Balloon tamponade In cases where endoscopic control of bleeding is not pos- sible or when i t will be some time before endoscopy will be possible, the use of balloon tamponade may be consid- ered. Once passed, the gastric balloon of the Sengstaken \200\223 Blakemore tube sh ould be in \202 ated with water ( soluble contrast medium) and gentle traction applied b y taping the tube to the side of the face. Effective control of bleeding will occur in 80 \200\22390% of cases. The risk of complications including oesophageal necrosis and perforat ion are high; therefore, de \201 nitive therapy must be performed within 24h. There is no evidence that the routine cooling of such tubes prior to use is helpful. Medical reduction of portal pressure Vasopressin is a potent splanchnic and peripheral vaso con- strictor that has been shown to reduce portal pressure. It has a short plasma half-lif e and must be given as a continu- ous infusion. It may be appropriate to give concurrent IV nitrates to ameliorate peripheral vasoconstriction. Terlipressin is a longer acting synthe tic vasopressin ana- logue that can be given as a 4-hourly bolus. It is associated with few er side effects than vasopressin. Somatostatin and analogs such as octreotide may also be g iven to reduce portal pressure in variceal bleeding. Pharmacological therapy to reduce port al pressure is the \201 rst-line treatment in the management of variceal bleeding and sho uld be initiated as soon as the diagnosis is sus- pected. Vasoactive drugs should continue for 2 \200\2235 days to reduce the risk of rebleeding. Although propranolol is proven to re duce the risk of bleeding, -blockade will reduce blood pressure and amel- iorate the comp ensatory tachycardia induced by hypovol- aemia. It is therefore contraindicated in the sett ing of an acute bleed but should be started once the initial episode is resolved. General measures in management of variceal bleeding Adequate IV access, with wide-bore peri pheral cannulae, should be obtained as a priority. Standard practice is to inset two 14G ca nnulae on the antecubital fossae. CVP monitoring may be useful in guiding resuscitation, bu t abso- lute pressures may be falsely elevated in patients with ascites. The response of CV P (or mixed venous saturation) to a \202 uid load remains a useful measure. Encephalopath y is common in cirrhotic patients and may be a consequence of the bleed or associated patho logy. It is standard practice to give regular lactulose to prevent encephalopathy, although this recommendation is not evi- dence based. Endotracheal intubation may be necessary to e nsure airway protection and is strongly recommended if prolonged therapeutic endoscopy or p lacement of a Sengstaken \200\223Blakemore tube is planned. Resuscitation There is experimental evidence that vigorous resuscitation may provoke reblee ding and increase mortality. Published international guidelines therefore promote prompt bu t cautious blood volume resuscitation with the aim of main- taining haemodynamic stability, adequate renal and cere- bral perfusion and a hemoglobin of 8g/dl. Endoscopic therapy Endoscopy is both diagnostic and therapeutic, and should be performed ur gently once the patient has been trans- fused and stabilized. Guidelines recommend endoscop y is performed within 12h of admission to hospital. A meta-analysis of 10 RCTs showed super ior early control of bleeding from oesophageal varices with endoscopic band ligation relati ve to sclerotherapy. Variceal band ligation is the recommended form of endoscopic therapy, but scle- rotherapy should be performed if band ligation is not tech- nically feasible. Correction of coagulopathy Coagulopathy and thrombocytopaenia are common in patients with d ecompensated chronic liver disease. FFP should be infused if the prothrombin time is prolon ged. Cryoprecipitate may be given if there is hypo \201 brinogenaemia. Recombinant activat ed factor VII did not improve outcome relative to standard therapy in a multi-center placeb o-con- trolled trial. A post hoc analysis of a subpopulation of 327 CHAPTER 20.5 Bleeding varices resuscitation and the correction of coagulopathy, empiric antibiotics and pharmacological t herapy to reduce portal pressure should be given. Endoscopic therapy with band ligation or sclerotherapy can be attempted but may lead to recurrent bleeding from iatrogenic ulceratio n. Local tam- ponade with a urinary catheter inserted per rectum is effective but carries a signi \201 cant risk of local necrosis if the balloon is left in \202 ated. TIPS is effe ctive in uncontrollable bleeding. Bleeding from gastric varices is harder to control than bleeding from oesophageal varices. Injection of cyanoacr- ylate tissue glue is effective in achieving haemostasis and prevents rebleeds. Not all endoscopists are experienced in the use of tissue glue, and in this case consideration should be given to temporary balloon tamponade prior to trans- fer or de \201 nitive therapy. Salvage therapy Rebleeding from oesophageal varices, de \201 ned as further haematemesis o r ongoing transfusion requirements >2h after endoscopic therapy, should be managed by repea t therapeutic endoscopy. If this is unsuccessful, consideration should be given to creation of a portal \200\223systemic shunt. This may be performed radiologically (TIPS) or sur- gi cally. The aim is to reduce the portal venous pressure to <12mm Hg. Early TIPS and surgery have been shown to improve survival in high risk patients. The performance of both surgery and TIPS is dependent upon local ex- pertise. All shunt procedures carry a risk of chronic encephalopathy. TIPS is effective in control of gastric variceal bleeding in 90% of cases. The threshold for TIPS should be lower in bleeding from gastric than oesophageal varices. Further reading Bosch J, Thabut D, Bendtsen F, et al. Recombinant factor VIIa for upper gas trointestinal bleeding in patients with cirrhosis: a rand- omized, double-blind trial. Gast roenterology 2004; 127: 1123-30. de Franchis R. Evolving consensus in portal hypertension. Report of the Baveno IV consensus workshop on methodology of diagnosis and therapy in porta l hypertension. J Hepatol 2005; 43: 167 \200\22376. Garcia-Pagan JC, Bosch J. Endoscopic ba nd ligation in the treatment of portal hypertension. Nature Clin Pract 2005; 2: 526 \200\22335. Garcia-Tsao G, Sanyal AJ, Grace ND, et al. Prevention and manage- ment of gastroesophageal varices and variceal hemorrhage in cir- rhosis. Hepatology 2007; 46: 922 \200\22338. Vangeli M, Patch D, Terreni N, et al. Bleeding ectopic varices \200\224 treatment with tran sjugular intrahepatic porto-systemic shunt (TIPS) and embolisation. J Hepatol 2004; 41: 560 \200\2236. Rectal varices Bleeding from rectal varices is uncommon, and the evi- dence base of most tr eatments is limited. In addition to 328 A REECE-SMITH & S MIDDLETON Intestinal perforation Drug history A variety of drugs can lead to perforation. Commonly NSAIDs and steroids cause gastric or duodenal erosions, but this may also occur with other drugs such as meth- otrex ate. Broad-spectrum antibiotics, chemotherapy or immunosuppressive medication can lead to p seudomem- branous colitis which may perforate if megacolon devel- ops. Patients suffering perforation of a GI viscus may present to the ICU under a variety of cir cumstances. Acute presenta- tion is common when perforation is the primary diagnosis. Howev er, perforation may also develop as a secondary phenomenon complicating critical illness. G I perforation is associated with the development of sep- sis. In addition, such a patient m ay undergo the further insult of surgical intervention to treat the underlying cause. Whils t sepsis is a \201 nal common pathway following perfora- tion, its presentation depends o n the speci \201 c anatomical site. As such, there may be a variety of different signs, sy mp- toms and investigative \201 ndings. The degree of sepsis also varies with the site of perforation, as the stomach and duo- denal contents provide a fairly sterile, albeit highl y caustic \202 uid, compared with the high bacterial load experienced in fecal peritoniti s, a difference re \202 ected in morbidity and mortality \201 gures. Examination \200 Signs of peritonitis Rigid abdomen \200 Guarding \200 Percussion tenderness \200 Dist ended abdomen Absent bowel sounds Shock secondary to sepsis Subcutaneous emphysema Loss of liver dullness to percussion \200 \200 \200 \200 Causes \200 Peritonism may be absent in patients taking steroids or sedatives, or obese or frail elderl y patients. In \202 ammation \200 \200 \200 Erosive, e.g. peptic ulcer, drug or chemical erosions Autoimmune, e.g. Crohn \200\231s or v asculitides Infective, e.g. diverticulitis, cholecystitis, C. dif \201 cile colitis Ischae mia, e.g. Ischaemic colitis Radiation, e.g. Radiotherapy Unknown, e.g. Appendicitis Investigations Biochemical Testing serum amylase is vital in the acute abdomen. This is a n on-speci \201 c test, with values elevated in almost any acute abdominal pathology, but it is very rare for levels to be as high as 4 times the upper limit of normal as would be exp ected in pancreatitis. Pancreatitis must be excluded as it will initially contraindicate su rgery. Non-speci \201 c markers of in \202 ammation such as CRP may be elevated, and elec trolyte abnormalities or evidence of acute renal failure should be sought. A low albumin ma y be an indicator of both chronic and acute ill health. \200 \200 Neoplastic, e.g. carcinoma of the colon Iatrogenic, e.g. endoscopy, anastomot ic leak Trauma, e.g. blunt force or Boerhaave syndrome Mechanical, e.g. obstruction or pseu do-obstruction \200 \200 \200 Clinical approach Presenting complaint Primary presentations As the majority of the GI trac t is in the abdomen, symp- toms of perforation are usually those of peritonitis. Pain is a common complaint, constant in nature and exacerbated by movement. Less commonly the esophag us is perfo- rated and a patient may complain only of pain in the chest or neck. Both group s of patients may suffer respiratory compromise either due to pain on movement of the dia- phragm or due to pleural effusion, which is likely in oesophageal perforation. Hematology Other non-speci \201 c markers of in \202 ammation and infection such as incre ased or decreased levels of either leucocytes or platelets may be present. Clotting abnorma lities require correction, and preparations should be made to ensure that any required bloo d products are available, particularly if surgery becomes necessary. Radiology Plain X-ray is of some use in the initial work-up of patients. The classic featur e of intraperitoneal perforation leads to free gas under the diaphragm on erect CXR in 80% of cases. In oesophageal perforations, a pneumomediastinum may be demonstrated. Gas will be seen in up to 60% of abdominal \201 lms, and normally only a supine \201 lm is availa- ble. Rigler \200\231s sign is the radiological effect of air on both sides of the bowel wa ll. Free gas also becomes visible against the contrasting density of the liver. Gas may hig h- light the inferior border of the liver or the ligamentum teres, or may be seen as bubble s between the liver and the anterior abdominal wall. If gas collects in the pouch of Ruther ford Morrison, a triangular bubble may also be seen just medial and inferior to the 11th ri b. CT scanning has largely replaced contrast studies due to rapid advances in technology. H owever, water-soluble contrast studies remain useful in speci \201 c circumstances when fr ee gas is expected to be present within a body Secondary presentations Intestinal perforation may occur secondary to a period of critical illness. Pseudomembranous colitis presents with diarrhea, either in immunocompromised patie nts or associated with antibiotics used to treat a previous source of sepsis. The colon bec omes colonized with C. dif \201 cile, which causes diarrhea by producing enterotoxins and cytotoxins. The major risk factor for erosive gastritis is respiratory fail- ure especially due to sepsis. It is suggested that erosive gastritis may occur as a result of compromised mucosal blood \202 ow during critical illness, and raised end-expiratory pressures durin g ventilation decrease blood \202 ow further. This prevents normal healing and also resul ts in a decreased production of protective factors such as prostaglandins. 329 CHAPTER 20.6 Intestinal perforation does not reduce the risk of a colonic perforation but miti- gates against the effects shoul d it occur. Subsequent reversal of an ileostomy is a relatively simple procedure which can be carried out a few weeks later and which rarely requires a full laparotomy. In cases of s evere contamination and in \202 ammation, a laparos- tomy may be formed, whereby the lapar otomy wound is left open and a \200\230Bogota \200\231 plastic bag or a vacuum dressing is sewn into the wound to maintain the moist, sterile environment in the abdomen. This allows the abdomen to be accessed for further washout and it provides an increased volume in the abdomen, thereby preventing abdominal compartment syndrome, which may occur when the abdome n is closed tightly over very inflamed and oedematous bowel. The laparaostomy can either be closed on return to theater when the swelling has settled or can be closed over time with the assistance of a suction dressing. Pseudomembranous colitis is normally successfully tre ated with conservative measures alone. However, should the patient develop a toxic megacolo n, surgery may be consid- ered to prevent or treat perforation or simply to remove the sour ce of sepsis. There is no evidence for treating the colonic distension with colonoscopy, as might be done in psuedo-obstruction. Total colectomy and formation of ile- ostomy is the o peration of choice, but mortality is high. Survival is improved with early surgery, but the morbidity and mortality associated with surgery make the decision to operate a matter of d elicate timing. cavity. This applies to situations when the peritoneum has been recently opened during surg ery or during chest trauma, when a pneumothorax may co-exist with a rup- tured esophagus. Treatment options Conservative Any septic collection must be adequately drained. If a cer- vical or thoracic perforation is particularly small, does not produce major sepsis and does not enter the pleural space it may be allowed to drain into the esophagus whilst a NG tube drains the stomach. Intra-abdominal perforations can sometimes become walled off within an in \202 ammatory mass. Examples of this include diverticular and appendix masses which ar e sometimes treated with IV antibiotics, enabling resolution of the in \202 ammation prior to elective resection. Surgery may sometimes be avoided with the use of radiologically gui ded drains placed in intra-abdominal collections. Operative Oesophageal perforations in the cervical portion require drains placed at operati on. If the perforation lies in the tho- racic portion, a variety of treatment options are p ossible, including repair, diversion, diversion and exclusion or stent- ing. Common to thes e is the necessity to drain the pleural cavity using a large bore chest drain. Intra-abdomi nal perforations will cause soiling of the peri- toneum that must be washed out and drained . Decontamination of the abdominal cavity is followed by repair of the perforation, whose s ize and site will deter- mine the nature of surgery performed. A small gastric or duodenal ulcer can be oversewn with an omental patch and this can be performed as an open or laparos copic pro- cedure. Small bowel perforation may be closed or a seg- ment excised with primar y anastomosis. Colonic perforation may be associated with major contamination, and segmenta l resection may be necessary. Traditionally, primary anastomosis is not performed because o f the risk of anastomotic dehiscence. Instead the proximal colon is exteriorized as a colos tomy (Hartman \200\231s procedure) and the rectal stump either exteriorized as a mucous \201 stula or simply oversewn. A Hartman \200\231s procedure can be reversed electively whe n the in \202 ammatory process has completely settled, some 6 \200\22312 months later. A d efunctioning ileostomy Further reading Chase CW, Barker DE, Russell WL, et al. Serum amylase and lipase in the eva luation of acute abdominal pain. Am Surg 1996; 62: 1028 \200\22333. Koss K, Clark MA, Sanders DS, et al. The outcome of surgery in fulminant Clostridium diffic ile colitis. Colorectal Dis 2006; 8: 149 \200\22354. Rubesin SE, Levine MS. Radiologic diagnosis of gastrointestinal per- foration. Radiol Clin North Am 2003; 41: 1095 \200\223115, Stollman N, Metz DC. Pathophysiology and prophylaxis of stress ulcer in intensive care unit patients. J Crit Care 2005; 20: 35 \200\22345. Williams N, Everson NW. Radiological con \201 rmation of intraperito- neal free gas. Ann R Coll Surg Engl 1997; 79: 8 \200\22312. 330 A REECE-SMITH & S MIDDLETON Intestinal obstruction bleeding could point to a colonic malignancy or in \202 amma- tory bowel disorder with ass ociated stricturing. Upper GI malignancy sometimes presents with obstruc- tion and a histor y of dysphagia or early satiety. Non-bowel- related intra-abdominal malignancies may imping e on small bowel or colon, and are relevant in a comprehensive history. Pseudo-obstruction can be initiated by various factors including electrolyte disturbance, hypothyroidism, seps is or simply old age. Surgery itself, anesthesia, analgesia and analgesic medication may al l contribute to electrolyte dis- turbance. It is particularly common in the ICU setting bec ause of the amalgamation of many of these factors. The generic term intestinal obstruction includes both small and large bowel obstruction. Un treated, obstruction may lead to perforation, discussed in Chapter 20.6. Large bowel is at risk of perforation if it becomes overdistended, whilst the small bowel will tend to perfor ate at an area of stric- ture or ischaemia created by the cause of the obstruction or venou s congestion. Obstructed bowel represents a single organ failure and leads to an array of m etabolic sequelae that can necessi- tate a higher level of care. Patients may also require inten- sive monitoring following the operative management of the obstruction, which is ofte n the only curative option. Causes Mechanical obstruction of the bowel will generally be caused by factors either withi n the bowel lumen, e.g. impacted foreign bodies, including feces and gallstones; factors in the bowel wall, such as benign and malignant strictures; or factors outside the bowel wall , such as her- nias, adhesions and congenital bands. Falling somewhere between these two \201 nal groups are problems such as vol- vulus and intussusception. Ileus and pseudo-obstr uction are conditions that are not distinguished as separate entities in continental Europe , and no biochemical distinction has been described. However, the terminology may be useful to describe the differing severity of a predictable dysmotility of the bowel, perhaps foll owing surgery, and the progressive distension originally described by Ogilvie . Examination \200 \200 \200 \200 \200 Evidence of dehydration Distended abdomen Irreducible hernias Non-speci \201 c tenderness Specific left iliac fossa tenderness (closed-loop obstruction) Palpable mass or lymphadenop athy, e.g. on per rectum examination Tympanic percussion Tinkling bowel sounds Absent bowel sounds \200 \200 Investigations Although a microcytic anemia might suggest an underlying GI in \202 ammator y or malignant process, routine blood tests are required to identify biochemical or hematol ogical dis- turbances rather than to establish the diagnosis. Clinical approach History Clinical presentation depends on the level of obstruction. More p roximal ( \200\230higher \200\231) obstruction tends to lead to col- icky abdominal pain an d early onset of vomiting with rela- tively little abdominal distension. Small bowel obstru ction presents in this manner. Vomitus is bilious if the obstruc- tion lies distal to the s phincter of Oddi, and will appear increasingly faeculent at levels further down the ileum a nd colon. Unless there is a \201 stula between the small and large bowel the onset of fae culent vomiting will be a relatively late symptom. More distal ( \200\230lower \200\231) ob struction may present with insidious constipation, abdominal distension and relatively litt le pain or vomiting. Diarrhea may be a sign of impending or subacute obstruction, whereas a bso- lute constipation indicates established obstruction. In small bowel obstruction, const ipation may be a late event. In general terms, vomiting tends to be the presenting feature in small bowel obstruction and constipation in large bowel obstruction. In established inte stinal obstruction, constant pain may simply re \202 ect abdominal distension, but it may herald ischaemia indicative of impending perforation. Radiology Plain radiograph may reveal dilated loops of bowel and an absence of gas distal t o the obstruction. Sometimes gas and \202 uid levels are visible. Small bowel loops are d ilated if >3cm wide, and large bowel should be <6cm except at the caecum where 9cm is the a cceptable limit. The speci \201 c point of colonic obstruction is often dif \201 cult to assess accurately on plain radiograph. Occasionally, an obstructing hernia can be seen on p lain \201 lms, and a soft tissue mass may be seen with intussuscep- tion. An important si gn to note is the \200\230coffee bean sign \200\231 seen with closed-loop obstructions as these inevitably require urgent surgical decompression. Contrast studies in small bowel obs truction may seem something of a paradox, but in adhesional obstruction water-soluble contr ast passing through to the caecum within 4 \200\2238h of ingestion suggests that the patien t has a subacute obstruction that is likely to resolve with conserv- ative measures. Treatment options Conservative The initial priorities are resuscitation and symptom con- tr ol. Patients are likely to be suffering dehydration, and electrolyte disturbances should be corrected. An NG tube will decompress the stomach and limit vomiting, whilst a urinary cat heter will help to assess \202 uid balance. Adhesional obstruction may settle with these simple measures. Combined surgical and medical gastroenterology care is Past medical history The two most common causes of small bowel obstruction in developed cou ntries are abdominal hernias and post- surgical adhesions. Colorectal and gynecological sur gery are frequently associated with the development of post- surgical adhesions. Appendicec tomy and pouch surgery are notorious for severe and extensive adhesions. A history of persi stent change in bowel habit, weight loss and rectal 331 CHAPTER 20.7 Intestinal obstruction essential in those patients with in \202 ammatory bowel dis- ease, where systemic steroids and broad-spectrum antibi- otic therapy may be effective. There is a role for further immu nosuppressive drugs in Crohn \200\231s disease, but this must be balanced with the risk of sepsis and so this a specialist decision. Colonic volvulus can sometimes be reduced by rigi d or \202 exible endoscope, with decompression tube placement if the bowel remains viable . Pseudo-obstruction will normally resolve with correction of metabolic abnormalities, and neostigmine may promote a return of motility. 80% of severe cases will resolve with colonos copy and decompression tube insertion, although some require a repeated procedure and there is a 3% risk of perforation each time. resection and anastomosis if the affected segment is too long to perform a stricturoplasty. Stricturoplasty involves making a longitudinal incision in the bowel wall across the stric ture and then sewing the defect back together in a transverse plane. This is preferable for short strictures as it is a smaller operation and preserves bowel length. High volvulus or malrotation may not resolve with con- servative measures and usually require surgery. Dela yed surgery for incarcerated hernias simply increases the likeli- hood of the bowel becomin g compromised and resection required. Obstructing tumors need either resection or a decom- pression operation, even if there is metastatic disease. Small bowel or right-sided colonic tumors can be excised with primary anastomosis, whereas left-sided colonic tumors are trad itionally treated by Hartman \200\231s procedure. However, experienced surgeons may perform primary anastomoses, defunctioned by means of an ileostomy. Patients considered not to req uire resection may bene \201 t from simple defunctioning, or from the positioning of a col onic stent. Operative Surgery is indicated if symptoms fail to settle with con- servative measures, alt hough the timing is still a matter of discussion in the literature. Water-soluble contrast studies in adhesional obstruction may indicate whether conserva- tive measures are likely t o be successful, but the timing of surgery remains an issue of debate, and requires experi- ence. Speci \201 c time scales have been suggested, but none has been widely endorsed. Th e development of right iliac fossa tenderness in the presence of closed-loop distal colonic obstruction may indicate imminent caecal perfora- tion and requires laparotomy. Crohn \200 \231s disease may produce strictures after the initial in \202 ammatory event has settled, and these may require Further reading Abbas S, Bissett IP, Parry BR. Oral water soluble contrast for the manageme nt of adhesive small bowel obstruction. Cochrane Database Syst Rev 2005; (1): CD004651. Ogilvie H. Large intestine colic due to sympathetic deprivation. Br Med J 1948; 2: 671 \200\2233. Saunders MD, Cappell MS. Endoscopic management of acute colonic pseudo-obstruction. Endoscopy 2005; 37: 760 \200\2233. 332 N DUNNE & H REECE-SMITH Lower gastrointestinal bleeding Acute lower GI tract hemorrhage is bleeding originating distal to the ileocaecal valve; how ever, brisk hemorrhage from the upper GI tract must also be considered. If bleeding from th e anal canal is excluded, then lower GI hemorrhage represents 20% of all cases of GI haemo r- rhage. Bleeding due to hemorrhoids is a common occur- rence, but only rarely will it cau se major hemorrhage necessitating hospitalization. In most patients, the bleeding is freque ntly relatively minor amounts, and can be investigated on an out-patient elective basis. Th is chapter will focus on the more infrequent pro- fuse lower GI hemorrhage which requires u rgent investi- gation and treatment. AXR: may show mucosal oedema consistent with in \202 am- matory bowel disease CXR: indicat ed in the presence of localized peritonism to examine for pneumoperitoneum. Endoscopy: \202 exible sigmoidoscopy and colonoscopy are both excellent for imaging the c olonic mucosa in a well prepared patient; however, visualization can be poor in the presenc e of profuse ongoing bleeding as clot and feces will obscure the mucosa. Thus, in the acute setting they have a limited role, but can utilize diathermy or injection therapies to cont rol the source of bleeding if it can be identi \201 ed. Arteriography: with bleeding rates of 1.0 \200\2231.5ml/min this technique can show extravasation of contrast into the lumen of the bowel and hence identify the source of bleed- ing. The superior mesenteric artery is selectively catheter- ized initially as it is usually found to be the source of the bleedi ng, but should this not be the case the inferior mesenteric artery can then be catheterized . Coil or sponge embolization can be used to arrest bleeding points; how- ever, the risk of ischaemic colitis needs to be borne in mind. Clinical approach History \200 Determine onset of the bleeding, along with its fre- quency and quantity. Patients and rela tives \201 nd it dif \201 cult to ascertain the latter but using objective measures such as a spoon-full, eggcup-full, cup-full or bowl-full can help. Establish the color and cons istency of the blood; is it mixed in with the stool or just pure blood; are there any clots , etc. Ask about any associated symptoms such as a recent change in bowel habit, abdominal pain, weight loss or anorexia. Ascertain any previous episodes of GI hemorrhage, and any tr eatment given. Obtain a drug history focusing on any anticoagulant drugs including warfarin , clopidogrel and aspirin. Common causes to consider The two most common causes are diverticular disease and angiodysp lasia, with carcinoma of the colon and in \202 amma- tory bowel disease comprising a relat ively small percent- age of cases. Rarer causes to consider if the above are excluded inclu de a bleeding Meckel \200\231s diverticulum, endometriosis and iatrogenic injury following endoscopic investigation of the colon. Diverticular disease accounts for >50% of cases, wit h bleeding occurring from the rupture of nutrient vessels passing through the neck of the d iverticulae. Vessel rupture is as a result of in \202 ammation of/trauma to the colonic mu cosa. The diverticulae are typically acquired herniations of the mucosa and submucosa throu gh the muscularis, seen most commonly in the sigmoid colon (95 \200\22398%) although they c an extend proximally and involve any part of the GI tract. These diverticulae are diagnosed in the non-acute setting via barium enema or endoscopic exami- nation of the colon. The bl eeding rarely needs treatment (<10%) and often stops spontaneously; however, long-term recu rrence of the bleeding remains a substantial problem particularly in patients on anticoagul ant drugs. Angiodysplasia is responsible for 5 \200\22310% of cases, with bleeding due to o verstretched, dilated fragile vessels run- ning in the colonic mucosa. 80% of the vascular malforma- tions occur on the right side of the colon, with the remaining 20% affecting the left-side and the sigmoid colon. Diagnosis requires angiography, as the endoscopic \201 n ding of a characteristic cherry-red spot is subtle and easy to miss in the profusely bleedi ng Examination: key points The initial approach should be according to the ABCD sys- tem as fo r any critically ill patient, particularly looking for evidence of haemodynamic instability . Pale conjunctivae suggest clinical anemia. Abdominal tenderness or masses may give clues as to the cause, and rectal examination con- \201 rms the presence and nature of blood an d again may identify a cause. Investigations Bloods: the following should be taken routinely at the time of insertion of 2 large bore IV cannulae \200 \200 FBC: to establish hemoglobin and platelet concentration U&E: for evidence of renal failure. Note that an isolated elevated urea can indicate upper GI hemorrhage due to breakdown of h emoglobin in the GI tract. LFTs: derangement may give clues as to the presence of metastase s. Clotting: abnormal clotting may be due to anticoagulant drugs, or may indicate the prese nce of disseminated intravascular coagulation (DIC). Group&save: vital to send this off ear ly, and if the need for transfusion is obvious cross-match the necessary amount of blood an d clotting products. Management Resuscitation First and foremost, the patient must be assessed and resu- ciated according to the ABCD approach. \200 Proctoscopy: will con \201 rm the presence of hemorrhoids, and may show evidence of recent bleeding. Rigid sigmoidoscopy: to examine the rectum and distal sig- moid colon for eviden ce of mass lesions, colitis or diver- ticulae, and con \201 rm the presence of blood. Radi ology: dependent on the causes being considered. Airway and breathing are not normally a problem, but if there has been severe blood loss th e patient can be tachypnoeic with low oxygen saturations due to severe anemia. 333 CHAPTER 20.8 Lower gastrointestinal bleeding Circulation can be compromised with the patient tachy- cardic and hypotensive, depending on the volume of blood lost and the patient \200\231s ability to compensate for the loss. Two large bore IV cannulae must be sited, and blood taken simultaneously. In the presence of h aemodynamic instability rapid infusion of crystalloid \202 uid should be commenced, whils t waiting for cross-matched blood to be made available. If the patient is severely unstable with ongoing hemorrhage, then O negative blood can be transfused, but this is rarely neces sary. An arterial blood gas sample can give immediate information as to the degree of anemi a and acid \200\223base status. A urinary cath- eter should be sited to monitor urine outpu t in the unstable patient. Disability is not normally an issue unless the patient is severe ly hypotensive thus compromising their cerebral perfusion. Exposure and examination of the abdomen is necessary to elicit any abdominal tenderness or the presence of any masses. Rect al examination will con \201 rm the pres- ence of blood. in the presence of profuse active bleeding is contentious, and, if available, angiography a nd subsequent embolization is the preferred treatment option. If this is not available and the patient is unstable, then surgery is the only option. Without an identi \201 able sour ce of bleeding, subtotal colec- tomy must be performed. If a source has been identi \201 e d by endoscopy or angiography but not treated, then a targeted colonic resection can be per formed aided by on-table washout. Surgery is preferable at an early stage, as mortal- ity i s increased with increasing transfusion requirement. Further reading Collins D, Worthley L. Acute GI bleeding: part I. Crit Care Resusc 2001; 3: 105 \200\22316. Collins D, Worthley L. Acute GI bleeding: part II. Crit Care Resusc 2001; 3: 117 \200\22324. Edelman D, Sugawa C. Lower GI bleeding: a review. Surg Endosc 2007; 21: 514 \200\22320. Green B, Rockey D, Portwood G, et al. Urgent colonoscopy for evaluation and management of a cute lower GI hemorrhage: a randomized controlled trial. Am J Gastroenterol 2005; 100: 2395 \200\223402. Keeling W, Armstrong P, Stone PA, et al. Risk factors for recurrent hemorrhage after succes sful arterial embolization. Am Surg 2006; 72; 802 \200\2236. Once the patient is adequately resuscitated, then diagnos- tic tests can proceed as above. 80% of lower GI bleeds will settle spontaneously, and inves- tigation as to the cause can b e done electively. For the remainder that don \200\231t settle, immediate investigation and treatment is somewhat dependent on the services availa- ble locally. As mentioned previous ly, the role of colonoscopy Lim C, Shridhar I, Tan L, et al. Contrast CT in localization of acute lower GI bleeding. Asian J Surg 2006; 29: 92 \200\2234. Strate L. Lower GI bleeding: epidemiology and diagnosis. Gastroenterol Clin North Am 2005; 34: 643 \200\22364. 334 N DUNNE & H REECE-SMITH Colitis Differential diagnosis See Figure 20.9.1. \200 \200 \200 Colitis (and proctitis) describes in \202 ammation of the colon (and rectum) of any etiolo gy. It usually presents with pass- ing bloody stool with an associated increase in frequenc y. The consistency of stool often depends on the extent of the disease, with more extensive involvement often leading to an increased looseness of stool. Severe proctitis can, in fac t, present with constipation, although the patient often passes blood and mucus independent of stool in these situ- ations. Abdominal pain is more common in more extensive and severe disease and in ischaemic colitis. Systemic symp- toms such as fever, anorexia and weight l oss are more indicative of severe ulcerative colitis (UC) or Crohn \200\231s. Abdominal exa mination is often unremarkable apart from mild tenderness. Signi \201 cant tympanitic dist ension or any evidence of peritonism are of great concern and need urgent attention. Ulcerative colitis Crohn \200\231s colitis Infective \200 \200 Recent contact with infectious patient E. coli, Salmonella, Shigella, Campylobacter, Yersin ia are common causes Recent antibiotic use; think C. dif \201 cile infection Diverticular colitis \200 \200 Rectum looks normal in these patients Bleeding diverticulae seen on endoscopy or divertic- ular disease noted on CT scan Radiation Bloody diarrhea Acute vs chronic Foreign travel Infectious contacts Family history of IBD Pelvic radiotherapy Tenderness or mass on examination Stool for MC&S \200 OC&P \200 C.difficile toxin Y N Infection Flexible sigmoidoscopy N Settles with antibiotics Inflammation in rectum? N Y Colonoscopy Associated with pseudomembranes Tumor N Crohn \200\231s with rectal sparing Y Diverticular colitis Biopsy & recheck C.difficile toxin Note distribution & biopsy Crohn \200\231s UC Indeterminate Fig. 20.9.1 Colitis \202 owchart. 335 CHAPTER 20.9 Colitis Ischaemic \200 IV and 4 \200\2239mg/kg orally) or oral azathioprine (1.5 \200\2232.5mg/ kg/day). This has been shown to reduce the colectomy rate in patients not responding to steroids, although th ere is a high relapse rate once the cyclosporin is stopped. Anticoagulation is essential in UC given the increased risk of DVT in these patients (e.g. SC tinazaparin 3500U once daily ). After 3 days treatment, patients with stool frequency >8/day or a CRP >45 are unlikely t o improve without a colectomy. Failure to improve within 5 days of treatment or deterio- ra tion within that period indicates that surgery is required \200\224usually a subtotal colec tomy with preserva- tion of the rectum. Older person with known vascular disease or recent surgery for an abdominal aneurysm. Often associated with signi \201 cant abdominal pain Be het \200\231s enterocolitis \200 Associated past history of genital ulceration, arthrop- athy, uveitis Investigation Bloods \200 \200 \200 Raised CRP, ESR, white cell count Low Hb, albumin Renal function in all patients presenting with severe acute colitis Autoantibodies if remaining doubts about diagnosis Complications of acute colitis Toxic megacolon Non-obstructive dilatation of colon >6cm in conjunction with pancolitis and systemic disturbance. Falling incidence. Patients are at gr eatest risk early after diagnosis \200\224espe- cially during the \201 rst attack. Often follows a prolonged attack of drug-resistant acute colitis. Precipitants are believed to in clude hypokalaemia, opioid analgesics, consti- pating drugs, anticholinergics and possibly superadded infections such as C. dif \201 cile and CMV. Examination reveals mild tympaniti c distension, but any evidence of localized or generalized peritonism should be an indicati on for emer- gency surgery. Perforation has mortality of 40%. Criteria for diagnosis are: \200 \200 \200 \200 \200 \200 Radiology \200 AXR: vital in cases of severe acute colitis to exclude toxic dilatation of the colon. Oedem a of the bowel wall can be seen as \200\230thumbprinting \200\231. Erect CXR: f any suspic ion of perforation Other \200 \200 Cautious sigmoidoscopy and biopsy for histology Stool culture for: microscopy culture and s ensitivity/ova and parasites/C. dif \201 cile Management of severe acute colitis Severe attacks are characterized by \200 \200 \200 \200 \200 Diagnosis of colitis Radiographic evidence of colonic distension >6cm Fever >38 C Heart ra te >120bpm Neutrophilia >10 x 109 One of the following: anemia, dehydration, electrolyte di sturbance, hypotension, reduced GCS Stool frequency >6 times per day plus 1 of the following: Temperature >37.8 C Pulse >90bpm Hb < 10.5g/dl ESR >30mm/h