Gastrointestinal Tract

 

VBMC TRAUMA CARE SERVICES GUIDELINE

Gastrointestinal Tract

            There is a widely held misconception that the gastrointestinal tract is quiescent following illness, injury, and/or surgery. The gut plays an active role in overall host defenses, gastrointestinal stress ulceration, and systemic inflammation.

The historical term attached to the clinical problem of post-operative gut dysfunction was “paralytic ileus”. This has been shortened in modern medical terminology to “ileus.” The traditional clinical practice is to withhold oral intake and maintain nasogastric decompression until there was clinical evidence indicating return of bowel function (passage of flatus, bowel movement, or audible bowel sounds). This practice is outdated and not consistent with what is currently known about bowel function in illness.

The stomach and small bowel function very well following illness, injury, and /or operative intervention unless there has been mesenteric ischemia or long-standing obstruction. The actual root cause of the clinical entity referred to as “ileus” is delayed return of colonic function. Although ingrained in our medical terminology, “ileus” is a misnomer and the proper term to use is colonic pseudo-obstruction.

            There are several clinical practices that either exacerbate or contribute to colonic pseudo- obstruction. Chief among these are bed rest, narcotic administration and fluid & electrolyte abnormalities. Depending on the clinical circumstances, the clinician also needs to consider other contributing factors such as fecal impaction, resolving peritonitis, intra- abdominal abscess, pneumonia, wound infection, retroperitoneal hematoma, and pseudomembranous colitis. Mesenteric ischemia and early mechanical bowel obstruction, although rare, must also be considered in the differential diagnosis.

For most patients, early mobilization, judicious use of narcotics, as well as attention to fluid & electrolytes can mitigate or prevent pseudo-obstruction. Routine use of an effective bowel regimen and/or early enteral nutrition is also effective depending on the patient and clinical circumstances. 

            The main risk to the patient with pseudo-obstruction is colonic ischemia and/or perforation which are dependent upon the degree of colonic distention. Perforation/ischemia is much more likely when colonic/cecal diameter is > 11cm. Under these circumstances, more aggressive management is warranted. For most patients, the treatment of pseudo-obstruction is relatively straightforward. Bowel rest, hydration, and correction of electrolytes are essential. Narcotics should be reduced as much as possible. Depending on the clinical situation, other treatable contributing factors need to be rectified or excluded. Nasogastric tubes are completely unnecessary for the vast majority of patients because they are not effective in reducing colonic distention. NG tubes should be withheld unless the patient is vomiting and/or has evidence of gastric distention on X-ray. A combination of stool softeners and cathartics accompanied by a prokinetic agent Reglan (metaclopramide) are usually effective. Cathartics and prokinetic agents are more effective when given orally but other routes of administration may be necessary depending on the clinical situation. Rectal stimulation with a suppository and/or enema may also produce results. For refractory patients or those with significant colonic distension, a parasympathomimetic agent (neostigmine) can be administered IV with excellent results. Routine use of neostigmine is precluded by side effects such as bradyarrythmias, bronchorrea, and diaphoresis. Patients should be monitored during drug administration particularly if they have known cardiac disease. Decompressive colonoscopy which is both diagnostic and therapeutic may be required for patients with significant colonic distention not responsive to the above measures.

Enteral Nutrition

            Not all patients require early enteral nutrition. Well-nourished patients who sustain mild to moderate injury or those undergoing elective operations tolerate up to seven days of fasting with little or no adverse consequences. However, patients with documented pre-injury or pre-operative malnutrition as well as those patients with complex critical illness/injury clearly benefit from early enteral nutrition. In fact, the evidence supporting early enteral nutritional support in the critically ill is clear and irrefutable. Infectious complications are significantly reduced in patients who receive early enteral nutrition. Early enteral nutrition also maintains gut integrity, reduces the risk of gastrointestinal stress ulceration, and increases the rate of wound healing.

Access routes

            The main difficulty with early enteral nutrition is achieving and maintaining a reliable feeding access. Gastric feeding is well tolerated, and most patients can be fed in the stomach. Unfortunately, tolerance is an issue for some patients, monitoring may be difficult, and the aspiration risk is higher than that for post-pyloric tubes. As the patient improves clinically, aspiration risk declines and the need for post- pyloric access diminishes.

Three approaches are used to establish feeding access: nasoenteral feeding tube, surgical jejunostomy, and percutaneous endoscopic gastrostomy (PEG).

For the vast majority of patients, a nasoenteral feeding tube is a safe, temporary access. These can be placed blindly (discouraged), via Cortrak image guidance, via endoscopy, fluoroscopy, or at the time of surgical intervention. Since these tubes frequently become dislodged, they should be secured in place with a bridle. Nasoenteral feeding tubes are not a reliable long-term access and should be replaced with a jejunostomy or gastrostomy tube. When a patient has significant foregut pathology, a surgical jejunostomy can be placed. This allows enteral feeding to proceed in the absence of an intact/functioning foregut. The most frequently utilized long-term feeding access is the PEG. This is a safe, effective way of delivering enteral nutrition for most patients.

 

Assessing enteral feeding tolerance

            Continuous feeding is the only method used for post-pyloric nasoenteral and jejunostomy feeding tubes. The small bowel will not tolerate bolus feedings. Continuous feeding is preferred even for PEG feedings early but can be changed over to bolus feedings over time. Feeding intolerance manifests clinically in a variety of ways. The key to delivering effective enteral nutrition is to be aware of the clinical manifestations of feeding intolerance and to realize that signs of intolerance vary depending on the feeding access used. Tube feeding reflux, high gastric residuals, vomiting, aspiration, abdominal distention, and diarrhea are all signs of feeding intolerance.

 

Tube feeding reflux

            In patients with a post-pyloric nasoenteral tube and a nasogastric tube, the first sign of intolerance can be tube feeding reflux in the nasogastric aspirate. The first maneuver should be to confirm tube positions with a radiograph. NG tubes can migrate distally and feeding tubes can be dislodged. Tubes should be repositioned if necessary. Once tube position has been confirmed, then a downward adjustment in rate and/or the addition of a prokinetic agent may be required. If reflux is significant and accompanied by abdominal distention, the best course of action is to hold tube feedings for 12-24 hours and reassess the patient. Sudden abdominal distention and reflux in a patient previously tolerating tube feeds is a very worrisome finding that warrants further investigation.

 

High gastric residuals

            In patients receiving continuous feeding via a PEG elevated gastric residuals are the first sign of intolerance. Residuals should be monitored every 4-6 hours and should not exceed the total of the tube feeding over that time period. When the residuals are elevated to > 500cc in a 6-hour monitoring period, should be withheld and rechecked after one period of rest. A prokinetic agent can be added with success in some patients. Again, elevated residuals and abdominal distention in a patient that previously tolerated feeds should alert the clinician to a change in clinical status that warrants investigation. Occasionally, patients will be fed into the stomach using a small bore nasoenteral feeding tube. Residuals cannot be checked via these tubes and no attempt should be made to do so.

 

Vomiting/Aspiration

            Vomiting and/or aspiration may be the first sign of feeding intolerance. In the awake patient, complaints of nausea will precede the event, so don’t ignore this complaint. This manifestation is more likely in patients being fed in the stomach via PEG or nasoenteral feeding tube. Remember that post-pyloric feeding reduces but does not eliminate vomiting/aspiration risk. The most prudent course of action is to hold feedings. Depending on the clinical suspicion for aspiration, an evaluation by a physician is warranted. Vomiting will usually dislodge a nasoenteral feeding tube, so replacement and/or verification of position is warranted.

 

Abdominal distention

            Frequently overlooked, abdominal distention and bloating are the earliest and most reliable signs of intolerance. All patients receiving enteral nutrition should be evaluated daily. Not all patients require an intervention, but this should be noted and brought to the attention of the physicians caring for the patient. Acute and/or significant distention may indicate mesenteric ischemia or colonic pseudo- obstruction.

Diarrhea

            Diarrhea is probably the most frequent complication of enteral nutrition. Oddly enough tube feeding is usually not the cause. Sorbitol containing medications are frequently to blame so a review of the medication record is warranted. If indicated, clostridium difficile colitis should be excluded. Higher tube feeding rates may produce diarrhea so a change in rate may be warranted. Anti-diarrhea agents can be utilized if the problem persists. Changes in formula can be made. If the volume of stool exceeds 500-1000cc per day, then holding the feeds may be necessary.

 

Tube maintenance

            Enteral access tubes are expensive and vital to patient care. Every effort should be made to maintain patency and protect against dislodgement.

 

Small bore feeding tubes

            Standard nursing guidelines for small bore feeding tubes should be rigorously followed to prevent clogging. The most effective way to maintain patency is to flush with tubes frequently with warm water and to avoid medication known to clog these tubes. Whenever tube feedings are interrupted or medications are administered, the tubes should be flushed with warm water.

 

PEG

            These tubes can and do become clogged and or dislodged. One of the most important aspects of daily PEG care is to assess the tube site and determine tube depth. Nurses should pay close attention to the insertion site for redness, swelling, and/or tube feeding reflux. Following placement, PEG tubes are secured in place using a silastic bolster. These bolsters are applied loosely to maintain the PEG at the original depth of insertion which is charted in the endoscopic procedure note. Each PEG tube has a centimeter marker on the side. The general depth for most patients is between 3-6 centimeters. The depth at insertion should be recorded on the nursing assessment. If the depth marker is more than 1cm less than or more than the insertion depth or there is tube feedings refluxing through the insertion site, feedings should be held and the physician notified immediately. Sustained tightening of the bolster, or sudden jerks on the tube, can bury the mushroom-shaped ‘bumper’, which normally lies in the stomach, into the wall of the stomach or abdominal wall. The result can be ‘feeding’ of the tract rather than the gastric lumen, resulting in severe infection. Remember, a sudden change in PEG feeding tolerance accompanied by abdominal distention can indicate PEG tube migration or dislodgement.

 

PEG Antibiotics

 

Guideline for Prophylactic Antibiotic for Percutaneous Endoscopic Gastrostomy

 

Translocation of endogenous microbial flora can occur during endoscopic procedures such as percutaneous endoscopic gastrostomy (PEG).1   While endoscopic related bacteremia carries a low risk, with certain patient comorbidities and history of previous procedures the risk increases.

Antibiotic prophylaxis can be useful for prevention of infections related to some invasive procedures and in specific clinical scenarios.  Patients undergoing PEG tube placement are at higher risk of bacteremia related to advanced age, compromised nutritional status, immunosuppression, and comorbidities.Prophylactic antibiotic therapy is recommended for these patients.1,2   The therapy is recommended as pre-procedural and as a one-time dose.1,2   Cefazolin that provides coverage for cutaneous organisms is adequate for this therapy.  In patients with methicillin-resistant Staphylococcus aureus (MRSA) decontamination is recommended.

 

Recommended antibiotic regimen:

Cefazolin 2g IV for patients weighing less than 120 kg
Cefazolin 3g IV for patients weighing 120 kg or greater

If a history of a severe allergy to penicillin is present, one of the following regimens may be used:

Clindamycin 900 mg IV or Vancomycin 15 mg/kg IV
PLUS
Gentamicin 5mg/kg IV or Aztreonam 2g IV or Levofloxacin 500 mg IV

 

1.     Antibiotic prophylaxis will be used in all patients receiving a PEG placement in the OR, endoscopy suite, and ICUs.

2.     Antibiotics dosing should be weight-adjusted

3.     Antibiotic administration should occur within 60 minutes prior to incision, except for vancomycin and fluoroquinolones which should be administered within 120 minutes prior to incision. 

4.     The antibiotic infusion should be complete before incision.

5.     Post procedure antibiotics are not warranted outside of a present infection or contaminated procedure

 

 

Diarrhea

            Not all liquid stools constitute diarrhea. Diarrhea is defined as frequent loose stools exceeding 1000cc per day and/or producing fluid/electrolyte abnormalities. The clinical objective is to identify and remove treatable causes of diarrhea. Medications are probably the most frequent cause of diarrhea. Drugs that produce diarrhea such as prokinetic agents, oral macrolides, cathartics, and sorbitol containing elixirs should be eliminated when possible. Adjustments in tube feeding rate and/or formula change may be required. Clostridium difficile colitis should be excluded or diagnosed and treated. Diarrhea may accompany a high-grade fecal impaction. Diarrhea may also be the only manifestation of intra- abdominal infection. Surgical resection of the small or large bowel (ileocecal valve in particular) may produce post-operative diarrhea. Diarrhea may follow resolution of pseudo-obstruction or surgical relief of a mechanical small bowel obstruction. In general, treatment is defined by the cause. Medications should be changed/eliminated. Fecal impaction should be cleared. Except for C. difficile colitis, symptomatic relief can be provided with anti-diarrhea agents such as combinations of lomotil, Imodium, paregoric, and narcotics.

 

Clostridium difficile (Pseudomembranous) Colitis 

            The Gram-negative bacterium Clostridium difficile is part of the normal colonic flora in roughly 20-25% of patients. The bacteria exist in small numbers in balance with other colonic flora and do not cause any problems. Pseudomembranous colitis develops because of an overgrowth of C. difficile allowing for increased toxin production and mucosal damage. The major mechanism is antibiotic administration that alters/reduces colonic flora allowing room for increased growth of the drug-resistant C. difficile bacterium. The disease can be produced by as little as one dose of antibiotics and most often follows single dose antimicrobial administration for perioperative prophylaxis. There is some data to suggest that mechanical bowel preparation/cleansing may produce the disease as well. The most frequent offending antimicrobials are cephalosporin (Rocephin), Clindamycin, ampicillin, and fluroquinolones such as levaquin. The primary manifestation of the disease is diarrhea which may occur up to 14 days after the last antibiotic administration. Occasionally the patients will have abdominal pain and distention. Rarely they will present with or have constitutional symptoms such as fever and systemic toxicity that accompany the diarrhea and abdominal pain. The diarrhea associated with the disease is quite distinct. The frequent passage of small amounts of foul-smelling liquid stools should raise clinical suspicion. The diagnosis is easily established by sending a stool specimen for toxin assay. Cultures are of no value because the bacteria are normal resident flora in many patients. First line therapy is metronidazole (Flagyl) administered 10-14 days via the enteral route. Intravenous flagyl is effective for patients who will not tolerate the oral route. Vancomycin given enterally is reserved for patients who present with severe disease and/or fail on Flagyl. Empiric therapy is appropriate after stool cultures have been obtained and can be stopped if the toxin assay is negative. Endoscopy to identify pseudomembranes is occasionally required to establish the diagnosis. Rarely, a patient will develop toxic megacolon and require emergent surgical intervention.

 

Constipation

There is overlap between constipation and colonic pseudo-obstruction. Abdominal pain, distension, nausea, and vomiting accompanied by absence of a bowel movement for more than several days are the most common symptoms. Unfortunately, these symptoms are identical to colonic pseudo-obstruction so the diagnosis is difficult in the hospitalized patient. Narcotics, bed rest, dietary changes, fluid & electrolyte abnormalities, particularly dehydration all predispose the patient to constipation. The key is prevention. Early mobilization of the patient and adequate hydration is essential. Patients who require pain medications should receive stool softeners as a routine. Once constipation develops attention should be turned to correcting the problem. Fecal impaction should be excluded by rectal exam. Remember that diarrhea may be a manifestation of fecal impaction. Stool softeners alone are usually not enough. Unless the patient is vomiting, oral cathartics should be tried initially. Oral Dulcolax tablets and/or milk of magnesia (MOM) can be administered along with oral metaclopramide (reglan) 10-20mg. Osmotic agents such as sorbitol are also effective particularly if administered with dulcolax. These regimens can be repeated. If the patient is vomiting or does not respond to oral therapy, digital rectal stimulation with a dulcolax suppository with or without enemas can be employed. Large volumes of laxatives such is Mirilax or citrate of magnesia should be avoided in patients who already have significant bloating. 

 

References:

1.     American Society of Gastrointestinal Endoscopy. Antibiotic prophylaxis for GI endoscopy. Gastrointestinal Endoscopy. 2015 81(1): 81-89. http://dx.doi.org/10.16/j.gie.2014.08.008

2.     Ban, KA; Minei, JP; Laronga, C; Harbrecht, BG; Jensen, EH; et al. American College of Surgeons and Surgical Infection Society: Surgical Site Infection Guidelines, 2016 update. Amer Coll Surgeons. 2016; 10: 59-73. http://dx.doi.org/10.1016/j.jamcollsurg.2016.10.029

3.     Bratzler DW; Dellinger EP; Olsen KM; et al. Clinical Practice Guidelines for Antimicrobial Prophylaxis in Surgery. AM J Health Syst Pharm. 2013 70(3):195-283. DOI: 10.2146/ajhp120568