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FIG. 2 Hand-assisted laparoscopic TAC. (A) 5-mm umbilical laparoscope port for the camera, 12-mm right working port at the site of the future stoma
(this is also the entry site), 5-mm left lateral assistant port, Pfannenstiel incision for hand assist and specimen extraction. (B) The entire colon is externalized through the Pfannenstiel incision.
199
■ Tilt operating table at appropriate angles to improve visualization
with gravity movement of abdominal contents.
■ Set up stirrups to keep legs no more than 10 degrees flexed at hips
to allow adequate motion of instruments.
■ Foley catheter should be in place before trocars are inserted.
■ Keep insufflation pressure below 15 mm Hg if possible.
■ Insert trocars under direct vision with camera.
■ Insert instruments with camera guidance if at all possible.
■ Lift tissue without grasping whenever possible.
■ Start dissection at the base of the mesentery at the vascular bun-
dle to make bloodless dissection possible.
■ Ensure no twist in the mesentery of the small bowel for ileostomy.
This may require reinsufflation of abdomen for laparoscopic view
of cut edge of mesentery without twist.
■ Know the protocol for air embolism: Trendelenburg and left lat-
eral decubitus positioning to move the air into the right atrium to
be aspirated.
POSTOPERATIVE MANAGEMENT
To date, there is no validated scoring system to stratify risk factors for postoperative recurrences. However, some of the known
risk factors include penetrating disease, two or more previous
CD surgeries, history of extensive small bowel resection of >10
cm, age <30 at diagnosis, an interval <10 years between diagnosis
and surgery, and presence of perianal disease. Finally, smoking is
an important modifiable risk factor that portends higher risk of
recurrence. The number of risk factors involved can help categorize
patients into low, moderate, and high risk of recurrence. Patients
with no risk factor are considered low risk. These patients may
stay off of medical therapy after surgery unless recurrence is noted
at 6-month surveillance colonoscopy. Presence of several risk factors put the patient at moderate risk of recurrence. These patients
should be aggressively managed with medical therapies including
anti-TNF therapy in combination with immunomodulator. Alternatively fecal calprotectin monitoring 3 months after surgery can
serve as an early indication for endoscopic examination.
CONCLUSION
Despite a century of advances in medical and surgical therapy, CD
remains a clinical challenge for the treatment team and a chronic
malady for patients. The complexity of the disease process and
multifaceted phenotypic presentations demand multidisciplinary
management. To date, the majority of patients suffering from CD
ultimately will require surgery, and therefore surgeons are an integral
part of this multidisciplinary team. A thorough preoperative workup
is imperative to establish a clear diagnosis of CC and to adequately
optimize nutritional status. A number of surgical techniques are
available as minimally invasive options enter the fray. Each technique
should be tailored to the patient’s condition and the surgeon’s skill
and clinical judgment.
S u g g e S t e d R e a d i n g S
Bartels SAL, Gardenbroek TJ, Aarts M, et al. Short-term morbidity and
quality of life from a randomized clinical trial of close rectal dissection
and total mesorectal excision in ileal pouch-anal anastomosis. Br J Surg.
2015;102:281–287.
Fazio VW, etal. Crohn’s disease and indeterminate colitis. In: Corman ML et
al, ed. Corman’s colon and rectal surgery. 6th ed.: Springer; 2013.
Feuerstein JD, Cheifetz AS. Crohn disease: epidemiology, diagnosis, and
management. Mayo Clin Proc. 2017;92:1088–1103.
Lightner AL, Vogel JD, Carmichael JC, etal. The American Society of Colon
and Rectal Surgeons clinical practice guidelines for the surgical management of Crohn’s disease. Dis Colon Rectum. 2020;63:1028–1052.
Lin AY. Completion proctectomy for Crohn’s disease. In: Fleshman JW
et al, ed. Atlas of surgical techniques for the colon, rectum, and anus.
Philadelphia: Elsevier; 2013.
200 ISCHEMIC COLITIS
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Ischemic Colitis
Ranim Alsaad, MD, and Pamela A. Lipsett, MD, MHPE
DEFINITION AND EPIDEMIOLOGY
Ischemic colitis (IC) is a condition that occurs when the blood supply
to colonocytes does not meet metabolic demands. It is the most common cause of gastrointestinal (GI) ischemia. Injury can occur in one
of two ways: at the initial incident of decrease in blood flow phase
and/or after reperfusion. If the injury occurred only at the mucosa,
it can be reversible. However, a transmural injury can present as
a life-threatening condition that can lead to stricture formation,
perforation, sepsis, and death. The incidence of IC ranges from 4.5
to 44 cases per 100,000 persons per year. Patients generally present
after the age of 60, and there is a higher prevalence in women. The
incidence of IC is expected to rise given the growing proportion of
elderly patients. It most commonly occurs after aortic or cardiac
surgeries. The severity of the disease dictates specific management
strategies. About 20% of patients diagnosed with IC will require
operative intervention, typically in an emergent setting.
ETIOLOGY
To understand the pathophysiology behind IC, we must consider
the arterial anatomy of the colon. As shown in Figure 1, the colon
is supplied by the superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the superior rectal artery. In
addition to these primary arterial branches, there is a rich collateral
circulation. Griffith’s point, at the splenic flexure, and Sudek’s point,
at the rectosigmoid junction, are particularly prone to ischemia,
cumulatively compromising 80% of IC cases. These high-risk, or
“watershed,” areas identify the regions in the colon between two
major arteries; the splenic flexure is the area between the SMA and
the IMA arterial supply, and the rectosigmoid junction is the region
between the IMA and the superior rectal artery supply. The former
area is mostly supplied by the marginal artery; however, in 50% of the
population, this artery is poorly developed. During aortic surgery,
when intraperitoneal, efforts should be made to ensure that the left
colon has adequate blood supply if the IMA is acutely sacrificed.
IC is classified according to the mechanism of decreased blood flow
to the colon. This is most commonly nonocclusive, as in cases of shock,
drugs, and colon obstruction. Less commonly, IC occurs after a vascular
insult, which could be due to an arterial thrombosis, embolism, or even a
venous occlusion. A special entity is the postoperative IC that can occur
after cardiac and vascular surgeries, in which there is an intraoperative
temporary cessation of blood flow to the colon. For example, following
abdominal aortic aneurysm repair or bypass, if the IMA was sacrificed
or if there was prolonged cross clamp time, IC can occur.
During periods of hypotension, blood flow is redirected to the brain
at the expense of the splanchnic circulation. At a histologic level, the
initial ischemic changes are always in the mucosa on the antimesenteric side. These changes will eventually spread through the colon wall
to the serosa if the insult continues. Mucosal injury will develop in 20
minutes to 1 hour of decreased blood flow, whereas transmural infarction occurs within 8 to 16 hours. Additional insult occurs when blood
flow is reestablished, causing reperfusion injury. Reperfusion injury is
associated with the release of reactive oxygen species, which causes lipid
peroxidation within cell membranes and leads to cell necrosis.
Risk factors for IC include advanced age, female gender, peripheral artery occlusive disease, coronary artery disease, heart failure,
chronic obstructive pulmonary disease, and inflammatory bowel
disease (IBD). Postoperative IC occurs most commonly after aortic surgery or after cardiac surgery with temporary GI vascular
FIG. 1 Colon blood supply. (From Araghizadeh F, Abdelnaby A, Colorectal surgery. In Anatomy and Physiology. Elsevier; 2013.)
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201
exclusion. In addition, the odds of developing IC are higher in cigarette smokers, both current and former (relative to never smokers).
The use of cardiovascular medications such as diuretics or digoxin
and psychotropic medications within the past month of presentation
is also significantly associated with IC.
CLASSIFICATION
One can classify IC into mucosal vs. transmural types with further
classification by severity as mild, moderate, and severe IC. Severe IC
often involves transmural infarcts of the colon wall, which leads to peritonitis, sepsis, perforation, and death. Another way to look at different
types of IC is by anatomic location or distribution: segmental colitis or
sidedness. A special entity is isolated right-sided colon ischemia (IRCI)
as it is associated with poor outcomes. IRCI has 30-day mortality rate of
20.3% compared with 9.0% in those with non-IRCI, higher frequency
of severe cases requiring surgical intervention (40.9% of patients compared with 10.3% in those with non-IRCI), and is associated with acute
mesenteric ischemia. Pancolitis and IRCI may be seen frequently in
patients with sepsis, and IRCI is associated more frequently in patients
with coronary artery disease and chronic kidney disease on hemodialysis. 61% of episodes of IC that required surgical intervention had either
IRCI or bilateral (pancolonic) patterns of ischemia.
PRESENTATION
The presentation of IC is often vague, and the diagnosis is often delayed
while other differential diagnoses are ruled out. The most common
symptoms of IC are acute onset abdominal pain, hematochezia, and
an urgent desire to defecate. Gangrenous colitis is characterized by
increasing abdominal tenderness, guarding, rebound tenderness, rising temperature, and paralytic ileus. The sudden onset of a toxic colitis
with signs of peritonitis and a rapidly progressive course are typical
of universal fulminant colitis, a rare variant of IC. Rectal bleeding
is found more frequently in non-IRCI (69.9%) compared with IRCI
(39.4%). One must have a high index of suspicion when patients
present with severe acute abdominal pain without bleeding, especially
if they have the common risk factors associated with IRCI. A timely
diagnosis of IRCI is important for patient survival.
Routine laboratory studies are unhelpful in reaching a diagnosis
of IC but are important for prognostication and assessing severity. Leukocytosis is a frequent finding. Elevated lactate, urea, and
creatinine are sometimes found. Some patients may present with
metabolic acidosis and a base deficit in cases of severe ischemia,
gangrene, and sepsis. Decreased hemoglobin levels, low serum
albumin, and the presence of metabolic acidosis can be used to
predict severity of IC.
Imaging usually involves a CT scan, but sometimes in entertaining other differential diagnoses, an abdominal x-ray is ordered.
Classic findings on an x-ray include thumbprinting, which indicates
mucosal edema. In cases of bowel perforation, an x-ray is a quick
way to see free air under the diaphragm. The use of contrast enemas
had previously been the diagnostic modality of choice, but has been
replaced, for the most part, by CT imaging and colonoscopy.
CT is the most helpful modality in the initial assessment of the
patient with abdominal pain. It can exclude other causes of abdominal pain, suggest a location and source of ischemia, and identify
complications associated with more advanced disease (Figs. 2 and 3).
CT will frequently show bowel wall thickening, thumbprinting, and
pericolonic stranding with or without ascites. After reperfusion,
there may be evidence of submucosal edema or hemorrhage. Emboli
or thrombi causing complete arterial occlusion are occasionally seen
with corresponding thin, unenhancing colonic wall due to complete lack of reperfusion. CT findings of colonic pneumatosis and
DIAGNOSIS
After a thorough history and physical examination looking for specific risk factors for IC, laboratory studies, imaging, and endoscopy
might be used to reach the correct diagnosis.
FIG. 3 A and B, Contrast enhanced axial CT image showing extensive dilatation and pneumatosis (arrow) of the small bowel. Pneumatosis was also seen in
the cecum, corresponding to the superior mesenteric artery vascular tract. Mesenteric venous gas is noted as well (arrow with *).
FIG. 2 Contrast enhanced axial CT image demonstrating foci of gas in
the portal veins (arrow). Peripherally branching air on CT helps differentiating portal venous gas from pneumobilia, which typically is more central.
Significant bowel distention is also noted.
202 ISCHEMIC COLITIS
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portomesenteric venous gas can be used to predict the presence of
transmural colonic infarction but can also be present with other
conditions like chronic obstructive pulmonary disease and infectious colitis. CT can also be diagnostic in severe cases, showing
bowel perforation and free air in the peritoneal cavity. Of course
this should be suspected on physical examination. In a patient
in whom the presentation of IC may be a heralding sign of acute
mesenteric ischemia (e.g., IRCI, severe pain without bleeding, and
atrial fibrillation) and the multiphasic CT is negative for vascular
occlusive disease, traditional splanchnic angiography should be
considered for further assessment. Angiography is otherwise rarely
helpful in diagnosing IC as most cases are caused by transient
hypoperfusion.
The gold standard for confirming diagnosis of IC is endoscopy,
where ischemic mucosa can be identified and biopsied for confirmation. Thus, early colonoscopy (within 48 h of presentation)
should be performed in suspected IC cases to confirm the diagnosis.
Typical findings of IC include segmental erythema, edema, mucosal
ulceration, submucosal hemorrhagic nodules, and involvement of
watershed areas. Occasionally, pseudomembranes related to mucosal
sloughing are observed. The colonic single stripe sign, a single linear
ulcer running longitudinally along the antimesenteric colonic wall,
is associated with IC (Fig. 4). After 48 hours, sloughing occurs, the
purple submucosal hemorrhages dissipate, and ulcerations develop.
In more severe ischemia with transmural infarction, the mucosa may
appear gray-green or even black (Fig. 5).
Endoscopy will also allow biopsies to be taken to further confirm
diagnosis. On histologic examination, signs of IC include mucosa
of normal architecture with necrosis and sloughing of the surface
epithelium, loss of epithelium in the superficial aspects of the crypts
(with or without ghosts of crypts), mucin depletion and reactive
changes in the residual crypt epithelium with nuclear hyperchromasia and increased mitoses, paucity or complete absence of acute
inflammatory cells, and the presence of hyalinosis in the lamina
propria (Fig. 6).
The classification is based on clinical, laboratory, imaging, and
endoscopic criteria. Management is driven accordingly. For mild
and moderate disease, treatment is supportive care, which includes
bowel rest, intravenous fluids, optimizing cardiac output, avoiding
medications that could worsen colonic ischemia like vasopressors,
correction of electrolytes and nasogastric tube decompression for
ileus. For confirmed IC, intravenous antibiotics are used to treat bacterial translocation that occurs when the mucosal barrier is damaged.
The antibiotic(s) selected should include both aerobic and anaerobic
pathogens. You should not expect to cover highly resistant pathogens. The duration of antibiotic therapy needed has yet to be studied
and determined, although some authors have recommended 2 weeks.
However, a period covering the time of mucosal injury when translocation is theoretically occurring seems reasonable.
SEVERITY
IC is classified into three categories: mild, moderate, and severe.
Most cases of IC are mild or moderate, and about 20% are severe at
initial presentation.
FIG. 4 Colonoscopic image of linear ulcerations placed along the lon-
gitudinal axis of the colon. (From, Maimone A, De Ceglie A, Siersema PD,
etal. Colon ischemia: A comprehensive review. Clin Res Hepatol Gastroenterol.
2021;45(6):101592.)
FIG. 5 Colonoscopic image showing cyanotic/black mucosal nodules
with deep ulcerations until mucosal necrosis. (From Maimone A, De Ceglie
A, Siersema PD, etal. Colon ischemia: A comprehensive review. Clin Res Hepatol
Gastroenterol. 2021;45(6):101592.)
FIG. 6 Ischemic colitis, H&E, 100×. This image shows characteristic features
of ischemic colitis, including superficial epithelial injury, crypts with atypia
including nuclear hyperchromasia, and hyalinized lamina propria. The crypts
appear closer together due to lamina propria collapse. (Image courtesy
Jacqueline Birkness-Gartman, MD.)
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203
A heart rate of >100 beats per min and systolic blood pressure
of <90 mm Hg at the time of diagnosis are associated with the need
for surgical intervention and/or mortality as are Hgb <12 mg/dL,
hyponatremia (Na <136 mEq/L), LDH >450 U/L, and blood urea
nitrogen (>28 mg/dL). A pancolonic distribution of disease and IRCI
also portend a poor outcome.
Patients who meet criteria for severe disease need a surgical evaluation and most often will require operative intervention. This was
the initial management in 53.6% of those with IRCI versus 14.5% in
those with non-IRCI.
Surgical intervention should be considered in the presence of IC
accompanied by hypotension, tachycardia, and abdominal pain without rectal bleeding; for IRCI and pancolonic IC; and in the presence
of gangrene.
SURGICAL APPROACH
Operative management of patients with IC is either in the acute setting or for treatment of the sequelae of colon ischemia. In the acute
setting, operative indications include peritonitis on examination,
massive bleeding, fulminant colitis, portal venous gas or pneumatosis on imaging with clinical picture of IC, or worsening clinical
condition on medical management alone.
The general principle of surgery is to remove all segments
of the colon that are grossly ischemic (Fig. 7). Surgery is usually
approached with a midline laparotomy; however, in certain circumstances, a diagnostic laparoscopy may be warranted. However, it can
be difficult to determine the extent of resection as the serosa can be
misleading as it will appear normal until transmural necrosis occurs.
Therefore, a preoperative CT scan or endoscopic evaluation of the
colon is important to establish the extent of bowel involvement.
Intraoperatively, one may use Doppler ultrasonography, endoscopy,
or photoplethysmography to assess mucosal viability or colonic
blood flow. After adequate resection has occurred, in patients where
there is concern for ongoing ischemia, it is not uncommon to leave
the fascia open and bowel in discontinuity and take the patient to
the intensive care unit for continued resuscitation for a planned
second-look laparotomy and closure in 12 to 48 hours to make sure
all necrotic tissue has been removed.
The decision to construct an anastomosis versus an ostomy
depends on many factors. The main concern is anastomotic leak
or nonhealing anastomosis. A primary anastomosis can be done
safely in uncomplicated isolated right colon ischemia when the rest
of the bowel appears very well perfused. However, for left-sided IC,
published opinion advocates for an end colostomy and rectal stump
(Hartmann procedure), which can be reversed later (i.e., no sooner
than 6–8 weeks postsurgery). In selected cases, it may be reasonable
even with left-sided disease to perform a primary anastomosis with
or without a protective diverting loop ileostomy. With additional
experience with preoperative localization of the extent of ischemia,
less invasive surgical approaches may become more attractive.
POSTOPERATIVE COURSE
Overall, the postoperative course of patients undergoing surgery for
acute IC is associated with high rates of morbidity and mortality.
Two-thirds of patients with severe IC requiring surgery develop
medical complications such as pneumonia, urinary tract infections,
atrial fibrillation, postoperative myocardial infarction, acute renal
failure, or the need for hemodialysis. There is a 37% in-hospital
mortality rate for severe IC.
Independent risk factors of mortality after emergent colectomy
for IC include elderly age, poor functional status, multiple comorbidities, low output heart failure (e.g., cardiac ejection fraction <20%
on echocardiogram), preoperative septic shock, preoperative blood
transfusions, preoperative acute renal failure, and delay from hospital
admission to surgery. Postoperative death is associated with the peak
preoperative lactate level (if above 2.5 mmol/L), amount of intraoperative blood loss, pre- and intraoperative catecholamine administration, subtotal or total colectomy, need for dialysis postoperatively,
and an American Society of Anesthesiologists (ASA) class 4.
Operative intervention is sometimes required for sequelae of IC
such as symptomatic colonic strictures or for ostomy reversal. Studies
showed high rates of complications after ostomy reversal (i.e., longer
length of stay, anastomotic leaks, and mortality). Other indications
for a second operation include facial dehiscence and wound complications. Patients with nongangrenous IC sometimes present with
abdominal pain, bloating, and obstructive symptoms weeks after
their initial episode. If a stricture is suspected, either a colonoscopy
or a contrast enema can identify it; the latter is helpful to describe
the length and location of the stricture. In 10% of the cases, strictures
develop as the colon heals. If clinically significant, causing obstruction or severe abdominal pain, strictures need operative intervention
by elective resection and primary anastomosis. Alternatively, there
are nonoperative methods to temporize symptoms when surgery is
not feasible, such as balloon dilation, and in some instances, stenting.
CONCLUSION
The incidence of IC has increased during the last few decades. Acute
IC continues to represent a very deadly disease associated with high
rates of morbidity and mortality. IC in the community typically
presents in older patients with multiple comorbidities. Patients who
survive their initial episode may require additional intervention, and
around 7% of patients will have another episode within 5 years. IC
is challenging to diagnose due to its nonspecific presentation, but
efforts should be directed to early consideration of this diagnosis
when risk factors and clinical conditions warrant.
FIG. 7 Portion of intestine with ischemia (cecum, top right of image).
Compare with normal pink-tan mucosa (bottom right of image).
(Image courtesy Arianna Rubinetti, MS, PA [ASCP] and Kevan Salimian, MD, PhD.)
S u g g e S t e d R e a d i n g S
Brandt LJ, Feuerstadt P, Longstreth GF, Boley SJ. American College of
Gastroenterology. ACG clinical guideline: epidemiology, risk factors, pat-
terns of presentation, diagnosis, and management of colon ischemia (CI).
Am J Gastroenterol. 2015;110(1):18–44 quiz 45.
Castleberry AW, Turley RS, Hanna JM, Hopkins TJ, Barbas AS, Worni M,
Mantyh CR, Migaly J. A 10-year longitudinal analysis of surgical manage-
ment for acute ischemic colitis. J Gastrointest Surg. 2013;17(4):784–792.
Yadav S, Dave M, Edakkanambeth Varayil J, Harmsen WS, Tremaine WJ,
Zinsmeister AR, Sweetser SR, Melton 3rd LJ, Sandborn WJ, Loftus Jr
EV. A population-based study of incidence, risk factors, clinical spec-
trum, and outcomes of ischemic colitis. Clin Gastroenterol Hepatol.
2015;13(4):731–738 e1-6; quiz e41.
204 MANAGEMENT OF CLOSTRIDIOIDES DIFFICILECOLITIS
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Management of
Clostridioides
DifficileColitis
Marylise Boutros, MD, Maria Abou Khalil, MD, and
StevenD. Wexner, MD, PhD (Hon)
lostridioides (formerly Clostridium) difficile infection (CDI) is an
important cause of community and nosocomial acquired diarrhea.
C
It is associated with significant morbidity and mortality, especially
amongst the immunosuppressed and elderly. This chapter will review
the clinical presentation and treatment options for patients with CDI.
BACKGROUND
While C. difficile was first described as an important cause of antibiotic-associated colitis in 1978, it was not until the early 2000s that CDI was
experienced as a threatening nosocomial problem due to an increase in
disease frequency, severity, and mortality. This change was attributed in
part to the emergence of hypervirulent strains, including NAP1/BI/027.
Antibiotic stewardship programs and strict infection control measures
allowed for early case identification and treatment, leading to a dampening of CDI incidence. Nonetheless, CDI remains an important cause
of nosocomial acquired infection and an increasingly recognized cause
of community acquired disease and transmission.
C. difficile is an anaerobic toxin-producing gram-positive bacillus that can exist in spore form (outside the colon) or vegetative
forms. The bacteria produce two exotoxins (toxin A and toxin B)
responsible for the colitis and diarrhea. Hypervirulent strains have
been associated with significantly increased toxin production and
subsequently a more severe clinical course. Ingestion of spores of C.
difficile via a fecal-oral route is a common cause of transmissibility,
and transmission is higher in patients with active disease compared
with asymptomatic carriers.
implicated. Antibiotic resistance patterns of C. difficile have also
been found to be correlated to virulence. Another important risk
factor for CDI is advanced age. Furthermore, immunosuppression,
inflammatory bowel disease (IBD), gastrointestinal surgery, and
length of hospitalization have all been associated with increased risk
of CDI. Special attention needs to be paid to patients with IBD, as
disease exacerbation can mimic C. difficile colitis. Although some
epidemiologic studies have implicated gastric acid suppression as a
risk factor, this association was not consistently found after adjusting
for confounding factors and is most likely to be the result of patient
illness and hospital length of stay.
CLINICAL PRESENTATION
Although some patients can be asymptomatic carriers of C. difficile,
CDI usually has clinical manifestations that can range from mild colitis
to fulminant severe disease with toxic megacolon. Patient factors and
pathogen characteristics have been implicated in the severity of the
clinical course. Increasing age, immunosuppression, and comorbidities
are amongst the most reported predictors of severe disease presentation.
Different CDI severity classification systems exist; however, there is
no universally accepted system. This limitation is likely because of the
inability of one scoring system to accurately predict the clinical course,
be simple enough to allow widespread point-of-care use, and allow for
time-dependent variables to be adjusted as the patient’s clinical course
evolves. In general, the existing CDI severity classifications include a
combination of factors associated with increased morbidity and mortality. These factors include physical examination findings, signs of
shock, and laboratory data. A useful disease classification system was
published in 2017 by the Infectious Disease Society of America and
Society for Healthcare Epidemiology of America (IDSA/SHEA) and
is summarized in Table 1. Thus, the evaluation of patients with CDI
should include a history, physical examination including vitals, urine
output, fluid requirements, as well as laboratory tests including complete blood count (with significant leukocytosis being a hallmark, but
not a pathognomonic feature, of CDI), renal function tests, albumin,
and lactate as a marker of end-organ perfusion.
Clinical Risk Factors for CDI
Several risk factors for contracting CDI have been identified. The
most widely recognized and modifiable risk factor for CDI is antibiotic use; CDI can occur up to 3 months after antibiotic discontinuation. Antibiotics result in a disruption of the balanced normal
colonic microbiota allowing pathogenic C. difficile bacteria to multiply and cause disease. While clindamycin was the first antibiotic
to be associated with CDI, many other antibiotics have since been
DIAGNOSIS
Testing is recommended for patients with unexplained new onset
diarrhea (3 stools/day) especially in the presence of risk factors
for CDI. Patients should be placed on preemptive isolation while
awaiting results. Hand hygiene with soap and water is superior to
alcohol-based hand-hygiene products for elimination of C. difficile
spores and is recommended in addition to contact precautions
including gloves and gowns.
TABLE 1 Disease Severity and Recommended Treatment
Disease Severity Clinical Characteristics Recommended Treatment
Nonsevere
disease
Severe disease Leukocytosis WBC ≥15,000 or
Fulminant
disease
Recurrent
disease
Leukocytosis, WBC ≤15,000 or
serum creatinine <1.5 mg/dL
serum creatinine >1.5 mg/dL
Hypotension/shock, ileus, or
megacolon
Vancomycin 125 mg PO QID × 10d OR fidaxomicin 200 mg PO BID × 10d
Use metronidazole 500 mg PO TID if none of the above available
Vancomycin 125 mg PO QID × 10d OR fidaxomicin 200 mg PO BID × 10d
Vancomycin 500 mg QID PO/PT (consider adding rectal vancomycin if ileus) + IV
metronidazole (500 mg q8h)
Pulse-tapered vancomycin regimen or fidaxomicin regimen is recommended.
Fidaxomicin, vancomycin with or without rifaximin, and fecal microbiota transplant (FMT) are used for second or subsequent recurrences.
With recurrences presenting with fulminant disease, in addition to the antibiotic
regimen administered, some advocate for the addition of FMT.
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TABLE 2 Diagnostic Tests for C. difficile
Test Details Sensitivity Specificity Substance Detected
Selective anaerobic
culture
Cell culture cytotoxicity
assay
Nucleic acid amplifica-
tion tests (NAAT)
Enzyme immunoassay
C. difficile glutamate
dehydrogenase (GDH)
Enzyme immunoassay
for C. difficile toxins
A and B
A variety of laboratory tests for C. difficile exist. They can detect
either the organism itself or the toxins in the stools. To avoid false
positive results, laboratory protocols recommend that only liquid
or loose stool samples be tested. Stool toxin tests are often used as
a multistep algorithm either with glutamate dehydrogenase (GDH)
assay or nucleic acid amplification tests (NAAT) assay followed by
toxin-recognition to help differentiate between asymptomatic carriers and patients with the disease. A summary of the commonly used
tests is presented in Table 2.
Rarely used
Takes a long time to finalize
Can be useful in patient with ileus (rectal swab)
Resource intensive and time consuming, not routinely done
Has been used as a gold standard test
Detects one or more genes specific to toxigenic strains
Capable of detecting asymptomatic carriers
GDH antigen is an essential enzyme produced by all
C. difficile isolates, but cannot differentiate between
toxigenic and nontoxigenic strains
Most strains produce toxins A and B although some
strains produce toxin B only, but CDI due to strains
producing toxin A alone has not been reported
High Low C. difficile vegetative
cells or spores
High High Free toxins
High Low/
Moderate
High Low C. difficile common
Low Moderate Free toxins
C. difficile nucleic
acid (toxic genes)
antigen
205
Endoscopy
Pseudomembranes are a characteristic endoscopic feature of CDI
that appear as raised white and yellow plaques and consist of toxin-induced ulcers with inflammatory cells and mucous (Fig. 1).
Confirmatory endoscopy with flexible or rigid sigmoidoscopy is not
necessary; however, it is often performed to exclude other causes of
colitis such as cytomegalovirus infection, graft-versus-host disease,
IBD exacerbation, or ischemic colitis. Endoscopic confirmation has
also been used in cases where a decision on surgical management
needs to be expediently made and the situation does not allow waiting for confirmatory laboratory testing.
Imaging
Abdominal imaging can aid in the diagnosis of colitis and identify
complications requiring operative intervention. Rarely, complications such as free air may also be seen. Classically, plain films were
used to assess for “thumb printing” secondary to submucosal edema
or toxic megacolon with colonic distention. Nowadays, an infused
computed tomography (CT) scan of the abdomen and pelvis is the
preferred imaging modality to assess the degree, extent, and complications of the colitis. Typical findings in severe or fulminant disease
include pancolitis with significant colonic thickening and ascites
(Fig. 2A). If gastrointestinal contrast is given, it can be seen trapped
between the edematous haustral folds (accordion sign) (Fig. 2B). Evidence of complications such as bowel perforation, toxic megacolon,
and ischemia can also be seen on CT.
MEDICAL TREATMENT
Given the role of antibiotics in the development of CDI and its potential recurrence, it is recommended to stop the inciting antibiotics as
soon as possible. Early treatment for CDI while awaiting confirmatory tests should be initiated, especially in patients with severe or fulminant disease. Although probiotics can decrease the occurrence of
FIG. 1 Endoscopic appearance of pseudomembranes. (From Iseman DT,
Hamza SH, Eloubeidi MA. Pseudomembranous [Clostridium difficile] colitis.
Gastrointest Endosc. 2002;56[6]:907.)
CDI, they have no role in the treatment of the disease. Metronidazole
was commonly used for treatment; however, vancomycin or fidaxomicin have been found to be superior to metronidazole and have
largely replaced it. The recommended treatment regimen with these
agents is based on disease severity and is outlined in Table 2. For the
first recurrence, a pulse-tapered vancomycin regimen or fidaxomicin
regimen is recommended. Fidaxomicin, vancomycin with or without
rifaximin, and fecal microbiota transplant (FMT) are used for second
or subsequent recurrences.
With recurrences presenting with fulminant disease, in addition
to the antibiotic regimen administered as outlined in Table 2, some
advocate for the addition of FMT.
Patients with severe colitis require special attention. They
should have large bore intravenous access and accurate measurements of intake and output to guide aggressive fluid resuscitation
206 MANAGEMENT OF CLOSTRIDIOIDES DIFFICILECOLITIS
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A
FIG. 2 Computed tomography scan showing fulminant Clostridioides difficile infection, with (A) and without (B) contrast.
with crystalloids. Acute kidney injury is a common complication
of severe colitis and resuscitation is generally the initial approach.
Patients should be kept fasting with complete bowel rest until their
symptoms improve. We recommend serial clinical examinations
of patients with severe disease including vital signs, abdominal
examination, and laboratory investigations as the clinical course
can evolve rapidly. Prompt recognition of complications associated
with the colitis will allow early management and improve outcomes. A multidisciplinary approach including surgeons, intensive
care and infectious disease specialists, may aid in the care of these
patients.
SURGICAL MANAGEMENT
Although rare (0.3%–6.2% depending on the epidemic status), surgical management is reserved for patients with fulminant disease who
fail to respond to medical management, worsen on treatment, or in
whom complications related to the colitis arise including hemodynamic compromise, abdominal compartment syndrome, or colonic
perforation (Box 1).
BOX 1 Indications for Surgical Management
• Colonicperforation
• Full-thicknessischemia
• Peritonitis,worseningabdominalexamdespiteadequatemedi-
cal treatment
• Abdominalcompartmentsyndrome
• Hemodynamicinstabilitywithongoingorincreasingneedfor
vasopressor support
• Needforintubationandmechanicalventilation
• Worseningend-organfailure(especiallyrenalfailure)
B
In the absence of absolute indications for surgery, no clear guidelines exist to define failure of medical management or the optimal
timing to intervene with surgery. Despite the morbidity associated
with emergency surgery in critically ill patients, evidence from retrospective studies suggests that earlier time to surgical intervention
with fulminant disease improves survival compared with continued
medical management alone.
Total Abdominal Colectomy with End Ileostomy
An open total abdominal colectomy (TAC) with an end ileostomy
remains the gold standard operation for patients with fulminant
C. difficile colitis (FCDC) requiring surgery and is the operation to
which all others are compared. Outcomes after segmental colectomies for the treatment of FCDC have been shown to be inferior to
TAC, and thus segmental colectomy is not recommended even if
the colitis appears to be limited to a part of the colon on CT imaging. Upon entry into the abdominal cavity, usually profuse ascites
is encountered. The colon usually appears dilated and edematous
but otherwise has a normal serosal surface, as this is a mucosal
disease. The distal extent of the resection is at the rectosigmoid
junction, where the rectum is transected and stapled; however, if
the rectosigmoid appears too friable and there is heightened concern for rectal stump blowout, the surgeon can consider a more
proximal transection to allow delivery of a distal stapled end of
more proximal sigmoid as a mucous fistula. It is our preference to
place a Malecot rectal catheter in the rectal stump for the first few
postoperative days to allow decompression while healing. Postoperatively, patients should remain in a monitored setting until
their vital functions are stable without the supportive measures
offered in the intensive care unit and until their systemic inflammatory response syndrome (SIRS) starts improving. Postoperative
length of stay is often prolonged by the patient’s comorbidities,
and rapid recovery is limited by the severity of the multiorgan
system involvement. After recovery, ileorectal anastomosis can be
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performed if the patient has returned to a functional baseline. This
usually occurs starting at 3 to 6 months postoperatively. Given the
significant postoperative morbidity associated with a colectomy for
severe CDI, many patients do not reach a level of fitness suitable to
endure another extensive operation for restoration of gastrointestinal continuity with an ileorectal anastomosis. In the literature, most
patients who undergo a TAC do not eventually have restoration of
gastrointestinal continuity.
Colonic Lavage and Diverting Loop Ileostomy
The creation of a diverting loop ileostomy (DLI) with colonic
lavage has been advocated as a less-invasive alternative to TAC in
this critically ill-patient population. In 2011, Neil et al. described
this approach, which consists of the creation of a DLI with colonic
lavage with warm polyethylene glycol solution and postoperative
antegrade installation of vancomycin flashes by the ileostomy
(Fig. 3). In their single-institution, single-surgeon series, the
authors compared 42 patients who underwent surgery for FCDC
with 42 historical patients who had undergone TAC. The authors
observed a decreased 30-day postoperative mortality for patients
who underwent a DLI compared with TAC. In addition to the
survival benefit, the authors demonstrated increased ileostomy
closure rates at six months. A minority of patients in the DLI
group required conversion to a TAC either due to the development of abdominal compartment syndrome or for failure of
improvement. Since the first description of this novel procedure,
few studies have compared it to TAC. There remains a lack of
high-quality prospective data comparing these two operations
given the difficulty in conducting such studies in the setting of a
disease associated with high mortality in the emergency setting.
A recent meta-analysis of 733 patients with DLI and 2950 patients
with TAC found no difference in postoperative morbidity or
mortality but found higher gastrointestinal restoration rates for
patients with DLI.
Thus, while no recommendations can be made on which
patients would best benefit from DLI vs. TAC, we believe patients
with severe disease early in their disease course, who do not have
any complications associated with their colitis necessitating a TAC
(perforation, ischemia, or toxic megacolon), can be offered a DLI
with colonic lavage. However, one must be cautious that patients
need close follow-up as the diseased colon is still in situ, and thus
there is a longer time to resolution of SIRS. Typically, patients may
take up to a few days to a week in this SIRS state before improving.
Tables 3 and 4 summarize the current evidence and the advantages
and disadvantages of each operation.
Theoretically, the creation of a DLI is relatively simple; however, there are a few technical challenges associated with fulminant
disease state and with performing the colonic lavage. We summarized the steps of the operation in Box 2 and at the following
link https://www.youtube.com/watch?v=1VMQrEI6jro&t=26s.
Furthermore, comorbidities such as elevated BMI may be challenging and may be overcome with the creation of an end loop
ileostomy.
SPECIAL POPULATION: PATIENTS WITH
INFLAMMATORY BOWEL DISEASE
IBD, particularly ulcerative colitis, is a risk factor for the development of CDI. Patients with IBD are also more likely to need surgical
intervention and have longer length of stay and increased mortality
with CDI.
TABLE 3 Comparison Between Total Abdominal Colectomy and Diverting Loop Ileostomy and Colonic Lavage
Pros Cons
Diverting loop ileostomy Less invasive operation and minimally invasive option
Higher gastrointestinal restoration rates
Improved postoperative morbidity compared with total
abdominal colectomy (TAC)
Total abdominal
colectomy
Definitive management
Faster resolution of the systemic inflammatory response
Limited data supporting its use
Optimal patient population not defined
Patients may require reoperation in the event of failure
Slower resolve of systemic inflammatory response
High morbidity and mortality
Low gastrointestinal restoration rates
TABLE 4 Summary of Published Papers Mortality Following Total Abdominal Colectomy and Diverting Loop
Ileostomy
Study Design and Location Study Interval Patient Population (n) 30-Day Postoperative Mortality
Neal etal. (2011) Prospective cohort, single
center
Fashandi etal. (2017) Retrospective, single center 2011–2015 DLI: 10
Ferrada etal. (2017) Retrospective, multicentric 2010–2014 DLI: 21
Hall etal. (2018) Retrospective review of pro-
spectively maintained database (ACS-NSQIP)
Juo etal. (2019) Retrospective review of
administrative database
(NIS database)
ACS-NSQIP, American College of Surgeons National Surgical Quality Improvement Program; DLI, diverting loop ileostomy; NIS, Nationwide Inpatient
Sample; TAC, Total abdominal colectomy.
2009–2011 DLI: 42
TAC: 42
TAC: 13
TAC: 77
2011–2016 DLI: 47
TAC: 410
2011–2015 DLI: 613
TAC: 2408
DLI 19% vs. TAC 50%
(P
= 0.006)
DLI 30% vs. 23% 50%, (P = 1)
DLI 17.2% vs. TAC 39.7%
(P = 0.002)
DLI 36% vs. TAC 31%
(P
= 0.451)
DLI 26.0% vs. TAC 31.1%
(P
= 0.28)
*In-hospital mortality
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A B
FIG. 3 Example of set-up for diverting loop ileostomy and colonic lavage. (A) Foley catheter inserted into distal limb of the ileostomy, sutured to the rod.
(B) Feeding access tubing used to administer vancomycin flushes.
BOX 2 Technical Details and Tips
• ExploratorylaparotomyordiagnosticlaparoscopyconfirmingdiagnosisandrulingoutcontraindicationstoDLI(laparoscopyispreferable if patient is a candidate and the surgeon is comfortable with this approach).
• Creationofadivertingloopileostomy20cmfromtheileocecalvalveinatypicalfashion(Brookeproximallimb,flushdistallimb;Fig. 3A).
• Insertingacatheter,typically18FFoleyurinarycatheterintothedistallimboftheileostomy,ideallypositionedinthececum(Fig. 3B).
• Lavageofthecolonisperformedwith8Lofpolyethyleneglycol(PEG)solutionwarmedto37°C.
• FoleycatheterconnectedtothebagcontainingthePEGsolutionusingurologicconnectiontubing(usedincystoscopy),allowingflow
control of the PEG solution to the diseased colon.
• PEGsolutionadministeredinincrements,ensuringthateffluentdrainageiscollectedintherectaltube.
• Iftheprocedureisperformedlaparoscopically,pneumoperitoneumcanbemaintainedat7–10mmHgduringlavage.Laparoscopic
bowel graspers may be used to aid in pushing the fluid along the colon.
• Ifperformedbyalaparotomy,theabdomeniskeptopen,andthesurgeoncanmanuallyaidthemovementofthefluidthroughthe
colon.
• Iftroubleisencounteredgettingfluidthroughthecolon,thepatientmaybemovedintotheTrendelenburg/reverseTrendelenburgpositions as well as left side up/down and right side up/down to move the fluid along the colon.
• Rarely,flexuremobilizationmaybenecessary.
• Duetofluidsequestrationinthediseasedandatoniccolon,anabdominalcompartmentsyndrome(ACS)mayoccurduringorafterthe
operation and the surgeon should be aware of this possibility.
• AbdominaldraincanbelefttoremoveexcessascitesandpotentiallyreducetheriskofACS
• Postoperatively,vancomycinflushes(500mgin500mLoflactatedRinger’s)aredeliveredtothediseasedcolonthroughtheFoley
catheter that was left in the efferent limb of the ileostomy. The first vancomycin flush is given after completion of the PEG flushes, and
administration should be continued every 8 h for 10 days or until the patient has clinically recovered (Fig. 3A and B).
Given that CDI can mimic IBD flares, it should be considered in
patients with worsening, smoldering, or relapsing IBD. While the
treatment for CDI in patients with IBD is identical to patients without IBD, given the increased morbidity and mortality in this population, they should be monitored closely and have a lower threshold for
early surgical intervention. It remains important to note that while
CDI enteritis is a very rare event, it can occur after TAC with end
ileostomy or following ileal pouch anal anastomosis, as a rare cause
of pouchitis, and should be excluded in the event of a high-output
ileostomy with SIRS.
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