4. Gastrointestinal

Abdominal perfusion pressure = Mean Arterial Pressure – Intraabdominal Pressure (APP = MAP – IAP)

ACS refers to multiple organ dysfunction due to increased intraabdominal pressure, typically >20 to 25 mmHg.

Abdominal hypertension refers to acute or chronic elevation of the intraabdominal pressure, typically >12 mmHg (normal abdominal pressure is around 5 mmHg).

Common Causes to Remember

Massive resuscitation and transfusions leading to bowel wall edema

Intraperitoneal or retroperitoneal hemorrhage

Bowel distention due to obstruction, ileus, or acute inflammation; bowel reperfusion injury from ischemia of any cause

Ascites/any space-occupying intraabdominal process, mass, or fluid

Loss of domain/abdominal closure under tension, usually after repair of complex ventral hernias

Types of ACS

Primary: primary etiology lies within the abdomen (e.g., excessive bowel wall edema or distention)

Secondary: from external causes (e.g., circumferential burn eschar)

Acute: e.g., acute bowel wall edema from massive resuscitation

Chronic: e.g., late stages of cirrhosis with massive ascites

Epidemiology

Incidence of intraabdominal hypertension in medical ICUs is 8%.

Incidence of true compartment syndrome in trauma patients is 2% to 9%.

Key Pathophysiology

Upward displacement of the diaphragm results in decreased thoracic volumes and pulmonary compliance, which lead to an increase in peak airway pressures, ventilation and perfusion mismatch, hypoxia, hypercapnia, and acidosis.

Compression of the inferior vena cava results in decreased cardiac venous return and increased peripheral vascular resistance. (As a result, blood pressure, cardiac output, cardiac index, and right atrial and pulmonary artery occlusion pressures decrease. Systemic delivery and consumption of O₂ decreases.)

Direct compression of the kidneys and obstruction of venous outflow result in a decrease in the glomerular filtration rate and urine output.

Compression of the mesenteric vasculature leads to a decrease in splanchnic perfusion, mesenteric venous hypertension, intestinal edema, and visceral edema.

Elevated central venous pressure interferes with cerebral venous outflow and results in increased intracranial pressure.

Previous pregnancy, cirrhosis, morbid obesity can chronically increase abdominal wall compliance and may be protective.

Clinical Manifestations

Distended, tense abdomen

Hypoxia, hypercapnia, and high peak inspiratory pressures with decreased compliance in the mechanically ventilated patients

Shortness of breath in extubated patients

Figure 4.1.1 Repeat frequently (every 4 to 6 hours). Monitor the trend.

Elevated central venous and pulmonary capillary wedge pressures

Oliguria and eventually anuria

Decreased cardiac output, hypotension, acidosis, vasopressor requirement

Decreased intestinal, renal, hepatic blood flow

Signs of increased intracranial pressure

Diagnosis/Measurement of Intraabdominal Pressure

Bladder pressure is an indirect measure of intraperitoneal pressure; 50 mL of sterile saline is instilled into the bladder via a Foley catheter with the drainage tube clamped, while the aspiration port is attached to a pressure transducer (zeroed at the level of the pubic symphysis, Fig. 4.1.1).

Management and Treatment

Surgical decompression is typically definitive! Abdomen is left open (usually with a negative pressure Vac dressing), until the etiology of the ACS improves.

Paralytics and diuretics may have a role in the management of intraabdominal hypertension.

Paracentesis is done for ascites and escharotomy for burn eschars.

SUGGESTED READINGS

Joynt GM, Wai JK. Intra-abdominal hypertension and abdominal compartment syndrome—making progress? Anaesth Intensive Care. 2012;40(1):11-13.

Khan S, Verma AK, Ahmad SM, et al. Analyzing intra-abdominal pressures and outcomes in patients undergoing emergency laparotomy. J Emerg Trauma Shock. 2010;3(4):318-325.

Malbrain ML, Cheatham ML. Definitions and pathophysiological implications of intra-abdominal hypertension and abdominal compartment syndrome. Am Surg. 2011;77(Suppl 1):S6-S11.

Malbrain ML, Chiumello D, Pelosi P, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med. 2005;33(2):315-322.

Raeburn CD, Moore EE, Biffl WL, et al. The abdominal compartment syndrome is a morbid complication of postinjury damage control surgery. Am J Surg. 2001;182(6):542-546.

4.2

Acute Pancreatitis

Antonios C. Sideris and Peter J. Fagenholz

Introduction

Inflammatory disease of the pancreas. Categories:

Mild (edematous, interstitial) acute pancreatitis

Severe acute pancreatitis (SAP): one or more of the following:

Failure of one or more organ systems (respiratory, renal, gastrointestinal, circulatory, disseminated intravascular coagulation (DIC)) at any time during the course of the disease

Three or more Ranson’s criteria (see “severity scoring”) or Apache II of eight or above

Local complications: necrosis, pseudocyst, and/or abscess

Moderate pancreatitis: SAP without organ failure

Common Causes to Remember

Epidemiology

Increasing incidence, ranging from 5 to 44 cases per 100,000 population

Severe pancreatitis incidence has remained stable over time (10% to 20% of all cases).

Slight increase with age, blacks more than whites, females more than males

Only 3% to 7% of patients with cholelithiasis and 10% of alcoholics develop acute pancreatitis.

Up to 75% have elevated amylase post-ERCP, but only 5% develop overt clinical pancreatitis.

Key Pathophysiology

Unregulated protease activation within pancreatic acinar cells, instead of inside the small bowel lumen

Protective mechanisms (enzyme compartmentalization, specific trypsin inhibitors such as serine protease inhibitor Kazal type 1 (SPINK1), low intracellular Ca⁺⁺) are overwhelmed.

Trypsinogen converted to trypsin by hydrolysis of N-terminal trypsinogen activating peptide (TAP), leading to activation of pancreatic proteases (phospholipase A2, chymotrypsin, elastase), complement, kallikrein-kinin, proinflammatory interleukins (TNFa, IL-1, IL-6, IL-8), coagulation, and fibrinolysis.

Autodigestion of the gland (with or without SIRS)

Mechanisms of trypsin activation depend on etiology, largely debated.

Mechanical: gallstone, ERCP, trauma, pancreas divisum

Obstruction of the ampulla by the stone, tumor or edema by the stone passage, and decreased flow from secondary pancreatic duct (Santorini) in pancreas divisum leading to increased intrapancreatic duct pressures and/or

Reflux of bile into pancreatic duct during transient ampulla obstruction

Systemic: EtOH, drugs, hypertriglyceridemia, hyper Ca⁺⁺, infections, and toxins: exact mechanisms remain unclear.

Diagnosis

Combination of clinical, laboratory, and imaging findings

Clinical

Epigastric pain, sometimes radiating to the back or shoulder, accompanied by nausea and/or vomiting is the most common clinical presentation.

Signs of shock in fulminant attacks

Tenderness on palpation +/– guarding

Jaundice if there is concurrent biliary obstruction

Palpable abdominal mass if a pancreatic collection or pseudocyst is present

Ecchymosis of the periumbilical (Cullen sign) and/or flank area (Grey-Turner sign) are rare and nonspecific (retroperitoneal hemorrhage).

Laboratory

Serum amylase and lipase more than three times the upper limit of normal is sensitive and specific for diagnosis of AP if clinical signs are present.

Serum amylase rises in 6 to 12 hours, remains elevated for 3 to 5 days. Level does not predict severity. Urine amylase offers no benefit over serum measurement.

Serum lipase is potentially more specific than serum amylase: useful in patients with delayed presentation, may remain elevated for up to 2 weeks.

ALT more than three times the upper limit of normal may be specific for gallstone pancreatitis.

Imaging findings

Imaging is not necessary to make the diagnosis if the clinical picture and serum tests are consistent with acute pancreatitis.

Abdominal CT with intravenous contrast

Gold standard imaging modality, but not necessary at presentation

Most useful at presentation to identify potential alternative diagnoses

Useful later in the course of disease to identify necrosis

Abdominal ultrasound

Best modality to identify cholelithiasis, common bile duct dilatation

Gallstones confirm etiology of gallstone pancreatitis in the absence of a more apparent cause. If seen, pancreas may appear edematous.

Endoscopic ultrasound is the most accurate modality for choledocholithiasis, but is invasive—rarely necessary.

Severity Scoring

No system is superior.

C-reactive protein ≥ 150 mg/L at 48 hours distinguishes mild versus severe attack.

Procalcitonin: similar to Apache II and Ranson criteria, cutoffs remain to be determined

Apache II: useful index to classify the severity of the disease, but cumbersome to use.

Ranson criteria: require 48 hours of clinical information to calculate (Table 4.2.1)

CT severity index: estimates the degree of necrosis and predicts higher morbidity and mortality. IV contrast administration is necessary (Table 4.2.2).

Bedside index of severity in acute pancreatitis (BISAP)

BUN ≥ 25 mg/dL

Impaired mental status

SIRS

Age > 60 years

Pleural effusion

Similar predictive ability for mortality as Apache II

Harmless acute pancreatitis score (HAPS)

Rebound tenderness/guarding

Creatinine ≥ 2 mg/dL

Hematocrit >43% in men and >39.6% in women

Can be calculated within 30 minutes of admission

98% predictive ability of patients with a benign course if all three parameters are negative

Differential Diagnosis

Other causes of epigastric/right upper quadrant abdominal pain: acute cholecystitis, perforated viscus, peptic ulcer, mesenteric ischemia, small bowel obstruction, ruptured abdominal aortic aneurysm (AAA), acute myocardial infarction, MI, pneumonia

Causes of hyperamylasemia: salivary tumor/inflammation, bowel obstruction, mesenteric ischemia, acute cholecystitis, ovarian tumor, ectopic pregnancy, macroamylasemia, renal failure, anorexia nervosa, liver disease

Always assess hyperamylasemia in conjunction with the clinical picture.

False negative amylase levels: hypertriglyceridemia, recurrent attacks of alcoholic pancreatitis, resulting in “burned out pancreas”

Management and Treatment

Fluid resuscitation

Patients with SAP need ICU level monitoring for management of end-organ dysfunction.

Fluid resuscitation is critical. The exact rate remains controversial, with renal dysfunction and systemic hypoperfusion complicating underresuscitation and ARDS and abdominal compartment syndrome complicating excessive fluid administration. Lactated Ringer’s has been shown to be superior to normal saline by reducing inflammatory mediator production—avoid in hypercalcemia-induced pancreatitis because it contains 3 mEq/L calcium.

Pain control

Intravenous opiates are standard.

Morphine has not been shown to cause or exacerbate AP attacks.

Nutritional support

Mild attacks: initially NPO, progress to oral feedings when the pain and nausea subside. Advance from clear liquids to solid food as tolerated

Alternatively, a low-fat solid diet has been shown recently to be as safe and may result in improved outcomes.

Patients not expected to resume oral feedings for 5 to 7 days (e.g., severe attacks) should receive nutritional support.

Enteral feeding is the preferred mode of nutritional support, as it prevents atrophy of the intestinal mucosa and bacterial translocation, thus leading to improved mortality, lower incidence of organ failure, systemic infection, need for surgery, and potentially a shorter hospital stay.

Oral or nasogastric feeding can be tried first, with jejunal feeding reserved for patients who cannot tolerate these approaches.

Total parenteral nutrition (TPN): use only in patients who cannot tolerate enteral feeding.

Avoid administration as an adjunct to enteral feedings, as it has been associated with a higher mortality, increased infectious complications, and longer ICU and hospital length of stay.

Antibiotic prophylaxis

This has no role in mild pancreatitis.

Prophylactic administration for noninfected necrosis remains highly controversial.

A recent Cochrane metaanalysis failed to show a mortality benefit or a decrease in infectious complications.

At present, prophylactic administration of antibiotics in noninfected necrosis is not advisable.

Prophylactic probiotic administration is discouraged, as it has been associated with bowel ischemia.

ERCP

This is not indicated in mild and non-gallstone pancreatitis.

Early (within 48 hours) ERCP is only indicated in patients with pancreatitis with concommitant cholangitis.

In patients without obstructive jaundice, early ERCP does not show a clear benefit and should be avoided.

Role of percutaneous or endoscopic intervention and surgery

The only clear indication for intervention is infected pancreatic or peripancreatic necrosis.

Whenever infected necrosis is suspected, a CT scan with intravenous contrast is the best first test.

Infection can be proven by the presence of gas in pancreatic necrosis on CT scan or by fine needle aspiration (FNA) with Gram stain and culture of the necrosis.

Neither of these is 100% sensitive, and in a severely ill patient with suspected infected necrosis, intervention should be performed even in the absence of definite proof of infection.

When infection is proven or suspected, the first intervention should be antibiotic administration (a carbapenem is standard) and percutaneous or endoscopic drainage.

Surgical debridement is reserved for when clinical improvement cannot be achieved by less invasive measures.

This progression from less invasive drainage procedures to more invasive surgical debridement is termed the “step-up approach.”

Surgery should be delayed until at least 4 weeks after the onset of pancreatitis whenever possible.

There are a variety of surgical techniques (open transabdominal debridement, laparoscopic debridement, video-assisted retroperitoneal debridement) with none that is clearly superior at this point.

Omission or delay of cholecystectomy in gallstone pancreatitis is associated with increased risk of recurrent attacks.

In mild to moderate pancreatitis, cholecystectomy should be performed during the index pancreatitis admission.

In severe disease, cholecystectomy should be delayed at least 6 weeks, as the complication rate is high after early cholecystectomy.

Outcomes

Mortality: 2% to 3% overall, may be up to 30% to 40% in SAP with organ failure

Complications

Systemic

ALI/ARDS, multiorgan failure, coagulopathy/DIC, acute renal failure (usually prerenal, confers worse progrosis)

Severe hypocalcemia

Local/mechanical

Acute fluid collection (30% to 50%)

Simple fluid accumulating in or near the pancreas within the first few days of acute pancreatitis

Usually resolves spontaneously and does not require treatment

Sterile pancreatic necrosis (20%)

No indication for surgery if asymptomatic, no consensus for prophylactic antibiotics

Supportive measures only

Infected pancreatic or peripancreatic necrosis (5% to 10%)

As above, diagnosed by CT or FNA

Usually gram-negative intestinal organisms, but may include gram positives or fungi

Treated with antibiotics and “step up approach” as above

Carbapenems are standard antibiotic therapy.

Pseudocyst (~10%)

Fluid collection formed due to walled-off disruption of the pancreatic duct

Many resolve spontaneously

If large, persistent, and symptomatic should be internally drained either endoscopically or surgically

Pancreatic fistulas (17% to 76% of severe cases)

High volume and amylase content coming from the pancreatic drains are indicative of pancreatic fistula formation.

Treatment is conservative.

Endoscopic transpapillary stenting may be as safe and decrease the time to fistula closure by decompressing the pancreatitic duct.

Other

Diabetes, pleural effusion/ pancreatic ascites (think about pancreatic duct disruption), splenic/mesenteric/portal vein thrombosis with gastric varices

SUGGESTED READINGS

Aboulian A, Chan T, Yaghoubian A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. 2010;251:615-619.

Al-Omran M, Albalawi ZH, Tashkandi MF, et al. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev. 2010;1:CD002837.

Bakker OJ, van Baal MC, van Santvoort HC, et al. Endoscopic transpapillary stenting or conservative treatment for pancreatic fistulas in necrotizing pancreatitis: multicenter series and literature review. Ann Surg. 2011;253:961-967.

Banks PA, Freeman ML. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 2006;101:2379-2400.

Bernhardt A, Kortgen A, Niesel H, et al. Using epidural anesthesia in patients with acute pancreatitis—prospective study of 121 patients. Anaesthesiol Reanim. 2002;27:16-22.

Besselink MG, van Santvoort HC, Buskens E, et al. Probiotic prophylaxis in predicted severe acute pancreatitis: a randomised, double-blind, placebo-controlled trial. Lancet. 2008;371:651-659.

Bradley EL 3rd. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, GA, September 11 through 13, 1992. Arch Surg. 1993;128:586-590.

Cannon JW, Callery MP, Vollmer CM Jr. Diagnosis and management of pancreatic pseudocysts: what is the evidence? J Am Coll Surg. 2009;209:385-393.

Casaer MP, Mesotten D, Hermans G, et al. Early versus late parenteral nutrition in critically ill adults. N Engl J Med. 2011;365:506-517.

Eatock FC, Chong P, Menezes N, et al. A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol. 2005;100:432-439.

Everhart JE, Ruhl CE. Burden of digestive diseases in the United States part III: liver, biliary tract, and pancreas. Gastroenterology. 2009;136:1134-1144.

Fagenholz PJ, Castillo CF, Harris NS, et al. Increasing United States hospital admissions for acute pancreatitis, 1988–2003. Ann Epidemiol. 2007;17:491-497.

Fagenholz PJ, Fernandez-del Castillo C, Harris NS, et al. National study of United States emergency department visits for acute pancreatitis, 1993–2003. BMC Emerg Med. 2007;7:1.

Forsmark CE, Baillie J. AGA institute technical review on acute pancreatitis. Gastroenterology. 2007;132:2022-2044.

Frey CF, Zhou H, Harvey DJ, et al. The incidence and case-fatality rates of acute biliary, alcoholic, and idiopathic pancreatitis in California, 1994–2001. Pancreas. 2006;33:336-344.

Frossard JL, Steer ML, Pastor CM. Acute pancreatitis. Lancet. 2008;371: 143-152.

Gardner TB, Vege SS, Pearson RK, et al. Fluid resuscitation in acute pancreatitis. Clin Gastroenterol Hepatol. 2008;6:1070-1076.

Hernandez V, Pascual I, Almela P, et al. Recurrence of acute gallstone pancreatitis and relationship with cholecystectomy or endoscopic sphincterotomy. Am J Gastroenterol. 2004;99:2417-2423.

Jacobson BC, Vander Vliet MB, Hughes MD, et al. A prospective, randomized trial of clear liquids versus low-fat solid diet as the initial meal in mild acute pancreatitis. Clin Gastroenterol Hepatol. 2007;5:946-951; quiz 886.

Jensen EH, Borja-Cacho D, Al-Refaie WB, Vickers SM. Exocrine Pancreas. Philadelphia, PA: Elsevier Saunders; 2007.

Kutsogiannis J, Alberda C, Gramlich L, et al. Early use of supplemental parenteral nutrition in critically ill patients: results of an international multicenter observational study. Crit Care Med. 2011;39:2691-2699.

McClave SA, Dryden GW. Issues of nutritional support for the patient with acute pancreatitis. Semin Gastrointest Dis. 2002;13:154-160.

Meng WB, Li X, Li YM, et al. Three initial diets for management of mild acute pancreatitis: a meta-analysis. World J Gastroenterol. 2011;17:4235-4241.

Mofidi R, Suttie SA, Patil PV, et al. The value of procalcitonin at predicting the severity of acute pancreatitis and development of infected pancreatic necrosis: systematic review. Surgery. 2009;146:72-81.

Moraes JM, Felga GE, Chebli LA, et al. A full solid diet as the initial meal in mild acute pancreatitis is safe and result in a shorter length of hospitalization: results from a prospective, randomized, controlled, double-blind clinical trial. J Clin Gastroenterol. 2010;44:517-522.

Munsell MA, Buscaglia JM. Acute pancreatitis. J Hosp Med. 2010;5:241-250.

Petrov MS, van Santvoort HC, Besselink MG, et al. Early endoscopic retrograde cholangiopancreatography versus conservative management in acute biliary pancreatitis without cholangitis: a meta-analysis of randomized trials. Ann Surg. 2008;247:250-257.

Quan H, Wang X, Guo C. A meta-analysis of enteral nutrition and total parenteral nutrition in patients with acute pancreatitis. Gastroenterol Res Pract. 2011;2011:698248.

Sathiaraj E, Murthy S, Mansard MJ, et al. Clinical trial: oral feeding with a soft diet compared with clear liquid diet as initial meal in mild acute pancreatitis. Aliment Pharmacol Ther. 2008;28:777-781.

van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010;362:1491-1502.

van Santvoort HC, Besselink MG, de Vries AC, et al. Early endoscopic retrograde cholangiopancreatography in predicted severe acute biliary pancreatitis: a prospective multicenter study. Ann Surg. 2009;250: 68-75.

Vege S, Yadav D, Chari S. Pancreatitis. Malden, MA: Blackwell Publishing; 2007.

Vege SS, Gardner TB, Chari ST, et al. Low mortality and high morbidity in severe acute pancreatitis without organ failure: a case for revising the Atlanta classification to include “moderately severe acute pancreatitis.” Am J Gastroenterol. 2009;104:710-715.

Villatoro E, Mulla M, Larvin M. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev. 2010;5:CD002941.

Wilson CT, de Moya MA. Cholecystectomy for acute gallstone pancreatitis: early vs delayed approach. Scand J Surg. 2010;99:81-85.

Wu BU, Conwell DL. Update in acute pancreatitis. Curr Gastroenterol Rep. 2010;12:83-90.

Wu BU, Hwang JQ, Gardner TH, et al. Lactated Ringer’s solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin Gastroenterol Hepatol. 2011;9:710-717, e711.

Yadav D, Lowenfels AB. Trends in the epidemiology of the first attack of acute pancreatitis: a systematic review. Pancreas. 2006;33:323-330.

4.3

Gastrointestinal Perforation

George Kasotakis

Introduction

Gastrointestinal perforation refers to complete penetration of the wall of the stomach, small or large intestine, allowing intestinal contents to flow into the peritoneal cavity.

Key Pathophysiology

Peptic ulcer perforation occurs when the injurious effects of acid and pepsin overwhelm the mucosal barrier and acid-suppression therapy has not been instituted or is inadequate to control the local acid environment.

In mechanical obstruction (obstructing tumor, volvulus, bowel herniation) without vascular compromise, ingested fluid and food, digestive secretions. and gas accumulate above the obstruction, leading to proximal bowel overdistention and eventually to microperforations or strangulating obstruction.

Intestinal ischemia (associated with hernia, volvulus, intussusception, severe calcific burden, or low flow states) can progress to infarction, gangrene, and perforation in as little as 6 hours.

Local obstruction by fecaliths (appendicitis, diverticulitis) may lead to localized luminal overdistention, compromised enteric wall blood supply, and finally severe inflammation and perforation.

Traumatic (more commonly with penetrating injuries) or iatrogenic perforations can also occur (typically during lysis of adhesions or endoscopy).

Common Causes to Remember

Untreated severe peptic ulcer disease

Malignant perforation

Untreated appendicitis

Cecal/sigmoid volvulus

Inflammatory bowel disease

Diverticulitis

Toxic megacolon

Excessive distention from bowel obstruction

Intestinal ischemia

Penetrating wounds to the abdomen

Iatrogenic (most commonly during colonoscopy, ERCP, or abdominal surgery)

Symptoms and signs

Gastric and duodenal perforations typically present with sudden pain in the epigastrium or right upper quadrant.

In contained perforated diverticulitis the symptoms are typically localized in the left lower quadrant.

In all other cases, location and quality of the pain depend on the part of the gastrointestinal tract that perforates.

In general, if the perforation is contained, local pain and tenderness may be present. Systemic manifestations of acute illness are typically mild. If the leakage of bowel contents is not contained, diffuse abdominal pain worsened by movement and associated with rigidity, guarding, and rebound tenderness is typically present. Fever and tachycardia are common.

Diagnosis

Peritoneal signs (diffuse abdominal pain, rigidity, guarding, and rebound tenderness) should alert the clinical staff for the possibility of bowel perforation. Fever, leukocytosis, and tachycardia are frequently present.

Figure 4.3.1 Free air under the diaphragm after iatrogenic duodenal perforation.

Free air in the subdiaphragmatic space can be identified on plain x-rays (Fig. 4.3.1).

Abdominal CT may provide information about the location of the perforation (localized bowel wall thickening, mesenteric and soft tissue stranding adjacent to the perforation) (Fig. 4.3.2).

Management and Treatment

Typically depends on the host’s physiology and whether the perforation is contained or not.

Broad-spectrum antibiotics, bowel rest, and percutaneous drainage of extraluminal collections may be used for the clinically well patient with localized peritoneal irritation.

In disseminated peritonitis, surgical exploration with cavity washout is usually warranted. Perforations may be patched (gastroduodenal), primarily repaired (intestinal), excised (gastric, intestinal), or proximally diverted (diverticulitis).

Figure 4.3.2 Localized sigmoid wall thickening, adjacent soft tissue stranding, and abscess in the lower abdomen with acute diverticulitis.

SUGGESTED READINGS

Beckham H, Whitlow CB. The medical and nonoperative treatment of diverticulitis. Clin Colon Rectal Surg. 2009;22(3):155-160.

Castellví J, Pi F, Sueiras A, et al. Colonoscopic perforation: useful parameters for early diagnosis and conservative treatment. Int J Colorectal Dis. 2011;26(9):1183-1190.

Horn AE, Ufberg JW. Appendicitis, diverticulitis and colitis. Emerg Med Clin North Am. 2011;29(2):347-368.

Rafferty J, Shellito P, Hyman NH, et al. Practice parameters for sigmoid diverticulitis. Dis Colon Rectum. 2006;49(7):939-944.

Spirt MJ. Complicated intra-abdominal infections: a focus on appendicitis and diverticulitis. Postgrad Med. 2012;122(1):39.

4.4

Acute Mesenteric Ischemia

Haytham M. A. Kaafarani

Introduction

Acute mesenteric ischemia (AMI) is caused by a sudden decrease in perfusion to the small or large bowel, resulting in a mismatch of metabolic supply and demand, with an ultimate risk of bowel necrosis.

Epidemiology

AMI is rare: its incidence increases with age and is reported to be around 1.09 per 100,000 person-years.

AMI is most common after the sixth decade of life, especially in patients with peripheral or coronary atherosclerosis.

Key Pathophysiology

The mesenteric blood supply is derived from three major arteries:

The celiac artery

The superior mesenteric artery (SMA = most commonly implicated vessel)

The inferior mesenteric artery (IMA)

The mesenteric arterial anatomy includes extensive collateral circulation connecting the major mesenteric vessels to each other as well as to the systemic circulation.

The probability of intestinal ischemia depends upon the adequacy of systemic and collateral perfusion, the number and caliber of affected vessels, and the duration of the insult.

The mesenteric vasculature can compensate for up to 75% acute reduction in perfusion for as long as 12 hours through increased oxygen extraction at the tissue level and increased collateral circulation.

Despite the extensive collateral mesenteric circulation, prolonged bowel hypoperfusion results in vasoconstriction, thus ultimately reducing collateral flow.

Ischemic damage is due to both hypoxic and reperfusion injury, often with vasoconstriction persisting after restoration of blood flow.

Ischemic injury to the bowel results in the systemic release of intracellular breakdown products and an increase in anaerobic metabolism.

Etiology and Risk Factors

The etiology of AMI may be categorized as

Mesenteric arterial embolism

Mesenteric arterial thrombosis

Nonocclusive mesenteric ischemia

Mesenteric venous thrombosis

Mesenteric arterial embolism

40% to 50% of cases

Most common cause: embolization from cardiac source to SMA

Occlusion usually at a branch of the SMA just distal to the middle colic artery, resulting in relative sparing of the proximal jejunum and distal large bowel

Risk factors

Cardiac arrhythmia (e.g., atrial fibrillation)

Myocardial infarction/ventricular aneurysm

Recent cardiac or aortic catheterization

Recent cardiac valve replacement

Endocarditis

Atrial septal defect (resulting in paradoxical embolus)

Mesenteric arterial thrombosis

25% of cases

Most common cause is atherosclerosis

Occlusion usually at the origin of the mesenteric vessel (SMA or celiac)

Less common causes include arterial dissection, arterial aneurysm, vasculitis, and iatrogenic injury (i.e., intraoperative)

Risk factors

Known atherosclerosis/vascular disease

Abdominal trauma

Infection

Nonocclusive mesenteric ischemia

20% of cases

Occurs most commonly due to a global reduction in cardiac output

Risk factors

Hypovolemia

Sepsis

Aortic insufficiency

Status post cardiac surgery

Digoxin use (may result in splanchnic vasoconstriction)

Cocaine abuse

Mesenteric venous thrombosis

5% to 10% of cases

Usually associated with the existence of a hypercoagulable state

Risk factors

Malignancy

Inherited coagulopathy (i.e., Factor V Leiden, Factor C, or Factor S deficiency)

Oral contraceptive use

Portal hypertension

Nephrotic syndrome

History of prior deep venous thrombosis or pulmonary embolus

Diagnosis

History and physical exam

History and physical exam alone are notoriously nonsensitive and nonspecific for AMI.

Embolic AMI: sudden onset of severe periumbilical pain, typically out of proportion to physical exam findings

Arterial thrombosis or nonocclusive ischemia, however, can occur more insidiously with 95% of patients reporting a 24-hour history of vague abdominal pain.

May also be accompanied by anorexia, vomiting, and diarrhea

Patients with transmural bowel necrosis can present with peritonitis, sepsis, and shock.

Laboratories

No single serologic value is diagnostic or prognostic, but a common presentation includes:

Leukocytosis with left shift

Hemoconcentration

Anion gap metabolic acidosis (lactic acidosis)

Hyperamylasemia

Elevated D-lactate

Usefulness is controversial

Estimated sensitivity of 70% to 100%

Estimated specificity of 40% to 90%

Improves with exclusion of shock, diabetic ketoacidosis, renal failure, and hepatic failure

Imaging studies

Plain abdominal radiographs

Nonspecific; normal in up to 25% of patients with ischemic bowel

Significant findings include “thumbprinting” suggestive of intestinal wall edema, pneumatosis intestinalis suggestive of bowel wall necrosis, or pneumoperitoneum suggestive of bowel perforation

Doppler-flow ultrasonography

Used in detection of stenosis or occlusion of mesenteric vessels (does not detect low-flow etiologies)

Often technically limited due to interference from air-filled bowel

Abdominal computed tomographic angiography (CTA)

Allows visualization of bowel wall thickening, pneumatosis intestinalis, portal venous gas and arterial occlusions, with both sensitivity and specificity above 90%

Higher accuracy for thromboembolic etiologies versus nonocclusive ischemia

Can also be used to rule out other causes of acute abdomen

Mesenteric angiography

Early angiography (within 12 hours of event) associated with improved survival

Allows simultaneous intervention to restore blood flow

Magnetic resonance angiography (MRA)

More detailed information about mesenteric vessels

More research needed to compare this modality to conventional and CT angiography.

Intraoperative diagnosis

Exploratory laparotomy is the gold standard and .zrequired for suspicion of any bowel infarction.

Treatment and Management

Goal of treatment is restoration of mesenteric perfusion.

Aggressive hemodynamic monitoring and support (isotonic fluids and/or vasopressors)

Broad-spectrum IV antibiotics

Immediate therapeutic intravenous anticoagulation

Correction of electrolyte and acid–base abnormalities

Mesenteric arteriography

Hypotension or hypovolemia may lead to false positive studies.

Therapeutic options include intraarterial vasodilators (papaverine), thrombolytic agents, angioplasty, stenting, and embolectomy.

Consider surgery for emergent situations when there is suspicion of intestinal infarction or perforation.

Mesenteric arterial embolism

Surgical embolectomy versus local thrombolytic therapy

Surgical embolectomy

Arteriotomy distal to embolus followed by advancement of balloon-tipped embolectomy (Fogarty) catheter

Examination for infarcted bowel 20 to 30 minutes following revascularization

Second look laparotomy within 24 to 48 hours

Local thrombolytic therapy

May be appropriate shortly after onset of symptoms if there is no clinical evidence of bowel infarction, and no contraindication to thrombolysis (tissue plasminogen activator, streptokinase, etc.)

>90% angiographic resolution of SMA occlusion with thrombolysis

Surgical intervention mandatory if no resolution within several hours or with worsening clinical status

Long-term anticoagulation to prevent future embolic events

Mesenteric arterial thrombosis

Treatment is primarily surgical.

Nonsurgical management with heparin anticoagulation is only in the absence of bowel infarction and with angiographic evidence of sufficient collateral perfusion.

Thrombectomy alone is unlikely to result in durable response given widespread atherosclerotic lesions. Therefore, combination of thrombectomy, revascularization techniques, and nonviable bowel resection is typically needed.

Arterial revascularization (open surgical visceral bypass) is associated with a high perioperative mortality (approximately 50%) but good long-term patency.

Endovascular stenting has been also reported in small case series.

Long-term antiplatelet agents may reduce risk of recurrence.

Mesenteric venous thrombosis

Initial management with heparin anticoagulation and workup for a hypercoagulable state

Close observation with serial abdominal exams is warranted; prompt laparotomy is necessary for any suspicion of infarcted bowel.

Small reports of successful venous thrombolysis; insufficient data to recommend thrombolysis over standard therapy

Prevention of recurrence with long-term anticoagulation

Nonocclusive mesenteric ischemia

Primary therapy is reversal of the underlying condition resulting in the low cardiac output state.

Successful use of local intraarterial angiographic papaverine infusion has been reported: may also be indicated postoperatively for 24 to 48 hours.

Long-term management with standard-dose aspirin.

Outcomes

Reported mortality approximates 60% to 70%.

Range is from 20% with early diagnosis and management to greater than 70% following bowel infarction.

Diagnosis prior to infarction is the single strongest predictor of survival.

Other predictors of mortality are advanced age, poor functional status, and prior cardiac surgery.

Reported 30-day postoperative morbidity approximates 60%.

Pulmonary and infectious complications are the most common.

SUGGESTED READINGS

Boley SJ, Brandt LJ, Sammartano RJ. History of mesenteric ischemia. The evolution of a diagnosis and management. Surg Clin North Am. 1997;77(2):275.

Cho JS, Carr JA, Jacobsen G, et al. Long-term outcome after mesenteric artery reconstruction: a 37-year experience. J Vasc Surg. 2002;35(3): 453.

Demirpolat G, Oran I, Tamsel S, et al. Acute mesenteric ischemia: endovascular therapy. Abdom Imaging. 2007;32(3):299.

Evennett NJ, Petrov MS, Mittal A, et al. Systematic review and pooled estimates for the diagnostic accuracy of serological markers for intestinal ischemia. World J Surg. 2009;33(7):1374-1383.

Gupta PK, Natarajan B, Gupta H, et al. Morbidity and mortality after bowel resection for acute mesenteric ischemia. Surgery. 2011;150(4):779-787.

Huerta C, Rivero E, Montoro MA, et al. Risk factors for intestinal ischaemia among patients registered in a UK primary care database: a nested case-control study. Aliment Pharmacol Ther. 2011;33(8):969-978.

Klein HM, Lensing R, Klosterhalfen B, et al. Diagnostic imaging of mesenteric infarction. Radiology. 1995;197:79.

Kumar, S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med. 2001;345(23):1683.

McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am. 1997;77:307.

Ofer A, Abadi S, Nitecki S, et al. Multidetector CT angiography in the evaluation of acute mesenteric ischemia. Eur Radiol. 2009;19(1):24-30.

Oldenburg WA, Lau LL, Rodenberg TJ, et al. Acute mesenteric ischemia: a clinical review. Arch Intern Med. 2004;164:1054-1062.

Park WM, Gloviczki P, Cherry KJ Jr, et al. Contemporary management of acute mesenteric ischemia: factors associated with survival. J Vasc Surg. 2002;35(3):445-452.

Schoots IG, Levi MM, Reekers JA, et al. Thrombolytic therapy for acute superior mesenteric artery occlusion. J Vasc Interv Radiol. 2005;16(3):317.

Vicente DC, Kazmers A. Acute mesenteric ischemia. Curr Opin Cardiol. 1999;14(5):453-458.

Wyers MC, Powell RJ, Nolan BW, et al. Retrograde mesenteric stenting during laparotomy for acute occlusive mesenteric ischemia. J Vasc Surg. 2007;45(2):269.

4.5

Gastrointestinal Bleeding

Kathryn L. Butler

Introduction

Upper gastrointestinal (GI) bleeding accounts for 80% of cases.

Jejunal/ileal bleeding is responsible for <5% of cases.

Remember vascular sources in postoperative patients

Visceral artery pseudoaneurysm after foregut surgery

Aortoenteric fistula after aortic aneurysm repair

Common Causes to Remember

Epidemiology

Annual incidence 170 cases per 100,000 adults

Incidence increases with advancing age

More common in men than women

Key Pathophysiology

Upper GI bleeding

Responsible for 80% of acute bleeds

Melena

Black, tarry schools

Usually from gastric acid degradation of hemoglobin to hematin

Can also occur secondary to digestive enzyme action in small intestine

Hematemesis

Can be bright red or coffee grounds

Brisk upper GI bleeding can present as hematochezia (bright red blood per rectum) without hematemesis or melena.

Most common causes: peptic ulcer disease (PUD) and varices

PUD

30% to 50% of upper GI bleeding cases

Bleeding most frequent indication for operation, and primary cause of death

Significant bleeding from erosion into artery of submucosa or larger vessel

Highest morbidity from erosion into gastroduodenal or left gastric arteries

Duodenal ulcers more common than gastric

Causes include Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs)

Varices

20% of upper GI bleeding cases

Secondary to portal hypertension

Compared with nonvariceal bleeding, there is increased mortality, risk of rebleeding, and need for transfusions.

Gastroesophageal (GE) varices most common

Although nonvariceal sources still account for most bleeds in cirrhotic patients, given high mortality rate of variceal bleeding, treat empirically for variceal hemorrhage (octreotide) until endoscopy identifies another source.