes-tine is very different depending whether they areoccurring in an immunosuppressed context or not.

In immunocompetent subjects, acute intestinalinfections are rarely investigated by a CT scan (Ma-cari et al. 2007). The possible causes include:• Giardia lamblia, a parasitosis found throughout the

world, the occurrence of which can be favoured byhypogammaglobulinaemia. This parasite attachesitself to the mucosa of the proximal small intestine(duodenum and jejunum) without invading it,

resulting in a local inflammatory response withparietal thickening by submucosal oedema andproblems of motricity, more difficult to assess oncross-sectional images than in opacifications.

• Ascaris lumbricoides is responsible for one of theworld’s most frequent parisitoses. Its diagnosis ispossible with CT scan, which shows the wormssurrounded by endoluminal liquid or distended bygas and thus appearing as linear clear areas(Hommeyer et al. 1995; Sherman and Weber 2005;Rodriguez et al. 2003). Occlusion by an endolu-minal ascaris cluster is a classic way of detectingthe parasite in countries where it is strongly ende-mic. It can be accompanied by perforation reveal-ing the condition.

Fig. 18 Ménétrier’s disease.The CT scan objectifiesconsiderable hypertrophywith an encephaloidappearance of the rugae of thestomach, major enhancementof the mucosa andsubmucosal oedema (a–c).The stomach ishypersecretory (c–d) andendoscopy (e) confirms theencephaloid hypertrophy ofthe gastric rugae

Acute Gastritis and Enteritis

• Anisakiasis is an acute infection caused by the larvaof Anisakis, a marine nematode ingested withpreparations made from raw fish (sushi, rawanchovies) or undercooked fish. The larva causesan inflammatory reaction of the intestinal wall,which can be of major importance and can extendover a length of about 10 cm. Lesions of the smallintestine may coexist with gastric and colicinvolvement and can be accompanied by allergicsymptoms. Occlusive forms have been reported,often combined with ascites. Blood hypereosino-philia occurs frequently. From the point of view ofa CT scan, the condition is very often situated in theterminal ileum and can extend into the adjacentcolon. The pathological examination confirms thepresence of an eosinophilic infiltration. An increasein specific IgE can support the diagnosis and musttherefore be systematically assayed when facedwith any histologically diagnosed ‘eosinophilicgastroenteritis’ (Fig. 19). Diagnostic certainty(endoscopic and/or in laboratory tests) can avoid asurgical procedure since the condition developsfavourably following drug-induced (or spontane-ous) elimination of the parasite (Repiso et al. 2003;Ishida et al. 2007; Ortega-Deballon et al. 2005).

• Strongyloides stercoralis causes parasitosis whichis particularly frequent in the tropics but also occursin temperate regions (e.g. the southeast of theUnited States). The larva of the parasite penetratesthe organism through the skin, migrates into therespiratory system then is coughed up and swal-lowed and reaches the duodenum at the adult stage.The process can repeat itself resulting in a cycle orendogenous reinfestation and visceral dissemina-tion, particularly encephalic in immunosuppressedpatients. The adult female infiltrates the laminapropria of the duodenum and jejunum causing aninflammatory reaction there of variable intensitydepending on the severity of the infestation.There is generally very marked hypereosinophilia.In severe forms, the dominant feature, in CT scan,is major liquid distension of the digestive lumengiving it the appearance of paralytic ileus orocclusion combined with more or less markedthickening of the wall. The colon can be simulta-neously affected with a scan appearance close tothat of ulcerative colitis (Kothary et al. 1999).

• Ileitis or enteritis due to Salmonella and Shigella,the most frequent acute infectious conditions foundin countries with a high standard of living, is seenas regular circumferential thickening of the last

Fig. 19 Gastric parietalpseudolipomatosis. Regularsubmucosal thickening offatty density has occurredover the whole gastric wall(white arrow). Thisappearance coexists with deepandroid adiposity. The patientis asymptomatic

D. Regent et al.

15 cm of the ileum wall readily extending to theadjacent colon to a lesser degree. The ‘target sign’appearance of the acute lesions is found particularlyin Shigella infections; satellite adenomegalymay be seen. The main sources of infection arepoultry meat, eggs, milk products and undercookedmeat. The severity of the symptoms is very variableand can be intense in immunosuppressed subjects.The ‘cholera-like’ very severe forms with waterydiarrhoea and the dysenteric, sometimes haemor-rhagic forms are combined with hyperallergicsymptoms with fever and possible multiple organfailure (Shigellosis) (Balthazar et al. 1966; VanWolfswinkel et al. 2008).

• Campylobacter jejuni also affects the ileocaecaljunction but it is generally a self-limiting disease.On the other hand, Salmonella typhi can lead tosevere, sometimes haemorrhagic inflammation,essentially affecting the small intestine causinghyperaemic and oedematous changes; the depthinvolved can result in perforation of the intestine.

• Yersiniosis is caused by Yersinia enterocolitica andYersinia pseudotuberculosis. They affect the rightileocolic region, presenting clinically as a pseudo-appendicitis or as acute feverish diarrhoea withterminal ileitis combined with mesenteric lymph-adenitis. Y. enterocolitica, along with the bacteriain the Salmonella order and Campylobacter, is thecause of the majority of generally self-limitingbacterial cases of gastroenteritis. Y. enterocoliticaabove all affects young subjects. The disease is dueto ingestion of contaminated food (pork meat, milk,water, tofu) or to blood transfusion. Faeces remaincontaminated for 90 days after clinical resolution.Diagnosis of yersiniosis using imaging techniquesis more the domain of echography than of CTscanning, considering the age of the subjects. Theinflammatory circumferential thickening of thewalls of the terminal ileum, the presence of regio-nal mesenteric adenopathy, the absence of an imageof appendicitis are all arguments in favour of thisdiagnosis. Severe septicaemia can be seen with thedevelopment of visceral abscesses specificallyduring treatment of iron overload with deferoxa-mine chelators (Abcarian and Demas 1991; Mat-sumoto et al. 1991; Antonopoulos et al. 2008).In subjects seropositive for human immunodefi-

ciency virus, opportunistic acute infections of thesmall intestine are now much less frequent due to the

efficacy of antiretroviral treatments which reduce theviral load and the frequency of all of these compli-cations. It is thus in cases of resistance or escapefrom these treatments (HAART or highly activeretroviral treatment) that a CT scan may be made ona patient with an acute abdomen or a febrile diar-rhoea syndrome in a seriously impaired general stateof health. The degree of immunosuppression mea-sured by the CD4 lymphocyte count is still the bestguide for the radiologist, when reading CT scanimages. The imaging technique only supplies a guideto a range of probable causes; it only providescharacteristic features in 12% of cases, and itsessential role is to contribute to evaluation of theseverity of the condition, and above all to screeningfor surgical complications (Wu et al. 1998; Kohet al. 2002).• A CD4 lymphocyte count [200/ml indicates rela-

tive immunocompetence and M tuberculosis is thenthe probable cause of the digestive disorders; with alymphocytes count between 200 and 100/ml, thereis some degree of immunosuppression and manyinfectious agents may be involved while below100 CD4/ml CMV infections, infections by MAIand cryptosporidiosis must be envisaged in the firstinstance. The other significant elements which canbe objectified and sought on CT scans include thepresence of hepatic and/or splenic infectious focallesions and light-centred adenopathies before andafter injection of contrast agent, indicating tuber-culosis, as well as the predominance of intestinallesions on the terminal ileum and caecum.

• In MAI infection on the contrary, the area affectedis frequently jejunal or diffuse and resembles bothradiologically and histologically that seem inWhipple’s disease (Figs. 20 and 21). Viscerallocations are rare, and the adenopathies are homo-geneous because in these patients, the very lowCD4 lymphocyte count, generally \100 and50 CD4/ml, does not allow a caseous necrosisimmune response to occur.

• Cryptosporidiosis is most often seen in deeplyimmunosuppressed states with CD4 lymphocytelevels \50/ml but it can occur months later in thedevelopment of the disease with levels of CD4/ml\200. The area affected is generally proximal,involving the duodenum/jejunum and upper ileum,but it can affect the whole digestive tract. It is notaccompanied by adenopathy. The intestinal walls

Acute Gastritis and Enteritis

are moderately and regularly thickened and theloops are the site of liquid distension which can beconsiderable (Fig. 22). Cryptosporidiosis, likeCMV infection, can be accompanied by cholangi-opathy shown on the CT scan images as a generallymoderate dilatation of the intra- and extra-hepaticbile ducts. The presence of a low stenosis of themain bile duct, in the papilla region, and the pre-disposition for developing alithiasic cholecystitis is

the other characteristic describing biliaryinvolvement.

• Gastrointestinal infections with Isospora bellicannot be distinguished clinically and radiologi-cally from cryptosporidiosis; only microscopicexamination of the faeces can provide an exactdiagnosis.

• CMV intestinal infections preferentially concernthe ascending caecum or the whole colon

Fig. 20 Eosinophilicenteritis. Regularcircumferential thickening ofthe walls of the duodenumand hypereosinophilyl.Biopsies confirmed thediagnosis of eosinophilicenteritis without a parasiticcause being found

Fig. 21 Portal ‘enteritis’. Ascitic oedematous decompensationof hepatic cirrhosis accompanied by diffuse submucosaloedema of the small intestine, colon and stomach. The

multifactorial causes of this submucosal oedema include portalhypertension and hypoproteinaemia

D. Regent et al.

(pancolitis); the small intestine is rarely affected.The regular parietal thickening can be massive insevere forms, or even have a pseudotumoral pol-ypoid appearance. It does not occur with adenop-athy. The coexistence of biliary involvement is adiagnostic argument.

• Histoplasmosis can, in countries where it is endemic,give rise to digestive involvement when the CD4count is\100/ml. As with tuberculosis, it can be aprimary infection or a reactivation. In the dis-seminated forms of histoplasmosis, the intestine isinvolved in 75% of cases. The aspects seen on a CTscan are identical to those encountered in tuberculosis:localisation on the terminal ileum and the ascendingcolon, generally regular concentric parietal thicken-ing, sometimes with pseudotumoral stenosis, infil-tration of the adjacent peritoneum, hypodenseregional adenopathy in the mesentery and retro-peritoneum and possible hepato-splenic, adrenalglands and peritoneal nodular infectious focal lesions.

• In neutropenic subjects, in particular during aplasiainduced to treat malignant haemopathy by stem celltransplantation, cancer chemotherapy or after organtransplant, it is essential to have good knowledge ofthe factors orientating the diagnosis of acute gas-trointestinal events after allogeneic haematopoieticstem cell transplantation, and in particular, thelength of time since the patient became aplasic(Schmit et al. 2008; Kirkpatrick and Greenberg2003; Beckett and Olliff 2005).

• Chemotherapy-related mucositis is the inevitableconsequence of lesions of the mucosal barrierbecause of the toxicity of the aplastic drugs used.The initially inflammatory epithelial lesions ulcer-ate (approximately at D 15) then heal. In the CTscan, diffuse or segmental circumferential thicken-ing of the wall of the digestive tube is seen withmucosal hyperaemia (alternation of hypoperfusedand hyperperfused areas within the thickenedwalls). In general, there is little or no infiltration ofthe mesentery, nor is there adenopathy. The gas-trointestinal tract is generally affected diffusely,and the clinical symptoms are moderate secretorydiarrhoea and/or abdominal pain.

• Neutropenic enterocolitis most often involves thecaecum (typhlitis or caecitis) but it is not unusualfor the terminal ileum to be affected which is agood argument in favour of the diagnosis andagainst that of infectious colitis, in particular ofpseudomembranous colitis due to Clostridium dif-ficile. The affects are multifactorial combiningmucositis lesions, deep neutropenia, disturbancesinduced in the microbial flora and a haemorrhagicnecrosis component of ischaemic origin. The CTscan shows circumferential thickening of the wallsof the caecum (typhlitis), of the ascending colonand the terminal ileum, combined with moderateinflammatory infiltration of the adjacent perito-neum. In general, there is little ascites and noadenopathy. In severe cases, signs of ischaemia

Fig. 22 Enteritis due toMAI in an HIV+ patient.Considerable submucosalthickening of the walls of thesmall intestine with thickenedand enhanced mucosa andserosa, abundant ascites.Laboratory investigationsconfirmed infection byatypical mycobacteria

Acute Gastritis and Enteritis

appear (parietal pneumatosis, lack of mucosalenhancement) or local complications: abscess,pneumoperiteum.

• The graft-versus-host reaction; After haematopoi-etic stem cell allotransplantation, the return tonormal in immunological terms occurs in threephases:– During the first 10–30 days, the immune system

is severely impaired by pancytopenia; localdefences are weakened by mucitis.

– Between 30 and 100 days after transplantation,the neutropenia corrects itself but with a delayfor the lymphocytes, the cause of continuedcellular and humoral immune deficiency. Infec-tious complications are thus frequent. An acuteform of graft-versus-host reaction appearing asabdominal pain, and secretory diarrhoea candevelop once the graft is functional. On CT scan,abnormally intense enhancement of the mucosaof the digestive tract is seen very clearly

predominating on the small intestine. This cor-responds histologically to a destroyed mucosa,replaced by richly vascularised granulation tis-sue. The intestinal loops are generally distendedwith liquid with a circumferential submucosaloedema and a comb sign in the correspondingmesentery; on the other hand, there is only rarelyinfiltration of the mesentery. The alternation ofhealthy areas with pathological areas and theclinical context of haematopoietic stem celltransplantation are obviously major factors formaking a diagnosis (Fig. 23).

– After 100 days, a chronic form of graft-versus-host reaction can be seen which occurs mainly asa malabsorption syndrome without expression inimaging techniques.

• Acute fungal infections, in particular the dissemi-nated invasive forms of aspergillosis which may bethe origin of necrotic ulcerative enteritis particu-larly concerns the ileum, the walls of which are

Fig. 23 Enteritis due to MAI in a young HIV+ patient. Jejuno-ileal parietal abnormalities (thickening, hyper-enhancement)accompanied by hypodense retroperitoneal mesenteric adenop-athies, suggestive of tuberculosis, but the clinical context and in

particular the very strong immunosuppression suggest more aMAI infection which will be confirmed by laboratoryinvestigations

D. Regent et al.

circumferentially thickened and the neighbouringmesentery infiltrated. There is a very high risk ofperforation and the symptoms are often not veryspecific, sometimes limited to a fever and abdom-inal pain without clear guarding. A CT scan istherefore of fundamental importance to confirm theparietal and peritoneal abnormalities of the ileo-colic junction (Tresallet et al. 2004).

• Mucormycosis. This is seen in subjects treated for amalignant haemopathy, in immunosuppressedtransplant patients, keto-acid diabetics, patientswith cardiac and renal impairment and duringchelator treatment for iron overload. Gastrointesti-nal involvement is uncommon, affecting the stom-ach more that the small intestine and colon. It isseen on CT scan as a circumferential diffusethickening of the walls of affected digestive seg-ments, which often coexist with hepatic focallocalisations (Suh et al. 2000).

2.3 Vascular Acute InflammatoryConditions of the Duodenumand Small Intestine

2.3.1 Acute Manifestations of Vasculitison the Small Intestine (Ha et al. 2000;Ahn et al. 2009)

The majority of forms of vasculitis, in any case thoseconcerning small- and medium-sized vessels, mayaffect the small intestine. We should think of themeach time; we see images in a young patient sug-gesting ischaemic lesions in an unusual site, forinstance in the stomach, above all the duodenum(ischaemia in the duodenum is practically alwaysrelated to vasculitis), or the rectum, or when the smallintestine and colon are simultaneously diffuselyaffected or when other viscera are affected, e.g. theuro-genital system.• Henoch-Schönlien purpura (sometimes called

rheumatoid purpura) is vasculitis of small vesselscharacterised by the presence of serum IgA andthe precipitation of immune complexes in thearterioles, capillaries and venules. Most frequentin children, where it usually develops benignly, aquarter of cases are seen in adults, more often inmen (sex-ratio 2/1), with a poorer prognosisbecause of more frequent and more severe renalinvolvement. The clinical triad of acute abdominal

pain, arthralgia and palpable purpura must bringthis diagnosis to mind. Abdominal pain occurs in44% of cases of Henoch-Schönlien purpura inadults, preceding the skin lesions in 10–15% ofpatients. The CT scan shows an inflammatorythickening with double halo signs of the digestivesegments affected, loss of mesenteric fat trans-parency with vascular engorgement, and ade-nopathy; ascites is present in the severest forms(Figs. 24 and 25). Complications due to perfora-tion or occlusion by invagination are less fre-quent in children and the digestive lesionsgenerally evolve favourably; the prognosis for thedisease depends on the kidneys (Chung et al.2006).

• Periarteritis nodosa (PAN) is a necrotising inflam-matory vasculitis which affects the wall of small- tomedium-sized muscular arteries leading to theformation of micro-aneurysms and stenoses. Itparticularly affects middle-aged men (in their 40 or50 s; sex-ratio 2–3/1) who, in 36% of cases, arecarriers of the hepatitis B virus. cANCAs are foundin laboratory tests in a large majority of cases butthey are not specific (since they are also found inWegener’s granulomatosis, in Churg–Strauss syn-drome and microscopic polyangiitis). The digestivetract is affected in 50–70% of PAN cases, essen-tially the jejunum which is the site of extensivesubmucosal oedema which can be spontaneouslyhyperdense when it is haematic, with a double haloimage on biphasic acquisitions after contrast med-ium injection. Perforations and stenoses are com-plications of the vascular lesions. The scan, evenwith the spatial resolution of current machines,cannot objectify the microaneurysms that are easilyshown by angiography (Rhodes et al. 2008; Jeeet al. 2000).

• Microscopic polyangiitis (hypersensitivity vasculi-tis; leukocytoclastic vasculitis) is a conditionidentical to PAN which affects small diametervessels (arterioles, venules, capillaries). cANCAsare present in the majority of cases. Renalinvolvement is found in 90% of cases in the form ofa necrotising glomerulonephritis. The effects on thedigestive tract are identical to those seen in theother types of vasculitis: regular inflammatorythickening of the (generally ileal) walls, vascularengorgement, loss of mesenteric fat transparency,and ascites.

Acute Gastritis and Enteritis

• Wegener’s granulomatosis histologically affects theintestinal tract in 24% patients but is only expressedclinically in 10%. It affects the small intestine andcolon. The appearance on CT scan is identical tothat seen in other forms of vasculitis. Acute formsare linked to intestinal perforations or extensivemassive ischaemic necrosis (fulminating necrotis-ing enterocolitis) (Pickhardt and Curran 2001).

• Churg–Strauss syndrome can exceptionally occuron intestinal-mesenteric structures (20% of cases),either in the form of ischaemic lesions secondary tovasculitis, or by eosinophilic infiltration of the wallwhich can be the cause of an occlusion or haem-orrhagic diarrhoea (Rha et al. 2000).

• Acute-disseminated lupus erythematosus (ADLE) isa necrotising vasculitis of autoimmune origin whichpreferentially affects young female subjects. Thedigestive effects are ischaemic, often haemorrhagiclesions consecutive to a real obliterating endarteri-tis. In physiopathological terms, the hypercoagula-ble state linked to the circulating antiphospholipidantibodies (anticardiolipin antibodies and lupusanticoagulant which are encountered in 30–40% ofpatients with ADLE, as against 2% in the generalpopulation) appears to be of decisive importance in

the occurrence of digestive symptoms. We speak ofan antiphospholipid antibody syndrome when thereare not enough diagnostic criteria for ADLE. Perf-orative and occlusive necrotic complications areclassic. The whole digestive tract can be affected butthe predilection is for the territory of the superiormesenteric artery. In acute situations, the CT scanshows circumferential thickening of the walls ofaffected digestive segments, engorgement of mes-enteric vessels with a particular arrangement of thevasa recta of the ileum related to its shortening(comb sign), and adenopathy. Polyseritis is frequent(peritoneal, pleural, pericardial liquid effusions,etc.) and evokes the diagnosis. A high incidence ofurogenital tract lesions has been reported (lupusglomerulonephritis, cystitis, hydronephrosis byfibrous changes to the ureterovesical junction orfollowing vesicoureteral reflux secondary to adetrusor spasm). In everyday practice, these data areof very limited interest because of their rarity(Pagnoux et al. 2003; Kaushik et al. 2001).

• Behcet’s disease. The gastrointestinal tract isaffected in 10–50% of patients with Behcet’s dis-ease. The lesions affect the ileo-caecal junctionwith a predilection for the terminal ileum and are

Fig. 24 Cryptosporidiosisand choleriform diarrhoeasyndrome in an HIV+ patientwith a CD4 level below50/ml. Diffuse submucosalthickening of all the ilealloops with increased mucosalcontrast, hypervascularisationwith the vasa recta showing acomb sign. Diagnosis ofcryptosporidiosis wasconfirmed by the laboratorytests

D. Regent et al.

the consequence of an inflammatory vasculitispreferentially affecting the venules. The deepulcerations typical of the disease may be transmu-ral, which explains the frequency of local compli-cations such as haemorrhage, perforation, fistulae,localised or diffuse peritonitis, for the diagnosis ofwhich the CT scan is particularly valuable. Parietalthickening can be massive, localised, asymmetricwith a polypoid appearance, pseudotumoral,ulcerated in the centre (Chung et al. 2001).

• Rheumatoid vasculitis. In longstanding severerheumatoid arthritis, with marked disorders in lab-oratory tests and in particular in male patients,acute intestinal inflammatory symptoms may beseen related to leukocytoclastic vasculitis of thesmall venules. The diffuse thickening of walls ofthe small intestine and colon with double haloenhancement, the possible infiltration of the mes-entery and the peritoneal liquid reaction are iden-tical to what is seen in the other forms of vasculitis.

Fig. 25 Graft-versus-hostreaction in a young patientwho had received a transplantof haematopoietic stem cells.Diffuse thickening due tosubmucosal oedema withincreased contrast in themucosa of all the smallintestine loops and the colon,in a graft-versus-host reaction

Acute Gastritis and Enteritis

2.3.2 Inflammatory Conditionswith a Vascular Origin ExcludingForms of Vasculitis

• Acute radiation enteritis of the small intestine (Lyeret al. 2001). This is seen during the weeks imme-diately following pelvic irradiation, most oftenafter doses higher than 45 Gy for uterine cervicalcancers. It appears as an oedematous parietalthickening of the loops of the small intestine in thepelvis and lower abdomen. Limitation of thelesions to the field of irradiation with cleardemarcation is highly evocative for this diagnosis(Fig. 26). The condition is usually resolved in a fewweeks with symptomatic treatment. This acuteeffect, related to the direct action of ionising radi-ation on the lining epithelium is different fromchronic radiation enteritis which is related to anobliterating endarteritis, the cause of fibrosinginflammation producing stenoses and fistulae,generally appearing several months to several years(2 months to 30 years) after irradiation.

• Angio-oedema (or angioneurotic oedema) of thesmall intestine. Angioneurotic oedema is a non-

inflammatory condition characterised by acuteepisodes of capillary hyperpermeability withoedema of the skin of the face and of the respira-tory and intestinal mucosae. The gastrointestinalcondition is expressed as an acute abdomen, gen-erally resolving within 24–72 h but there is apotential risk of death by hypovolaemic shock. Theappearance of watery diarrhoea in the final phase ofthe attack is good diagnostic evidence. CT scanimages combine extensive inflammatory thickeningof the walls of the digestive tract (stomach andsmall intestine) with liquid distension of thedigestive lumens, congestion of mesenteric vesselsand peritoneal fluid effusion. The cause of thisdisease is a hereditary or acquired lack of C1-esterase inhibitor, which should be determined bylaboratory investigations. A personal or familialhistory of Quincke’s oedema or minor forms (epi-sodes of urticaria, transitory dyspnoea) should besought but the digestive events may precede cuta-neous and respiratory symptoms by several years.There are paraneoplastic forms associated withlymphoproliferative syndromes, autoimmune

Fig. 26 Acute painfulepigastric symptoms in a 29-year-old patient. The scanobjectifies oedematouscircumferential thickening ofthe proximal jejunal loopswith discrete peritoneal fluideffusion accompanied bysmall mesenteric andperitoneal adenopathies.Purpura eruptions were seenon the lower limbs withinhours of the examinationconfirming the diagnosis ofHenoch-Schönlein purpura

D. Regent et al.

diseases or cancers. Certain cases of this conditionmay be seen during treatment with conversionenzyme inhibitors (ACE inhibitors) (De Baker et al.2001).

• Buerger’s disease (thromboangiitis obliterans). Inyoung subjects who are usually heavy smokers thiscondition affects the vasa vasorum of arteries ofintermediate size, leading to thrombosis and severeparietal inflammatory reactions. Digestiveinvolvement is infrequent. Intestinal parietalsymptoms are of the same type as those seen invasculitis but an angioscan shows the segmentalthromboses of the medium-sized arteries. Thecontext (young subject, heavy smoker) is funda-mental to the diagnosis (Marder and Mellinghoff2000).

• Vasculitis linked to cocaine. After just one inha-lation of cocaine, the picture of an acute abdomencan be seen on a CT scan with images analogousto those seen in acute or subacute ischaemia of thedigestive tract (Fig. 27). The colon is most oftenthe site but the small intestine alone can beaffected, essentially the ileum. The histologicalsimilarities between Buerger’s disease and vascu-litis due to cocaine have led some authors tosuggest that there are close links between thesetwo conditions (Herrine et al. 1998; Hagan andBurney 2007).

2.3.3 Drug-Induced Enterocolitis (Chatelainet al. 2007)

Drug-induced enteropathies, particularly colic condi-tions, are frequent but in general are not investigatedusing imaging techniques because of the usuallyminor character of their clinical symptoms.• Drug-induced Ileitis

– Ulcerated ileitis lesions can be seen after inges-tion of NSAIDs, but are much less frequent thancolic conditions. One of their particularities asthey develop is the formation of diaphragm-likestenoses (Fig. 28).

– Corticosteroids, tablets of iron salts or potassiumchloride may lead to lesions similar to thosecaused by NSAIDs.

– In all cases, the clinical picture can be acute withbloody diarrhoea, and peritonitis through perfo-ration may be seen. The severity of the conditionis not related to how long treatment has beenadministered.

• Enteropathy due to NSAIDs. Diaphragm disease isa rare but specific complication of chronic pro-longed use of NSAIDs. It is seen above all inmiddle-aged women taking NSAIDs over the longterm for a rheumatic condition. It may be revealedclinically by an acute occlusive syndrome butusually attention is drawn to the condition bysubocclusive episodes, chronic diarrhoea and

Fig. 27 Acute painfulepigastric symptoms in a21-year-old female patient.Considerable circumferentialsubmucosal (a–c) oedema ofthe duodenum confirmed byendoscopy (d) which showsthe hyperaemic (d, e) andhaemorrhagic character oflesions due to Henoch-Schönlein purpura

Acute Gastritis and Enteritis

weight loss. Fine fibrous circular membranes, per-forated in the centre, develop in the ileal lumen,opposite valvules with which they interact. Histo-logically the submucosa is the site of fibroustransformation which would seem to correspond tothe development of the ulcerous lesions caused bythe NSAIDs (Zalev et al. 1996).

• Necrotising ileocolitis due to treatment with kay-exalate and sorbitol. An ulcerated condition of thedistal ileum and the right colon, often accompaniedby partial or transmural necrosis, which can then becomplicated by perforation with peritonitis, may beseen in renally impaired subjects treated withkayexalate for hyperkalaemia. In fact it is the sor-bitol, a hypertonic solution administered to coun-teract the constipation induced by kayexalate,which would seem to be the cause of the necrotis-ing ileocolic lesions, through its direct toxic actionon the mucosa and the local hypovolaemia that itinduces due to its hypertonicity, and which causes alow local flow that can lead to parietal necrosis.

• Ileal melanosis. Like the much more frequent colicmelanosis with which it can be associated, thisis the consequence of long-term treatment for

constipation by laxatives of the anthraquinonegroup. It is a feature of pathological anatomy whichis not visible using imaging techniques.

• Clofazimine enteropathy. Clofazimine belongs tothe phenazine group used in the treatment of lep-rosy, atypical mycobacterial infections and some-times in graft-versus-host reactions, and after beingused for several months can accumulate in themucosa of the small intestine, the mesenteric gan-glia and the greater omentum, giving them abrown-black or orangey colouration by which thecondition can be identified in a pathological anat-omy examination. The clinical picture is a combi-nation of abdominal pain, vomiting and diarrhoea.

2.4 The Acute Appearance of Crohn’sDisease in the Small Intestine(Madureira 2004; Gourtsoyianniet al. 2009)

Crohn’s disease can be revealed by an acute painfulfeverish episode with diarrhoea, or by an acutecomplication, such as an intestinal occlusion, deep

Fig. 28 Acute radiationenteritis. Regular moderatecircumferential submucosaloedema of all the pelvic loopsof the small intestine in afemale patient irradiatedduring the previous 3 weeksfor a neoplasia of the cervixof the uterus

D. Regent et al.

abscess, fistula, perforation or digestive haemorrhage.In all these circumstances, a CT scan is often per-formed quite quickly, and one must be able to identifythe disease on the images produced, and its possiblecomplications (Meyers et al. 1995; Lee et al. 2002).

It is obvious that, given an acute picture, even ifquestioning the patient or the clinical examinationpoints towards Crohn’s disease, the use of enteroc-lysis should be avoided and the examination per-formed usually without modifying the content of theloops or by performing enterography without a cath-eter, by ingestion of water or opacifying agent and inall cases taking care to minimise the dose of ionisingradiation delivered to these patients, who are oftenyoung and who will be repeatedly exposed to CTscans as the condition develops.

Crohn’s disease in the small intestine preferentiallyinvolves the terminal ileum, but, particularly inacutely revealed forms, it can affect almost the wholeileum or a shorter or longer segment of the jejunumand evidently the whole or part of the colon.

Positive CT scan diagnosis of Crohn’s disease inthe small intestine is based on the criteria for trans-mural inflammation seen as:• more than 3 mm of parietal thickening;• parietal stratification visible with double halo

images in the active inflammatory forms;• the presence above all, of the classic modifica-

tions of vascularisation on the mesenteric side ofthe loops affected: vascular jejunisation of theileum (i.e. increase in the number of vasarecta per unit length, tortuosity and dilatation ofthese vessels), and a comb sign, which essen-tially reflect the shortening of the digestivesegments involved and their mesentery whichis, moreover, the site of fibrofatty infiltration(sclerolipomatosis);

• the presence of mesenteric adenopathy.The mesenteric vascular abnormalities indicate an

active, developed, widespread condition seen in anacute clinical context. There is close correlation withthe clinical Crohn’s disease activity index.

Fig. 29 Vasculitis in a heroine addict. The scan was per-formed for acute hyperalgesic pain which shows acute lesionspredominantly on the proximal jejunum and characterised by

considerable circumferential submucosal oedema with targetsign enhancement, accompanied by small quantities of perito-neal fluid effusion

Acute Gastritis and Enteritis

In contrast, fibrostenotic lesions appear in the scan as:• regular uniform thickening, with no or little

enhancement after injection of a contrast agent.However, it must be emphasised that the fibrosiscan be enhanced, sometimes considerably, ondelayed acquisitions. Delayed enhancement istherefore not a decisive predictive element for theefficacy of the medical treatment;

• stenosis of the lumen and upstream distension itwith regular infundibuliform connection of thenormal wall;

• absence of mesenteric vascular modifications, inparticular the comb sign.Target or double halo enhancement images are

also not themselves specific, even if this feature wasinitially described in Crohn’s disease. Differentialdiagnosis should consider ischaemia, vasculitis,infectious enteritis, haematoma (Fig. 29), radiationenteritis and graft-versus-host reaction. Submucosalfatty metaplasia (or submucosal pseudolipomatosis)

can lead to hesitation even more here than in thestomach. Its typical appearance of fatty density (thefat halo sign) and its existence in an overweightpatient with excessive deep abdominal fat makes itseasy to identify (Fig. 30).

An emergency CT scan, even if it lacks precisionand does not allow as fine an analysis as CT enter-oclysis (Kohli and Maglinte 2009), does permit Cro-hn’s disease to be diagnosed and shows the activity ofthe disease (Minordi et al. 2009). Obviously, ithighlights local complications: inflammatory orfibrous stenosis, abscesses, fistulae, perforations andany possible remote lesions such as urinary calculi,venous and more rarely arterial thrombosis, spond-yloarthropathy, sclerosing cholangitis, etc. (Figs. 31,32, and 33).

Meta-analyses have shown that there are no sig-nificant differences in diagnostic accuracy betweenCT and MRI (Horsthuis et al. 2008a, b). Given thenecessity of limiting irradiation as much as possible,

Fig. 30 Acute enteropathydue to non-steroidal anti-inflammatory drugs.Moderately stenosing parietalcircumferential thickening ofthe jejunum, withconsiderable lastingenhancement (white arrow).Double balloon enteroscopyconfirmed the diagnosis ofenteritis due to NSAIDs

D. Regent et al.

Fig. 31 Acute attackrevealing Crohn’s disease.Regular circumferentialthickening of the final ilealloops with target sign imageby enhancement of themucosa and signs oftransmural inflammation withcomb sign appearance of thevasa recta

Fig. 32 Acute attack ofCrohn’s disease with pelvicperitonitis. Presence ofimages of acute inflammatorythickening of the ileal wallwith signs of transmuralinflammation. Multiple pelviccollections with one largerorganised collection withthick wall and gas bubbles(white arrow)

Acute Gastritis and Enteritis

Fig. 33 Phlegmoncomplicating an ileal Crohn’sdisease extending to therectosigmoid junction. The CTscan shows the typical imagesof ileal Crohn’s disease (blackarrow). In the pelvis there ismassive inflammatoryinfiltration of the adjacentmesenteric structures (straightwhite arrow) (a–c) withcontinuous extension at therectosigmoid junction (whitecurved arrow) (d)

Fig. 34 Duodenal-jejunalparietal haematoma afteringestion of large dose ofAspegic�. Presence ofconsiderable circumferentialthickening extending to thewall of the proximal jejunalloops. The patient hadingested relatively largequantities of Aspegic� duringthe days prior to the acuteincident which revealed this

D. Regent et al.

particularly in young patients, it therefore seems bestto direct these patients wherever possible to MRI, allthe more so as the additional information from dif-fusion sequences allows very effective assessment ofthe degree of activity of the disease, correlated per-fectly with clinical/laboratory activity indices.Injected sequences can thus be avoided and T2-weighted sequences used, at the equilibrium stateand in diffusion, to effectively follow the spontane-ous development of the disease and/or duringtreatment.

2.4.1 To summarizeThe appearance in a CT scan of localised or diffusehypodense parietal thickening of the stomach and/orsmall intestine, with visible stratification afterinjection, in the context of an acute abdomen,should mean that several hypotheses need to beconsidered for which exploration of the rest of theabdominal cavity may provide pros and cons of usefor the aetiological diagnosis. It is usually, aboveall, the clinical history and carefully searching thepatient’s medical history which will guide thisaetiological orientation. A radiologist is a clinicianwho must go well beyond the description of imagesif he wishes to provide the medical community withthe services which the latter has the right to expect(Figs. 34 and 35).

References

Abcarian PW, Demas BE (1991) Systemic Yersinia enterocoliticainfection associated with iron overload and deferoxaminetherapy. AJR Am J Roentgenol 157:773–775

Ahn E, Luk A, Chetty R, Buttany J (2009) Vasculitides of thegastrointestinal tract. Semin Diagn Pathol 26:77–88

Antonopoulos P, Constantinidis F, Charalampopoulos G,Dalamarinis K, Karanicas I, Kokkini G (2008) An emer-gency diagnostic dilemma; a case of Yersinia enterocoliticacolitis mimicking acute appendicitis in a thalassenia majorpatient; the role of CT and literature review. Emerg Radiol15:123–126

Asrani A, Avelline R, Abujudeh H, Lawrason J, Kaewlai R(2007) Intramural gastric abscess-preoperative diagnosiswith CT. Emerg Radiol 14:253–256

Balthazar EJ (1979) Effects of acute and chronic pancreatitis onthe stomach pattern of radiographic involvement. Am JGastroenterol 72:568–580

Balthazar EJ, Charles HW, Megibow AJ (1966) Salmonella andshigella-induced ileitis: CT findings in four patients.J Comput Assist Tomogr 20:375–378

Beckett D, Olliff J (2005) Non infectious manifestations ofstem cell transplantation. Brit J Radiol 78:272–281

Brown BM, Federle MP, Jeffrey RB (1982) Gastric wallthickening and extragastric inflammatory process: a retro-spective study. J Comput Assist Tomogr 6:782–785

Buyt L, Smeets P, Verstraete K (2003) Infectious emphysema-tous gastritis in multiple sclerosis. JBR-BTR 86:148–149

Chatelain D, Mokrani N, Flejou JF (2007) Entérocolitesmédicamenteuses. Ann Pathol 27:439–447

Chen TA, Lo GH, Lin CK, Lai KH, Wung HY, Yu HC, Hsu PI,Chen HH, Tsai WL, Chen WC (2007) Acute pancreatitis

Fig. 35 Jejunal segmentalsubmucosal metaplasia in anoverweight patient. Theseimages of parietal thickeningwith a fatty density seen in thecontext of painful abdominalsymptoms led wrongly to thediagnosis of ischaemia of thesmall intestine and amisunderstanding of the realorigin of the condition, whichwas biliary

Acute Gastritis and Enteritis

associated acute gastro-intestinal mucosal lesions: inci-dence, characteristic and clinical signification. J ClinGastroenterol 41:830–834

Chung SY, Ha HK, Kim JH, Kim KW, Cho N, Cho KS,Lee YS, Chung DJ, Jung HY, Yang SK, Min YI (2001)Radiologic findings of Behcet syndrom involving thegastrointestinal tract. Radiographics 21:911–924

Chung DJ, Park YS, Huh KC, Kim JH (2006) Radiologicfindings of gastrointestinal complications in an adult patientwith Henoch Schönlein purpura. AJR Am J Roentgenol187:w396–w398

Curvelo LA, Brabosa W, Rhohr R, Lanzoni V, Parise ER,Ferrari AP, Kondo M (2000) Underlying mechanism ofportal hypertensive gastropathy in cirrhosis: a hemodynamicand morphological approach. J Gastroenterol Hepatol24:1482–1483

D’Almeida A, Juse J, Onetto J, Restrepo R (2008) Bowel wallthickening in children: CT findings. Radiographics 28:727–746

De Baker AI, De Schepper AM, Vandevenne JE, Schoeters P,Michielsen P, Stevens WJ (2001) CT of angio-oedema ofthe small bowel. AJR Am J Roentgenol 176:649–652

Gelfand DW, Ott DJ, Chen MY (1999) Radiologic evaluationof gastritis and duodenitis. AJR Am J Roentgenol173:357–361

Gore RM, Miller FH, Pereles FS, Yaghmai VY, Berlin JW(2000) Helical CT in the evaluation of acute abdomen. AJRAm J Roentgenol 174:901–913

Gourtsoyianni S, Zamboni GA, Romero JY, Raptopoulos VD(2009) Routine use of modified CT enterography in patientswith acute abdominal pain. Eur J Radiol 69:388–392

Ha HK, Lee SH, Rha SE, Kim JH, Byum JY, Lim HK,Chung JW, Kim JG, Kim PN, Lee MG, Auh YH (2000)Radiologic features of vasculitis involving the gastrointes-tinal tract. Radiographics 20:779–795

Hadas-Halpren I, Hiller N, Guberman D (1993) Emphysema-tous gastritis secondary to ingestion of large amounts ofCoca Cola. Am J Gastroenterol 88:127–129

Hagan IG, Burney K (2007) Radiology of recreational drugabuse. Radiographics 27:919–940

Harisinghani MG, Wittenberg J, Lee W, Chen S, Guttierez AL,Muller PR (2003) Bowel fat halo sign in patients withoutintestinal disease. AJR Am J Roentgenol 181:781–784

Herrine SK, Park PK, Wechsler RJ (1998) Acute mesentericischemia following intranasal cocaine use. Dig Dis Sci43:586–589

Hommeyer SC, Hamill GS, Johnson JA (1995) CT diagnosis ofintestinal ascaridiasis. Abdom Imaging 20:315–316

Horsthuis K, Stokkers PC, Stoker J (2008a) Detection ofinflammatory bowel diseases: diagnostic performance ofcross sectional imaging modalities. Abdom Imaging33:407–416

Horsthuis K, Bipart S, Bennink RJ, Stoker J (2008b) Inflam-matory bowel diseases diagnosed with US MR scintigraphyand CT: metaanalysis of prospective studies. Radiology247:64–79

Ishida M, Harada A, Egawa S, Watabe S, Ebina N, Unno M(2007) Three successive cases of enteric anisakiasis. DigSurg 24:228–231

Jee KN, Ha HK, Lee IJ, Kim JK, Sung KS, Cho KS, Kim PN,Lee MG, Lim HK, Choi CS, Auh YH (2000) Radiological

findings of abdominal polyarteritis nodosa. AJR Am JRoentgenol 174:1675–1679

Jung C, Choi YW, Jeon SC, Chung WS (2003) Acute diffusephlegmonous oesophagogastritis: radiologic diagnosis. AJRAm J Roentgenol 180:862–863

Jung JH, Choi HJ, Yoo J, Kang SJ, Lee KY (2007) Emphy-sematous gastritis associated with invasive gastric mucormycosis: a case report. J Korean Med Sci 22:923–927

Kaushik S, Federle MP, Schur PH, Krishman M, Silverman SG,Ros PR (2001) Abdominal thrombotic and ischemic man-ifestations of the antiphospholipid antibody syndrome: CTfindings in 42 patients. Radiology 218:768–771

Kim DH, Pickhardt PJ (2007) The stomach. In: Pickhardt PJ,Arluk GM (eds) Atlas of gastrointestinal imaging. Radio-logic–endoscopic correlation. Saunders-Elsevier, Philadel-phia, pp 61–112

Kim TU, Kim S, Woo SK, Lee JW, Lee TH, Jeong YJ, Heo J(2008) Dynamic CT of portal hypertensive gastropathy—significance of transient gastric perfusion defect sign. ClinRadiol 63:783–790

Kirkpatrick ID, Greenberg HM (2003) Gastrointestinal com-plication in the neutropenic patient: characterization anddifferentiation with abdominal CT. Radiology 226:668–674

Koh DM, Langroudi B, Padley SPG (2002) Abdominal CT inpatients with AIDS. Imaging 14:24–34

Kohli MD, Maglinte DD (2009) CT enteroclysis in small bowelCrohn’s disease. Eur J Radiol 83:398–403

Kothary NN, Muskie JM, Mathur SC (1999) Resident’steaching files. Strongyloides stercoralis hyperinfection.Radiographics 19:1077–1081

Lee SS, Ha HK, Yang SK, Kim AY, Kim TY, Kim PN, Lae MG,Myung SJ, Jung HH, Kim JH, Min YI (2002) CT of prominentpericolic or perienteric vasculature in patient with Crohn’sdisease: correlation with clinical disease activity and findingson barium studies. AJR Am J Roentgenol 179:1029–1036

Levine MS (2008) Inflammatory conditions of the stomach andduodenum. In: Gore RM, Levine MS (eds) Textbook ofintestinal radiology, 3rd edn. Saunders-Elsevier, Philadelphia,pp 563–592

Loi TH, See JW, Diddapur RK, Issac JR (2007) Emphysema-tous gastritis: a case report and a review of the literature.Am Acad Med Singapore 36:72–73

Lyer RB, Jhingran A, Sawaf H, Libshitz HI (2001) Imagingfindings after radiotherapy of the pelvis. AJR Am JRoentgenol 177:1083–1089

Macari M, Balthazar EJ (2001) CT of bowel thickening:significance and pitfalls of interpretation. Am J RoentgenolAJR 176:1105–1106

Macari M, Megibow AJ, Balthazar EJ (2007) A pattern approachto the abnormal small bowel; observation at MDCT and CTenterography. AJR Am J Roentgenol 188:1344–1355

Madureira AJ (2004) The comb sign. Radiology 230:783–784Marder VJ, Mellinghoff IK (2000) Cocaine and Buerger

disease. Arch Intern Med 160:2057–2060Matsumoto T, Ida M, Sakai T, Kimura Y, Fushima M (1991)

Yersinia terminal ileites: sonographic findings in eightpatients. AJR Am J Roentgenol 156:965–967

Mazzie JP, Wilson SR, Sadler MA, Khalili M, Javors BR,Weston SR, Katz DS (2007) Imaging of gastrointestinaltract infection. Semin Roentgenol 42:102–116

D. Regent et al.

Meyers MA, McGuire PV (1995) Spiral CT demonstration ofhypervascularity in Crohn disease ‘vascular jejunization ofthe ileon’ or the ‘comb sign’. Abdom Imaging 20:327–332

Minordi LM, Vecchioli A, Buidi L, Poloni G, Fedeli G,Bonomo L (2009) CT findings and clinical activity inCrohn’s disease. Clin Imaging 33:123–129

Muldoney SM, Balfe DM, Hammeman A, Wick MR (1995)‘Acute’ fat deposition in bowel wall submucosa: CTappearance. J Comput Assist Tomogr 19:394–399

Ortega-Deballon P, Carabias-Hernandez A, Martin-Blasquez A,Garaulet P, Benoit L, Kretz B, Limones-Esteban M, Favre JP(2005) Anisakiase: une parasitose que le chirurgien doitconnaître. Ann Chir 130:407–410

Pagnoux C, Mahr A, Guillevin L (2003) Manifestationsabdominales et digestives des vascularites. Ann Med Interne(Paris) 154:457–487

Pickhardt PJ, Curran VW (2001) Fulminant enterocolitis inWegener’s granulomatosis. AJR Am J Roentgenol 177:1335–1337

Repiso OA, Alcantara TM, Gonzalez de Frutos C, de Artaza VT,Rodriguez MR, Valle MJ, Martinez PJL (2003) Gastroin-testinal anisakiasis. Study of a series of 25 patients.Gastroenterol Hepatol 26:341–346

Rha SE, Ha HK, Lee SH, Kim JH, Kim JK, Kim JH, Kim PN,Lee MG, Auh YH (2000) CT and MR imaging findings ofbowel ischemia from various primary causes. Radiographics20:29–42

Rhodes ES, Pekala JS, Gemery JM, Dickey KW (2008) Case129: polyarteris nodosa. Radiology 246:322–326

Rodriguez EJ, Gama MA, Ornstein SM, Anderson WD (2003)Ascariasis causing small bowel volvulus. Radiographics23:1291–1293

Schmit M, Bethge W, Beck R, Faul C, Claussen CD, Horger M(2008) CT of gastrointestinal complications associated withhaematopoietic stem cell transplantation. AJR Am JRoentgenol 190:712–719

Sherman SC, Weber JM (2005) The CT diagnosis of ascariasis.J Emerg Med 28:471–472

Suh WS, Park CS, Lee MS, Lee JH, Chang MS, Woo JH,Lee IC, Ryu JS (2000) Hepatic and small bowel mucormy-cosis after chemotherapy in a patient with acute lympho-cytic leukemia. J Korean Med Sci 15:351–354

Thoeni RF, Cello JP (2006) CT imaging of colitis. Radiology240:623–638

Tresallet C, Nguyen-Thanh O, Aubriot-Lorton MH, Akakpo JP,Al Jijakli A, Cardot V, Chigot JP, Menegaux F (2004) Smallbowel infarction from disseminated aspergillosis. Dis ColonRectum 47:1515–1518

van Wolfswinkel ME, Lahri H, Wismans PJ, Petit PLC, vanGenderen PJJ (2008) Early small bowel perforation andcochleovestibular impairment as rare complications oftyphoid fever. Travel Med Infect Dis 7:265–268

Wu CM, Davis F, Fishman EK (1998) Radiologic evaluation ofthe acute abdomen in the patient with acquired immunode-ficiency syndrome (AIDS): the role of CT scanning. SeminUltrasound CT MR 19:190–199

Zalev AH, Gardiner JW, Warren RE (1996) NSAID injury tothe small intestine. Abdom Imaging 23:40–44

Acute Gastritis and Enteritis