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Ischemic Colitis
AlodiaGabre-Kidan andDavidJ.Maron
57
Refer toAlgorithm inFig. 57.1
A. Colonic ischemia is the most common form
of intestinal ischemia with an estimated incidence of 7–16/100,000-patient years. While
colonic ischemia can present as severe, lifethreatening disease, most cases are mild, selflimited, and reversible. Given its transient
nature, many patients may not even seek
medical attention, which leads to a likely
underestimation of the true incidence in the
medical literature.
B. The most common presenting symptoms in
patients with colonic ischemia are abdominal pain over the affected portion of the
colon, an urge to defecate, and bloody diarrhea. None of these ndings are necessary
for a diagnosis and all three will only be
present in half of cases. Rather, the clinician
should be aware that in the presence of signicant risk factors any of these symptoms
should raise suspicion.
C. Risk factors include any comorbidities or
clinical features that predispose to hypoperfusion of the colon. In particular, signicant
A. Gabre-Kidan
Division of Colorectal Surgery, Johns Hopkins
School of Medicine, Baltimore, MD, USA
D. J. Maron (*)
Department of Colorectal Surgery, Cleveland Clinic
Florida, Weston, FL, USA
e-mail: marond@ccf.org
cardiovascular comorbidities such as coronary artery disease, congestive heart failure,
diabetes, or a known history of vascular disease. Although colonic ischemia is largely
due to reversible local hypoperfusion, or
“non-occlusive” disease, emboli to the
colonic vasculature are possible and patients
with a history of atrial brillation or other
arrhythmias should raise suspicion as well.
Other, more specic elements of the history
that should be elicited include a history of any
abdominal surgery where the IMA may have
been sacriced (prior colonic resection;
abdominal aortic aneurysm repair), irritable
bowel syndrome, illicit drug use, or long distance running, as all have been shown to be
risk factors. In patients in whom colonic ischemia is high on the differential diagnosis who
present with peritonitis and/or hemodynamic
instability unresponsive to resuscitative
efforts, operative exploration should be pursued as this is worrisome for full-thickness,
irreversible ischemia. If left unaddressed, this
would lead to sepsis, shock, and ultimately
death.
D. Although the diagnosis of colonic ischemia
can often be made with a thorough history and
physical exam alone, adjunctive investigations
can help better localize the disease and predict
the severity of the ischemic insult. Many prospective and retrospective studies have sought
to identify laboratory markers to aid in diagnosis. Routine laboratory investigations should
© Springer Nature Switzerland AG 2020
S. R. Steele etal. (eds.), Clinical Decision Making in Colorectal Surgery,
https://doi.org/10.1007/978-3-319-65942-8_57
437
438
A. Gabre -Kidan and D. J. Maron
Fig. 57.1 Algorithm for ischemic colitis
57 Ischemic Colitis
439
include a CBC, BMP, LDH and lactate.
Elevated BUN and LDH are the markers with
the greatest specicity for colonic ischemia
but many studies have found elevated WBC,
decreased bicarbonate levels, and increased
creatinine as surrogates for acid/base and volume status. Perhaps more important than the
absolute values are their trends as treatment is
initiated. Laboratory abnormalities should
start to normalize with resuscitation; any worsening acidosis or leukocytosis are worrisome
for progression of ischemia.
E. Imaging should begin with a plain radiograph
of the abdomen. Although the ndings will
often be non-diagnostic, X-rays are quick and
inexpensive. Furthermore, more ominous
ndings such as free air, portal venous gas, or
pneumatosis can be seen on plain lms and
suggest severe, full thickness ischemia and
the need for urgent surgical intervention.
Although similarly non-specic, the classic
sign of “thumbprinting” can be seen on plain
lms and suggests bowel wall edema and
thickening. More often than not, however,
plain X-rays will be inconclusive and the next
step should be a CT scan with intravenous
and oral contrast.
F. A CT scan serves four main purposes: (a)
supporting the diagnosis of colonic ischemia
with ndings of fat stranding, bowel wall
edema or ndings of severe ischemia such as
portal venous gas, pneumatosis, or free air,
(b) rule out other pathology whose symptoms
can overlap with colonic ischemia such as
diverticulitis, infectious colitides, or inammatory bowel disease (c) localize the segment of colon involved and any potential
small bowel involvement, and (d) evaluate the
mesenteric vasculature for atherosclerosis,
stenosis, or occlusion. Given that most
colonic ischemia is due to a transient, lowow state, the major arteries will usually be
patent, however clues such as stenosis or atherosclerosis can help identify a patient that
may be at risk for ischemia.
G. Recent studies have shown that isolated right
sided colonic ischemia may represent a specic entity with a different clinical course
than other sites of colonic ischemia. Montoro
and Brandt compared patients with colonoscopically or surgically conrmed isolated
right colon ischemia to patients with other
distributions of ischemia. Patients with ischemia of the right colon were generally sicker
with increased comorbidities at baseline and
had worse outcomes with a higher rate of
operative intervention and higher eventual
morbidity and mortality. Many authors have
hypothesized that this is because right-sided
ischemia is a manifestation of acute mesenteric ischemia given that the right colon is
supplied by the SMA.
H. Although CT scan may offer signicant
information, colonoscopy remains the gold
standard for diagnosis. Findings can represent a spectrum of mild disease including
hemorrhagic nodules, edema, erythema, and
friability, to manifestations of severe ischemia, including ulcerations and gangrene.
Findings will vary depending not only on the
severity but also on the timing of colonoscopy relative to time of initial insult. It is recommended that colonoscopy be performed
within 48h of presentation and that the colonoscope only be inserted to the distal most
extent of the ischemic changes for fear of perforation from manipulation and insufation
of an ischemic segment of colon. A “single
stripe sign,” a single longitudinal ulcerated or
inamed colon strip, is considered diagnostic
of colonic ischemia but is rarely seen on colonoscopy. Pathognomonic biopsy ndings
include mucosal infarction and ghost cells,
however these are seen in less than 10% of
overall cases and ghost cells are only seen
20% of cases requiring surgery.
I. Management of colonic ischemia includes
bowel rest, aggressive intravenous uid
resuscitation, antibiotic administration, and
serial abdominal exams. Given that the pathophysiology of colonic ischemia is relative
hypoperfusion, optimization of intravascular
volume status is crucial. While there is little
evidence supporting the use of antibiotics in
the literature, the loss of the mucosal barrier
is believed to put patients at risk for bacterial
440
A. Gabre -Kidan and D. J. Maron
translocation. Antibiotics should be directed
at gram negative and anaerobic pathogens
and should continue for at least 7 days from
diagnosis.
J. Patients who present with or develop signs of
peritonitis or hemodynamic instability should
be operatively explored. The specic
approach is surgeon and patient dependent. If
the diagnosis of colonic ischemia is in doubt,
it may be useful to perform a diagnostic laparoscopy to evaluate the colon and small
bowel. However, in a patient who is hemodynamically unstable, laparotomy with the goal
of quickly identifying and resecting the segment at risk is more prudent.
K. Any segment of colon with signs of irrevers-
ible ischemia should be resected. Areas of the
colon that appear questionable but have not
progressed to full thickness ischemia may be
left behind with the intention of performing a
second look laparotomy after aggressive
resuscitation in the intensive care unit.
Ultimately, all diseased segments of colon
should be resected so that the patient is left
with only healthy, well-perfused colon.
L. The decision to perform a bowel anastomo-
sis (with or without proximal diversion) or
an end colostomy/ileostomy depends largely
on the patient’s underlying comorbidities
and current hemodynamic state. The surgeon must weigh the risks of performing an
anastomosis versus the risks of a stoma. As
many patients with colonic ischemia are
elderly with comorbidities that put them at
high risk for elective surgery, there is a high
likelihood of permanent stoma in this patient
population.
Suggested Reading
Brandt L, Feuerstadt P, Blaszka M. Anatomic patterns,
patient characteristics, and clinical outcomes in ischemic colitis: a study of 313 cases supported by histology. Am J Gastroenterol. 2010;105:2245–52.
Brandt L, Feuerstadt P, Longstreth G, Boley S. ACG
clinical guideline: epidemiology, risk factors, patterns of presentation, diagnosis, and management of colon ischemia (CI). Am J Gastroenterol.
2015;110:18–44.
Feuerstadt P, Brandt L. Update on colon ischemia:
recent insight and advances. Curr Gastroenterol Rep.
2015;17:45.
Longstreth G, Yao J.Epidemiology, clinical features, high-
risk factors, and outcome of acute large bowel ischemia. Clin Gastroenterol Hepatol. 2009;7:1075–80.
Montoro M, etal. Clinical patterns and outcomes of isch-
aemic colitis: results of the working group for the
study of ischaemic colitis in Spain (CIE study). Scand
J Gastroenterol. 2011;46:236–46.
Colonic Conditions: Infectious Colitis
WilliamC.Cirocco andShandraR.Day
58
See Algorithm inFig. 58.1
A. Acute diarrhea is typically categorized as
symptoms lasting <14 days while chronic
diarrhea continues >30days. Acute inammatory colitis includes organisms such as
Campylobacter, Salmonella, Shigella,
Enterohemorrhagic and Enteroinvasive E. coli
(EHEC and EIEC) and E. histolytica as well
as Clostridium difcile. Several other infec-
tious agents may cause chronic colitis such as
other strains of E. coli (Enteropathogenic—
EPEC, Enteroaggregative—EAEC), mycosis,
mycobacterium (TB) and parasitic infections.
Patients with chronic infection usually present
with symptoms for weeks or months including
fever, abdominal pain, weight loss, diarrhea
and malabsorption. See Table58.1 for a list of
common causes of infectious colitis and
Table 58.2 for treatment of specic causes of
infectious colitis.
B. Severe colitis is typically associated with
dehydration, fever and weight loss and may
present with hypotension and leukocytosis.
W. C. Cirocco (*)
Head, Section of Colon and Rectal Surgery, Banner
MD Anderson Cancer Center, Phoenix, AZ, USA
S. R. Day
Division of Infectious Diseases, Department of
Internal Medicine, The Ohio State University Wexner
Medical Center, Columbus, OH, USA
An abdominal/pelvis CT scan may show a
thickened colon wall, colon dilation or exudative uid. For C. difcile colitis, specic
severity scoring systems have been described
to categorize mild-to-moderate, severe and
complicated disease (see Table58.3).
C. Recurrent infectious colitis is frequently seen
in patients with Clostridium difcile infection (CDI) and is typically categorized as
recurrent CDI within 8weeks of completion
of therapy (see Table58.4). Other infections
known to cause recurrent disease include
Salmonella (typically recurrent bacteremia
or a chronic carrier state), Cryptosporidium,
Cystoisospora and Cyclospora primarily in
immunocompromised patients. In patients
with recurrent symptoms, consider repeat
infection or alternative pathogens based on
risk factors and exposure.
D. Diarrhea is due to increased water content in
stool caused by either decreased water absorption in the small bowel or active secretion of
water throughout the bowel (through toxin production, invasion or tissue penetration).
Diarrhea is typically dened as three or more
loose or watery bowel movements within 24h.
E. Fever and tenesmus suggest an inamma-
tory proctocolitis that may be caused by
Campylobacter, Shigella, E. histolytica, C.
trachomatis and N. gonorrhea as well as
other opportunistic pathogens in HIVinfected patients. Symptoms lasting
© Springer Nature Switzerland AG 2020
S. R. Steele etal. (eds.), Clinical Decision Making in Colorectal Surgery,
https://doi.org/10.1007/978-3-319-65942-8_58
441
442
W. C. Cirocco and S. R. Day
Fig. 58.1 Algorithm for evaluation of patients with diarrhea/colitis
Table 58.1 Common causes of infectious diarrhea/colitis
Bacterial Parasitic Viral Fungal
Shigella E. histolytica CMV Histoplasmosis
Salmonella Strongyloides HSV Candida
Campylobacter Giardia
a
EHEC/EIEC Cryptosporidium
C. difcile (see Fig.58.2) Cystoisospora belli
Yersinia enterocolitica Cyclospora
Vibrio spp.
b
Microsporidia
a
a
a
a
Rotavirus
Ebola
Norwalk virus
a
a
TB Schistosomiasis
Aeromonas Chagas
Traveler’s Diarrhea
EPEC/EAEC
a
a
C. trachomatis (proctocolitis)
N. gonorrhea (proctocolitis)
a
These pathogens are a common cause of infectious diarrhea but do not typically cause inammation
b
Vibrio cholera does not invade the cell wall and there are few neutrophils in the stool. Diarrhea is caused by enterotoxin
that causes watery diarrhea. Other species of Vibrio such as Vibrio parahaemolyticus cause diarrhea through both
enterotoxin production as well as small bowel inammation
>10days with associated weight loss should
raise concern for Giardia, Cyclospora or
Cryptosporidium. Bloody diarrhea (especially in the absence of fecal leukocytes)
suggests infection with EHEC or E. histo-
lytica (leukocytes are destroyed by the parasite). Consider Yersinia enterocolitica if
there is unexplained abdominal pain and
fever or appendicitis-like symptoms.
F. Risk factors for CDI include both the number
of hospitalizations and prolonged duration of
hospitalization (>50% of patients had CDI
with hospitalization >4 weeks) along with
the use of antibiotics and proton pump inhibitors. Patients should be questioned regarding travel, especially travel outside of the
USA to tropical areas where there is increased
risk for traveler’s diarrhea as well as viral and
parasitic pathogens. It is also important to
investigate for illness in family members and
other close contacts. Patients with a history
of anoreceptive sex may develop proctitis
58 Colonic Conditions: Infectious Colitis
443
Table 58.2 Antimicrobial treatment for common causes of infectious diarrhea/colitis
Pathogen Treatment
Shigella Ciprooxacin 500mg PO BID or Levooxacin 500mg PO daily or Azithromycin 500mg PO
Daily×3days
Salmonella Mild illness—none, Possible bacteremia—Ciprooxacin 500mg PO BID (Ceftriaxone 2g IV
Q24h if Cipro resistant)×5–7days
Campylobacter Mild illness—none, severe or immunocompromised—Azithromycin 500mg PO daily or
Ciprooxacin 750mg BID PO×3days if uncomplicated, 7–14days if complicated
Yersinia Ciprooxacin 500mg PO BID or TMP/SMX PO×5days
Vibrio Doxycycline 300mg PO×1 dose or Ciprooxacin 1g PO×1 dose or Azithromycin 1g
PO×1 dose
Aeromonas Mild illness—none, severe diarrhea or immunocompromised—Ciprooxacin, Ceftriaxone or
TMP/SMX
EHEC None
TB Typical TB treatment
C. difcile See Fig.58.2
Giardia Metronidazole 250mg PO TID×5–7days
E. histolytica Metronidazole 750mg TID PO×5–7days followed by a luminal agent Paromomycin 30mg/kg/day
PO in three divided doses×5–10days or Diloxanide PO 500mg TID×10days
Schistosomiasis Praziquantel 20mg/kg PO TID×1day
Strongyloidiasis
Ivermectin 200μg/kg daily×2days, Albendazole 400mg PO BID×10–14days
Cryptosporidium Supportive care, reduce immunosuppression, +/-Nitazoxanide 500 to 1000mg PO BID
(×14days)
Cystoisospora
belli
TMP/SMX 1 tablet PO BID×10days followed by chronic suppression until immune system
recovers
Cyclospora TMP/SMX 1 tablet PO BID×7–10days followed by chronic suppression until immune
system recovers
CMV Ganciclovir, Valganciclovir (dose adjusted based on renal function)
HSV Acyclovir, Valacyclovir (dose adjusted based on renal function)
Norwalk virus,
None
Rotavirus, Ebola
Histoplasmosis Amphotericin B (dose dependent on formulation used), Itraconazole 200mg PO TID×3days
followed by 200mg PO BID
TMP/SMX trimethoprim/sulfamethoxazole
Table 58.3 Special populations of patients with infectious colitis
Risk factor Details
HIV/AIDS Greatest risk for OIs when CD4
count is less than 200
Solid organ
Immunosuppressed
transplant
Bone marrow
Immunosuppressed
transplant
IBD (Crohn’s/
ulcerative colitis)
Immunosuppressed or altered
immunity
Chronic steroid use Immunosuppressed
Underlying
malignancy
Recent
Altered immunity (including
leukemia and lymphoma)
Immunosuppressed
chemotherapy
Table 58.4 C. difcile infection severity scoring system
(adapted from Suarwicz etal.)
Severity Criteria
Mild-to-
moderate
Diarrhea, not meeting criteria for
Severe or complicated disease
disease
Severe
disease
Serum albumin <3g/dl plus one of the
following:
– WBC ≥15,000cells/mm
3
– Abdominal tenderness
Severe and
complicated
disease
Any of the following (due to CDI):
– ICU admission
– Hypotension (with or without
vasopressor use)
– Fever ≥38.5°C
– Ileus or signicant abdominal
distention
– Mental status changes
– WBC ≥35,000 or <2,000cells/mm
3
– Serum lactate >2.2mmol/l
– End organ failure (mechanical
ventilation, renal failure, etc.)
444
W. C. Cirocco and S. R. Day
secondary to multiple sexually transmitted
infections (HSV, Gonorrhea, Chlamydia,
Syphilis) or colitis due to enteric pathogens
(Campylobacter, Shigella, C. difcile,
Chlamydia) with the location determined at
colonoscopy. Of note, these patients are also
at risk for Giardia which causes a noninammatory diarrhea.
G. Immunosuppressed patients, including those
with a history of organ and stem cell transplant as well as HIV/AIDS are at increased
risk for multiple bacterial, viral and parasitic
infections. These patients may also have
more than one pathogen, therefore continued
monitoring of their symptoms and continued
work-up is appropriate. One pathogen to
note, Norovirus, typically causes a selflimited gastroenteritis but in immunocompromised patients may lead to chronic
infection and severe complications.
H. Patients with inammatory bowel disease
(IBD) may have colitis due to their underlying disease, but they are also at risk for other
infections including CDI as they are frequently on immunosuppression for their
IBD, thus increasing their risk for opportunistic infection (OI).
I. Initial evaluation should be done for signs of
systemic toxicity including hypotension,
lethargy and altered mental status or
dehydration with postural hypotension,
tachycardia and dry mucous membranes.
Abdominal examination should evaluate for
the presence of bowel sounds, abdominal
distention or peritoneal signs (rebound,
guarding, rigidity).
J. Non-inammatory diarrhea suggests one of
the following infectious organisms: Giardia,
Cryptosporidium, Vibrio, E. coli (not EIEC or
EHEC), Staphylococcus aureus, Bacillus
cereus, or Norwalk virus. The presence of
blood without fecal leukocytes is suggestive
of EHEC or amebiasis. Inammatory diarrhea
suggests infection with Shigella, Salmonella,
Campylobacter jejuni, EIEC or CDI.
K. Initial laboratory evaluation may include
CBC with differential (bandemia, anemia,
thrombocytopenia, with profound leukocytosis suggests severe CDI), chemistry (electrolyte abnormalities and creatinine for renal
function), liver function tests and serum
lactate.
L. Initial work-up depending on symptoms and
exposures may include stool culture or stool
enteric PCR for Salmonella, Campylobacter,
Shigella/EIEC, Shiga toxin, parasite testing for
Giardia, E. histolytica and Crypto sporidium
and C. difcile toxin titers (see Algorithm #2).
Consider stool studies for fecal lactoferrin,
comprehensive ova and parasites and special
studies for Cryptosporidium, Cystoisospora,
Cyclospora and Microsporidia. Yersinia
enterocolitica, Vibrio spp. and Aeromonas
requires special culture media and can be specically requested. Special stool studies are
required to evaluate for viral pathogens including rotovirus and Norwalk virus. Serologic
testing for Strongyloides and E. histolytica
may be considered if there are any risk factors
or peripheral eosinophilia (especially with
Strongyloides).
M. Abdominal plain lms may show colon dila-
tion or toxic megacolon concerning for severe
CDI (see Algorithm 2). An abdominal/pelvis
CT scan may show colon wall thickening suggestive of active colitis but has limited sensitivity and specicity. Flexible endoscopy may
be very helpful in evaluating causes of inammatory colitis. Colonic ulcers are suggestive
of amebiasis or Crohn’s disease, but necrotic
ulcers can also be seen in Shigella. The presence of pseudomembranes are diagnostic of
CDI, but they are not always identied. Testing
for N. gonorrhoeae, C. trachomatis, HSV and
syphilis should be undertaken if localized
proctitis is visualized, especially in patients
with a history of anoreceptive intercourse.
Biopsies of visible lesions of the colorectal
mucosa may be very helpful in differentiating
infectious colitis from IBD as well as identifying specic pathogens on staining including
cryptosporidium, E. histolytica, CMV, HSV,
TB and Histoplasmosis. Patients with known
underlying IBD such as ulcerative colitis (UC)
or Crohn’s disease are challenging because
they are at increased risk for infectious complications although biopsies will frequently
show non-specic colitis so that it is very
important to ask for special, pathogen specic
staining.
58 Colonic Conditions: Infectious Colitis
445
N. Supportive care for patients with infectious
colitis can range from IV uid and electrolyte replacement in patients with dehydration
to ICU care with mechanical ventilation and
vasopressor support in patients with multiple
organ system failure (see Algorithm 3). In
patients with mild diarrhea/colitis, oral rehydration should be encouraged. Appropriate
isolation and hand hygiene, especially in
patients admitted to the hospital, should also
be instituted depending on the pathogen.
Contact isolation and hand washing with
soap and water in patients with diarrhea due
to CDI is critical to decrease the risk of nosocomial transmission. See Table58.2 for specic antimicrobial therapies (if indicated)
depending on the type of pathogen.
See Algorithm inFig. 58.2
A. Presenting symptoms include the onset of
diarrhea (>3 loose, frequent stools per day),
fever, loss of appetite, nausea and abdominal
pain with distension and/or abdominal
cramping/bloating.
B. A change in vital signs may be absent entirely
or only include fever early in the clinical course
versus the other end of the spectrum with more
fulminant infection leading to systemic sepsis
and hemodynamic instability requiring vasopressor support (see Table58.4).
C. Severe CDI frequently causes leukocytosis
and WBC count >35,000cells/mm3 is associated with severe and complicated infection.
Leukopenia with WBC count <2,000 cells/
mm3 may also be seen in severe and complicated disease. Patients with severe CDI
should have additional laboratory evaluation
including measurements of electrolytes and
renal function (serum creatinine), albumin
(<3 g/dl in severe disease) and lactate
(>2.2mmol/l in severe and complicated disease). The CDI severity scoring system is
presented in Table58.4.
D. Underlying illnesses including renal failure
and malignancy places patients at increased
risk for CDI.Immunosuppressed patients are
at increased risk for severe infection including
transplant recipients, patients receiving chemotherapy, and patients with HIV/AIDS.HIV/
AIDS patients who require emergent subtotal
colectomy have a dramatically increased mortality rate up to 100% in one series.
E. There is no established preferred test for the
diagnosis of CDI as the diagnostic testing
available varies based on the institution and
lab. It is important that only stools from
patients with diarrhea (not formed or semiformed stool) be tested for C. difcile toxin.
Fig. 58.2 Algorithm for evaluation and management of patients with C. difcile infection
446
W. C. Cirocco and S. R. Day
F. The guidelines for the diagnosis, treatment
and prevention of CDI from 2013 recommend the use of nucleic acid amplication
tests for C. difcile toxin such as PCR for the
diagnosis of CDI over toxin A + B Enzyme
Immunoassay (EIA).
G. Glutamate dehydrogenase (GDH) EIA
screening tests can be used as part of an algorithm with subsequent toxin A + B EIA
testing.
H. Cell culture cytotoxicity assay is typically a
send out test but may be helpful clinically in
patients with multiple potential causes of
diarrhea and colitis, including patients with
underlying IBD.A positive C. difcile cytotoxicity assay indicates that the diarrhea is
due to CDI while a negative test suggests
another etiology may be the primary cause of
the diarrhea.
I. C. difcile culture alone is not sufcient to
diagnose CDI since not all strains of C. dif-
cile produce toxin.
J. Imaging studies such as abdominal plain
lms may show increased dilation of the
colon. A CT scan of the abdomen may also
reveal colon wall thickening, perhaps
‘ascites’ (more accurately, exudative uid
from the colon) or even perforation in later
stages.
K. Flexible endoscopy may reveal the presence
of pseudomembranes on direct visualization (the origin of the moniker ‘pseudomembranous colitis’, the original name
attached to CDI). The presence of pseudomembranes is not always identied and is
not required in order to establish a diagnosis of CDI.Biopsy will merely conrm the
presence of colitis of a non-specic inammatory origin. Underlying IBD (UC or
Crohn’s disease), will further complicate
the work-up, establishment of a diagnosis
and potential treatment. Patients on chronic
immunosuppressive therapy (IBD, transplant, cancer patients or patients on chronic
steroid therapy) may prove especially
challenging.
L. Discontinuation of systemic antibiotics, if
possible, is the cornerstone of the management of CDI. If antibiotics are required for
management of a concurrent infection, a prolonged course of CDI treatment may be indicated. The use of any anti-peristaltic agents
should be avoided because this may prolong
CDI and perhaps even precipitate the development of toxic megacolon. Discontinuation
of PPIs and H2 Blockers, if possible, is especially important to reduce the risk of recurrent CDI.
M. Fecal microbiota transplant (FMT) should be
considered for patients with ≥2 episodes of
CDI who have failed maximal medical therapy which typically includes either a prolonged taper of oral vancomycin or rifampicin
(Table 58.5). Indications, contraindications
as well as preparation and post FMT management are presented in Table58.6.
Table 58.5 Medical management of C. difcile
infection
Clinical
denition Medical management
Initial
episode,
mild
disease
Initial
episode,
moderate
disease
Initial
episode,
severe
disease
First
recurrence
Second
recurrence
Vancomycin 125 mg PO QID×10–14
days or Fidaxomicin 200 mg PO
BID×10 days
Vancomycin 125mg PO
QID×10–14days or Fidaxomicin
200mg PO BID×10days
Vancomycin 500mg PO four times
daily plus Metronidazole 500mg IV
Q8h or Fidaxomicin 200mg PO
BID×10days plus Metronidazole
500mg IV Q8h
Consider surgery for patients with ileus
Vancomycin 125mg PO×10–14days
or Fidaxomicin 200mg PO
BID×10days for rst recurrence
Fidaxomicin 200mg PO BID×10days
or Vancomycin 125mg PO tapered
regimen (four times daily×14days,
then BID×7days, then daily×7days,
then every other day×7days, then
every 3days×14days, then stop) or
consideration for fecal microbiota
transplant (FMT) (Table58.6)