PERFORATED VISCUS AND THE ACUTE ABDOMEN Faculty of Medicine , University of British Columbia. Department of Surgery Division of General Surgery Photography and text by D.B. Allardyce MD, FRCS. Technical Assistance by: Steve Toews Transcription by: Lisa Bahn PERFORATED VISCUS AND THE ACUTE ABDOMEN OBJECTIVES Presumed Knowledge: 1. The student is able to describe the structure and relationships of the GI Tract and peritoneum. 2. They are able to describe the nerve pathways and the features of visceral and parietal [somatic] pain. 3. They can describe the secretory function of the segments of the GI tract and the digestive organs. 4. They have a working knowledge of the natural history and gross pathology of inflammatory and neoplastic diseases of the GI tract. Knowledge to be Acquired: 1. The student should be able to develop a differential diagnosis based on the patient’s initial presentation. 2. They should be able to take then a full history, asking indirect questions and direct questions when necessary, which reflect knowledge of the most likely diagnoses.. 3. The student should be able to conduct a physical examination which accurately portrays the patient’s general status and identifies ventilatory and circulatory problems quickly. The student then should be able to complete the examination of the abdomen, recognizing the physical signs of peritoneal irritation, and be able to localize the process to an abdominal quadrant when this situation exists. 4. The student should be able to initiate monitoring and appropriate early diagnostic and resuscitative measures. 5. The student should be able to arrive quickly at a provisional diagnosis. 6. The student should know those conditions which may require very early operative management. 7. The student should be able to describe in basic terms the operative strategies for management of perforation of the intestinal tract based on the underlying pathology and the site of the perforation. 8. The student should be able to write appropriate post-operative orders. Approach to the Patient with an Acute Abdomen Although this presentation will eventually have a focus on the problem of perforated viscus, it is important initially to bring a general knowledge of the conditions which cause acute abdominal pain and their relative risks, to the bedside. A grouping into general categories is seen below. 1. Intra-abdominal or retroperitoneal hemorrhage. 2. Ischemia or infarction of the intestinal tract. 3. Perforated viscus. 4. Obstructed hollow viscus. 5. Acute intra-abdominal or retroperitoneal inflammation. 6. Extra-abdominal or non-GI causes of abdominal pain. 7. Factitious causes of abdominal pain. Blood in the peritoneal or retroperitoneal space appears to be a signifigant irritant. Although an uncommon cause of acute abdomen, the unpredictable course and critical nature of blood volume contraction makes early diagnosis mandatory. Sepsis and ECF contraction may also eventually result in shock, but will not do so within minutes of the onset of pain, as in this case of ruptured, pathologic spleen [infectious mono.] As in any acutely ill patient, the issues of Airway, Breathing, and Circulation need to be addressed. Airway obstruction seldom accompanies complaints of acute abdominal pain but needs to be quickly excluded. Usually a few seconds of observation, noting the absence of stridor and presence of a normal quality voice, is sufficient. Ventilatory compromise may occasionally be caused by severe abdominal distention and pain, aggravated by pre-existing pulmonary diseases and narcotics, severe acidosis and hypotension caused by the intra-abdominal process. Many of the processes causing acute abdominal pain will result in contraction of the circulating blood volume. Hemorrhage, as in rupture of an abdominal aortic aneurysm, may critically reduce blood pressure and result in a recognizable picture of decompensated hypovolemic shock, with pallor, diaphoresis, and cool and mottled extremities. Severe acute pancreatitis, or mesenteric arterial occlusion with mid-gut infarction, may also result in shock, but require longer periods in which to evolve. Small bowel obstructions cause contraction of the effective volume of the extracellular fluid by third spacing into the lumen of the obstructed gut. Again, the contraction of the plasma volume requires time, compensation occurs and the reduced blood volume and cardiac output may not be obvious. Acute pancreatitis with positive Ranson’s major criteria is a potent cause of rapid and massive “third spacing” The plasma volume contracts quickly in the first hours after onset. Hemo concentration, hypotension, anuria may be established by the time the patient presents. This patient underwent an early laparotmy with the mistaken diagnosis of perforated viscus .A hemorrhagic ascites, pancreatic phlegmon, and extensive fat necrosis was found. Useful surgical options are few. The obstructed small bowel sequesters litres of fluid with electrolyte concentrations similar to ECF .Plasma volume contracts. Adults seldom develop hypovolemic shock, but a compensated picture evolves with postural drop in BP, low cardiac filling pressures[CVP] and pre-renal failure.If strangulation occurs[as in this case] toxemia and/or bacteremia will be superimposed on the volume deficit. If not properly resuscitated, these individuals tolerate narcotics and anesthetic agents poorly. Patients with acute abdominal pain should be examined carefully for compensated loss of blood volume, looking for a postural drop in blood pressure, collapsed peripheral veins, absence of jugular filling, poor quality peripheral pulses, cool skin, and slow capillary refill. Patients with an acute abdomen presenting to emergency rooms are usually assessed in a triage area. Young patients who are ambulatory and have stable vital signs, for example, a possible appendicitis, may then be assessed in a fast track or short stay area. [ Refer to the flow chart at the end of this section for a quick overview] Older individuals and all those exhibiting significant distress or displaying objective signs of a potentially dangerous condition (rapid pulse, temperature over 38, low blood pressure) would be then directed to an acute bed where monitoring should be established. Monitoring would consist of a 3-lead electrocardiogram display, O2-sat monitoring, and intermittent display of blood pressure and pulse. A peripheral intravenous should be quickly established and venous blood taken for laboratory tests. Specific tests to be requested may be decided later as the differential diagnosis is developed. The patient with an acute abdomen needs to be seen by a physician as soon as the early nursing assessment is completed and monitoring is set up. Hemorrhage as a cause of abdominal pain needs to be given first consideration. The course of arterial bleeding into the peritoneum or retroperitoneum in these conditions is unpredictable and exanguination can occur without warning. The most common cause of sudden collapse, abdominal pain and shock is a ruptured abdominal aortic aneurysm. A free rupture into the peritoneal cavity results in exsanguination and death so rapidly that no intervention could be taken; even if the patient were in an emergency room at the time it occurred. Most abdominal aortic aneurysms, however, leak initially and then are contained by the retroperitoneal tissues. During this timeframe, which may be only measured in minutes or hours, there is time for a diagnosis and transport to an operating room. As blood dissects through the retroperitoneum pain is experienced in the back and flank. A sensation similar to tenesmus may be described by the patient as blood dissects into the pelvis. Pallor, diaphoresis and hypotension are present almost immediately and should alert the examiner. Many of these individuals are obese and the characteristic pulsatile mass in the upper abdomen may be difficult to feel. Although an intravenous should be started and blood taken for other baseline values and cross-match, attempts at resuscitation are fruitless and waste time. Trying to insert nasogastric tubes and place Foley catheters in the emergency room cause further delay. A trip to the x-ray department for a CT scan or ultrasound may prove fatal. Often the patient is best taken, by a vascular surgeon, quickly to the operating room, diagnosis based only on a strong clinical suspicion. Other causes of intra-abdominal hemorrhage, although also threatening, are at least amenable to resuscitation and may stabilize enough to permit a more thorough assessment, including imaging. These include diagnosis such as ectopic pregnancy, rupture of a corpus luteum cyst, ruptured hepatic tumors, rupture of a previously diseased spleen, or rupture of a visceral artery aneurysm. Once hemorrhage has been considered and ruled out as a cause of the abdominal pain, attention may then be focused on other causes. During the development of the history and the physical exam, it is appropriate to initiate fluid replacement if there are indications that a deficit exists. Patients who are suffering from nausea and vomiting are best managed by insertion of a nasogastric tube and placed on continuous suction. A Foley catheter is necessary to monitor the effectiveness of IV infusion. Analgesics may be given, usually as small, frequent, intravenous doses. Patients who are stabilizing, with indications of reversal of hypovolemia and have a functioning NG tube in place may then be sent for imaging (three views of abdomen, CT abdomen or ultrasound of abdomen.) Aspiration is a continuing threat to patients with an acute abdomen. The darkness and sometimes remote area of the Xray suite is poor location to suffer a massive emesis. Obstruction of the small bowel is particularly dangerous in this respect. The NG tube will not confuse the xray findings, and its proper position can be confirmed on the films. CT of the abdomen has emerged as a definitive imaging in the investigation of SBO. Look for complete obstruction. If present, the correlation with strangulation is very high. Complete the resuscitation and proceed to OR. Laboratory test results should soon be available. A differential and provisional diagnosis can then be developed based on the evidence from the history, physical exam, imaging and laboratory results. Ischemia of the gut, although not as likely to cause sudden death as a ruptured abdominal aortic aneurysm, is associated with a very high mortality rate. Mesenteric vascular occlusion usually occurs proximally in the superior mesenteric artery leading to ischemia or infarction of the entire mid-gut. Ten to 20 cm of proximal jejunum may be spared, as is the left colon. Most of these patients are elderly, with significant collateral diseases (diabetes, coronary artery disease, peripheral vascular occlusive disease, renal failure). If a laparotomy is performed and infarction of the mid-gut is found, it would not be an appropriate decision to resect the infarcted bowel, leaving these frail patients only ten inches of jejunum and the left colon. This length of bowel is insufficient gut to allow maintenance of even fluid balance, much less provide adequate nutrition. Unfortunately, very few of these patients with proximal occlusion of the SMA are diagnosed and have an appropriate intervention quickly enough to save the ischemic bowel. Results have been best in centers where there is an interest in this specific condition and management protocols are in place. Given the relatively short warm ischemia time for irreversible hypoxic injury to the bowel, many patients do not present until after the bowel is infarcted. An all to common scenario is that of a frail,elderly vasculopath who suddenly developes agonizing general abdominal pain .Distention may not be signifigant, and the degree of rigidity or guarding may not impress the examiner. Vital signs tend to deteriorate earlier than in cases of mechanical SBO,. The patient may prove difficult to stabilize, remaining acidotic and hypotensive, despite concerted efforts. Some cases of bowel ischemia can be salvaged, however, and it is disappointing to miss these opportunities. Push quickly through the imaging and to the operating room. This is a vascular complication and a direct approach to the occlusion of the mesenteric vessel will increase the chances of a favourable outcome; i.e. get the opinion of a vascular surgeon early and do the correct imaging; a clear demonstration of the anatomy of the occlusion will be very helpful in the OR Ischemic bowel may appear congested, as above, or it may exhibit diffuse pallor.The bowel in the two cases to the left was ischemic but viable; the most likely etiologies of this picture are a stenosis of the proximal SMA or a low flow state. Restoration of blood flow is the operative treatment of proximal stenosis. Resection alone, leaving the vascular occlusion in place, is a poor option, even if a signifigant length of gut seems to sustain perfusion.. Another salvageable situation presents when a shorter segment of intestine is ischemic or infarcted. Often the explanation for the the loss of perfusion to the affected region is obscure [? Small, peripheral embolus, thrombotic disorder, low flow state] Diagnosis may be difficult. Obstruction may not be complete and peritonitis is slow to evolve as the infarcted bowel retains mechanical integrity for some time, often for several days, before frank necrosis and perforation occurs. Opportunities to successfully manage ischemic bowel are often lost when the diagnosis is not considered and patients are identified as having “small bowel obstruction” and treated expectantly with intravenous fluids and analgesics. By the time hypotension, acidosis and anuria have evolved, the situation is irretrievable. As in the instances of intra-abdominal or retroperitoneal hemorrhage, ischemic bowel needs to be included in the early differential diagnosis and then excluded by timely diagnostic imaging if there is sufficient suspicion. Once the threatening conditions of hemorrhage and bowel ischemia have been considered and excluded, management of the other causes of the acute abdomen may be proceeded with. Obstruction of a hollow viscus, perforation of a viscus and localized inflammatory processes should now be given sequential consideration. Although many of these conditions are also life threatening and will require a timely operative intervention, they do not present the same potential for sudden death or mortal loss of an organ system. Obstruction of a hollow viscus usually presents with pain suggestive of colic. The patient is restless and even agitated and the intensity of the pain varies.. Acute cholecystitis begins as biliary colic. The patient is restless and complains of severe epigastric pain, usually radiating to the RUQ and scapular region. They are afebrile with stable BP and little elevation of pulse rate. There is no evidence of volume depletion. If the stone remains impacted, inflammatory changes slowly evolve. A low-grade fever develops and the patient has RUQ tenderness. A mass may eventually be palpable Because of the pressure in the lumen, patchy necrosis of the GB wall occurs and a localized perforation will eventually follow. US confirms the diagnosis Early OR [48 hrs] is preferable to conservative strategies. Mechanical small bowel obstruction is usually incomplete. For this situation to occur, the compressing band needs to be softer [omentum, in this case] There is no internal hernia, hence the mesenteric vessels are not compromised. Proximal dilation is not as marked, as bowel content continues to get by the compression point. Bowel sounds may be audible without the stethoscope as peristalsis is quite violent[note the hemorrhage on the antemesenteric border] Continuous NG suction is a critically important part of conservative management. Approx. 60% of incomplete obstructions will resolve with “suck and drip” “It’s a bowel obstruction. See the fluid level” If the intestine contains a mix of air and fluid,. “fluid levels” may be seen on an upright abdominal film. A fluid level will usually be evident in the stomach but gas and liquid normally will pass through the small bowel so rapidly, and gas bubbles are so small, that they cannot be discriminated radiologically. Gas is always seen in the colon but fluid levels are rarely seen. Fluid levels seen on upright radiographs are not pathognomonic of obstruction Alternative causes include ileus of any cause, gastroenteritis, purgatives and ischemia. Paradoxically, a complete SBO may display no fluid levels if the intestine is completely filled with fluid. The signifigance of fluid levels on upright films should be assigned only after the “total” clinical picture has been elucidated. Obstruction of a hollow viscus (biliary system, small or large bowel or ureter) will include a subset of situations which do not immediately and seriously threaten the patient. For example, 1. Stone in the cystic duct causing biliary colic and acute cholecystitis. 2. A simple obstruction without strangulation of the small bowel. 3. A neoplastic or diverticular stricture with obstruction of the colon. Obstruction is incomplete, or the ileocecal valve is incompetent. 4. The passage of a ureteral calculus. However, there are also scenarios which evolve which increase the risk and need to be identified as separate from the above. 1. A stone in the cystic duct with empyemia of the gallbladder or emphysematous cholecystitis. 2. A stone in the common bile duct with ascending cholangitis and septicemia. 3. A complete strangulating small bowel obstruction. 4. A complete colonic obstruction with competent ileocecal valve and impending cecal rupture. 5. A colonic volvulus with ischemia. 6. A complete ureteral obstruction with pyonephrosis. A stone in the CBD is a serious complication of cholelithiasis Pancreatitis and cholangitis are much more threatening problems than acute cholecystitis. The epigastric pain of biliary colic is similar for a stone in the gallbladder neck and in the ampulla, but rigors, high fever and jaundice indicate that the patient has CBD stones and cholangitis. Bacteremia is the rule and septic shock should be anticipated.. Effective volume expansion and antibiotics may result in some improvement, but decompression of the CBD is mandatory. There is nothing wrong with an open surgery and choledochotomy; The CBD may be filled with pus. Just place a T-tube and close.-The patient is often too ill for formal duct exploration and cholangiograms. A small bowel obstruction which has an acute onset, with no flatus passed since the onset of pain, should be considered to be complete. When volume expansion is well underway, and the NG tube is positioned, imaging should happen-start with 3 views-if there is still doubt about the completeness of the obstruction, obtain A CT of the abd/pelvis If the obstruction is complete, .proceed to the OR Do not “sit” on this problem. The mortality is 6-10 times higher if the strangulated bowel is gangrenous.. Large bowel obstruction, often gradual in onset, may suddenly become complete if fecal material plugs the remaining passage. Should the ileal cecal valve be competent, the cecum can become so distended that it bursts,. releasing enormous amounts of gas into the peritoneal cavity. Massive fecal peritonitis is also the rule;, survivorship is unlikely. This patient had an obstructing cancer of the hepatic flexure. The cecum ruptured, but fortunately for this frail individual, fecal soiling was minimal. In large bowel obstructions with marked cecal dilation and no dilation of the small bowel [competent valve] the situation is emergent. Sigmoid volvulus often presents in a recurrent and seemingly manageable way [endoscopic decompression]. Occasionally a critical situation evolves when distention and compromise of the mesenteric vessels leads to patchy necrosis of the colon. Ventilation may be inadequate in the presence of high intra abdominal pressures. Attempts to sigmoidoscope unstable patients who may have sigmoid ischemia are ill-advised. Stat laparotomy, trans-anal intubation and decompression of the loop, resection of the sigmoid and end colostomy may be the best option in this latter group of patients.… Amongst patients with perforated viscus there are also subsets of variable degrees of risk and therefore a variation in the urgency with which diagnosis and intervention must occur. The outcome in these individuals varies with the site of the perforation, the underlying pathology, the age of the patient, and collateral diseases. The major issue influencing the pace of early management is the degree to which the perforation has been contained or localized by peritoneal defense mechanisms. 1. Perforation of peptic ulcer; contrast via a nasogastric tube shows evidence of a duodenal ulcer but no continuing leakage.[there may be an option for conservative management] 2. Appendiceal perforation with a localized abscess. 3. A diverticular perforation with a localized pelvic abscess. Scenarios of greater urgency include: 1. Perforation of a peptic ulcer with free air and fluid and continuing extravasation demonstrated. 2. Perforation of the small bowel suspected. 3. Perforation of the appendix with a spreading peritonitis. 4. Perforation of a colonic diverticulum with generalized peritonitis.