Page 78 – Practical Gastro

Case Presentation

A 48-year-old woman who was initially diagnosed with Hepatitis C, subsequently developed compensated cirrhosis of liver and portal hypertension with a complication of hepatocellular carcinoma. She presented to the hospital with lower abdominal pain. On examination, vitals were stable. She was noted to have massive splenomegaly, without hepatomegaly, hepatic bruit, ascites or pedal edema. In the periumbilical region were distended superficial veins similar in appearance to caput medusae, but without any bruit around the umbilicus. The CT of the abdomen is as shown in Images 1 and 2.

What is the abnormality seen?
What are the implications of the abnormality and treatment options?
What is the diagnosis if there was an additional finding of a bruit around the umbilical area?

DISCUSSION

Caput medusae are a network of dilated veins around the umbilicus and are one of the manifestations of portal hypertension from cirrhosis of the liver. The term is Latin for Head of Medusa and originates from its similarity to Medusa’s hair.

Caput medusae may be left alone. Embolization or transjugular intrahepatic portosystemic shunt may be used to decompress the collateral route in cases of hemorrhage. Knowledge of the other collaterals is essential since they may undergo spontaneous hemorrhage or bleeding from disruption of these vessels during surgical procedures.¹ They also had lesser episodes of bleeding from esophageal varices. At times this could be mistaken for paraumbilical hernia.

Cruveilhier-Baumgarten (CB) syndrome, described by Cruveilhier (1835) and Baumgarten (1908), refers to a murmur over the umbilicus often in the presence of caput medusae, resulting from portal hypertension, usually with hepatic cirrhosis. Recanalization of the umbilical vein with reverse blood flow from the liver into the abdominal wall veins creates the murmur.²

Embryologically, the left umbilical vein undergoes gradual atrophy to form the ligamentum teres in the falciform ligament. A small portion of the umbilical vein at its junction with the left portal vein may remain patent throughout life. CB syndrome represents spontaneous portosystemic collateralization between the paraumbilical vein and the veins of the anterior abdominal wall in a patient with portal hypertension.

A Case Report

Hepatic Abscesses Caused by a Rare Fistulous Tract

Neha Sahni,Dhiraj Gulati,Kamran Heydarpour

Introduction

We present a case of a fistula, between the portal vein and the left hepatic duct, discovered during an endoscopic retrograde cholangiopancreatography (ERCP). Fistulas between the portal vein and biliary tract are rare and occur in less than 1 % of patients with biliary tract disease.¹ Current literature reports that portobiliary fistulas may occur spontaneously, after biliary stent placement, following biliary surgery, after trauma, post trasjugular intrahepatic portosystemic shunt (TIPS) placement and also following liver biopsies;^{1 ,2,3,7,8} the case we present was likely a complication of cholangitis. A literature review accompanies this case.

CASE REPORT

A 79 year-old African American female with a history of cebrovascular accident, hypertension, congestive heart failure and hyperlipidemia presented to the hospital after having been found at home on the floor with altered mental status. Upon initial evaluation, she complained of vague chest pain and right upper quadrant abdominal pain. On physical examination, her temperature was 100.9 degrees; her blood pressure, heart and respiratory rates were normal. The remainder of the physical examination was unremarkable.

Initial blood tests were as follows: aspartate aminotransferase, 267 IU/L (<33 IU/L), alanine aminotransferase, 105 IU/L (<32 IU/L), total bilirubin of 2.1 mg/dl (0.0-1.5 mg/dl), direct bilirubin 1.3 mg/ dl (0.0-0.3 mg/dl), alkaline phosphatase 397 IU/L (35105 IU/L), international normalized ratio (INR) of 2.0, and a prothrombin time of 17.2 sec (10.6-13.4 sec). The complete blood count revealed a white cell count of 15.3 (4.8-10.8 k/mm cu) and a hemoglobin of 9.3 (12-16 g/dl). A CT of the abdomen revealed multiple hypodense nodules throughout the liver (Figure 1) with a dilated common bile duct. An ERCP was performed for suspicion of acute cholangitis. The common bile duct was injected and a ﬁlling defect in the gallbladder was noted to be consistent with a large gallstone. As the biliary tree branches were completely ﬁlled (Figure 2), there was a ﬂuid accumulation at the proximal portions of the biliary tree suggesting abscesses. These ﬂuid collections were draining through a ductal structure completely different from that of the biliary tree. Thus, a fistula between the biliary tree and the ductal structures was exposed. Further evaluation revealed that the ductal structure was, in fact, the portal vein. A 7-French 10-cm stent was placed to assure adequate drainage of the bile duct (Figure 3). A CT guided biopsy of the liver lesions demonstrated acute cholangitis with microabscesses. The patient was successfully treated with intravenous antibiotics. The follow-up ERCP performed two months later revealed complete resolution of the fistula.

DISCUSSION

This case is a good demonstration of a rare ﬁstula in the gastrointestinal (GI) tract. Portobiliary ﬁstulas can occur spontaneously, following biliary stent placement, biliary surgery, trauma, post TIPS placement, as a result of liver biopsy ^1,2,3,7,8,10 and, in our case, as an unusual complication of ascending cholangitis. Repeated inﬂammation, with development of scar tissue between adjacent organs, can cause the formation of ﬁstulas.^1,5 In this patient, it was the upsurge of pressure in the hepatic duct from prolonged cholangitis that led to an outpocketing and an eventual ﬁstulous tract between the hepatic duct and portal vein, which lie in close proximity. Per previous case reports, portobiliary ﬁstulas may present with right upper quadrant pain, hemobilia and bleeding per rectum resulting in anemia.^1,4,6,9 The pathophysiology of rectal bleeding is that leakage of blood from the portal vein into the hepatic duct, common bile duct and then to the GI tract occurs. The lack of bleeding in the patient presented above can be explained by Figures 4 and 5. Magnetic resonance imaging (MRI) revealed a thrombus in the portal vein, proximal to the fistula, blocking the vein from bleeding into the GI tract. It was also suspected that the thrombus contributed to the fistula formation by eroding the portal vein wall.

Given the elevated liver enzymes, INR and bilirubin and the hepatic nodules seen on the abdominal CT, cancer was highly suspected. Liver biopsy confirmed cholangitis and ruled out malignancy. Blood cultures were positive for Staphylococcus simulans and Enterococcus species, most likely starting in the biliary ducts spreading through the fistula into the portal vein to the liver creating abscesses.

Ultimately, a stent was placed to maintain drainage of the duct as well as relieve the high pressures in the duct due to the cholangitis. It was the relief of this pressure that allowed for the natural closure of the fistula, as proven by the repeat ERCP done two months later. Treatment may also have included surgical resection of the fistula had it not resolved.

Unusual Causes of Abdominal Pain, #2

Unusual Causes of Abdominal Pain

George W. Meyer

CASE

A 12 year old girl presents with a several month history of daily episodes of abdominal pain with some diarrhea (loose bowel movements). Her bowel movements were 3-4 per day without nocturnal defecation. She had no weight loss and her growth and Tanner development were normal compared to an older sister. She has complained of daily headaches without aura since age 8. She also gave a history of motion sickness, especially in automobiles. On physical examination her vital signs were normal and there were no abnormalities in the physical examination. A therapeutic trial was initiated.

Answer and Discussion

This young person had abdominal migraine. She responded to Inderal 10 mg by mouth thrice daily. Not only did her abdominal pains find relief but she no longer complained of headaches. Ninety percent of recurrent abdominal pain in pediatrics is functional, the farther from the umbilicus, the greater the chance for significant disease. The differential diagnosis includes cyclic vomiting, tachygastria, and, perhaps, abdominal epilepsy. Abdominal migraine is said to affect 2-4 % of children, 60 % are female, with the age of onset between 2 and 10 years. The pain is associated with other complaints, such as anorexia, nausea, vomiting, and pallor. Sixty percent of children are said to have a family history of migraines. Most children outgrow their abdominal pains but they may develop or continue to have migraine headaches. Propanolol and cyproheptadine have been described as beneficial in preventing these episodes. During the acute episode some find that acetaminophen or ibuprofen may be helpful; anti-nausea medications such as triptans are best administered rectally; intravenous valproic acid has been reported to be successful in the Emergency Department.

Inflammatory Bowel Disease: A Practical Approach, Series #88

Hepatobiliary Disease and Inflammatory Bowel Disease

Emily Schonfeld,

James S. Park,

Seymour Katz

Ten to twenty percent of patients with inflammatory bowel disease (IBD) have liver disease. This article will encompass important inflammatory conditions, such as primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC), drug-induced liver injury, cholelithiasis, steatosis and rare liver diseases associated with IBD, such as amyloidosis and granulomatous hepatitis.

IntroductIon

Ten to twenty percent of patients with inflammatory bowel disease (IBD) have liver disease.¹ This article will encompass important inflammatory conditions, such as primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC). We will also discuss drug-induced liver injury, cholelithiasis, steatosis and rare liver diseases associated with IBD, such as amyloidosis and granulomatous hepatitis.

Primary Sclerosing Cholangitis

PSC is a chronic inflammatory condition of the intra- and extrahepatic bile ducts that leads to strictures and fibrosis of the bile ducts (Figure 1).^2-4 The prevalence of PSC is 6-16 cases per 100,000 people in North America and Europe.^2,5,6 The disease is more commonly found in men than in women.^2,4 About 70% of patients with PSC also have IBD, usually ulcerative colitis (UC), but it can also be seen in Crohn’s disease (CD).^1-4

The pathogenesis of PSC is unknown. There may be a genetic predisposition to PSC as there is an increased risk of PSC in patients having a first-degree relative with the disease.²

Patients are often asymptomatic at the time of diagnosis and the most common laboratory abnormality is an elevated alkaline phosphatase.^2,4 Diagnosis can be made with magnetic resonance cholangiopancreatography (MRCP), endoscopic retrograde cholangiopancreatography (ERCP) (Figure 1), and percutaneous transhepatic cholangiography (PTC).^2,4,7 When comparing MRCP to the other imaging modalities, the sensitivity and specificity of MRCP for the diagnosis of PSC have been reported at ≥80% and ≥87% respectively.⁷ These imaging modalities will demonstrate a “beaded” appearance of the intra- and extrahepatic bile ducts.^4,7 This appearance of the bile ducts represents multiple stricturing areas interspersed with normal or dilated areas.^2,7

There are a number of adverse outcomes associated with PSC. PSC can lead to cirrhosis and the adverse effects of end-stage liver disease.^4,8 It is also associated with recurrent episodes of cholangitis.⁷ There is an increased risk of colorectal cancer in patients with PSC and ulcerative colitis compared to patients with ulcerative colitis alone.^2,9,10 Patients should therefore start screening colonoscopies when they are diagnosed with both diseases.⁹ Patients with PSC not only have an increased risk of colorectal cancer, but they also have an increased risk of cholangiocarcinoma, which is seen in 7-15% of patients.^3,7,11 It is important to note that PSC has a course independent of IBD and it is unchanged by colectomy.^2,4,9

Ursodeoxycholic acid (UDCA) has been studied for the treatment of PSC, but it has not been shown to be beneficial in PSC.² High dose UDCA (28-30 mg/ kg/day) has demonstrated an increased risk of adverse events in PSC patients.^12,13 Definitive treatment for PSC is a liver transplant, but PSC can recur in patients posttransplant.^2,7

One type of PSC, small-duct PSC, can only be diagnosed by liver biopsy since it does not have the typical imaging findings seen in large-duct PSC.^2,4,7 Small-duct PSC demonstrates similar laboratory findings and histology to large-duct PSC and it can progress to large-duct PSC.^2,4,7

An overlap syndrome between autoimmune hepatitis and PSC occurs in IBD patients.^2,4,7 These patients have the classic imaging findings seen in PSC and laboratory findings that suggest autoimmune hepatitis, such as elevated aminotransferase levels, gamma-globulin levels, anti-nuclear antibody levels, and anti-smooth muscle antibody levels.^2,7 Liver biopsy is usually required for this diagnosis.²

Primary Biliary Cirrhosis

PBC is characterized by destruction of the intrahepatic bile ducts.¹⁴ It is an autoimmune disease that is seen more often in women, with increased risk in first-degree female relatives.^14,15 Although PBC is not specifically associated with IBD, it should also be suspected in patients with an elevated alkaline phosphatase or cholestasis.¹⁵ PBC can lead to fibrosis and cirrhosis of the liver.¹⁵ 90-95% of patients with PBC have antimitochondrial antibodies.¹⁴ Elevated alkaline phosphatase, mild transaminase elevation, and increased immunoglobulins, usually immunoglobulin M (IgM), are common laboratory abnormalities seen in PBC.¹⁵ The diagnosis of PBC is based on two of the three following criteria: positive antimitochondrial antibodies, elevated alkaline phosphatase and a liver biopsy that demonstrates destruction of bile ducts in the portal triad.¹⁵

Osteoporosis, hyperlipidemia, and vitamin deficiencies are found in PBC with advanced disease.^14,15 UDCA is used in the treatment of PBC and it can delay the progression of early stage disease.^14,15 Colchicine and methotrexate have been used as second and third-line agents.¹⁴ When patients have advanced liver disease, the only treatment is orthotopic liver transplantation, but PBC can recur in the transplanted liver.^14,15 A normal or low bilirubin level is the best predictor of survival in PBC.¹⁵

Cholelithiasis and Choledocholithiais

Cholelithiasis can be seen in patients with IBD, especially in patients with CD with ileal involvement.⁴ These patients can have an increased biliary cholesterol saturation and this may increase cholelithiasis.¹⁶ Choledocholithiasis occurs in 15% of patients with cholelithiasis and can lead to cholecystitis, cholangitis and pancreatitis.¹⁷ It is therefore important to evaluate for gallstones in all IBD patients with abnormal liver function tests.

Drug Induced Liver Injury

The most common type of drug-induced liver injury is an idiosyncratic reaction that is not dose-dependent and can occur days after starting the medication.⁴ Methotrexate, cyclosporine and azathioprine can cause hepatotoxicity in a dose-dependent method.⁴

5-aminosalicylate (5-ASA) compounds can lead to an elevation in aminotransferase levels.⁴ There are case reports of granulomatous hepatitis secondary to sulfasalazine.¹⁸

Azathioprine and 6-mercaptopurine (6-MP) can cause liver disease in a hepatocellular or cholestatic method, but usually laboratory values improve after stopping the drugs.^1,4,19 Mild transaminase elevation can be managed by lowering the dose of the drugs.^1,4 Azathioprine and 6-MP can also cause nodular regenerative hyperplasia of the liver, which is a rare long-term complication that can lead to portal hypertension.^1,20,21

Methotrexate can cause a transaminitis.1 Methotrexate hepatotoxicity can eventually lead to cirrhosis and should be used with caution in patients with pre-existing liver disease.^4,22 Hepatotoxicity occurs in a dose-dependent fashion.⁴

Cyclosporine can also cause hepatotoxicity based on the dosing of the medication.⁴ The liver injury is usually a cholestatic pattern.⁴

Infliximab-induced hepatotoxicity is rare and can cause a transaminitis.^1,23,24 Infliximab can also cause an exacerbation of hepatitis B.²⁵ All patients should be tested for hepatitis B prior to treatment with infliximab.²⁵

All Others – Rare Diseases
Steatosis

Steatosis can occur in patients with IBD and often presents as elevated transaminases.¹ Ultrasound, CT and MRI can help diagnose patients with non-alcoholic fatty liver disease (NAFLD).^1,26 Sourianarayanane et al. used imaging techniques and found the prevalence of NAFLD to be 8.2% in IBD patients, which is lower than that seen in the general population. The study also found that IBD patients with NAFLD had a higher BMI, more obesity, and more signs of metabolic syndrome.²⁶ The patients with NAFLD in this study were more likely to have had previous small intestinal surgery, to take steroids at the time of imaging, and less likely to have received anti-TNF-α medications.²⁶ The gold standard for diagnosis is liver biopsy and can evaluate for nonalcoholic steatohepatitis (NASH).¹

Hepatic Amyloidosis

Amyloidosis occurs in 0.9% of patients with CD and 0.07% of patients with ulcerative colitis.⁴ Amyloid can deposit in multiple organs, including the liver.²⁷ Systemic AA amyloidosis is associated with IBD.^27,28 Liver biopsy is needed for diagnosis.⁴

Granulomatous Hepatitis

Granulomatous hepatitis can be seen in patients with CD with an elevated alkaline phosphatase.⁴

Liver Abscess

Liver abscesses can occur in patients with IBD, especially CD, and can present with fever, right upper quadrant pain, leukocytosis and an elevated alkaline phosphatase.^4,29 Diagnosis can be made with imaging studies, such as an abdominal ultrasound or CT scan.⁴ Liver abscesses are usually treated via percutaneous drainage.²⁹

Cancers – HCC and Cholangiocarcinoma

Patients with PSC are at increased risk of cholangiocarcinoma, with a prevalence of 7-15%.^3,7,11 It is difficult to diagnose cholangiocarcinoma since it resembles the strictures seen in PSC and there is often a high mortality rate at the time of diagnosis.^4,7,30 Risk factors for cholangiocarcinoma in PSC include elevated bilirubin, variceal bleeding, proctocolectomy, and ulcerative colitis with colorectal cancer or dysplasia.¹¹ Cholangiocarcinoma arises in both the intra- and extrahepatic bile ducts and it is divided into intrahepatic, perihilar and distal disease.³⁰ When imaging the biliary tree in PSC, long strictures may indicate an underlying cholangiocarcinoma.^2,3,11 An elevated CA 19-9 can be helpful; however, patients who are Lewis antigen negative will not be positive for CA 19-9.^3,4

ERCP with brush cytology may aid in the diagnosis of cholangiocarcinoma, but its sensitivity is low.2-4 Flourescence in situ hybridization (FISH) increases the sensitivity of ERCP brushings.^2,3

Cholangiocarcinoma is frequently diagnosed at advanced stages and it is therefore difficult to treat, often palliative.^4,7,31 Liver transplant has been used in treatment of early cholangiocarcinoma.^2,31 The American Association for the Study of Liver Diseases (AASLD) guidelines recommend liver transplant in patients with a single unresectable mass that is ≤ 3cm and no metastatic disease.^2,4,7 Patients are given radiation and chemotherapy prior to transplant.^2,4,7

Hepatocellular carcinoma (HCC) occurs in patients with PSC when PSC has progressed to cirrhosis.^4,8,32 AASLD recommends surveillance for HCC every 6 months in patients with cirrhosis.³² The diagnosis of HCC can be made with four-phase CT scans or MRI scans which demonstrate early arterial enhancement and delayed washout of the HCC mass.^32,33 Smaller lesions, usually < 2 cm, often need serial imaging and biopsy to help with diagnosis.³³

Treatment of HCC is based on the size of the lesion and extent of underlying liver disease.³⁴ Surgical resection, orthotopic liver transplantation, radiofrequency ablation, transarterial chemoembolization (TACE), and chemotherapy are the treatment modalities used for HCC.^33,34 The Barcelona Clinic Liver Cancer (BCLC) staging helps determine prognosis in patients with HCC.^34,35 The Milan Criteria is used to determine if a patient is eligible for an orthotopic liver transplant.^32-34 Patients with one mass < 5 centimeters or three masses < 3 centimeters are eligible for orthotopic liver transplantation.^32-34 The 5-year survival rate for orthotopic liver transplantation following the Milan Criteria is 70%.³²

CONCLUSION

IBD is a chronic inflammatory condition that involves the gastrointestinal tract.⁹ There are multiple hepatobiliary diseases associated with IBD and these diseases should be investigated when an IBD patient presents with abnormal liver function tests.

PSC is one of the more common manifestations of liver disease in IBD.^1-4 Patients with an elevated alkaline phosphatase and IBD should be evaluated with the appropriate imaging tests for possible PSC.^2,4 Medications used to treat IBD can lead to drug-induced liver injury, which may precipitate discontinuation of these medications. Cholelithiasis and steatosis, similar to the general population, are seen in patients with IBD.^1,4 Rare complications of IBD include amyloidosis and liver abscesses.^27,29 These diseases are associated with systemic symptoms, such as renal and cardiac involvement in amyloidosis and fever and leukocytosis in liver abscesses.^4,27,29

Nutrition Issues in Gastroenterology, Series #127

Clogged Feeding Tubes: A Clinician’s Thorn

Charles Fisher,

Bethany E. Blalock

Clogged feeding tubes are responsible for significant lost delivery of enteral feeding. They also increase risks and costs to patients in the event that they must be replaced. This article will present evidence-based guidelines to clinicians for feeding tube clog prevention and declogging. The current products and techniques for declogging feeding tubes will be discussed with emphasis on practical declogging methods.

IntroductIon

Enteral feeding tubes are a lifeline for those patients who rely on them every day for nutrition, hydration and medication administration. According to the American Society for Enteral and Parenteral Nutrition (ASPEN), data from 2009 revealed that more than 245,000 patients per year require at least a temporary feeding tube during a hospital stay, along with another nearly 31,000 who are on enteral nutrition at home; numbers are not available for what are surely many thousands more in long term care facilities.¹ Estimates of the incidence of clogged feeding tubes range widely, from 12.5 – 45% over the life of a tube.^1-4 The cost of supplies, nursing care, and confirmatory abdominal x-rays required for simple nasoenteric tube replacement is therefore significant when multiplied across such a large scale, and this is not even to speak of the dollars that could be saved by preventing the need for more involved tube replacements such as via fluoroscopy or endoscopy. Though reliable data on the healthcare costs of tube replacement are scarce, a single trip to fluoroscopy to replace a clogged J-arm at our facility can cost upwards of $1,000, for example.

As many clinicians know all too well, clogged feeding tubes may result from several factors, including narrow tube diameter, insufficient water flushes, and inattention to proper medication administration.³ There are many anecdotal practices to declog feeding tubes such as using cranberry juice, cola, meat tenderizer and enzymes such as pancrealipase, papain, and chymotrypsin, but several studies cast doubt on the effectiveness of these remedies.^5,6 A review of the literature indicates that the best way to manage clogged feeding tubes is by preventing them,^1,2,7 but in the event that a feeding tube does become occluded, there are safe and effective methods established for restoring tube patency. Declogging methods include warm water flushes, enzymatic clog dissolvers, and mechanical clog removal tools, all of which are reviewed here. Suggestions for how to avoid clogged tubes in the first place are outlined as well. Declogging

Despite a lack of evidence to support them, many practices persist regarding how to “properly” unclog a feeding tube. As is often true, the internet is as much a source of misinformation as it is of reliable advice when it comes to unclogging feeding tubes. A casual search, such as one that a home patient might undertake, yields erroneous and sometimes even unsafe information, including recommendations to use hot water, coffee, carbonated beverages, pipe cleaners, and tenderizer. These common but unsupported methods were repeated often on a number of different sites. Notably, these are only examples from a recent search, and some sites do offer the internet user sound advice; the danger lies in the lay person using an ineffective even unsafe method, which in the worst case could lead to damaged GI mucosa, or more likely, a costly trip to the emergency department for a new tube. Water

Research clearly supports water as the best choice for initial declogging efforts, as carbonated beverages, juices, and meat tenderizer have been shown to be ineffective.^5,8,9 In fact, because of their acidic pH, juices and carbonated beverages may even cause formula protein precipitation within the tube, making the clog worse or leading to more clogging later on.² When clogs do occur, and they will, it is best to attempt clearance immediately using warm water and a gentle back and forth motion with the plunger of the syringe.² Alternating pressure and suction with the syringe should not be done with great force because ruptured feeding tubes have occurred.² Thus, syringes of 30 mL or larger are appropriate for gastrostomy tubes, but a 60 mL syringe should be used with smaller-French nasoenteric �2012 Actuated Medical, Inc. + 310 Rolling Ridge Drive + Bellefonte, PA 16823 USA or jejunostomy tubes since smaller syringes generate excessive pressure.^1,10 After instilling the lukewarm water, clamp the tube and let it soak for up to 20 minutes if a stubborn clog does not immediately allow for the back on forth motion.

Enzymes

If water does not work, then enzyme solutions are a second-line option. Current products in the United States include Viokace and Clog Zapper™. Aside from Viokace, all other pancrealipase brands available in the U.S., such as Creon and Zenpep, are enteric coated and therefore cannot be used for this off-label purpose. Since it requires a prescription, Viokace is primarily used only in institutional or clinic settings unless the patient already has it at home for pancreatic enzyme replacement therapy. To use, one tablet of Viokace must be crushed and dissolved with one 324 mg nonenteric-coated tablet of sodium bicarbonate (or 1/8 teaspoon baking soda) and 5 mL water in order to create the alkaline pH for clog dissolving. Clog Zapper™ is a commercially available product from Corpak that requires only water for preparation and may be recommended for home use with training.¹¹

Mechanical Devices

There are currently three approved mechanical devices for clearing feeding tubes. The Bard brush and the Bionix Feeding Tube Declogger are for use only in shorter tubes such as gastrostomy and jejunostomy tubes, not nasoenteric tubes. The Bard brush, which is designed to fit 20 Fr and larger PEG tubes, is a flexible nylon stem with soft bristles on the end that are intended to minimize mucosal injury.¹² Its recommended use is actually prophylactic tube cleaning and it is not recommended as a tool to clear clogs, though it does have the advantage of being commercially available online. The Bionix, on the other hand, is specifically designed to remove clogs. A flexible plastic stem with a “screw and thread design,” this tool comes in varied sizes to fit gastrostomy or jejunostomy tubes sizes 14 to 24 French.¹³ However, it is only for use by trained professionals in a medical setting.

Finally, the latest device is the TubeClear® system, which only recently received FDA clearance for use in hospital settings and may be a remedy for resolving clogged nasoenteric, gastrostomy, and jejunostomy tubes sizes 10-18 Fr (see Table 1).¹⁴ TubeClear® uses single use stems paired with a control box that plugs into AC power to create a jackhammer-like motion inside the tube. The advantage is its use in long, narrow Dobhoffstyle tubes, which are more prone to clogging in the first place and which are time consuming and uncomfortable to replace. TubeClear® also has stems in development for clearing 8 Fr tubes and Gastro-Jejunostomy tubes – the most costly and time consuming to replace, however, these versions are not yet FDA cleared. A summary of declogging tips is presented in Table 2. See Table 3 for commercially available products.

Clog Prevention

As is true in so many cases in the medical setting, an ounce of prevention is worth a pound of cure. While clogged feeding tubes are impossible to prevent 100% of the time, there are a few simple procedures that will save patient discomfort, time, lost feeding delivery, lots of frustration, and money.

Tube Diameter

Common sense tells us that the smaller the tube diameter patient comfort and should therefore be considered, (and also the longer the tube), the more likely the tube particularly if smaller tubes have failed. In addition, we is to clog. While flexible, small-bore feeding tubes are use a 24 Fr PEG with a 12 Fr jejunal extension for the the obvious choice for nasoenteric feeding (as opposed same reason. Similarly, 12 Fr jejunal extension tubes to Salem SumpTM type tubes), our anecdotal experience through 24 Fr PEGs clog significantly less often than at our institution has been that 12 Fr feeding tubes clog 8-10 Fr tubes, and some case series have borne out this less often than 8 or 10 Fr tubes without sacrificing observation.¹⁵

Medications

Combining a clear plan for medication delivery with flushing will limit clogged tubes. Medication lists should be given a thorough review by a pharmacist to promote the use of available liquid alternatives; to limit the use of capsules and extended release forms; and to identify which pills can be finely crushed using a mortar and pestle (or other crushing device such as the Silent Knight Pill Crusher by Medline Industries) and dissolved.6 Pharmacists might also suggest alternative delivery modes such as intravenous, subcutaneous, intramuscular, transdermal, or rectal in order to limit the number of different medications that must be flushed down the feeding tube.^3,16,17 Finally, pharmacists should be enlisted to advise regarding incompatible medications and when they should be separated by 30-60 minutes.³

Water Flushes

Routine, proactive flushing during feeding and medication administration is the best way to prevent many clogged tubes, yet up to 57% of nurses do not flush before giving medications according to various reports.^3,16-18 Therefore, proper flushing instructions for both home and institution feeding should be clear to the end provider or caregiver. There are variations in practice such as using sterile water when the tap water is not proven safe, and varied flushing frequencies, but consistent flushing before and after medication administration and bolus feedings, and periodically with continuous or cyclic feedings, is the most important intervention to prevent clogging.

For continuous feedings, a minimum volume 30 mL water flush should be administered at least every 8 hours to maintain tube patency and more as indicated for hydration needs.^1,16,19 Enteral feedings should be stopped and the line flushed prior to giving medications and again before turning the feedings back on. For bolus or intermittent feedings, at least 60 mL should be flushed before and after the enteral formula. The same goes for medications: flush 5, 15, or 30 mL or more between each medication.^1,3,16,19 Finally, if medications are given at the same time as formula boluses, they should all be separated by water, i.e., water-medicationwater-formula-water. See Table 4 for the University of Virginia Health Systems handout for home patients. Table 5 summarizes the recommendations for clog prevention.

CONCLUSION

Clogged feeding tubes increase health care costs and decrease nutrient delivery. Consistent and scheduled
flushing of all types of feeding tubes is the best defense
against clogs. However, while avoiding clogged feeding tubes is a worthy goal, they can and will occur. When they do, the front line for declogging is to use lukewarm water as described, and failing that, commercial products are available. Importantly, there is a gap in health care provider knowledge when it comes to best practices for declogging feeding tubes, and addressing this barrier will help prevent lost nutrition for patients, along with wasted time and money. Finally, as declogging devices become more sophisticated and mainstream, tube replacements due to occlusion will hopefully become a rare occurrence.

Nutrition Issues in Gastroenterology, Series #126

Yogurt: Nutritious Food or Sugary Treat?

Angie Hasemann

Introduction

The importance of consuming adequate calcium through daily intake of milk products has been a health focus of Americans for many years.¹ However, liquid milk consumption has declined in the United States in recent years.² This has been matched by an increase in the consumption of frozen, drinkable, and spoonable yogurt, which has caused a boom in yogurt production. Considering that overall dairy consumption has been below recommended daily intakes, the dairy industry has responded by an increase in development and marketing of other dairy products.^3,4 Specifically, yogurt manufacturing has responded to consumer Angie Hasemann, RD, CSP Outpatient Pediatric Dietitian, Children’s Fitness Clinic, University of Virginia Children’s Hospital, Charlottesville, VA demands, resulting in both healthier and more flavorful products emerging. No longer is yogurt the high fat dairy product it was decades ago. Not only have lower fat versions been developed, but now there are a variety of other nutrients being added to yogurt. Companies have responded to consumer concerns regarding healthier options and have developed products to meet the needs of convenience and flavor demanded by consumers today.² With this abundance of options, many consumers feel lost in the yogurt aisle of the grocery store.

What Happened to Yogurt?

Twenty years ago, there were not many options for yogurt. A quick glance down the dairy aisle in a grocery store shows just how much things have changed. Over time, the industry has grown significantly, and global sales are projected to reach $494 billion by 2015. Included in this, retail sales of frozen, drinkable, and spoonable yogurt increased 7.5% to nearly $6.4 billion in 2011 and are predicted to grow even further, at a rate of 5-7% per year through 2017. This growth is partly due to America’s desire to eat healthier while not sacrificing flavor or convenience.² Yogurt manufacturers have risen to this challenge.

Healthier Enhancements

The first health-enhancing adjustment by the yogurt industry was the development of reduced fat, low fat, and eventually, fat-free versions. These changes helped to establish yogurt as a true “health food.” With the addition of “live and active cultures,” touted health benefits grew. The wide variety of probiotics currently found in yogurt are purported to rejuvenate gut flora and are being researched for a variety of potential health benefits, including lowering cholesterol and increasing brain cognition. Almost half of dairy producers are working on new products which are low fat or fat-free, have reduced amounts of sodium and sugar, are available in lactose-free versions, are organic, include probiotic cultures, and are fortified with nutrients, specifically calcium and protein. The appeal of the lower sugar and higher protein content of Greek yogurt has helped this section of the yogurt industry explode in recent years, now accounting for about one-third of all yogurt consumption.²

Flavor-Enhancing Changes

While the nutrient profile of yogurt has changed in recent years, so have the multitude of flavors available in the supermarket. Yoplait alone boasts 99 distinct flavors on its website.⁵ It is now possible to find flavors that sound more like luxurious desserts, kid-friendly treats, and unhealthy indulgences rather than the calcium-packed dairy product yogurt was once known to be.

What’s in Your Yogurt?

Research shows that four brands rule the yogurt industry. Chobani currently offers 7 products online⁶ and recently was chosen as the supplier for the USDA Greek Yogurt Pilot Program, which will bring this product into schools across the nation as part of the national school lunch program.⁷ Dannon Activia promotes 8 products online, with a variety of options touting the live and active cultures for which Activia has become known.⁸ 38 Stonyfield Farm is a leading organic yogurt supplier, with 9 different products.⁹ Yoplait has been a player in the industry for years and currently has 18 product types online. With so many options, the difference among products can be difficult to digest. Table 1 shows a simple breakdown of some of the basic yogurt products on the market. The variance in container size can be distracting to the consumer. Table 1 also contains an analysis of these same basic yogurt types, comparing each product’s nutrients per 8 oz. serving for a fair comparison.

Dessert-Inspired Yogurt

With the demand to develop better tasting yogurts and the desire to find healthier sweets; dessert-inspired yogurts have overwhelmed the market. Companies now compare yogurt to tempting sweets in television advertisements, and food scientists have continued to work to develop yogurt options that will rival the desserts people crave. Manufactures have marketed them as such. Table 2 reviews versions of dessert-inspired yogurt products. In comparison per 8 oz., the huge gap in nutrition is evident.

Kid-Friendly Yogurt

Yogurt is a food commonly consumed by children, offering the consistency that is safe for toddlers and the ease in packaging and on-the-go eating that parent’s desire. Companies have done their research to appeal to this population. Table 3 shows the broad product development targeted directly at parents who are inclined to search healthy and convenient products their children will enjoy. These products are often offered in kid-friendly portions, varying in size from 2 oz. tubes to the typical 6 oz. adult serving. Table 4 shows the level of calcium available in these products.

While many parents consider these products to be a healthy option for their children, few recognize the high level of sugar in such products. While a plain yogurt would contain around 1.5 grams of sugar per ounce, Table 5 shows how these products include much more. In fact, all but two products have double the amount of sugar per ounce as plain yogurt.

Drinkable Yogurt

While efforts have been made to appeal to children, yogurt products have begun to compete with alternative beverages by marketing drinkable forms. Adults have responded favorably to this convenience item, as it fits well with the on-the-go lifestyle of busy parents and adults. In recent years, the acid whey byproduct of Greek yogurt is being used to create these drinks, thereby making the production process of both products more efficient. Table 6 exhibits the variety of drinkable yogurt products currently on the market. Typical serving size can vary greatly by product and targeted audience. Comparison by 8 oz. serving is included in the shaded rows of this table.

How Do These Products Add Up?

Yogurt has long been revered for its calcium content; however, in an effort to better meet the evolving needs of consumers, the nutrient profile has changed. Nutrition content also varies greatly across the industry and no two products have identical nutrient content. Education for the public to simplify nutrient label reading is essential to help the busy shopper to understand what nutritional value is present in the yogurt product they grab off the shelf. Unfortunately, many assume they are all equal, which could not be further from the truth.

Back to Bones

While yogurt originally was known as a good source of calcium (defined as: 100-199 mg or 10-19% DV/ serving), many current products fall short of the calcium offered in other dairy products. While 8 oz. of milk and 1.5 oz. of most cheeses contain 300 mg of calcium, many yogurt products have far less. Table 1 shows multiple products which offer only 150-200mg of calcium per serving. In fact, only two of the basic yogurt products contain 300mg of calcium. Over half of the kid-friendly versions highlighted in Table 4 have only 100 mg of calcium and none reach the level present in a cup of milk. This is largely due to the smaller serving size of the products; however, it is a sign of inferior nutrition value when comparing a kid-friendly yogurt cup or tube to other snack choices. It is also a reminder that kid-friendly yogurt products are not dependable as a traditional excellent source of calcium ( ≥ 200 mg or 20% DV/ serving) which yogurt was once thought to be. Although dessert-inspired yogurts often are served in the larger sizes, their calcium content often falls short as well. Some drinkable yogurts also lack the calcium of other dairy foods, although the amount of calcium can vary greatly by product.

How Sweet It Is

While dairy products have natural sugar present, flavored yogurts have greatly increased this amount. Some yogurt products have pushed the limits of sugar content, while not always maintaining the benefits of calcium seen in rival products. While sugar content per 8 oz. serving can be as low as 9-12 g, you’ll find numerous products that feature 30g of sugar or more per 8 oz. serving. In fact, half of the products featured in Table 1 have flavors that contain 30g of sugar or more per 8 oz. serving. In looking at the dessert-inspired yogurt products, most have well over 30g sugar per 8 oz. serving, and the kid-friendly products are not much better. Utilizing unflavored yogurt and adding natural sugar via fresh or fresh frozen fruit may be the healthiest option available to consumers.

On the Horizon

In the vastly expanding yogurt industry, many current trends are on the horizon. Experts predict greater industry consolidation, limiting the number of production companies but likely increasing the specialty products available from the four largest yogurt companies (Chobani, Dannon, Stonyfield Farm, and Yoplait), as well as more large scale dairy farms to meet the growing needs of a population that is turning to yogurt as an on-the-go “healthy snack” or even a dessert substitute. With the expected increase in consumption of dairy products, specifically yogurt, the industry is turning to more sustainable packaging. Creating efficiencies in the production process will likely establish packaging that better meets the needs and peaks the interests of consumers. This ongoing variance in serving size will require greater attention to the details on the packaging. With a demand for more lactose-free products, more alternative products will be developed, and more liquid versions of yogurt will likely be created in an effort to rival other drink competitors. Retailers and consumers alike are always looking for new flavors, innovative packaging, and novel products. Utilizing probiotic cultures, applying sustainable materials to extend shelf life, and fortification through added nutrients are also trends that will be present on the grocery store shelf in the coming years.²

Summary

Yogurt varieties have drastically changed in the past decade and will likely continue to evolve. As manufacturers look for innovative ways to meet the needs of consumers’ palates and busy schedules, healthcare providers will need to use the same innovation and show equal dedication to educating consumers. As with all aspects of nutrition, the quality and health value of yogurt may not be visible from the front of the packaging and likely requires some investigation through careful evaluation of the nutrition facts label.
With the wide variety of yogurt products available, educating the public regarding the differences is vital in order to allow the consumer to determine the difference between a “Nutritious Food or Sugary Treat.”

Frontiers in Endoscopy, Series #9

Direct Percutaneous Endoscopic Jejunostomy: Who, When, How, and What to Avoid

Christopher John Murphy,

John C. Fang

While direct percutaneous endoscopic jejunostomy (DPEJ) is not yet widely practiced, advantages include longer durability compared to percutaneous endoscopic gastrostomy with jejunal extension (PEGJ) and less invasiveness than surgical methods with similar rates of complications. DPEJ placement does not require special equipment and is similar in technique to widely practiced percutaneous endoscopic gastrostomy (PEG), and thus should be more widely available. This article will review the current state of DPEJ, specifically addressing when and in whom it should be considered, the technical approaches to placement, and complications to avoid.

Introduction

Direct percutaneous endoscopic jejunostomy (DPEJ) was first described by Shike in 1987 as a method establishing long term enteral feeding in cancer patients with previous gastric resection.¹ DPEJ is an endoscopic procedure that places a percutaneous feeding tube directly into the jejunum similar to a percutaneous endoscopic gastrostomy (PEG) that places a feeding tube directly into the stomach. There are several approaches to long-term jejunal access, each with unique advantages and disadvantages (Table 1). Percutaneous endoscopic gastrostomy with jejunal extension (PEGJ) remains the most common endoscopic approach due to high reported initial success rates, but tube malfunction is common and requires frequent re-interventions. Percutaneous gastrojejunal feeding tubes are increasingly being placed fluoroscopically, which while not requiring sedation, does involve radiation exposure and may have similarly high tube malfunction rates. Direct percutaneous jejunostomy can also be performed through interventional radiology (IR-J), though there are only limited reports in the literature and it is not widely available.2 There are several surgical jejunostomy (SJ) methods including laparoscopic and needle-catheter techniques, which have success rates approaching 100%. However they require multiple skin incisions, general anesthesia, and if attempted laparoscopically may need conversion to open surgery.³ While DPEJ is not yet widely practiced, advantages include longer durability compared to PEGJ and less invasiveness than surgical methods with similar rates of complications. DPEJ placement does not require special equipment and is similar in technique to the widely practiced PEG, and thus should be more widely available. This article will review the current state of DPEJ, specifically addressing when and in whom it should be considered, the technical approaches to placement, and complications to avoid.

WHO
General Indications for Jejunal Feeding

General indications for jejunal feeding are the need to bypass the stomach due to gastric dysfunction or previous resection. Previous gastric resection can render the stomach dysfunctional both from impaired emptying and increased propensity to reflux. In addition, gastric resection may make the stomach difficult to access percutaneously. More specific indications for direct jejunal feeding include: gastric obstruction, gastroparesis, high risk of aspiration, previously failed gastric feedings, post-surgical or other anatomy that precludes gastric access, or need for jejunal decompression/venting. Gastrostomy is generally avoided in patients with anticipated esophagectomy due to concern that PEG may compromise the integrity of a future gastric conduit.^4,5

DPEJ Indications

Indications for DPEJ are summarized in Table 2. Maple et al. ⁶ reported the largest series of 307 patients undergoing DPEJ. In this report 28% of DPEJ were placed due to GI cancer, 21% for gastroparesis, 19% due to previous gastric surgery including partial or total gastrectomy and 13% due to high clinical risk of aspiration. The outcomes of DPEJ placement for specific clinical indications are summarized below.

Aspiration

Patients with recurrent aspiration pose a difficult challenge for clinicians and suffer high morbidity and mortality.⁷ Percutaneous gastrostomy has not been shown to decrease aspiration and aspiration pneumonia. In patients with a history of aspiration, recurrent aspiration after gastrostomy placement has been reported in 1162% of patients.⁸ Outcomes after PEGJ placement have also been disappointing with multiple studies unable to demonstrate decreased aspiration.^9,10,11,12 The poor results of PEGJ with recurrent aspiration may be explained by several factors: frequent PEGJ tube malfunction with clogging and proximal migration into the duodenum or stomach and possibly increased duodenal-gastric reflux due to an extension tube crossing the pylorus.

A few studies have reported decreased aspiration with direct jejunal feeding using SJ¹³ and DPEJ.^14,15 Panagiotakis et al.reported 11 patients who underwent DPEJ for recurrent aspiration.¹⁵ After DPEJ placement monthly aspiration events decreased significantly from 3.39 to 0.42. Another retrospective analysis compared 205 DPEJ and 58 PEGJ patients and reported aspiration in 18.1% of DPEJ vs. 31.0% of PEGJ patients though this difference was not statistically significant once adjusted for bed-bound status.¹⁶ In another report 16/18 patients with aspiration pneumonia who underwent surgical jejunostomy did not have recurrent aspiration.¹³ While the literature is limited, direct percutaneous jejunostomy feeding may reduce aspiration in high-risk patients.

Gastroparesis

Gastroparesis is a common indication for DPEJ placement.⁶ Good outcomes were recently reported in 14 patients undergoing DPEJ due to severe gastroparesis secondary to perioperative vagus nerve injury during lung transplantation.¹⁷ In these patients, DPEJ placement led to prolonged successful enteral feeding in 90% of patients. If PEG is required for gastric venting, a separate gastrostomy tube can be placed during the same procedure. Combined PEG/DPEJ has been shown to have decreased re-intervention rates and improved patient satisfaction compared to PEGJ alone.¹⁸

Chronic Pancreatitis

Up to 5% of patients with chronic pancreatitis will fail conservative treatment and are candidates for long term enteral feeding. In these patients, jejunal feeding provides nutritional support while minimally stimulating the exocrine pancreas. In one report, long term jejunal feeding in CP obtained by PEGJ or DPEJ decreased the percentage of patients with pain from 96% to 23% while increasing mean weight by 4.5kg over 6 months.¹⁹ A majority of the literature on jejunal feeding in pancreatitis has utilized PEGJ; however DPEJ has been reported successfully in patients with chronic pancreatitis as well.^20,21 While more studies are clearly needed, this preliminary data suggests that DPEJ may be an effective means for providing nutritional support in these patients.

Critically Ill Patients

Percutaneous feeding tubes are not often required in the critical care setting due to shorter length of stay, however indications for percutaneous jejunal feeding are similar to those in non-critically ill patients. Successful DPEJ use has been reported in 17 mechanically ventilated ICU patients requiring long-term jejunal feeding for previous aspiration pneumonia (9), failing gastric feeds (4), post-operative anastomotic leak (3) and duodenal obstruction (1).²² All had successful DPEJ placement with one complication of colonic perforation. The remaining 16 tolerated jejunal feedings at goal rates with no episodes of aspiration and 13 were ultimately discharged from the hospital with continued jejunal feedings.

Comparison of PEGJ vs. DPEJ

When considering long-term jejunal access, the endoscopist must choose between PEGJ and DPEJ approaches. PEGJ has higher reported success rates,^16,23 is generally considered less technically challenging, and is more widely taught in fellowship programs. However, with its longer and smaller caliber tube, PEGJs are prone to frequent clogging and tube migration. Fortunato et al. reported of 102 PEGJs in children, the mean number of jejunal tube replacements was 2.2 tubes per patient (range 1-14) with median tube functional duration of 39 days (range 2-274).²⁴ Tube failure was most commonly due to displacement (31%), clogged tube (22%), and mechanical failure (19%). Similarly high PEGJ malfunction rates were reported in a study following 75 adults with PEGJ placement over 9 months, 53% of patients had tube dysfunction and 41% of patients requiring tube removal or exchange.²⁵ A limited number of studies have directly compared PEGJ and DPEJ with results supporting longer durability and fewer malfunctions with DPEJ. Zopf et al. performed a retrospective analysis of 205 DPEJ and 58 PEGJ procedures and found that DPEJ functioned longer (272 days ± 414 vs. 130 days ± 223, p = 0.023) with less clogging (9.9% vs. 40%, p= 0.002) and tube migration (5.4% vs. 33.3%; p = 0.005).¹⁶ Fan et al. found that over 6 months follow-up, DPEJ was associated with signiﬁcantly longer feeding tube patency and less re-intervention (13.5% DPEJ vs. 55.9% PEGJ, p= 0.002).²³ These results are consistent with a retrospective study reported in abstract only demonstrating longer durability of combined PEG plus DPEJ compared to PEGJ alone.¹⁸ Finally a randomized prospective trial also reported only in abstract form reported fewer re-interventions and higher patient satisfaction with DPEJ over PEGJ.²⁰

DPEJ Contraindications

Contraindications to DPEJ (Table 2) are similar to PEG and include uncorrected coagulopathy (with standard threshold INR < 1.5 and platelets > 50,000), proximal GI obstruction that would prevent passage of the endoscope to the jejunum, and inability to oppose the small bowel to the anterior abdominal wall. Management of antithrombotics should follow published guidelines. PEG is considered a high-risk procedure for bleeding by the ASGE (American Society of Gastrointestinal Endoscopy) guidelines and similarly so should DPEJ placement.²⁶ Relative contraindications include severe obesity, peritoneal dialysis, ascites and neoplastic, inflammatory, or infiltrative diseases of the small bowel and/or anterior abdominal wall. In addition, other standard general contraindications to endoscopy apply as well.

WHEN

As recommended by ASGE Practice Guidelines²⁷ nasoenteric feeding is the preferred approach for patients expected to be able to resume oral feeding within 30 days. Therefore DPEJ should be considered in the management of patients with an indication for jejunal access expected to require enteral feeding for greater than 30 days.

If it is highly likely that jejunal feeding will be needed for > 30 days, it is not necessary to wait until then to place DPEJ. Alternatively, DPEJ placement is never urgently indicated and thus naso and oro-enteric feeding tubes can be used until clinical parameters are maximized for safe percutaneous placement or to determine if clinical improvement will eliminate the need for longer term jejunal feeding.

HOW
Pre-procedural Preparation

As an extension of ASGE guidelines for PEG, preprocedure laboratory evaluation is generally not required for DPEJ placement. Prophylactic antibiotics, typically cefazolin 1gm IV, are indicated unless the patient is already receiving other adequate antibiotic coverage. Anti-spasmodics such as glucagon and hyoscine can be used during the procedure to help reduce jejunal peristalsis. The procedure is performed with the patient in the supine position. DPEJ may be performed under conscious sedation, monitored anesthesia care, or general anesthesia. Procedure times are greater compared to PEG and therefore at our institution we now perform all initial DPEJ placements under general anesthesia to decrease aspiration risk during a prolonged procedure in the supine position. Use of CO2 for insufflation is also useful to reduce postoperative discomfort and risk of bowel over insufflation. Standard commercially available PEG kits can be used for the procedure with the only caveat that the looped guide wire and snare are long enough to pass through whatever enteroscope is used for the procedure. The authors most commonly use a pediatric colonoscope for DPEJ placement, but use of dedicated balloon and non-balloon enteroscopes have been reported as well.

Technique (see Figure 1)

DPEJ is technically similar to a pull PEG procedure with the main difference that additional procedural time is required to reach the small bowel and identify an appropriate area for direct jejunal puncture. The enteroscope is advanced into the jejunum and an appropriate puncture site is identified by observing transillumination of light in a discrete area on the anterior abdominal wall. To further confirm the site, external pressure using a single finger should produce a discrete indentation in the jejunal wall visualized by the endoscope. Both excellent transillumination and discrete ﬁnger indentation are required for safe jejunal puncture. After sterile skin preparation and local anesthesia, a sounding needle (typically 21 gauge 1.5-inch needle) is advanced into the jejunal lumen using the “safe-track” technique (see Table 4). Once visualized in the jejunum (Image 1), the tip of the sounding needle is immediately secured with a snare to prevent migration of the jejunum away from the abdominal wall. Using a scalpel, a stab incision is made immediately adjacent to the sounding needle and the larger trochar/needle cannula (~14 gauge) is inserted into the jejunum parallel to the sounding needle again using safe track technique and the snare is transferred from sounding needle to the trocar. From this point the procedure follows the same steps as a standard pull PEG technique. The looped guidewire is fed through the trochar, snared and withdrawn with the endoscope through the mouth. The jejunostomy tube is attached to the wire and pulled into place until the bumper is seated in the jejunum (Image 2). Endoscopic re-visualization can be performed at the operator’s discretion to conﬁrm placement, but is not necessary in uncomplicated procedures.

Leaving the jejunal port open immediately after successful placement facilitates small bowel decompression. Tube feeding can be initiated immediately at 25-50mL/hour and titrated to goal rate as tolerated. Feeding with standard polymeric formulas can be used in almost all patients unless there is concern for malabsorption or pancreatitis. There is little information regarding the time for secure adherence of the jejunum to the abdominal wall, thus it is advisable to wait at least 4 weeks prior to removal of a DPEJ. It is likely that mature stoma tract formation occurs much earlier unless the patient has poor wound healing from steroids, diabetes mellitus, immunosuppression, or severe malnutrition.

Success Rates

In the larger studies DPEJ success rates have ranged from 65-86% (Table 3).^6,16,28,30 Increased success is consistently reported in patients with prior gastric or esophageal resection. This is likely secondary to postoperative anatomy being conducive to passing the endoscope further into the small bowel and adhesions ﬁxing the jejunum to the anterior abdominal wall facilitating site identiﬁcation. In the largest series of DPEJ placement the most common reasons for failure were absent transillumination/finger indentation (20%), suboptimal transillumination/finger-indentation (5.5%), inability to reach the jejunum (2.6%), inability to pass the scope concomitant with failure to transilluminate (1.9%), and sedation complication (1.3%).⁶

As with other endoscopic procedures, DPEJ placement success appears to follow a learning curve. One study reported success rates of inexperienced operators (<66 procedures) was 63.7% compared to 77.5% and 74.5% in medium (67-187 procedures) and highly experienced endoscopists (>188 procedures) respectively.16 Obesity has also been shown to decrease successful DPEJ placement in two studies. The first reported patients with abdominal wall thickness on CT scan <3cm (vs. ≥3cm) had successful placement 73% vs. 39% (p= 0.003) of the time with no successful placements when thickness exceeded 4 cm.²⁹ In the second study, increasing BMI was directly associated with decreased success rates with BMI < 18.5 (96% success), BMI 18.5-24.9 (81% success), BMI 25-29.9 (73% success) and BMI > 30 (60% success).³⁰

If DPEJ is initially unsuccessful, PEGJ can be placed during the same procedure, although there is data that repeat DPEJ attempt under general anesthesia with a dedicated balloon enteroscope is often successful.³¹ A number of helpful hints have been described to aid in successful DPEJ placement (Table 5).

Adjunctive Techniques

Several adjunctive methods to the standard DPEJ technique described above have been reported. Adding fluoroscopy to the procedure allows confirmation that the endoscope has passed the ligament of Treitz and can be a useful tool to visually guide the sounding needle to the snare.³² A success rate of 97.5% was reported in a series of 40 patients utilizing the selective use of a 15 cm long drainage needle with intermittent fluoroscopic guidance.³³ The authors felt that using a longer needle facilitated deeper penetration in obese patients in whom traditional transillumination or jejunal indentation may not be feasible. The use of ultrasound during DPEJ has also been described to help delineate a targeted loop of jejunum, confirm close proximity to the anterior abdominal wall, and rule out intervening viscus when transillumination has failed. ³⁴ Routine use of fluoroscopy and ultrasound have not been widely adopted, but they remain useful modalities to consider in potentially difficult patients.

Perhaps the most promising adjuvant technique for DPEJ placement has been the use of single³⁵ and double-balloon enteroscopy (DBE). Song et al. reported a series of 10 patients who failed standard DPEJ with pediatric colonoscopes and subsequently underwent repeat DPEJ with DBE with 100% success.³¹ The reasons for initial failures were inability to transilluminate (5 patients), altered anatomy of efferent limb (3 patients), and limited endoscopic advancement due to looping and small-bowel angulation (1 patient each). The authors further reported 93% success (27/29 patients) utilizing DBE for initial DPEJ placements. In this series repeat DPEJ with DBE was performed under general anesthesia in almost all patients. The authors hypothesized that improved outcomes with DBE were due to the ability to pass further into the small bowel from reduced instrument looping and a more flexible tip on the DBE scope allowing passage through small bowel angulation and narrowing.

WHAT TO AVOID
Inappropriate Indications

DPEJ placement should be considered only with extreme caution for patients with small bowel motility disorders or for patients with eating disorders such as anorexia or bulimia, functional nausea or vomiting, or patients with chronic pain (Table 2). If there is concern that small bowel feeding would not be tolerated, a trial of nasojejunal feeding prior to more invasive DPEJ placement is warranted.

Complication Rates

Reported complications from the larger DPEJ studies are summarized in Table 3. Complications are generally rare, but severe adverse events reported in 2-6.3% of cases. These include jejunal volvulus, necrotizing fasciitis, bowel perforation, and bleeding. Small bowel volvulus is a potential complication of jejunostomy regardless of placement technique as the relatively unfixed small bowel can rotate around the single point fixation of the jejunostomy. Small bowel volvulus is likely less common in patients with previous abdominal surgery due to adhesions that may fix the small bowel at multiple locations. Use of T-fasteners to establish additional points of jejunal fixation near the site of the DPEJ may reduce the risk of jejunal volvulus. As noted previously obesity decreases success rates and it has 34 also been associated with a trend towards more adverse events. In one series the adverse event rate was 19% in patients with BMI > 25 and 4 of 5 severe adverse events also occurred in patients with BMI > 25.³⁰

CONCLUSION

DPEJ provides direct jejunal access without the morbidities of surgery. It should be considered whenever long-term jejunal access is required. The most common indications are altered gastric anatomy, gastroparesis, GI malignancies, and recurrent aspiration. Limited data suggests that DPEJ provides more reliable long-term functionality, fewer re-interventions, and decreased risk for aspiration compared to the more commonly practiced PEGJ. DPEJ use has been limited due to
perceived need for greater technical expertise, however
the procedure is very similar to the pull PEG technique with the distinction that greater time and caution is required while identifying the site for direct jejunal access. Placement success can be improved by using a number of helpful hints and adjuvant techniques including use of balloon enteroscopy. Complication rates are similar to other methods of direct jejunal feeding tubes and include volvulus, necrotizing fasciitis
and persistent jejunal fistula. At this time improvements
in DPEJ techniques and further prospective studies comparing DPEJ to other methods of jejunal access are needed, but present data suggest that DPEJ should be more frequently practiced.

Inflammatory Bowel Disease: A Practical Approach, Series #87

Diagnosis and Management of Microscopic Colitis: A Review of the Literature

Jesse A. Green

The vague presentation of microscopic colitis is similar to celiac disease, irritable bowel syndrome (IBS), or inflammatory bowel disease (IBD). Its diagnosis can be complicated further with concurrent celiac disease or IBD. Treatment is usually aimed at shortening the duration of symptoms. In this paper we will discuss current methods of diagnosis, confounding issues, and treatment.

Introduction

The term microscopic colitis encompasses two separate diagnoses: lymphocytic colitis and collagenous colitis. The names describe the change to the colonic mucosa that is not due to an infectious cause, ultimately causing chronic watery, non-bloody diarrhea without other physical findings. It affects women more commonly than men and presents usually above the age of 65.¹ Microscopic colitis can be confused with diseases that present similarly, such as celiac disease, IBS or IBD.

A colonoscopy is often normal and biopsies of the colonic mucosa are required to make a definitive diagnosis. It is easy to distinguish collagenous colitis from lymphocytic colitis by the presence of a thick subepithelial collagen band whereas the telltale sign of lymphocytic colitis is infiltration of the colonic epithelium with lymphocytes. The two conditions under the umbrella of microscopic colitis have an association with other autoimmune disorders like celiac disease, rheumatoid arthritis, thyroid disease or diabetes mellitus. In patients with concurrent celiac disease or IBD, the diagnosis of microscopic colitis is often difficult. The goal of treatment is to shorten the duration and control symptoms and can be accomplished successfully in most cases.² In this paper we will discuss current methods of diagnosis, confounding issues and treatment.

Definition

Microscopic colitis is defined by symptoms of chronic, watery diarrhea without identification of an infectious cause, often without endoscopic lesions or radiographic findings but only with histologic abnormalities.^{3, 7}

Epidemiology

With increased awareness and improved diagnostic capabilities, microscopic colitis has become a common diagnosis. The incidence of microscopic colitis is 10/100,000 in the United States.⁴ Lymphocytic colitis is slightly more prevalent and has a 5.5/100,000 incidence,⁵ whereas collagenous colitis currently has an incidence of 4.6/100,000.⁶ The average age of diagnosis in microscopic colitis is 60-65 and patients older than 65 have five times the risk of developing microscopic colitis.⁶ The other risk factors for developing microscopic colitis include female gender, personal history of malignancy, hypothyroidism or celiac disease.⁶

Pathogenesis

The etiology is multifactorial and the exact mechanism remains unknown. However, it is believed that a dysregulated immune response to a luminal agent leads to reduced sodium and chloride absorption as well as active chloride secretion.⁷ The diarrhea can be defined as secretory. One study showed that the thick collagen band found in collagenous colitis may act as a diffusion barrier and down-regulate tight junction molecules.⁸ Medications that have been implicated in causing microscopic colitis include H2 blockers, PPI, SSRI’s, carbamazepine, simvastatin, and ticlopidine.^{9 10, 11} Lansoprazole, for example, a potent and commonly used PPI has been extensively studied for its association with microscopic colitis.^12,13,14 A case study of 850 patients who were switched from omeprazole to lansoprazole showed direct correlation of lansoprazole with intermittent diarrhea characterized as lymphocytic and collagenous colitis on histology. When lansoprazole was discontinued, follow-up biopsies revealed resolution with normalization of colonic histology.¹⁵

Clinical Findings

Symptoms may include some or all of the following: intermittent or persistent watery diarrhea, abdominal cramps, fecal urgency or incontinence, weight loss, or nausea. A complete history helps differentiate this disease from other causes of chronic, watery diarrhea. It is important to obtain a thorough medication list, which includes both prescription and over-the-counter drugs. Physical exam is usually unremarkable.

Laboratory markers are generally not useful for the diagnosis or for assessing disease activity. A stool sample should be collected as a first step. Although not routinely used for diagnosis, there are an increased number of CD3+ T cells found in the lamina propria and intraepithelial compartments in both lymphocytic and collagenous colitis.^{16, 17} There are no specific autoantibodies implicated as markers for microscopic colitis.¹⁸ Autoantibodies against GnRH or GnRH-R, seen in IBS are not frequently observed in microscopic colitis patients.¹⁹ Interestingly, there is an increased incidence of HLA DQ2 in both subtypes of microscopic colitis.

Diagnostic Modalities (Table 1)

The test of choice is a colonoscopy with biopsies. Histology of colonic biopsies which show inflammation of the mucosa and thickening of the subepithelial collagen layer, as in collagenous colitis, or an increase in the number of lymphocytes in the surface epithelium as in lymphocytic colitis.²⁰ Flexible sigmoidoscopy may be sufficient; however, negative findings do not exclude the possibility of this disease.²¹ It is important to take multiple biopsies throughout the colon, as collagenous and lymphocytic colitis may be patchy. However, greater than 90% of findings are present in the left colon.^{22, 23, 24}

Endoscopy and Pathology

Colonoscopy is usually grossly normal (figure A). However, a coarse and nodular surface of the mucosa may be seen in collagenous colitis. Erythema and tortuous vasculature with diffuse cloudiness of the mucosa have been noted in early development of collagenous colitis.²⁵ Mild edema and loss of vascularity can be seen (figure B). A “cat-scratch” appearance of the colonic mucosa may occur in collagenous colitis, further defined as “mucosal tears” (figure C).²⁶ This finding is explained by the barotrauma in the colon with decreased compliance due to the rigidity of collagen in the subepithelium. Histologically, collagenous colitis is described by colonic mucosal subepithelial collagen deposits 7-100 micrometers in diameter (figure D) (normal being 1-7 micrometers). Subepithelial collagen layer that is greater than 10 micrometers is a common finding. Lymphocytic colitis is characterized by mononuclear infiltrates with few neutrophils and eosinophils in the lamina propria and intraepithelial lymphocytes greater than 20 per 100 surface epithelial cells (figure E) (normal are 3-5/100 cells). Focal cryptitis (figure F) is sometimes present. Epithelial damage, such as cellular flattening and mucin depletion may occur.²⁷

Diagnostic Dilemmas and Associations with the Disease (Table 2)

Microscopic colitis may be diagnosed in patients with concomitant IBS, IBD or celiac disease. Others include chronic ischemia or infectious colitis, hyperthyroidism, carcinoid, VIPoma, or persistent NSAID. A‘quick way’to distinguish chronic diarrhea in a patient with microscopic colitis from a patient with IBD is the preserved mucosal architecture.²⁸ One study found that there is a 70-fold increase in risk for an individual with celiac disease to develop microscopic colitis when compared with the general population.²⁷ Concomitant celiac disease is present in approximately 5% of the patients with microscopic colitis.²⁹ IBD may have focal areas of microscopic colitis. It is more common to have concurrent autoimmune disease, including celiac disease, with collagenous colitis as compared to lymphocytic colitis (53% to 26% respectively).³⁰ Distinguishing celiac disease from microscopic colitis requires serological tests, such as anti-tTG antibodies.^{31, 33} Collagenous colitis must be differentiated from ischemic colitis, as both will demonstrate a thickening of the connective tissue band, seen with a three-color histologic staining protocol, [Masson’s trichrome].³¹ Collagenous colitis may be a systemic autoimmune disorder with extraintestinal manifestations such as arthritis and thyroiditis. A Duke study revealed an association between seronegative spondyloarthropathy with collagenous colitis in 7% of patients with confirmed collagenous colitis.³² There is an increased relative risk of lung cancer in women with collagenous colitis.³³ Smoking and chronic alcohol uses have been implicated as risk factors for development of microscopic colitis.³⁴

Management Goals and Treatment

Quality of life is directly proportional to disease activity in patients with microscopic colitis.³⁵ Clinical remission is not always associated with histological remission and relapses are common. The goal of pharmacological treatment is to improve symptoms while minimizing side effects.A treatment algorithm is outlined in Figure F. Prior to initiating pharmacologic treatment, it is important to remove any drugs that may be contributing to symptoms. Next, associated conditions should be properly managed. Dietary modifications are helpful in those patients who notice an association between certain foods. However patients with isolated microscopic colitis, sans celiac disease, do not adequately respond to dietary gluten withdrawal.³⁶ Symptomatic treatment with anti diarrheal agents such as loperamide is appropriate Colloidal bismuth, cholestyramine, sulfasalazine, and mesalamine may be added if diarrhea is not controlled. Failing these patients require systemic steroids, but they have a high chance of relapse following steroid cessation.^37,38,39 Budesonide is more effective and has fewer side effects. Oral budesonide is the first-line therapy to induce remission in microscopic colitis ⁴⁰ with more than 80% of patients experiencing clinical and histologic remission.²⁷ However, in unresponsive patients or those unable to tolerate steroids, immunosuppressive agents should be considered. Induction therapy with infliximab for 6 weeks and then maintenance with adalimumab every 2 weeks has been shown to be effective in refractory disease.⁴¹ Methotrexate and azathioprine have also shown efficacy in intractable disease.⁴²

Summary

Lymphocytic colitis and collagenous colitis can be both categorized under the general umbrella of microscopic colitis. Clinical symptoms include chronic, non-bloody, watery diarrhea and histologic findings of lymphocytic proliferation or collagen thickening in the colonoscopic mucosa. These diseases are thought to be autoimmune in origin and have associations with celiac disease, thyroid disease, and diabetes mellitus. The etiology still remains unclear. Goals of treatment remain the elimination of exacerbating factors and controlling symptoms.

A Case Report

The Use of Epsilon Aminocaproic Acid in a Case of Massive Hemorrhage from Cytomegalovirus Colitis in a Patient with Multiple Myeloma Treated with Bortezomib

Steven D. Deas,Marc D. Hopkins,Louis M. Varner

Introduction

Epsilon aminocaproic acid (EACA) blocks fibrinolysis by binding competitively to plasminogen and preventing binding to fibrin. It has been primarily used following thoracic surgery as an adjunctive therapy to help treat persistent postoperative bleeding.¹ We report a patient with lower gastrointestinal bleeding from cytomegalovirus (CMV) colitis who was treated successfully with EACA.

Case Report

A 56-year-old African American man presented to our medical center with a single episode of hematochezia associated with diffuse, cramping abdominal pain. The patient, who had been diagnosed with multiple myeloma several months before, had received two rounds of bortezomib and dexamethasone induction chemotherapy, and was hemodialysis dependent because of myeloma cast nephropathy. In addition to chemotherapy, he had received a single dose of radiation therapy to a lumbar vertebral lesion.

The patient’s medical history was otherwise significant for diabetes mellitus, hypertension and hypothyroidism. He was on insulin and antihypertensive medications as well as acyclovir and fluconazole for infectious prophylaxis while on chemotherapy. He reported no drug allergies. Though he had a history of heavy alcohol use over a period of decades, he quit drinking after he was diagnosed with myeloma. He denied tobacco or illicit drug use.

On presentation, he was tachycardic but normotensive and his physical exam was remarkable only for the presence of bright red blood in the rectal vault. He was noted to have a hemoglobin level of 7.5g/ dL (from a baseline of 10g/dL). His leukocyte count was 10,700 with a neutrophilic predominance and his platelet count was 241,000. He had a normal coagulation profile, blood urea nitrogen and transaminase levels. His alkaline phosphatase was mildly elevated, but stable over time.

After admission to the medical ward, he had several more episodes of hematochezia, which required transfusion of two units of packed red blood cells. Colonoscopy on the following day revealed discontinuous areas of non-bleeding ulcerated mucosa at the splenic flexure, the transverse colon and the ascending colon. The ulcers appeared superficial and irregular with normal intervening mucosa.

The differential diagnosis for hematochezia with ulcerated mucosa included infectious and ischemic colitis as well as inflammatory bowel disease. He had no history of previous bleeding or abdominal pain to suggest undiagnosed inflammatory bowel disease, and though he was on hemodialysis, had no significant hypotension to suggest ischemic colitis. He had received a single treatment of radiation therapy to a lumbar spine lesion in recent weeks, but the pattern of his disease was not consistent with radiation-induced injury to the gastrointestinal tract. Clostridium difficile toxin evaluation was negative. Therefore, due to the endoscopic appearance of the lesions, as well as his immunocompromised state, viral etiology was suspected.

Multiple biopsies were obtained and revealed marked acute and chronic inflammation with granulation tissue. Within the granulation tissue were a number of cells with atypical cytologic features including nuclear pleomorphism, irregular nuclear contours and nuclear hyperchromasia. Rare cells showed putative intranuclear inclusions. Though immunohistochemical studies for cytomegalovirus failed to highlight biopsied tissue, the lesions were highly suspicious for cytomegalovirus 50 (CMV) colitis and the patient was found to be CMV IgG positive. He was treated empirically with intravenous gancyclovir. CMV colitis often develops as a result of reactivation during immune suppression, but interestingly has never before been reported as an adverse effect of bortezomib therapy.

There was no active bleeding at the time of colonoscopy, however the patient developed repeated episodes of hematochezia the following day and ultimately required transfer to the intensive care unit and multiple transfusions of blood and blood products. Transfusion requirement eventually came to a total of fifteen units of packed red blood cells as well as multiple units of fresh frozen plasma and platelets. The surgical consultant felt that total colectomy carried a high risk in this patient with multiple co-morbid conditions and recommended supportive care and continued treatment with gancyclovir, while reserving colectomy as a last therapeutic option.

In an effort to limit blood product transfusions, he was treated with epsilon aminocaproic acid (EACA) which was dosed intravenously at 4 grams every twelve hours. On days of dialysis, it was dosed following the hemodialysis session. Following the initiation of EACA therapy, there were no further episodes of hematochezia for the remainder of his hospital course. EACA was discontinued and the patient was monitored for three days prior to discharge.

On the night after discharge, he experienced recurrent rectal bleeding and was readmitted. EACA was restarted and hematochezia improved. Repeat colonoscopy showed non-bleeding ulcerated mucosa throughout the entire colon which was improved from prior endoscopy as well as an actively bleeding ulceration in the proximal ascending colon with a bleeding vessel which was endoscopically treated with an injection of epinephrine and hemostatic clipping. Bleeding did not recur and he was discharged home.

Discussion

Epsilon aminocaproic acid binds competitively to plasminogen, blocking the binding of plasminogen to fibrin and subsequent conversion to plasmin, effectively inhibiting fibrinolysis. Adverse effects reported with EACA use include thrombosis, myalgia and myopathy and intrarenal obstruction from ureteral clots or glomerular capillary thrombosis. It is contraindicated for use in patients with disseminated intravascular coagulation or an active intravascular thrombosis.

In a recent Cochrane review of 16 trials in a total of 1035 surgical patients, it has been shown to reduce the need for allogeneic blood transfusions in the perioperative period, especially during cardiac surgery. In cardiac surgery, there also appeared to be a significant decrease in perioperative blood loss. While there was no significant improvement in mortality, there was no significant increase in rate of occurrence of myocardial infarction, stroke, or thromboembolism.² EACA has also been used successfully in the treatment of hemorrhage following complicated dental extractions,³ in patients with aneurysmal subarachnoid hemorrhage,⁵ recurrent epistaxis due to hereditary hemorrhagic telangiectasia,5 and in traumatic hyphema.⁶

The use of oral EACA in radiation-induced hemorrhagic gastritis has been described in a single case report,⁸ but until now there are no reported cases describing the use of EACA in hemorrhage from a lower gastrointestinal source. In patients with diffuse hemorrhagic colitis, in which endoscopic therapy is not adequate and surgery is not a preferred option, treatment with EACA may be an additional treatment strategy to reduce the need for the transfusion of blood and blood products. Further study is needed to determine the true efficacy and safety of EACA in gastrointestinal hemorrhage.

The opinions or assertions herein are the private views of the authors and are not to be construed as reflecting the views of the United States Air Force or the Department of Defense.

A Case Report

Epiploic Appendagitis: Underappreciated, Easily Misdiagnosed and Often Masquerading as an Acute Abdomen

January 2014 • Volume XXXVIII, Issue 1

Stanley Yakubov,Po Cheng Chu,Kadirawel Iswara,Ira Mayer

Introduction

Epiploic appendagitis (EA), also known as appendicitis epiploica, is an uncommon, benign condition of the epiploic appendages that occurs due to torsion or spontaneous venous thrombosis of a draining vein.³ The resulting strangulation and inflammation leads to localized abdominal pain.⁵ Moreover, EA is a self-limited condition that often mimics other serious surgical conditions such as acute diverticulitis, appendicitis and even cholecystitis.³ We report a case of left lower quadrant pain presumed to be acute diverticulitis with possible abscess formation and diagnosed as epiploic appendagitis by computed tomography (CT) scan of abdomen/pelvis.

Case Description

A 44 year-old male with past medical history of gastroesophageal reflux and peptic ulcer disease presented with four days of severe left lower quadrant abdominal pain, nausea and constipation. At the onset of his symptoms he was seen at a local emergency department (ED) where he was diagnosed and treated for presumed diverticulitis with metronidazole and ciprofloxacin. However, the pain subsequently worsened and he was referred to our institution for evaluation and treatment.

His vital signs upon arrival in the ED were a temperature of 97.4°F, blood pressure 110/71 mmHg, heart rate 67 beats/min and respiratory rate of 18 breaths/min. He described his pain as sharp, 10/10 in intensity, localized to left lower quadrant (LLQ), non-radiating and it was associated with nausea, but no vomiting. On physical examination his abdomen was tense, non-distended, tender in the LLQ with positive guarding, but no rebound and normal bowel sounds were present. Laboratory analysis showed a white blood cell (WBC) count of 6.7 K/Ul with 67% neutrophils. The remainder of the laboratory tests and physical exam were unremarkable.

He was started on broad-spectrum antibiotics for presumed diverticulitis with possible abscess formation, and he was given morphine for symptomatic relief. CT scan of abdomen/pelvis with contrast was performed showing an oval-shaped fat density (Figure 1) in the left lower quadrant anterior to the sigmoid colon characteristic of epiploic appendagitis. His clinical presentation improved with conservative treatment including non-steroidal anti-inflammatory drugs (NSAIDs) and he was discharged home after resolution of his symptoms.

Discussion

Epiploic appendagitis can affect anyone including young and healthy individuals, although obesity and heavy exercise are thought to be potential risk factors.² It most commonly occurs in the second to fifth decades of life, with slightly higher incidence in middle aged males.^1,3 First described by Vesalius in 1543, about 100 pedunculated fatty structures, also known as epiploic appendages, protrude from the serosal surface of the colon from the cecum to the recto-sigmoid junction.³ In 1956, Lynn et al. created the term epiploic appendagitis to describe inflammation of epiploic appendages.¹ The size and number of epiploic appendages increase in the lower abdominal quadrants, with the sigmoid colon accounting for approximately 57% of epiploic appendages, followed by the cecum 26%, ascending colon 9%, transverse colon 6% and descending colon 2%.⁴

EA can be either primary or secondary. Primary EA is caused by torsion or spontaneous venous thrombosis of a draining vein of the epiploic appendage.¹ Secondary EA is related to lymphoid hyperplasia or is secondary to an inflammatory process in adjacent organ such appendicitis, diverticulitis, cholecystitis or colitis.⁴ Patients most commonly present with acute abdominal pain, more often in the left lower than right lower quadrant, without associated leukocytosis or fever.¹ Our patient presented with the classic presentation of EA. It is recognized and diagnosed with the use of ultrasound or CT scan, with CT scan being more sensitive and speciﬁc. EA should be entertained when diverticulitis, appendicitis and other causes of acute abdomen are ruled out. EA appears on CT as an oval-shaped fat density (Figure1), paracolic mass with fat stranding and thickened peritoneal lining.² Complete resolution of symptoms typically occurs within two weeks with conservative treatment, primarily anti-inﬂammatory agents.⁴

CONCLUSION

The infrequency of epiploic appendagitis makes this condition an unusual and difﬁcult diagnosis for many physicians. Therefore, improved awareness and recognition of EA can lead to fewer misdiagnoses, thereby decreasing redundant medical procedures as well as unnecessary surgical interventions.