Diarrhea

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25 Diarrhea

Rajeev Dhupar, Juan B. Ochoa

Diarrhea is one of the most common abnormal manifestations of gastrointestinal (GI) dysfunction in the intensive care unit (ICU); the reported incidence is between 2% and 63%.¹ Diarrhea is best defined as bowel movements that, owing to increased frequency, abnormal consistency, or increased volume, cause discomfort to the patient or the caregiver. This definition demonstrates the subjectivity in diagnosing diarrhea, a fact that complicates interpretation of the literature and limits applicability of guidelines. The impact of diarrhea on patient care in the ICU, including its cost in morbidity and mortality, is unknown. However, it is undeniable that diarrhea remains a persistent problem in many ICUs.

Criteria

Several criteria are used to diagnose diarrhea:

1 Abnormal frequency. Normal frequency is described as one or two bowel movements per day and is in part determined by the amount of fiber in the diet. Three or more bowel movements per day are considered abnormal.¹

2 Abnormal consistency. Abnormal consistency is described as either nonformed stool or stool having excessive fluid content that causes “inconvenience” to the patient, nursing staff, or caregiver. Normal stool water content is 60% to 85% of the total weight.¹

3 Abnormal amount. Stool amount and volume vary significantly with the amount and type of enteral intake. Insoluble fiber adds a significant amount of bulk volume. A “normal” amount is considered to be approximately 200 grams per day.¹ Abnormal amounts are considered to be greater than 300 grams/d, or volumes greater than 250 mL/d.^1,²

To date, clinicians are lacking a consistent scale or index that allows a reliable and practical way of measuring stool volume, consistency, and frequency. In its absence, the bedside nurse remains the most reliable person to diagnose the presence of diarrhea.

Pathophysiology

Bowel movements with normal physiologic volume, consistency, and frequency are the result of a GI tract that integrates motility, secretion, and absorption of fluids and adapts to the quality of the food bolus given. The result is a fecal bolus that is produced once or twice every 24 hours and has consistency and fluidity within the boundaries of normal.

Diarrhea results when there is a disorder of GI physiology or when GI tract function is incapable of handling the food bolus. There are several classifications of diarrhea, suggesting that no classification is ideal at helping the clinician plan for patient care. Perhaps the most useful approach is to classify diarrhea according to alterations of physiologic events:

1 Increased fluid secretion that overwhelms absorption. On average, up to 9 liters of fluid is secreted into the GI lumen in addition to the normal oral intake. Less than 1% of that fluid is contained in stool, owing to the amazingly large absorptive capacity of the small and large bowel. Within the intestinal mucosa, passive and active transport of sodium determines the amount of water that is absorbed. Stimulation of the active secretion of fluids into the GI lumen occurs when intracellular levels of the second messenger, cyclic adenosine monophosphate (cAMP), increase within enterocytes. Increased intracellular cAMP concentration promotes chloride secretion.³ Thus, diarrhea caused by excessive secretion of fluids is called secretory diarrhea. Secretory diarrhea characteristically contains large amounts of fluid and is described as watery. Secretory diarrhea is observed in certain infectious diseases such as cholera or infections with rotavirus. Secretory diarrhea also can be observed in endocrine disturbances associated with carcinoid syndrome or vasoactive intestinal peptide (VIP)-secreting tumors.

2 Increased mucous secretion from the large bowel. Overproduction of mucus by the large bowel can lead to development of diarrhea. Excessive mucus secretion is observed in colonic infections such as Clostridium difficile colitis and amebiasis.⁴ The incidence of infectious diarrhea in the ICU is unknown.

3 Contaminated food products. Of particular concern is the contamination of the food being given in the ICU. Contamination of enteral formulas can occur at multiple levels, including preparation of the enteral product, use of “open units,” addition of modular dietary components, and contamination of the enteral access port (i.e., feeding tube, gastrostomy tube). The incidence of diarrhea due to contaminated feeding tubes is unknown.

4 Diarrhea due to increased osmotic load. Many substances that are taken orally and are not fully absorbed can exert a significant osmotic force, overwhelming the physiologic absorptive capacity of the GI tract. A significant number of patients with diarrhea in the ICU fall into this category.

a Osmotic diarrhea caused by medications. Sorbitol is frequently and inadvertently given to patients in the ICU as a means of preparing many medications for delivery via feeding tubes and is an often overlooked culprit causing diarrhea.⁵ Other osmotic agents include Golytely and magnesium-containing medications.

b Incomplete digestion and malabsorption. The incidence of malabsorption in the ICU is unknown. However, there are many instances where malabsorption should be considered as a cause of diarrhea in the critically ill patient. These include:

i Incomplete protein digestion (azotorrhea). Protein digestion occurs mainly in the stomach by pepsin (only activated at low pH) and hydrochloric acid. In the ICU, virtually all patients receive medications to raise intragastric pH, such as histamine receptor type 2 (H₂) blockers or proton pump inhibitors.^6,⁷ In addition, feeding tubes frequently “bypass” the stomach, eliminating both gastric acid and gastric proteolytic digestion.

ii Undigested carbohydrates. In addition to sorbitol (see earlier discussion), excessive glucose, lactose, or fructose in tube-feeding formulas can overwhelm the absorptive capacity of the small bowel, causing an osmotic influx into the gut lumen.⁸

iii Undigested fats. Steatorrhea (diarrhea caused by undigested fats) is characteristically observed in patients with pancreatic insufficiency. Inadvertent lack of mixing pancreatic enzymes with the food bolus can occur in patients with intestinal bypass, pancreatic fistulas, or in patients who have undergone pancreatectomy. It is also observed in patients with incomplete bile production, such as patients who have a biliary diversion.

iv Excessive dietary load. Diarrhea due to excessive load (overfeeding) of any of the main dietary components (protein, carbohydrate, or fat) can be observed in the ICU. Iatrogenic overfeeding occurs in up to 33% of patients in the ICU, and is a result of inappropriate estimations of caloric and protein needs or inadequate metabolic surveillance.⁹ Excessive loads of protein, carbohydrate, or fat also occur with “specialized” formulas that contain altered amounts of one or more of these components. For example, certain diets may contain high amounts of fat, overwhelming digestive and absorptive processes.

v Atrophy of the GI tract. Atrophy of the intestinal brush border is associated with decreased capacity of digestion and absorption. Atrophy is observed in malnourished patients; thus, diarrhea is observed commonly in patients with hypoalbuminemia. Atrophy also occurs when enteral intake is interrupted for more than a few days. This is a particular problem in surgical patients when prolonged “bowel rest” is ordered.

5 Abnormal motility. Intestinal dysmotility is a frequent problem in the ICU. The use of promotility agents (e.g., erythromycin) can inadvertently cause diarrhea in these patients.

6 Abnormal gut flora. Colonic flora is essential for normal absorption and function of the large bowel. Antibiotics create massive disruptions in colonic flora and can sometimes lead to nosocomial infections with resultant diarrhea. Currently, C. difficile is the leading cause of nosocomial diarrhea and accounts for 30% of patients with antibiotic-associated diarrhea.¹⁰ The gut microflora can be modulated through the use of probiotic agents, but this topic is under intense investigation, and no current guidelines exist regarding their use to treat or prevent diarrhea in ICU patients.¹¹

Clinical Consequences of Diarrhea

Untreated, diarrhea can lead to multiple problems. These include:

1 Wound breakdown and secondary soft-tissue infection. Diarrhea can cause a moist, contaminated environment; if left untreated, this can lead to skin breakdown and eventual soft-tissue infection. Particularly concerning are the presence of decubitus ulcers; diarrhea can be either a causative factor or worsen or complicate management.

2 Fluid and electrolyte disturbances are particularly frequent in patients with secretory diarrhea. In these patients, clinicians need to pay attention to fluid replacement and correct metabolic acidosis and/or hypokalemia.

3 Malnutrition. Inadequate nutrient absorption can lead to poor nutrient utilization.

4 Increased workload for nurses and caregivers. Diarrhea imposes a substantial burden on nurses and other caregivers. In addition, the presence of a soiled patient evokes a sense of poor quality of care. Maintaining a clean patient with diarrhea requires additional ICU personnel time and resources that could be better used.

Diagnosis

Careful and complete evaluation of diarrhea is necessary for good patient care. Unfortunately, diarrhea is often ignored or hastily “treated” while clinicians pay more attention to other organ systems. Diagnostic laboratory tests often do not exist, making it ever more difficult to identify and treat the patient. We propose the following approach:

1 Does the patient really have diarrhea? Clinicians rarely will question the diagnosis of diarrhea. Most diagnoses are probably made without a clear understanding of the definition of diarrhea. A concerted effort to diagnose diarrhea by all members of the ICU staff is essential. The creation of scales or indices could become particularly useful as a means of communication. These could also aid in following the effectiveness of treatment.

2 Can an iatrogenic cause explain the presence of diarrhea?

a Is the patient on prokinetic agents or stool softeners?

b Is the patient receiving medications with high concentrations of sorbitol?

c Is the patient being overfed?

d Is the patient intolerant to any of the components of the diet?

e Is a specialized diet providing an excessive amount of a substance (e.g., fat) that the patient is having difficulty digesting?

f Is bypassing the stomach or inhibiting acid secretion affecting the digestion of protein?

g Is the patient on any other medication that can cause diarrhea?

3 Assessing the patient’s absorptive or digestive capacity.

a Does the patient have gut atrophy, as seen with prolonged bowel rest? Would this patient benefit from an intestinal rehabilitation strategy?

b Is the patient malnourished?

c Does the patient have a condition (e.g., pancreatitis) that alters the secretion of digestive enzymes?

d Does the patient have a chronic disease process (e.g., short gut syndrome) that alters absorption?

4 Does the patient have an infection?

a Is there any evidence of contamination of feeding tubes? Are you using a closed system? How often is it being changed?

b Is there cause for nosocomial bowel infection? Is the patient C. difficile toxin negative?

c Has colonic flora been altered significantly with antibiotics?

Treatment

Treatment is dependent on identification of the underlying cause. One or several reasons for the presence of diarrhea generally can be identified. Once identified, the causes of diarrhea should be eliminated, modified, or treated. In particular, iatrogenic causes of diarrhea should be identified and corrected whenever feasible. For example, prolonged courses of prophylactic antibiotics are no better than short courses for the prevention of surgical site infections; therefore, adherence to current guidelines to limit antibiotics is important.^12,¹³

Modification of the diet may be important if the GI tract is being overwhelmed with high quantities of a particular nutrient. This is particularly important for patients receiving formulas that deliver excessive fat loads.

Digestive enzymes such as pancreatic enzymes or bile substitutes should be supplemented when the disease process (or treatment) is associated with decreased production of these enzymes.

Agents that inhibit GI motility, such as loperamide, should be used with caution. These drugs are often ordered empirically and may worsen underlying pathology, especially when the causative agent is infectious.

Bulk-forming agents are sometimes given to patients to improve the consistency of the fecal bolus. These agents have to be used in the appropriate amount, since they can also be a cause of diarrhea.¹⁴

Antibiotics to treat infectious diarrhea also should be used with caution. If the diarrhea is causing minimal discomfort and is of no physiologic consequence, waiting for arrival of results of tests for C. difficile may be advised.¹⁵

Restoring normal colonic flora has become an increasingly frequent practice in the ICU. Provision of prebiotics and probiotics in different presentations is now being suggested, but the implications of such therapies are not clear and require further investigation.^11,¹⁶ Soluble fiber may have a role in restoring normal colonic function and flora.

Stopping or decreasing the rate of enteral nutrition is often done; however, this is only advocated if the patient is being overfed or exhibits intolerance to the diet. Only under exceptional circumstances should stopping oral intake and giving total parenteral nutrition be advocated as a treatment for diarrhea.

Conclusions

Diarrhea is a poorly studied clinical manifestation of GI dysfunction in the ICU. The true incidence of diarrhea in ICU patients is unknown because of the lack of a universally accepted definition or a concerted effort to study the problem. Despite these limitations, when discovered, diarrhea can be effectively treated with careful clinical evaluation of the patient and easily implemented therapeutic measures.

Annotated References

Cunha BA. Nosocomial diarrhea. Crit Care Clin. 1998;14:329-338.

This article reviews both noninfectious and infectious causes of nosocomial diarrhea.

Dallal RM, Harbrecht BG, Boujoukas AJ, et al. Fulminant Clostridium difficile: an underappreciated and increasing cause of death and complications. Ann Surg. 2002;235:363-372.

This article is a single-institution review of the epidemiology and outcomes of patients with C. difficile colitis.

Nelson RL, Glenny AM, Song F. Antimicrobial prophylaxis for colorectal surgery. Cochrane Database Syst Rev 2009;1:CD001181.

This reviews the evidence for the duration of antibiotics in the post-colorectal surgery patient and makes recommendations based on the most recent data.

Pilotto A, Franceshi M, Vitale D, Zaninelli A, DiMario F, Seripa D, et al. The prevalence of diarrhea and its association with drug use in elderly outpatients: a multicenter study. FIRI; SOFIA Project Investigators. Am J Gastroenterol. 2008;103:2816-2823.

This is a multicenter study of the incidence of diarrhea in nonhospitalized elderly patients on different medication regimens including antibiotics and PPIs.

Wiesen P, van Gossum A, Presier JC. Diarrhoea in the critically ill. Curr Opin Crit Care. 2006;12:149-154.

This article reviews the causative factors, pathophysiology, and potential treatments of ICU-associated diarrhea.

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2 Wiesen P, van Gossum A, Presier JC. Diarrhoea in the critically ill. Curr Opin Crit Care. 2006 Apr;12(2):149-154.

3 Krishnan S, Ramakrishna BS, Binder HJ. Stimulation of sodium chloride absorption from secreting rat colon by short-chain fatty acids. Dig Dis Sci. 1999;44:1924-1930.

4 Cunha BA. Nosocomial diarrhea. Crit Care Clin. 1998;14:329-338.

5 Hyams JS. Sorbitol intolerance: an unappreciated cause of functional gastrointestinal complaints. Gastroenterology. 1983;84:30-33.

6 Pilotto A, Franceshi M, Vitale D, Zaninelli A, DiMario F, Seripa D, et al. The prevalence of diarrhea and its association with drug use in elderly outpatients: a multicenter study. FIRI; SOFIA Project Investigators. Am J Gastroenterol. 2008 Nov;103(11):2816-2823.

7 Leonard J, Marshall JK, Moayyedi P. Systematic review of the risk of enteric infection in patients taking acid suppression. Am J Gastroenterol. 2007 Sep;102(9):2047-2056.

8 Fernandez-Banares F, Esteve M, Viver JM. Fructose-sorbitol malabsorption. Curr Gastroenterol Rep. 2009 Oct;11(5):368-374.

9 Edes TE. Nutrition support of critically ill patients. Guidelines for optimal management. Postgrad Med. 1991;89:193-198. 200

10 OKeefe SJD. Tube feeding, the microbiota, and Clostridium difficile infection. World J Gastroenterol. 2010 Jan 14;16(2):139-142.

11 Morrow LE. Probiotics in the intensive care unit. Curr Opin Crit Care. 2009 Apr;15(2):144-148.

12 Wistrom J, Norrby SR, Myhre EB, et al. Frequency of antibiotic-associated diarrhoea in 2462 antibiotic-treated hospitalized patients: a prospective study. J Antimicrob Chemother. 2001;47:43-50.

13 Nelson RL, Glenny AM, Song F. Antimicrobial prophylaxis for colorectal surgery. Cochrane Database Syst Rev 2009 Jan 21;(1):CD001181.

14 Nakao M, Ogura Y, Satake S, et al. Usefulness of soluble dietary fiber for the treatment of diarrhea during enteral nutrition in elderly patients. Nutrition. 2002;18:35-39.

15 Dallal RM, Harbrecht BG, Boujoukas AJ, et al. Fulminant Clostridium difficile: an underappreciated and increasing cause of death and complications. Ann Surg. 2002;235:363-372.

16 Meier R, Burri E, Steuerwald M. The role of nutrition in diarrhoea syndromes. Curr Opin Clin Nutr Metab Care. 2003;6:563-567.

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