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 Management depends on the etiology, but should include \200 Frequent clinical evaluation including stool charts by gas- troenterologists, surgeons & intensivists Daily blood (FBC, CRP, electrolytes, albumin) assessment Daily abdominal radiograph if any suspicion of colon ic dilatation. IV electrolyte-rich \202 uid blood as required (beware hypokalaemia) Av oid antidiarrhoeal drugs (e.g. loperamide, codeine), opioids, anticholinergics and if possi ble NSAIDs, all of which increase the risk of perforation. Remember that signi \201 cant p ain may indicate perforation. Broad-spectrum antibiotics can be used in those show- ing sig ns of septic complications, except in bacterial causes where they should be targeted speci \201 cally to the infecting organism. Acute GI hemorrhage Severe bleeds occurs in <5% of all colitis patients but accounts for 1 0% of the emergency colectomies per- formed for UC. Risk of signi \201 cant hemorrhage inc reases with the extent of the disease. \200 Further reading Carter MJ, Lobo AJ, Travis SP, et al. Guidelines for the management of in \202 ammatory bowel disease in adults. Gut 2004; 53 Suppl 5: V1 \200\22316. Dunckley P, Jewell D. Management of acute severe colitis. Best Pract Res Clin Gastroenterol 2003; 17: 89 \200\223103. Travis SP, Farrant JM, Ricketts C, et al. Predicting outcome in severe ulcerative colitis. Gut 1996; 38: 905 \200\22310. Truelove SC, Witts LJ. Cortisone in ulcerative colitis; \201 nal report on a therapeutic trial. Br Med J 1955; 2: 1041 \200\2238. For acute severe UC also consider: \200 Van Assche G, D \200\231Haens G, Noman M, et al. Randomized, double- blind comparison of 4 mg/kg versus 2 mg/kg intravenous cyclosporine in severe ulcerative colitis. Gastroenterolog y 2003; 125: 1025 \200\22331. High dose IV steroids (e.g. hydrocortisone 100mg qds) and topical steroids administered rec tally (e.g. pred- nisolone enemas bd) IV cyclosporin if no signi \201 cant improvement aft er 3 days, followed by oral cyclosporin when in remission (2mg/kg 336 S STRACHAN & N SONI Intra-abdominal sepsis A septic focus present in the abdomen. Peritonitis (in \202 am- mation of the serosal memb rane that lines the abdominal cavity and organs) may follow. It can be thought of as surgi- cal or non-surgical. 2 Secondary \200\224beware! In disease relating to bowel pathology CT and ultrasound give l imited yield and increase time to laparotomy, which may be crucial. 3 Tertiary \200\224CT a nd contrast studies may be helpful in de \201 ning bowel leaks and collections which may b e amenable to percutaneous drainage or require re- laparotomy. Terminology May be divided into primary, secondary and tertiary. \200 Primary: spontaneous bacterial peritonitis \200\224uncommon, almost exclusively found in pa tients with liver cirrhosis. Causative organism usually E. coli, Enterococcus or Pneumococc us. Treatment with -lactam antibiotics. Secondary: related to pathological process in a v isceral organ which can remain localized or focal, or become generalized, leading to perito nitis; may be further subdi- vided into operative and non-operative causes. \200 Surgery: laparotomy is frequently the investigation and treatment of choice. Treatment Principles of treatment are: 1 To correct the underlying cause \200\224rapid surg ery crucial if problem surgical. 2 Systemic antibiotics \200\224to limit the infection as soon as Operative: ruptured viscus \200\224upper or lower bowel perforation, biliary obstruction, a ppendicitis, diver- ticulitis. Non-operative: pancreatitis, enteritis, toxic megaco- lon. possible. 3 Supportive therapy to limit/prevent complications from subsequent organ failure. Important components are: \200 \200 Adequate and early resuscitation Broad-spectrum antibiotics \200\224speci \201 c antibioti c once organism known. Surgery (laparotomy vs laparostomy, see abdominal compartment syndro me below). Supportive therapies, e.g. inotropes, respiratory support. Nutrition: enteral (c onsider NJ placement at laparotomy and feeding if NG feeding contraindicated); or parental nutrition. Tertiary: persistent or recurrent infection after initial treatment (usually laparotomy) ha s occurred, e.g. abscess and \201 stulae formation, pancreatic pseudocyst formation. Thes e patients show ongoing sepsis with persistent organ failure and raised in \202 ammatory m arkers. There may be frankly infected material from drains or they may have positive cultur es. \200 Differential diagnosis Includes causes of pain and raised in \202 ammatory markers in the abdominal region, identifying problematic organ: bowel, tubo-ovarian, biliary tract and pan creas, renal tract. Importance placed on early identi \201 cation of operative vs non-oper ative causes. Special considerations Abdominal compartment syndrome may occur in the closed septic abdome n. An acute increase in intra-abdominal pressure results in organ dysfunction (especially r enal, maybe hypotension or respiratory). The abdominal pressure can be measured via a urina ry bladder pressure. If intravesical pressure is >25mm Hg laparostomy is indicated. Further reading Hutchins RR, Gunning MP, Lucas DN, et al. Relaparotomy for sus- pected intraperito neal sepsis after abdominal surgery. World J Surg 2004; 28: 137 \200\22341. Symptoms and signs \200 \200 Onset: acute or insidious. Spectrum of disease: mild, limited (generally not seen on ICU) t o severe systemic/septic shock. Sepsis \200\224general malaise, pain, anorexia, nausea, fev er Non-speci \201 c abdominal \200\224pain, diarrhea, hyperactive bowel sounds, peritoniti s. \200 Malbrain ML, Chiumello D, Pelosi P, et al. Prevalence of intra- abdominal hypertension in c ritically ill patients: a multicentre epidemiological study. Intens Care Med 2004; 30: 822 \200\2239. Investigations \200 Blood tests: to aid diagnosis and establish severity of local and systemic illness include: FBC, U&E, glucose, LFT, Ca, amylase, CRP, clotting, lactate. ABG for PO2, PCO2, acid \200 \223base including base de \201 cit. Microbiological specimens for culture. Radiology: 1 P rimary \200\224ultrasound useful to aid paracentesis, ultra- Paugam-Burtz C, Dupont H, Marmuse JP, et al. Daily organ-system failure for diagnosis of pe rsistent intra-abdominal sepsis after post-operative peritonitis. Int. Care Med 2002; 28: 5 94 \200\2238. \200 \200 Rogers PN, Wright IH. Postoperative intra-abdominal sepsis. Br J Surg 1987; 74: 973 \200\223s5 Internet resources Surviving Sepsis Campaign: www.survivingsepsis.org sound Doppler portal \202 ow. This page intentionally left blank 338 CS WALDMANN Pancreatitis After adequate resuscitation, a CT scan of the abdomen (with IV contrast in the absence of contraindications) should be performed to con \201 rm the diagnosis and, if pos- sible, th e CT should be repeated after a few days to identify local complications, such as necrosis which might not be visualized earlier. Acute pancreatitis occurs with an incidence of 100 \200\223200 per million of the populati on and represents a spectrum of disease ranging from a mild to a rapidly progressive illnes s with multi-organ dysfunction syndrome (MODS). Most patients (80 \200\22390%) settle with conservative management of IV \202 uids and analgesia. Gallstones or alcohol abuse are th e most common causes of pancreatitis, and the eventual solution to preventing further attac ks of pancreatitis may require cholecystectomy or an alcohol withdrawal pro- gramme. Those patients that do not settle with conserva- tive management are a problem and may require th e input of the critical care team. 2. Role of antibiotics The routine use of prophylactic antibiotics in patients with necroti zing pancreatitis is not recommended. Where an infected abscess has been demonstrated follo w- ing \201 ne needle aspiration (FNA) and in the presence of sepsis elsewhere, antibioti cs should be prescribed accord- ing to local policies. Selective decontamination of the dig estive system has been proposed for patients with SAP; however, on the available evidence t his technique is not routinely recommended. Candida infection of the pancreas is an indepen dent risk factor for mortality; in a study by Hoerauf et al., mortality was 12.5% when Cand ida was not grown, but 53.9% with Candida present in the pancreas. Severe acute pancreatitis (SAP) 10 \200\22320% of patients admitted to hospital with pancre atitis will develop SAP. Of these, 1/3 will develop infected necrosis of the pancreas whic h carries with it a mortality of up to 80%. In a study by Rau and colleagues in 2000, steri le necrosis was associated with a 33% incidence of multi- organ dysfunction (MOD) and a mor tality of 6%, whereas infected necrosis was associated with an incidence of 81% MOD and 62% mortality. A rise in serum amylase and clinical assessment are poor indicators of severity in the \201 rst 48h. Ultrasound has been used extensively to detect gallstones, but cont rast-enhanced CT is now the investigation of choice and will detect early abscess formation and necrosis of the pancreas, con \201 rm the diagnosis and reveal gallstones should they be present. Endoscopic retrograde cholangiopancreatography (ERCP) is employed if available in the presence of jaundice. The variation in management worldwide triggered the need for a multidisciplinary consensus conference in Washington in 2004 comprising 5 critical care s ocieties: \200 \200 \200 \200 \200 3. Nutrition There is no bene \201 t in the routine use of TPN; early enteral feeding is i ncreasingly used to maintain a high caloric intake. Early feeding via an NJ tube has been a dvocated as the method of choice and should probably be used, but the NG route should be at tempted if this fails. It is reasonable to wait up to 7 days before TPN is started because of fail- ure of the NJ and NG routes. Strict glycaemic control should be used, but the rout ine use of immune-enhanced feed is not recommended. 4. Indications for surgery CT-guided FNA is recommended in order to determine whether necro tic pancreatic tissue has become infected. Only in the presence of infected pancreatic tiss ue and radiological evidence of gas should antibiotics and drain- age/debridement be recomm ended. Drainage and debri- dement can be achieved percutaneously, laparoscopically or by la parotomy. Where appropriate, operative necrosec- tomy and/or drainage should be delayed at least 2 \200\2233 weeks to allow for demarcation of the necrotic pancreas. Delaying surgery is associated with increased survival; Mier et al. in 1997 demonstrated that mortality if surgery is performed in the \201 rst 72h is 56%, which reduces to 27% if surgery is delay ed by at least 12 days. European Society of Intensive Care Medicine Society of Critical Care Mediciine American Tho racic Society European Respiratory Society Societe de Reanimation de Lange Francais The aim was to try and simplify and rationalize the man- agement of SAP. Evidence-based rec ommendations were developed by a jury of 10 people. There were 6 recom- mendations: 1. Admission to a critical care unit These patients usually require early and aggressive \202 uid resuscitation and adequate analgesia. The use of epidural blockade has to be tempe red by concern around the pos- ssiblity of the patients developing a coagulopathy. These pa tients are at risk of developing MODS and local compli- cations of pancreatitis. They need close supervision and monitoring preferably in a critical care area. Lack of ICU beds may m ean they are not admitted to an ICU until they require level 3 care and are often initially managed with the help of an outreach team. Scoring systems used include the Ranson, Imrie and APACHE II. Routine measurement of all or most of the parameters should be carried out i n the \201 rst 48h, as well as regular clini- cal examination and evaluation of the patie nt with SAP. A Ranson score of >3/11 is associated with a mortality of 60%. 5. Management of gallstone induced pancreatitis Where pancreatitis is accompanied by jaundice, con \201 rmed as obstructive by LFTs, then ERCP is often bene \201 cial in remov- ing a common bile duct stone. Care needs to be exer cised to ensure that coagulation is restored to near normal prior to the procedure. If poss ible, ERCP should be performed within 3 days of admission. If ERCP cannot be accomplished b ecause it is not technically feasible or available, alternative methods of biliary drainage must be considered. 6. Targeting in \202 ammatory response General measures used in the critically ill includi ng tight blood glucose control, and lung protective ventilation 339 CHAPTER 20.11 Pancreatitis strategies for patients with ALI, should be employed in patients with SAP. In the presence of severe sepsis, the patient with SAP can be managed according to Surviving Sepsis Campaig n guidelines. This may necessitate consid- eration of the use of recombinant activated prot ein C (even though there is an as yet unproven concern that it may be responsible for causi ng retroperitoneal haemor- rhage in patients with SAP). only indicated if the cyst causes signi \201 cant symptoms such as pain, vomiting, infecti on or inability to tolerate oral intake. Treatment is by endoscopic drainage or percutane- ous aspiration and catheter drainage. Outcome Overall mortality from SAP is in the range of 7 \200\22310% but remains high in tho se in whom necrosis occurs; if necrosis is <30% of the pancreas, the mortality rate is 7%, whereas if the whole pancreas becomes necrotic mortality is of the order of 50%. SAP leads to death in 25% of elderly patients. Complications Pancreatic abscess Early scanning of patients who are failing to progress and appropriate treatment of necrosis should minimize the risk of an abscess forming. Abscess formation can occur some weeks after the initial attack, and rarely appears until the secon d week. Pain, persistent temperature, nausea, vomit- ing and a palpable mass could be indic ators of either an abscess or a pseudocyst. A raised platelet count and a leu- cocytosis ma y be found on investigation. Imaging with CT is the gold standard, but an ultrasound in ICU may some- times be necessary in a very ill patient. Treatment with per- cutaneous drainage is the ideal solution, but operation may be required where the collection is very extensiv e or not amenable to radiological intervention. Further reading Hoerauf A, Hammer S, Muller-Myhsok B, et al. Intra-abdominal Candida infect ion during acute necrotizing pancreatitis has a high prevalence and is associated with incr eased mortality. Crit Care Med 1998; 26: 2010 \200\2235. Mier J, Leon EL, Castillo A, et al. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg 1997; 173: 71 \200\2235. Nathens Avery B, Curtis J, Randall MPH et al. Management of the critically ill patient with severe acute pancreatitis. Crit Care Med 2004; 32: 2524 \200\22336. PACT module on Pancreatitis www.esicm.org Ranson JH, Rifkind KM, Roses DF, et al. Prognosti c signs and the role of operative management in acute pancreatitis. Surg Gynaecol Obstet 19 74; 139: 69 \200\22381. Pancreatic pseudocyst Pseudocysts occur in 15 \200\22350% of patients after an attack of pa ncreatitis. There is usually no communication between the pancreatic duct and the psuedocys t. Intervention is Surviving Sepsis Campaign www.survivingsepsis.org/ 340 SF LEDWIDGE & RB GALLAND Acute acalculous cholecystitis De \201 nition Acute acalculous cholecystitis (AAC) is in \202 ammation of the gallbladde r in the absence of gallstones. Immunosuppression For example, disseminated malignancy, chronic systemic disease, prolonged ICU stay, premature infants, HIV and AIDS often associated with Cryptosporidium or CMV, tr ans- plantation associated with Candida and CMV, bone mar- row transplantation (incidence 4 %), Incidence AAC accounts for 2 \200\22315% of all cases of cholecystitis undergoing cholecyst ectomy and up to 50 \200\22370% of cases in children. In a mixed intensive care population, the incidence is 0.6 \200\2231%. In trauma patients, this may be up to 18%. Diagnosis High index of suspicion and serial monitoring The average stay of a patient with concurrent AAC in intensive care prior to diagnosis and subsequent cholecys- tectomy has be en found to be as long as 19 days. Therefore, it is important to have a high index of suspi cion and early radiographic evaluation. It has been suggested that trauma patients with a h igh Injury Severity Score >12 who are tachycardic and have required several units of packed red blood cells should be monitored by ultrasound for the development of AAC. Risk factors Men account for 80 \200\22390% of AAC seen after trauma or operation. Mean age in intensive care is 50 \200\22361yrs with a mean APACHE II score of 17. Mortality is 50 \200\22385% without treatment, reduced by early diagnosis and intervention. Organisms Most commonly E. coli and Klebsiella pneumoniae. Other organisms implicated are E nterococcus faecalis, Pseudomonas, Staphylococcus, Enterobacter, anaerobes such as Clostrid ium or Bacteroides, or fungi. Anaerobes are particularly com- mon in diabetics and patients >70yrs of age. Symptoms and signs \200 \200 Fever or unexplained sepsis Right upper quadrant pain \200\224only present in 25% of patien ts with AAC Recent jaundice Palpable right upper quadrant mass Ultrasound-induced Murphy \200\231s sign \200 \200 Pathogenesis Opportunistic infections, e.g. \200 Investigations \200 Leucocytosis \200 Elevated CRP \200 Hyperamylasaemia \200 Eleva ted aspartate aminotransferase (AST) Bacterial: Brucella, Coxiella, Leptospira, Mycobacterium tuberculosis, Salmonella, Mycoplas ma, Vibrio cholerae Fungal: Candida spp. Parasitic: Leishmania, Plasmodium spp., Schistosom a spp. Viral: Epstein \200\223Barr virus (EBV), CMV, varicella-zoster, Dengue virus \200 \200 Ultrasound \201 ndings \200 \200 \200 Gallbladder hypoperfusion and ischaemia For example, shock due to trauma, multiple injuries , spinal injury, burns, recent operation particularly cardiopulmo- nary bypass, multi-syste m organ failure, congestive cardiac failure, haemodialysis \200 Thickened gallbladder wall >3.5mm Hydrops/pericholecystic \202 uid or subserosal oedema S ludge in gallbladder These three have often been referred to as the diagnostic triad, although they are not path ognomonic for AAC and may be present in up to 50% of medical ICU admissions; therefore, cor relation with clinical and laboratory param- eters is required. Shock, use of vasopressors and low cardiac output result in splanchnic vasoconstriction lea ding to gallbladder ischaemia Mechanical ventilation with PEEP increases hepatic venous pre ssure decreasing portal perfusion Disturbed microcirculation may play a role due to intra- vascular coagulation and visceral atherosclerosis in vas- culopaths and those with vasculit ides, e.g. primary antiphospholipid syndrome, SLE, Sjogren \200\231s syndrome, Churg \200 \223Strauss, giant cell arteritis, polyarteritis nodosa, Henoch \200\223Schonlein purpura H epatic artery embolism in trauma or chemoembolization Special investigations Cholescintigraphy involves IV administration of a 99mTech- netium-la beled analog of iminodiacetic acid with hepatic uptake and subsequent concentration in bile . Failure to opacify the gallbladder is highly sensitive and speci \201 c for acute calcul ous cholecystitis due to cystic duct obstruc- tion. In AAC, cholescintigraphy has a sensiti vity of 79% and a specificity of 87%. False-negative results may occur because of cystic du ct patency. False-positive results may occur because of fasting, liver disease or TPN, and may be as high as 30 \200\22340% in critically ill patients. Morphine-aug- mented cholescin tigraphy may minimize false-positive results by increasing gallbladder \201 lling by elev ating the pressure in the common bile duct. Morphine-augmented cholescintigraphy has the hi ghest sen- sitivity for AAC of up to 90%, followed by CT with a sensitiv- ity of 67% and ul trasound 27 \200\22330%. False positives occur when ascites or hypoalbuminaemia mimic a thi ckened gallbladder wall. Bile stasis leading to sepsis \200 Opiate analgesics cause spasm of the sphincter of Oddi and induce increased biliary pressur e Prolonged fasting or TPN (incidence up to 30%) inhibits gallbladder emptying, leading to bile stasis and toxic con- centration of bile salts Obstruction, e.g. gallbladder polyp, mu lti-septate gall- bladder, ampullary stenosis, tumor, Echinococcus, Ascaria spp. 341 CHAPTER 20.12 Acute acalculous cholecystitis CT has the disadvantage of not being able to be performed at the bedside, but has the advan tage of diagnosing other causes of intra-abdominal sepsis. Laparoscopy in the ICU with loca l anesthesia and IV seda- tion has also been used as a diagnostic tool. ERCP ERCP can be performed when surgery or PTC are con- traindicated. This involves selecti ve cannulation of the cystic duct and placement of a nasobiliary catheter within the gallbl adder for drainage. Aspiration and lavage with 1% NAC dissolves luminal mucus and sludge. T he complications are acute pancreatitis, cholangitis, intestinal perforation and hemorrhage . Management Optimization of haemodynamic status Antibiotics according to cultures Prophylaxi s Prophylactic measures include cholecystokinin or ceru- letide. It is debateable whether t hese should be initiated in all ICY patients to promote gallbladder motility. Conservative management In primary antiphospholipid syndrome the diagnosis is based on posi tive lupus anticoagulant or anticardiolipin antibodies. The treatment is LMWH and oral anti coagu- lants, not cholecystectomy. AAC in SLE, Henoch \200\223Schonlein purpura, Sjogren \200\231s syn- drome and Churg \200\223Strauss syndrome may be treated suc- cessfully with corticosteroid treatment alone, providing intestinal perforation has been excluded. In chil dren, serial ultrasound monitoring has been employed successfully in an attempt to avoid th e need for cholecys- tectomy. Laparoscopic cholecystectomy This is essential for those with perforation/gangrene as these risk peritonitis. It is safe and curative, even in the immunocompromised where the operati ve morbidity is 9.1%. Major complications are rare (4%) with a low morbidity of 12 \200\223 13%, although this may rise to 14 \200\22330% in high risk patients. CT- or ultrasound-guided percutaneous transhepatic cholecystostomy (PTC) CT or ultrasound-g uided PTC should be the management of choice in high-risk surgical candidates or elderly pa tients. PTC involves perforation of the gallbladder under ultra- sound or CT guidance by a transhepatic approach to mini- mize the risk of bile peritonitis. A pigtail catheter is ins erted into the gallbladder and irrigated with 5 \200\22310ml sterile saline daily to avoid occlusion. It is contraindicated in coagulopa- thy, ascites or colonic interposition. In th e elderly, PTC has been shown to result in prompt clinical improvement in 95% of patients, with morbidity and mortality each of 3%. Complications from PTC include hemorrhage, vagal r eactions and hypotension from proce- dure-related bacteraemia, sepsis, bile peritonitis, pl eural effusion, pneumothorax, respiratory distress, perforation of the intestinal loop, sec ondary infection or colonization of the gallbladder, and catheter dislodgement. During mean follow-up of 1.8yrs, no elderly patient with AAC developed a recurrent episode after cathe ter removal, and it has therefore been suggested that the drain may be removed 3 weeks afte r insertion without further intervention. It is important to perform cholecystocholangiogra phy to ensure cystic duct patency prior to catheter removal. Complications Clinical presentation is non-speci \201 c, resulting in a high inci- dence o f gangrene (up to 63%), perforation (up to 15%), abscess (4%), ascending cholangitis, perit onitis, sepsis and death (up to 41%). Gallbladder perforation is particularly common in tho se with systemic diseases such as periph- eral vascular disease, intrinsic heart disease or diabetes, and those who are chronically immunosuppressed. Cystic duct perforation has also been reported. Further reading Barie PS, Eachempati SR. Acute acalculous cholecystitis. Curr Gastroenterol Rep 2003; 5: 302 \200\2239. Kalliafas S, Ziegler DW, Flancbaum L, et al. Acute acalculous chole- cystitis: incidence, r isk factors, diagnosis, and outcome. Am Surg 1998; 64: 471 \200\2235. McChesney J, Northup P, Bickston S. Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoper- fusion: a case series and review of pathophysiology. Dig Dis Sci 2003; 48: 1960 \200\2237. Owen CC, Jain R. Acute acalculous cholecystitis. Curr Treat Options Gastroenterol 2005; 8: 99 \200\223104. Vogt DP. Gallbladder disease: an update on diagnosis and treatment. Cleveland Clin J Med 2002; 69: 977 \200\22384. 342 M JAVID & RB GALLAND Splanchnic ischaemia the dressings after formation of laparostomy, hence, con- tinued IAP monitoring may be nece ssary. Inadequate gut perfusion, due to imbalance of oxygen delivery compared with demand, leading to bowel damage and infarction if of suf \201 cient duration. Splanchnic hypoper- fusion is thought to have a signi \201 cant impact on the out- come of many critically ill patien ts. Diagnosis Rapid diagnosis and institution of treatment can signi \201 - cantly improve sur vival. Early clinical features include severe pain out of proportion to the physical \201 ndings. Peritonitis, fever, leucocytosis and lactic acidosis later develop. Abdominal comp artment syndrome may cause abdominal distension, shortness of breath, renal failure and syn cope Pathophysiology In shock, cardiac and CNS blood \202 ow are maintained at the expense of the mesenteric circulation. Current hypoth- eses suggest that GI tract barrier function is impaired dur- ing periods of insufficient gut perfusion, leading to translocation of enteri c bacterial endotoxin into the sys- temic circulation. A generalized in \202 ammatory resp onse is triggered, mediated by macrophage products, such as TNF- , which is released as a result of endotoxin stimulation. Ultimately this can lead to multiple organ failure. Gut r eperfusion may have similar deleterious effects as a result of oxidant-mediated damage. Investigations Gastric tonometry Measures intraluminal pCO2 as a measure of mucosal pCO2 (a nd, hence, pH) in the GI tract via a catheter in the stomach. It monitors splanchnic hypope rfusion and can guide resuscitative measures according to gastric pH levels. Maintenance of gastric mucosal pH of \211 7.32 can reduce morbidity and mortality; however, there are di f \201 culties in interpreting results, and some studies have shown no ben- e \201 t of s uch monitoring. When initially introduced it was thought that this form of monitoring would be popular; however its use has been con \201 ned to a few centers. Causes \200 \200 \200 \200 \200 \200 \200 All forms of shock Burns Trauma; multiple injuries Compromised MI Haemodialysis with ultra \201 ltration. Abdominal compartment syndrome Occlusive mesenteric ischaemia due to a thro mboem- bolic event. May be arterial, usually involving the supe- rior mesenteric artery, ve nous or combined. Obstructive sleep apnoea Weaning from mechanical ventilation Protein maln utrition Treatment Clinical \200 \200 Deal with underlying cause Volume resuscitation: crystalloids or colloids; blood in cases o f haemorrhagic shock. NB: those requiring >5l of \202 uid are at risk of abdominal compar tment syndrome. Assessment of volume status is, therefore, vital. End- diastolic volumetric or echocardiographic indexes will give more accurate estimates than CVP and PAoP meas- ure ments in these patients. Vasoactive drugs. Abdominal perfusion pressure (APP = MAP \200 \223 IAP) should be optimized. Inotropes may be nec- essary if APP <60mm Hg. Norepinephrine has no nega- tive effects on gut perfusion. Avoid epinephrine and dopamine as they have be en shown to reduce splanchnic perfusion. Early enteral nutrition, particularly containing i mmnu- nomodulating ingredients (e.g. glutamine and arginine), may improve clinical outcome in some clinical states. Surgery. Resection of ischaemic or gangrenous bowel; re-exploratio n at 24h may be advisable when demarcation of viable and non-viable bowel can be more obvio us. \200 \200 Prevention Prompt recognition/measurement of gut hypoperfusion and instigation of treatment . Monitoring of intra-abdominal pressures (IAPs) every 1 \200\2232h in those at high risk o f abdominal compartment syndrome and decompression prior to onset of end-organ failure can dramatically improve prognosis. Even mild elevations in IAP (>12mm Hg) worsen outcomes. Cri tical IAP values leading to higher incidences of complications are: \211 23mm Hg for delay in post-operative ventilatory weaning; \211 24mm Hg for renal dysfunction; and \211 25mm Hg for death. Non- surgical preventative measures may be used to reduce IAP prior to end-s tage complications: sedation and pain con- trol; gut emptying by NG tube placement, laxativ es and enemas; neuromuscular blockade to relax the abdominal wall and improve organ perfusi on; paracentesis in those with ascites or retroperitoneal collections; continuous haemofilt ration in those with interstitial oedema. Continuous negative abdominal pressure devices ha ve been designed, but require further research into their effects. Emergency surgery, i.e. formation of laparostomy, is required to prevent bowel ischaemia if IAP continues to rise a nd abdominal compartment syndrome develops. There are no established guidelines as to a cut -off pressure when surgery is necessary, and the pressure at which abdominal compartment sy ndrome occurs is dependent on host factors. The whole clinical picture should be taken into account, but early decompression may lead to improved outcomes. NB: \202 uid can re-accu mulate beneath Experimental \200 Small intestinal mucosal tissue oxygenation is improved after resuscitation with blood or g elatine infusions when compared with lactated Ringer \200\231s solution in pig models. Dobu tamine and enoxamone (PDE inhibitor) and fenoldopam (dopamine D1 receptor agonist) have bee n shown to maintain splanchnic blood \202 ow during hypop- erfusion in animal models. Dop examine may be an option; no clinical study has shown a bene \201 cial effect to date, and remains contro- versial. IL-1 . IV administration improves mesenteric blood \202 ow in pig models. 343 CHAPTER 20.13 Splanchnic ischaemia Complications \200 \200 Jakob SM, Clinical review: splanchnic ischaemia Crit Care 2002; 6: 306 \200\22312. Bowel infarction Liver dysfunction. Hepatic arterial \202 ow increases at times of reduce d portal venous \202 ow, thereby maintain- ing hepatic perfusion; however, this compensat ory mechanism is limited, after which further decreases in splanchnic and/or systemic \202 ow lead to liver failure. Sepsis Systemic in \202 ammatory response leading to multi- organ failure Kirton OC, Windsor J, Wedderburn R, et al. Failure of splanchnic resuscitation in the acute ly injured trauma patient correlates with multiple organ system failure and length of stay in the ICU. Chest 1998; 113: 1064 \200\2239. Lisbon A. Dopexamine, dobutamine and dopamine increase splanchnic blood \202 ow: what is the evidence? Chest 2003; 123: 460S \200\2233S \200 Malbrain MLNG, Chiumello D. Prevalence of intra-abdominal hypertension in critically ill pa tients: a multicentre epidemiologi- cal study. Intensive Care Med 2004; 30: 822 \200\2239.