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INFECTIONS OF COLON AND RECTUM INCLUDING AIDS RELATED INFECTIONS
Deepak Amarapurkar*, Rajiv Baijal
*Department of Gastroenterology, Bombay Hospital and Medical Research Centre, and Jagjivan Ram Western Railway Hospital, Mumbai.
INTRODUCTIONAcute diarrhoea represents a non-specific response of the intestine to a number of different kinds of insults including infections, adverse drug reactions, inflammatory bowel disease and ischaemia. Acute infectious diarrhoea causes a wide spectrum of illness ranging from minor inconvenience to a severe illness resulting in profound volume depletion and death. Infection is acquired predominantly through oral ingestion of pathogenic microorganism and/or toxins produced by microorganisms. Patients present with complaints of diarrhoea that may be noticeably bloody and is the result of an organism causing an inflammatory reaction either by direct invasion of colonic/ileal epithelium or by tissue damage. Symptoms associated with diarrhoea may include abdominal pain and cramping, tenesmus, fever and dehydration (Table 1).
On a clinical basis it is useful to categorize infectious diarrhoea into (1) inflammatory or bloody diarrhoea and (2) noninflammatory or watery, nonbloody diarrhoea, because the differential diagnosis of aetiologic organisms, the site of intestinal involvement and the outcome and management are different (Table 2). Stool examination must be done in all cases for occult blood, bacteria and parasites. Stool should also be tested for Clostridium toxin if the patient has been on antibiotics. Microscopic examination of a stool smear for the presence of faecal leucocyte is useful in distinguishing inflammatory and non inflammatory diarrhoea. The faecal leucocytes examination is considered positive if 3 or more polymorphonuclear leucocytes are present per high power field in four or more fields (Table 3).
Viral Bacterial Protozoal Rota virus
Norwalk virus
Enteric adenovirus
Calcivirus
Astrovirus
Small round virus
Coronavirus
Herpes simplex virus
CytomegalovirusShigella
Salmonella
Campylobacter
Escherichia coli
Yersinia
Clostridium difficile
Clostridium perfingens
Staphylococcus aureus
Bacillus corus
Vibrio cereus
Chlamydia
Nisseria
Treponema pallidum
N. gonorrhaea
Entamoeba histolytica
Cryptosporidium
Giardia lamblia
Inflammatory Diarrhoea Non inflammatory Diarrhoea Faecal leucocyte count Positive Negative Clinical Presentation Bloody, small volume diarrhoea,lower left quadrant abdominal cramps, may be febrile and toxic Large volume, watery diarrhoea, may have nausea, vomiting cramps. Causes Shigella, Salmonella,campylobacter, Yersinia,Invasive E. coli, YersiniaClostridium difficile Viruses, vibrio, Giardia,Enterotoxigenic E. coli enterotoxin producing bacteria, foodborne gastroenteritis Site of involvement Colon Small intestine Diagnostic evaluation Indicated If severely volume depleted or toxic
Infectious causes Non infectious causes Shigella
Salmonella
Campylobacter
Invasive E coli
Yersinia
Clostridium difficileInflammatory bowel disease
Radiation colitis
Ischaemic colitis
Sigmoidoscopic examination helps to differentiate between conditions that cause mucosal disruption from those that have no mucosal changes or only microscopic changes. Biopsies obtained from normal and abnormal mucosa may provide distinguishing information. The final diagnosis may depend on identifying a specific organism, toxin, allergen or drug, finding other GI lesion or noting the response to certain medications (Tables 4,5 and 6).
Bloody Diarrhoea Diarrhoea Inflammatory bowel disease Pseudomembranous colitis Drugs
Diversion colitis
Solitary rectal ulcer
Radiation induced colitis
Ischaemic colitis
EndometriosisCollagenous colitis
Microscopic colitis
Laxative/diuretic use
Pseudomembranous colitis
Drugs
Irritable bowel syndrome
Food allergy
Malabsorption
Colitis cystica profunda
Faecal impaction
Pneumatosis cystoides intestinalis
Crohn’s disease
Proctitis Proctocolitis or Enterocolitis Chlamydia trachomatis
N gonorrhoeae
Herpes simplex virus
T pallidum
Human papilloma virus (anal warts)Campylobacter
Shigella
E. histolytica
Salmonella
Shigella
Campylobacter
Mycobacterium avium intracellulare
Mycobacterium tuberculosis
Cryptosporidium
Isospora
Cytomegalovirus
Herpes simplex virusSPECIFIC DISEASES AFFECTING THE COLON AND RECTUM
Bacterial Infections of the Colon (Fig. 2)
1. Infection with Shigella speciesShigella is a gram-negative bacillus. Shigella infections are caused by S. sonnei, S. flexeneri, S. dysenterie and S. boydi. Shigellosis is most common in children between ages 6 months and 5 years. S. sonnei usually is the cause, whereas S. flexneri is the more common isolate in persons older than 15 years, S. dysenterie has produced epidemic shigellosis. The organism is transmitted by faecal-oral contact. It is highly infectious and intestinal damage occurs with ingestion of as few as 10-100 organisms. Intestinal damage occurs primarily from direct invasion of the organism into the colonic epithelium and to a lower extent, by the production of an enterotoxin. The shigella toxin is composed of an subunit which is catalytic and a B subunit, which is responsible for binding. The endoscopic appearance of shigellosis shows intense involvement of the rectosigmoid with varying levels of proximal colonic involvement. Approximately 15% of shigella cases will have a pancolitis. In children, shigella infection has been associated with the occurrence of seizures. Antibiotics reduce the duration and severity of symptoms in shigellosis and shorten the period of faecal excretion of the organisms. Ciprofloxacin, tetracycline, ampicillin and trimethoprim - sulphamethoxazole are effective against the organism.In addition oral or intravenous rehydration should be given. Antidiarrhoeal agents are contraindicated. Oral vaccines are being developed against infections with shigella organisms.
Organism Risk Factors/Reservoirs Therapy Campylobacter* Contaminated food,water, raw milk, infected animals and humans. Erythromycin
CiprofloxacinSalmonella* Food (Milk, eggs,poultry, meat) water,infected humans Ampicillin TMP/SMX Shigella* Food, water,infected humans Ciprofloxacin
TMP/SMX
Ampicillin
TetracyclineEscherichia coli Beef, raw milk, direct contact Supportive care Aeromonas* Untreated Water TMP/SMX Plesiomonas Uncooked shellfish TMP/SMX Yersinia* Food (Milk product Tofu) water TMP/SMX Entamoeba histolytica Travel to endemicareas (Food, water, fruit) Metronidazole Clostridium difficile Antibiotic use,Chemotherapy Metronidazole
Vancomycin
Cholestyramine*Mild to moderate symptoms do not require therapy;
TMP/SMX = trimethoprim/sulphamethoxazole
Water - soluble contrast media (e.g. Gastrograffin)
Hydrogen peroxide.Agents that induce ischaemia :
Oral contraceptives
Vasopressin
Ergotamine
Cocaine
Dextroamphetamine
Neuroleptics
DigitalisLaxatives
Anthraquinones (e.g. Cascara sagrada, aloe rhubarb, senna, frangula) induce melanosis coli and cathartic colon.Miscellaneous
NSAIDs
Gold
Isotretinoin
Antibiotics
Chemotherapy (e.g. cyclophosphamide, methotrexate 5 FU and cytosin) arabinoside)
Methyldopa
Flucytosine
Type of ulcers Primary location Size in cms Features Therapy Non specific 0.5-6.5 Antimesenteric
locations,
oval to roundSurgery for
perforation haemorrhage or abscess formationsDieulafoy’s (Fig. 9) Variable < 2 mm Erosions into large
submucosal arteryDiagnosis by mesenteric angiography.
Surgical resectionStercoral Sigmoid,
rectosigmoid1-4 cm Associated with faecal impaction,
antimesenteric
locationSurgical resection Solitaryrectal(Fig. 10) Anteriorrectum < 1 cm Associated with rectal prolapse,motor disturbances of
the pelvic floorBowel retraining,
bulk laxatives,
abdominal
rectopexy for
rectal prolapseCrohn’sdisease(Fig. 11) Right colon 0.2-2.0 cms Multiple ulcers,nodularity, strictures.
Involvement of small intestineAnti inflammatory drugs, steroids Ischaemic(Fig. 7) Splenic flexure,
descending colon1-10cms Circumferential
shallow diffuse,
dusky mucosaSurgical resection Malignant Variable Variable Associated with mass stricture Surgical resection followed by chemotherapy Tubercular(Fig. 12) IleocaecalR colon Variable Circumferential. IC valve abnormal,terminal ileal disease, pseudo polyps may be present ATT surgeryfor perforation,
obstruction
2. Infection with Campylobacter species
C. jejuni accounts for 98% of isolates reported. Direct contact with faecal matter from infected persons or animals and the ingestion of the contaminated food or water have been implicated in transmission of Campylobacter infection. Incubation period is 1-7 days. Symptoms include diarrhoea (often bloody), abdominal pain, malaise, headache and fever. Most patients recover within 7 days, with or without antibiotic therapy but relapse may occur. Complications include bacteraemia, toxic megacolon, Reiter’s syndrome and hemolytic-uraemic syndrome. Recurrence in patients with AIDS may stem from persistence of the organism in gallbladder. The sigmoidoscopic findings in the rectum and sigmoid colon are indistinguishable from those of ulcerative colitis. A tentative diagnosis of campylobacter infection can be made if Gram stain of the stool shows commashaped, gram negative bacteria. The diagnosis is confirmed by positive stool cultures. The main stay of therapy is fluid and electrolyte replacement. Erythromycin is often given for severe dysentery or relapsing infection, but there is no evidence that it reduces the duration or severity of symptoms. Ciprofloxacin is an alternate choice, but quinolone resistant strains have been described.
3. Colitis Induced by Escherichia Coli
E. coli belongs to the family Enterobacteriaces and are facultative, anaerobic, gram-negative bacteria.
Enteroinvasive E. Coli (EIEC)
It is an important cause of traveller’s diarrhoea, food borne gastroenteritis and diarrhoea in children in developing countries. This strain can invade the intestinal mucosa and usually presents with bloody diarrhoea, fever, abdominal cramping tenesmus and myalgias. The disease is usually self-limited. The role of antibiotic therapy is undefined, but it is reasonable to give trimethoprim-sulphamethoxazole, ampicillin, or ciprofloxacin to patient with dysentery.
Enterohaemorrhagic E. Coli (EHEC)
Infection with EHEC is caused by 0157 : H7 strain, which can be formed in poorly cooked ground beef unpasteurized dairy products, and faecally contaminated water. The patient usually presents with severe abdominal cramps and watery diarrhoea which then progresses to bloody diarrhoea. The organism is not invasive but produces disease from Shiga-like toxin that is cytotoxic to vascular endothelial cells in vitro. Complications include haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) which occur most commonly in children or in those with severe bleeding and leucocytosis. Recovery without sequelae is the usual outcome, although patients with HUS and TTP may have renal failure and neurologic deficit. Antibiotics are not recommended because they may increase toxin production.
Enterotoxigenic E. Coli (ETEC)
It accounts for most of traveller’s diarrhoea. Transmission is by faecal-oral route, through ingestion of contaminated food or water. Disease is produced by adherence of ETEC to the mucosa, followed by production of toxins. Invasion of the mucosa does not occur. The usual course of the disease is a self limited, 3-5 days illness characterized by watery diarrhoea and abdominal cramping. Occasionally, a low grade fever and rarely, a bloody diarrhoea are associated with this illness.
Enteropathogenic E. Coli (EPEC)
This strain also lacks invasive properties. Illness primarily affects the young (< 2 years of age) and must be considered as a probable cause in out breaks of diarrhoea in hospitalized infants. Profuse watery diarrhoea, which can become chronic is the usual presentation. It rarely results in bloody diarrhea.
4. Infection with Yersinia Enterocolitica
The most common presentation is diarrhoea, abdominal pain and low grade fever. Most cases are self limited and do not require antibiotic therapy. Approximately 25% of the diarrhoea cases are grossly bloody. Children and young adults can present with a pseudo-appendicular syndrome manifested by symptoms of right lower quadrant pain and tenderness fever and leucocytosis. Microscopic stool examination usually shows red and white cells. Findings at surgery show nesenteric lymphadenitis and terminal ileitis. On rare occasions, a patient may progress to a fulminant enterocolitis with possible perforation, peritonitis, and major intestinal haemorrhage. Pharyngitis is common in children and is seen in upto 10% of adult cases. Patients with an iron-overload state (haemochromatosis) are susceptible to sepsis from Yersinia. Post infectious manifestations of reactive arthritis, erythema nodosum, Reiter’s syndrome, thyroiditis, myocarditis and glomerulonephritis have been reported.
5. Infection with Vibrio Parahaemolyticus
It is a member of the vibriolonacease family and is a halophilic organism (grows only on media containing salt). This organism has been isolated in fish, crutacenous and shellfish. The resulting diarrhoea is commonly watery, but upto 15% of patients present with bloody diarrhoea.
Other organisms that cause dysentery and are associated with seafood ingestion are Pleisomonas Shigelloides and Campylobacter.
Enterocolitis induced by Clostridium Difficile (Fig. 3)
Pseudomembranous colitis (PMC) is caused by C. difficile, a gram positive, spore forming, anaerobic bacillus. It is mediated by two toxins enterotoxin A and cytotoxic B. Patients are susceptible to C. difficile diarrhoea during and after cessation of antibiotic therapy. The incidence of C. difficile carriage in patients ranges from 7-21%, however, diarrhoea develops in only one-third of these patients. Clindamycin, the penicillin and the caphalosporins are most frequently associated with this syndrome. Other risk factors are cancer chemotherapy, Immunosuppression and hospitalization. A stool assay for C. difficile toxin should be obtained in any patient suspected of having PMC. Culture is very sensitive but not very specific, because upto 20% of hospitalized patients are colonized with C. difficile. The endoscopic appearance of the involved colonic mucosa can range from normal to a classic appearance of a pseudomembrane i.e. 1-3 mm yellow-whitish plaque - like lesions, that are scattered or confluent over the colonic mucosa. The histologic appearance of pseudomembrane shows a “Summit” lesion on the surface of the colonic epithelium which is composed of inflammatory cells, fibrin and mucus. Treatment consists of stopping the incriminated antibiotic and drug therapy consisting of oral bacitracin or metronidazole or vancomycin in patients with moderate to severe symptoms. An alternative to antibiotic therapy is the oral anion exchange resin cholestyramine. The resin binds C. difficile toxin while the colonic flora reconstitutes itself. Resin is indicated in mild cases and treatment of relapse which occurs in 15-20% cases. Faecal enema and probiotics (e.g. oral saccharomyces boulardi) have been used experimentally to re-establish colonic bacterial flora.
Colorectal Disease and HIV (Table 6)
As with non-immunosuppressed patients, colitis secondary to invasive bacteria (salmonella, shigella, campylobacter and Yersinia) bacteria that produce cytotoxic (EHEC) and amoebiasis must be considered. Proctitis and bloody diarrhoea can occur due to rectal gonorrhoea, lymphogranuloma venereum (Chlamydia trachomatis), primary anorectal syphilis and herpes simplex. The hallmark of herpes proctitis is severe rectal pain, purulent, rectal discharge and difficulty in urination. Inguinal lymphadenopathy and perianal ulcerations may be noted.
CMV colitis is characterized by abdominal pain, diarrhoea haematochezia and fever. Patchy involvement of colonic mucosa is seen on colonoscopy and diagnosis is aided by the identification of cytomegalic inclusion cells. Pseudomembranous colitis must also be in the differential diagnosis for individuals with AIDS who are taking or have recently completed antibiotic therapy (Fig. 4).
Cryptosporidium, isospora belli, microsporidia, giardia, mycobacteria avium intracellulare and lymphoma all of which can cause diarrhoea in this population typically affect the small bowel but do not cause a bloody diarrhoea. Patients who have inflammatory bowel disease and then acquire AIDS may show improvement in their IBD probably secondary to immunosuppression from HIV.
Sexually Transmitted Colorectal Pathogens (Table 5)
Gonorrhoeal Proctitis
Asymptomatic rectal carriage of N gonorrhoea is common in promiscuous gay men. The symptoms of acute rectal gonorrhoea include a creamy rectal discharge, haematochezia, constipation or obstipation and anal dyspareunia. Complications include perirectal abscesses, fistulae, strictures and sepsis. Sigmoidoscopy reveals rectal erythema and friability. The diagnosis is based on positive cultures obtained from rectal swabs. Therapies for rectal gonorrhoea that produce cures in 95% of cases include intramuscular procaine penicillin G (4.8 million units) with oral probenecid (1 gm) or intramuscular spectinomycin (2 gm). Third generation cephalosporin are effective against penicillin resistant strains.
Proctitis Caused by Chlamydia Trachomatis (Fig. 5)
Infections with C trachomatis, the causative agent of lymphogranuloma venereum, accounts for 20% of proctitis in gay men. Asymptomatic carriage occurs in 2-5% of gay men. Patients usually present with bloody diarrhoea, mucopurulent discharge and less commonly tenesmus, constipation and fistulae. Physical examination may reveal tender, enlarged inguinal lymph nodes (buboes). Biopsy specimens of rectum show granulomatous inflammation with giant cells, inflammation with neutrophils, esoinophils and crypt abscesses and visible organism on Giemsa staining. The diagnosis of proctitis caused by C-trachomatis is confirmed by culture of rectal swabs. The treatment of choice is tetracycline 500 mg qid for 2-3 weeks.
Proctitis Caused by Herpes Simplex Virus (HSV) (Fig. 6)
It presents with intense anal pain, tenderness, tenesmus, discharge, constipation, urinary symptoms (retention, weak stream), pain (in abdomen, buttocks, thighs) impotence and sacral paraesthesia. Sigmoidoscopy may reveal focal ulcers and vesicles. Diagnosis depends on viral isolation from rectal swabs or biopsy specimens showing acute and chronic inflammation microabscesses and superficial ulcerations. Acyclovir appears to hasten clinical recovery.
Anorectal Syphilis
Proctitis caused by Treponema pallidum is characterized by rectal pain, discharge and tenesmus. Primary syphilis may produce anal chancres, the exudate of which may reveal spirochaetes on dark field microscopy, secondary syphilis produces flat wart like perianal and penile lesions called condylomata lata. The diagnosis is confirmed by serologic testing, although false negative tests are common in early disease.
Therapy includes intramuscular benzathine penicillin (2.4 million units, single dose) or tetracycline (500 mg qid for 15 days).
Anal Warts
Condylomata acuminata are verrucous skin coloured or pink papilliform skin lesions resulting from infections with human papilloma virus (HPV). Warts occur on glans penis in men and on the labia, vulva and cervix in women. Anal warts in men are frequently but always associated with receptive anal intercourse. They may cause strictures, discharge and bleeding. The therapies include podophyllin, cryotherapy and surgical fulguration, but recurrences and post therapy strictures are common.
COLORECTAL DISEASES MIMICKING INFECTIOUS COLITIS
1. Collagenous and lymphocytic colitis
These are syndromes characterized by chronic watery diarrhoea with histologic evidence of mucosal inflammation but normal endoscopic and radiographic appearances. Both disorders exhibit infiltration of lamina propria with mononuclear cells, epithelial cells damage, preserved crypt architecture without cryptiis. Collagenous colitis is distinguished from lymphocytic colitis by presence of a subepithelial band of collagen that is 10-100 µu thick (normal/4 µu). The mean age at presentation is 60-65 years, and most patients are women.
These disorders are immunologically mediated and many histologic features resemble those of coeliac sprue, which is associated with collagenous and lymphocytic colitis, as are arthritis and other autoimmune disorders. Proposed aetiologic agents include NSAIDs, bacterial cytotoxins, bile salt malabsorption and a genetic predisposition. Diarrhoea is caused by defective sodium and chloride absorption and defective chloride/bicarbonate exchange. The diagnosis of these disorders is made by colonoscopy with biopsy, which will be positive in 80% of patients. Drugs that have shown efficacy in treating these conditions include 5-aminosalicylate, sulphasalazine and prednisone. Coeliac sprue should be excluded and antihistamines should be considered for patients with large numbers of mast cells in biopsy specimens.
2. Diversion Colitis
Diversion colitis is an inflammatory process that is seen in the portion of colon from which the faecal stream has been diverted. This is usually seen in Hartmann’s pouch that is formed after sigmoid resection. The endoscopic and histologic appearance of the mucosa is similar to that of ulcerative colitis. These changes resolve promptly following anastomosis of the bowel and restoration of faecal stream. Proposed theories as to the cause of this inflammatory reaction include overgrowth of normal bowel flora and a nutritional deficiency of short-chain fatty acids which are produced by anaerobic bacteria and are used as an energy source by the colonic epithelial cells. Therapy is not needed for mild cases, In severe cases, short chain fatty acid enemas induce remission in most cases. 5-ASA enemas may be useful, however, corticosteroid enemas are usually ineffective.
3. Ischaemic Colitis (Fig. 7)
Most patients are middle aged or elderly and have a history of atherosclerotic heart disease and/or peripheral vascular disease. Medications that have been implicated in colonic ischaemia include digitalis, NSAIDs diuretics, vasopressin, gold compounds and some cancer chemotherapeutic agents. A common complication of surgical repair of an abdominal aortic aneurysm is colonic ischaemia.
The left colon is the segment most commonly affected (75%). The next most common segments are the transverse colon (15%) and right colon (5%). The rectum is rarely involved due to its rich blood supply.
The patients complain of sudden onset of abdominal pain. The degree of bloody diarrhoea is variable. An acute abdominal series may show “thumbprinting” of the colonic mucosa. Flexible sigmoidoscopy is the mainstay of diagnosis. The rectum is usually spared due to its collateral blood flow. Above the rectum, the mucosa becomes friable, and oedematous, and there may be areas of haemorrhage and ulceration resembling those of Crohn’s disease. Angiography is generally not helpful in the evaluation of ischaemic collitis. Ischaemia colitis is a small vessel disease (nonocclusive), as oppposed to mesenteric midgut ischaemia of the small bowel, which involves thrombosis or embolism in the superior mesenteric artery (occlusive). A barium enema is contraindicated in suspected ischaemic colitis. Treatment is supportive with frequent abdominal examination and monitoring of vital signs. Most patients recover with supportive treatment. Some patients improve but develop a colonic stricture. Other patients may progress to bowel infarction with development of peritonitis and possible perforation requiring laparotomy and intestinal resection.
4. Radiation Enterocolitis (Fig. 8)
Therapeutic radiation usually for prostate, bladder, and gynaecologic or rectal cancers - results in a dose dependent acute injury to the bowel that is within the treatment port. This injury develops shortly after the onset of radiotherapy, leaving the bowel mucosa oedematous, erythematous and friable. Histologically, there is an acute inflammatory cell infiltrate, and often there are crypt abscesses composed of eosinophils. The patients have symptoms of diarrhoea, tenesmus, abdominal cramping and sometimes blood in stools. Symptoms may develop from 6 months to 30 years after irradiation. The incidence is generally reported as 2-10%. The most serious problems are severe bleeding, significant stricturing and fistula formation between bowel loops and other organs such as the vagina.
Predisposing factors include hypertension, diabetes mellitus, pelvic inflammatory disease, thin physique, prior abdominal or pelvic surgery concomitant chemotherapy and amount of radiation exposure. Interestingly having acute radiation injury does not seem to correlate with the development of chronic radiation injury. The delayed injury seems to be due to vasculitis with endarteritis. All layers of the bowel wall are affected, including the serosa. Barium studies help by showing lack of haustra, mucosal effacement, narrowing, ulcerations and fistula in involved segments of bowel. The endoscopic findings include ulcerations, inflammatory change, atrophic mucosa, luminal narrowing or telangiectasia.
Antidiarrhoeal and anticholinergic drugs treat acute radiation injury. Anti-inflammatory drugs are rarely required.
Delayed injury is treated with anti-diarrhoeal agents, anti-inflammatory agents, topical or systemic steroids depending upon the severity of symptoms. Bleeding telangiectasias can be treated by ablative therapy using endoscopically applied energy from an Nd : YAG laser. Surgery for major complications may be undertaken but is difficult due to extensive intra-abdominal adhesions. Consequently, bypass or diversion surgery rather than direct corrective interventions are done.
Typhlitis
It is an acute necrotizing colitis primarily of the caecum, occurs mainly in immunosuppressed patients with leukaemia, cancer chemotherapy, aplastic anaemia, bone marrow transplant and AIDS. Involved segments of intestines exhibit ulcers, wall - thickenings, haemorrhagic necrosis and luminal dilatations. Histologic findings include submucosal oedema, necrosis, and presence of fungal and bacterial organisms in small vessels. Typhlitis must be considered in febrile neutropenic patient with abdominal pain, nausea, vomiting, distension, diarrhoea and associated stomatitis and pharyngitis. Blood cultures positive for pseudomonas, candida or other enteric organisms suggests sepsis.
Medical therapy includes nasogastric suction, intravenous hydration; antibiotics to treat pseudomonas organisms. Amphotericin B is added if fever persists for > 72 hours. Surgery is indicated for perforation, severe haemorrhage, uncontrolled sepsis and refractory disease. Typhlitis has a high mortality rate (40-50%).
Colitis Cystica Profunda
It is a benign disease characterized by presence of large, submucosal, mucous filled cysts usually in the rectum. The lesions can be solitary or multiple in localized, segmental or diffuse distribution. The condition is associated with local trauma of the bowel and the symptoms regress after a diverting colostomy. It is a manifestation of a spectrum of disease states including solitary rectal ulcer syndrome and rectal prolapse. Patients present at a mean age of 30 years with bloody or mucous rectal discharge, diarrhoea abdominal or rectal pain, tenesmus or obstruction. Endoscopic findings include obvious cysts with overlying normal mucosa or it may show erythema, oedema, friability, ulcerations, mass, prolapse or stricture, usually on the anterior rectal wall within 12 cms of the anal verge. Histologic findings include submucosal enlargement with benign cysts, replacement of lamina propria with collagen and smooth muscle cells and mucosal oedema, ulcerations, inflammation, pseudomembranes and crypt distortion. Minimal symptoms can be managed by dietary fibre supplementation. Local surgical procedures (cyst excision, posterior proctectomy, electrocautery, injection sclerosis) are needed to treat patients with haemorrhage, obstruction, pain or stenosis. Recurrence is common and diverting colostomy is reserved for the most disabled patients.
Pneumatosis Cystoides Intestinalis
It is characterized by multiple thin walled gas filled cysts varying in size from few to several millimeters with no epithelial lining. It is associated with COPD, intestinal obstruction, scleroderma, bowel infarction, pseudomembranous colitis and necrotizing enterocolitis. It may occur after surgery or endoscopy. The cysts contain hydrogen gas and are located in the submucosa or subserosa near the mesenteric border. It may occur due to mechanical introduction of gas into the bowel wall, invasion of bowel wall by gas producing bacteria and trapping of excess intraluminal gas produced by bacterial carbohydrate fermentation within the bowel wall. Patients may be asymptomatic or may present with diarrhoea abdominal discomfort, distension, haematochezia, and mucus discharge and weight loss. Complications include volvulus, haemoperitoneum, obstruction, intussusception haemorrhage and perforation. A CT scan is more sensitive than barium radiography in detecting intramural gas and portal vein mesenteric gas. On endoscopy the cysts are multiple, pale blue, rounded soft masses. Cysts usually resolve with treatment of underlying condition but some patients may benefit from high flow oxygen on even hyperbaric oxygen therapy. Metronidazole and ampicillin have been used in some patients. Surgery is reserved for severe refractory symptoms or complications, but post operative cyst recurrence is common.
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