Toxic Megacolon

Toxic megacolon is rare, but it’s an emergency. It can happen when you have a severe
case of colitis, inflammation in your colon. Inflammation that penetrates to the muscles
in your colon causes them to stop working. Food and gas build up inside, your colon
walls widen and stretch, and toxins begin to leak out into your bloodstream

 What is toxic megacolon?

Toxic megacolon is a rare but serious complication of severe colitis. Colitis is
inflammation in your colon (large intestine). Colitis typically affects the mucous
lining of your intestine. But severe and prolonged inflammation can eventually
spread to the deeper layers of your colon, including the muscles. This can begin
to break down the structural integrity of your colon.
Deep inflammation disables the muscles in your colon wall that contract to move
substances through. It causes those substances (food and gas) to build up in
your colon while the walls weaken, stretch and widen (dilate). Ultimately, toxic
substances build up inside your colon and leak through the weakened walls into
your bloodstream. This causes systemic toxicity.

 What is the difference between toxic megacolon and other types of

megacolon?
Other conditions can cause your colon to become blocked and backed up with
food and gas, stretching and widening the walls. Large intestinal
obstructions and pseudo-obstructions may cause megacolon. However, systemic
toxicity may not always occur. Inflammatory and infectious colitis are often more
associated with systemic toxicity, resulting in symptoms such as low blood
pressure, fast heart rate and altered mental status.

 What are the possible complications of toxic megacolon?

Toxic megacolon is a medical emergency that puts you at risk of several life-
threatening complications, including:
 Gastrointestinal perforation/rupture.
 Severe gastrointestinal bleeding and blood loss.
 Systemic infection and sepsis.
 Abdominal compartment syndrome.

 How does toxic megacolon cause death?

Weakened and stretched colon walls are especially vulnerable to tearing. A
perforation or rupture in your colon wall could lead to serious internal bleeding
and infection in your abdomen (peritonitis). This can quickly spread to your
bloodstream and puts you at risk of toxic shock. Severe abdominal pressure can
also cause organ failure by depriving your organs of blood and oxygen.

 SYMPTOMS AND CAUSES

 What are the symptoms of toxic megacolon?
Symptoms may include:
 Diarrhea (often bloody).
 Abdominal pain and tenderness.
 Distended abdomen.
 Gas and gas pain.
 Nausea and vomiting.
 Dizziness.
 Dehydration.
 Rapid heart rate.
 Fever.
 Low blood pressure.
 Mental confusion.
 Fatigue/malaise.

 What is the most common cause of toxic megacolon?

Technically, any type of colitis can lead to toxic megacolon if it’s severe enough.
However, it’s most commonly associated with inflammatory bowel disease (IBD).
IBD is an umbrella term for several conditions that cause chronic and incurable
colitis. IBD that isn’t well managed with diet and medication is more likely to
eventually penetrate to the deeper layers of your colon.
 What causes toxic megacolon?
Toxic megacolon is a complication of severe colitis, which can have many
causes. There are many different types of colitis that may lead to toxic
megacolon, including:

 Ulcerative colitis. Ulcerative colitis is one of the most common types of

inflammatory bowel disease, and one of the most common causes of toxic
megacolon. Most cases occur within the first few years after diagnosis.
 Crohn’s disease. Crohn’s disease is another type of inflammatory bowel
disease. It more often affects your small intestine, but can also affect your colon
(large bowel). Crohn’s disease is highly susceptible to toxic megacolon in its
early stages.
 Ischemic colitis. Ischemic colitis is a side effect of intestinal ischemic
syndrome, which is when your intestines aren’t getting enough blood supply. As
this is a relatively difficult problem to solve, ischemic colitis has the opportunity to
advance to toxic megacolon.
 Radiation colitis. Colitis or enteritis is usually a short-term side effect
of radiation therapy, but some people develop chronic symptoms that can lead to
complications.
 Infectious colitis. Infections from bacteria, parasites or viruses can cause colitis.
Certain types may affect certain people more severely. Common food
poisoning and stomach flu infections can cause severe colitis in some people.
Those with compromised immune systems are especially vulnerable
to cytomegalovirus.
 Pseudomembranous colitis. The bacterium C. diff (clostridioides difficile)
causes this type of infectious colitis. Pseudomembranous colitis is often
mentioned as a risk for toxic megacolon. The infection commonly affects people
 taking antibiotics for a separate infection. The antibiotics kill helpful bacteria in
your gut that usually keep the C. diff bacterium in check, allowing C. diff to run
wild. C. diff infection can become severe very quickly.

 What risk factors contribute to toxic megacolon?

You may be more likely to develop toxic megacolon if you have:

 Inflammatory bowel disease.

 Autoimmune disease.
 HIV/AIDS.
 An organ transplant or take immunosuppressants.
 Diabetes.
 Kidney disease.
 Chronic obstructive pulmonary disease.
 Congestive heart failure.

Certain medications that you may be taking can make conditions worse for toxic
megacolon, including:

 Opioids.
 NSAIDs.
 Antidepressants.
 Anticholinergics.
 Antidiarrheals.
 Bowel prep for colonoscopy.

 DIAGNOSIS AND TESTS

 How is toxic megacolon diagnosed?

Your healthcare provider will ask you about your symptoms and your complete history
of health conditions and medications. Certain conditions or medications may make toxic
megacolon more likely. Some medications, such as steroids, may mask the symptoms
of toxic megacolon. They’ll examine you physically before moving on to more specific
tests.

Your physical exam may show a swollen abdomen, abdominal tenderness and an
overall appearance of toxic illness. Your healthcare provider may listen to your bowel for
decreased bowel sounds resulting from decreased movement. They’ll take your vital
signs to check for fever, low blood pressure and fast heart rate, which are all signs of
toxicity.

Your provider will also need to take a blood test and imaging test of your abdomen to
confirm your diagnosis. Imaging may mean an X-ray, an abdominal ultrasound or a CT
scan. They’ll be looking for colon dilation and any related complications. The blood
test will show evidence of deep inflammation by counting your red and white blood cells.
The criteria to diagnose toxic megacolon include:

 Evidence that your colon dilation is greater than 6 centimeters.

 At least three of the following:
o Fever over 100.4 degrees Fahrenheit (38 degrees Celsius).
o Heart rate greater than 120 beats per minute.
o High white blood cell count.
o Anemia (low red blood cell count) .
 At least one of the following:
o Dehydration.
o Electrolyte/fluid imbalance.
o Altered mental status.
o Low blood pressure.

In addition, your healthcare provider may want to test your blood or your poop for
specific infections.

 MANAGEMENT AND TREATMENT

 What is the treatment for toxic megacolon?

You’ll need treatment in the hospital for a few days. The goal of initial treatment is to
stabilize your condition and reduce the severity of your colitis. If you have sepsis, you
may need critical care, such as mechanical ventilation for respiratory failure
or dialysis for kidney failure. Otherwise, treatment for toxic megacolon will typically
begin with:

 IV fluids for rehydration and electrolyte replacement.

 Antibiotics to treat or prevent infections.
 Corticosteroids for inflammation.
 Bowel rest with enteral nutrition (tube feeding).

If your condition doesn’t improve with steroids, your provider may try another type of
medication, such as an immune modulator. This may help reduce the overactive
immune response that’s causing too much inflammation and too many white blood
cells in your tissues.

Surgery

About 50% of people may be successfully treated with medication alone. Others will
need surgery, especially if there are life-threatening complications involved. Healthcare
providers consult surgeons early on when someone has toxic megacolon to help in the
decision-making. Your healthcare provider may judge that it’s safer to remove the
affected portion of your colon to prevent further risk or complications. When you have
a colectomy, you’ll probably need an ostomy as well.
An ostomy is an opening in your abdomen. Poop exits your body through the ostomy
when your intestines aren’t working the way they should. You may need a temporary or
permanent ostomy, depending on what kind of colectomy you have. Whether short-term
or long-term, an ostomy can be a big adjustment to process, especially in an emergency
setting.

 OUTLOOK / PROGNOSIS
 Can you survive toxic megacolon?

Your chances are good if you seek treatment soon enough. The overall survival rate for
those treated for toxic megacolon is around 93%. Those who have complications, such
as a perforation, have a survival rate closer to 75%. Complications mostly occur when
toxic megacolon goes untreated for too long, so it’s important to recognize the
seriousness of your condition.

 A note from Cleveland Clinic

Toxic megacolon is a medical emergency that can develop quickly and unexpectedly.
It’s more of a risk if you’ve been recently diagnosed with inflammatory bowel disease
and the disease isn’t yet managed. But it can also happen during an acute infection, or
in other cases of severe colitis. Pay attention if your usual symptoms begin to worsen or
change.

If you begin to feel generally ill and toxic during severe colitis, seek medical attention
right away. Early management is key to preventing life-threatening complications, and it
may prevent the need for surgery. If you do need an emergency colectomy and ostomy,
know that you’ll have ample support to help you adjust to these changes going forward.

SHOW MORE
When toxins damage your enzymes, they prevent the production of hemoglobin in your
blood, which can accelerate aging. It also can lead to the failure of energy production
and lower your protection against oxidated stress. Failure of these normal body
functions increases your risk of diseases like: Cancer.

What are the different parts of the large intestine?

The large intestine is one long tube, but slightly different things happen in different parts of it.
Its three parts are the colon, the rectum and the anus. The colon can also be divided into parts.
The entry point, about six inches long, is called the cecum. The rest of the colon is divided into
segments: the ascending colon (traveling up), the transverse colon (traveling across to the left),
the descending colon (traveling down) and the sigmoid colon (headed back across to the right).
Because there is no real division between the parts, people divide up the large intestine
differently in their minds. Some people think of the large intestine as everything but the anus.
They might say the three parts of the large intestine are the cecum, the colon and the rectum.
Or they might call it the colon, but mean the same thing: the cecum, the rest of the colon and
the rectum. Here we consider the cecum part of the colon, and everything part of the large
intestine.

A person may develop toxic megacolon if they have colon inflammation due to conditions such
as Crohn’s disease, or ulcerative colitis, or infections such as C. difficile. The colon may expand
rapidly, which can prevent gas and feces from leaving the body. This can result in a colon
perforation, which can be fatal.

Depending on the severity and progression of the condition, a doctor or healthcare professional
may treat a person with medication in hospital, such as antibiotics and IV fluids. If a person
requires surgery, a surgeon may remove part of the colon.

Toxic megacolon is a medical emergency, and anyone with symptoms should seek medical
attention immediately. The outlook for the condition is significantly better for people who
receive early diagnosis and treatment.

Megacolon: What Is It, Causes, Symptoms, Treatment, and More

What Is Megacolon?

Megacolon is an abnormal dilation of the colon that is not caused by mechanical obstruction. It is
usually accompanied by symptoms such as abdominal discomfort, but may result in serious
complications (colonic perforation, peritonitis, and/or sepsis) if left untreated.

Types of megacolon

Megacolon can be classified as acute or chronic depending on whether the dilation is temporary
or ongoing. All cases of acute megacolon are acquired, whereas chronic megacolon can be both
acquired or congenital.

Acute megacolon can be further categorized depending on whether there is inflammation of the
colon. If inflammation is present, this usually results in systemic toxicity, so the resulting
condition is referred to as toxic megacolon. If no inflammation is present, the resulting condition
is referred to as Ogilvie syndrome, or just acute megacolon.
What Causes Megacolon?

Megacolon has a wide range of causes, including infection, disease, medication, and various
congenital disorders. It may also occur following a major surgery; however, the condition is
often idiopathic, which means the exact cause is not known. 

Infection

One of the most common causes of megacolon is infection. This includes bacterial infections
such as Clostridium difficile, Salmonella, Shigella, and Campylobacter, as well as parasitic
infections such as Trypanosoma cruzi (commonly known as Chagas disease) and Entamoeba
histolytica.

Disease

Megacolon can also be caused by a variety of neurological and systemic diseases. Common
neurological causes are diabetic neuropathy and Parkinson's disease, while systemic causes
include some muscular dystrophies, scleroderma, and systemic lupus erythematosus.

Medication

In rare cases, megacolon may be the adverse effect of a medication. Most notably, drugs such as
risperidone, clozapine, and loperamide are associated with increased risk of megacolon.

Congenital disorders

Megacolon can also be caused by some congenital disorders, as is true in the case of
Hirschsprung’s disease, where functional obstruction of the intestines is often observed.

Other

Other possible causes of megacolon include electrolyte imbalances (e.g. hypokalemia) and
hypothyroidism.

Pathophysiology

The exact mechanism by which megacolon develops is not known. However, the end result is the
same: severely decreased intestinal motility causes a buildup of feces, air, and intestinal
secretions in the colon, which presents as dilation of the colon.

There are several suggested mechanisms by which intestinal motility might be decreased:

 In acute, non-toxic megacolon, there is damage to the autonomic nervous system

  In chronic megacolon, there is inherent neurological and/or muscular dysfunction in the
bowels

 In toxic megacolon, there is reduced smooth muscle activity, likely as the result of
inflammation. This may be related to increased nitric oxide synthesis.

What Are the Symptoms of Megacolon?

Common symptoms of megacolon include constipation, bloating, and abdominal pain or

tenderness. In more severe cases, hard fecal masses called fecalomas may also be present.

Depending on the cause, megacolon may have additional symptoms. In toxic megacolon, usually
caused by infection, additional symptoms include fever, tachycardia, and shock. In disease-
related cases of megacolon, additional symptoms are those of the disease itself.

How Is Megacolon Diagnosed?

Megacolon can be diagnosed by observing the size of the colon on an abdominal x-ray scan.
Most physicians agree that a colon diameter greater than 12 centimeters at the cecum should be
classified as megacolon.

A contrast enhanced CT scan is used to confirm these findings, additionally showing the colon is
free of mechanical obstruction.If a CT scan is not possible, colonoscopy can be performed to
verify the colon is free of mechanical obstruction. However, in toxic megacolon, colonoscopy
should not be performed due to high risk of perforating the colon.

How Is Megacolon Treated?

Treatment for megacolon starts by addressing the underlying cause (such as the offending
medication or disease), if known. In acute megacolon, all food and drink should be withheld and
a nasogastric tube placed. If non-toxic, neostigmine should be administered, and if necessary, the
colon itself should be decompressed by means of a colonoscopy. If toxic, steroids and broad
spectrum antibiotics should be given.

In chronic megacolon, both dietary and pharmacological methods should be used to increase
intestinal motility. Laxatives and enemas may also be used to prevent fecal impaction.

If the patient does not respond to these treatments within one to three days, it may be necessary
to use surgery to remove all or part of the colon. Following colectomy, options include ileorectal
anastomosis and ileostomy.

Is megacolon reversible?

In most cases, megacolon is reversible. This depends on whether it is possible to treat the
underlying cause. In acute and toxic megacolon, the underlying cause can usually be treated or
otherwise resolves itself naturally, so dilation of the colon is reversed. However, chronic
megacolon involves a progressive or congenital pathophysiology that cannot be resolved.

Summary

Megacolon is an abnormal dilation of the colon that can be categorized as acute, toxic, or
chronic. Acute megacolon, also known as Ogilvie syndrome, is associated with damage to the
autonomic nervous system and often occurs in ill or postoperative patients with no clear cause.
Toxic megacolon is characterized by concurrent systemic toxicity, usually as the result of colon
inflammation following an infection. Chronic megacolon is caused by bowel dysfunction as a
result of neurological or muscular disorders.

In all three types, symptoms include constipation, bloating, and abdominal pain. Diagnosis of
megacolon relies on the use of x-ray and CT scans, and a variety of treatment options can be
employed depending on the cause and nature. In rare cases, surgery may be needed to treat
megacolon.

Inflammatory bowel diseases are mainly broken down into two autoimmune conditions
- ulcerative colitis and Crohn's disease - both of which cause chronic inflammation in
the gastrointestinal tract.

Ulcerative colitis mostly appears in individuals aged from 20 to 30 years old.

The chronic inflammation only involves the mucosal layer of the colon or the rectum and
inflammation usually starts in the rectum and goes retrograde through the colon.

Ulcerative colitis can involve only the rectum, in which case it’s called ulcerative proctitis, can
involve the rectum and the sigmoid colon - called ulcerative proctosigmoiditis, or can involve
the rectum, sigmoid colon and the colon up to the splenic flexure - called distal ulcerative colitis.
In some cases, it can also pass the splenic flexure, but spare the cecum - called extensive colitis
and finally it can involve the entire colon including the cecum - called pancolitis.

The onset of the disease is gradual and symptoms are progressive over a few weeks. There may
be systemic symptoms, such as fatigue, fever, unintentional weight loss, as well as dyspnea and
palpitations due to iron deficiency anemia caused by blood loss.

Gastrointestinal symptoms include bloody diarrhea, colicky abdominal pain, and tenesmus.

Systemic toxicity refers to toxic effects that occur when a toxic substance is carried
to distant locations in the body, causing an adverse effect 123. Systemic toxicity is
typically evaluated in studies of acute, sub-acute, sub-chronic, and chronic duration
based on the device’s intended exposure1. Symptoms of systemic toxicity may include
CNS excitement, such as circumoral and/or tongue numbness, metallic taste,
lightheadedness, dizziness, visual and auditory disturbances, disorientation, and
drowsiness4.

Intestinal ischemia
Intestinal ischemia is a medical condition in which injury to the large or small intestine
occurs due to not enough blood supply. It can come on suddenly, known as acute
intestinal ischemia, or gradua…
TOXIC MEGACOLON

Background
Toxic megacolon is a life-threatening condition characterized by nonobstructive
segmental or pancolonic dilatation of at least 6 cm with systemic toxicity.  [1] It was
recognized by Marshak and Lester in 1950. [2] Although inflammatory bowel disease
(IBD) is a common reason for toxic megacolon, other etiologies including infections,
inflammation, bowel ischemia, radiation, and certain medications can lead to the
development of this condition. 

Toxic Megacolon. A 22-year-old man presented with abdominal pain, passage of blood
and mucus per rectum, abdominal distention, fever, and disorientation. Findings from
sigmoidoscopy confirmed ulcerative colitis. Abdominal radiographs obtained 2 days
apart show mucosal edema and worsening of the distention in the transverse colon. The
patient's clinical condition deteriorated over the next 36 hours despite steroid and
antibiotic therapy, and the patient had to undergo a total colectomy and ileostomy.

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 To
xic Megacolon. Gross pathology specimen from a case of pseudomembranous colitis
demonstrating characteristic yellowish plaques.

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To
xic Megacolon. Computed tomography scan from a patient with pseudomembranous
colitis demonstrating the classic accordion sign.

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It is important to differentiate toxic megacolon from other conditions that present with
megacolon without systemic toxicity such as Hirschsprung disease,  [6] idiopathic
megacolon/chronic constipation, chronic long-standing constipation of any etiology,
and intestinal pseudo-obstruction (Ogilvie syndrome). [1]  Patients with these conditions
do not develop signs of systemic toxicity and, therefore, do not fall into the category of
having toxic megacolon (see the image below). (See also Etiology, Presentation,
and Workup.)

Toxic Megacolon. A 72-year-old woman presented with vomiting and abdominal

distention. The supine (right) and erect (left) plain abdominal radiographs show gross
dilatation of the colon with multiple air-fluid levels. On further questioning, the patient
revealed that she was taking diuretics for hypertension. Blood biochemical tests
revealed markedly lowered potassium levels. After potassium replacement therapy, the
patient's pseudo-obstruction completely resolved.

Toxic Megacolon

Pathophysiology

Although the precise pathophysiology of toxic megacolon is unproven, several factors

may contribute to its development and precipitation. In cases of uncomplicated colitis,
the inflammatory response is confined to the mucosa. The microscopic hallmark of toxic
megacolon is inflammation extending beyond the mucosa into the muscularis propria.
Whereas the typical ulcerative colitis inflammatory response is limited to the mucosa,
toxic megacolon is characterized by severe inflammation extending into the smooth
muscle layer, thus paralyzing the colonic smooth muscle and leading to dilatation. The
extent of dilatation seems to be correlated with the depth of inflammation and
ulceration. [1]
Studies by Mourelle et al showed significantly increased amounts of inducible nitric
oxide (NO) synthetase in the muscularis propria of patients with toxic megacolon,
particularly in the more dilated colonic segments.  [7, 8, 9]
As inflammation progresses into the smooth-muscle layers of the colon, NO and local
inflammatory modulators appear to be involved in toxic megacolon pathogenesis.
Neutrophils invade the muscle layer in toxic megacolon and directly damage the
myocytes by the release of proteolytic enzymes, cytokines, and leukotriene B 4.
Systemic uptake of cytokines and other inflammatory mediators leads to fever,
tachycardia, hypotension, and other signs of systemic toxicity. NO is generated by
macrophages and smooth muscles cells in the inflamed portions of the colon, inhibiting
smooth muscle tone and leading to colonic dilatation.  [1]
These findings were supported by the idea that, in animal models, giving
dexamethasone and/or decontaminating the bowel with broad-spectrum antibiotics led
to decreased NO levels and improvement in colonic dilatation.  [8] According to a study by
Schworer et al, patients with toxic megacolon were successfully treated with NO
synthase inhibitor. [10]
A number of other precipitating factors have been identified, including antimotility
agents, opiates, anticholinergics, antidepressants, barium enemas,
colonoscopies/bowel preparations, and immunotherapies.  [5, 11, 12]
Myenteric plexus involvement is not consistent and likely does not contribute to colonic
dilatation.

Etiology

Inflammatory causes of toxic megacolon include the following:

 Ulcerative colitis [4, 13]
 Crohn colitis [14]
Infectious causes of toxic megacolon include the following:
 Salmonella species [15]
 Shigella species [16]
 Campylobacter species [17]
 Yersinia species
 Clostridium difficile [18, 19, 20]
 Entamoeba histolytica: About 3% of patients with amoebic infections
develop severe colitis and a small percentage of these will have toxic
megacolon; use of loperamide in this setting increases the risk of developing
toxic megacolon [21]
 Cryptosporidium [22]
 Cytomegalovirus [23]
 Rotavirus [24]
 Invasive aspergillosis [25]
Other etiologies of toxic megacolon include the following:
 Radiation colitis
 Ischemic colitis
 Nonspecific colitis secondary to chemotherapy [11, 26, 27]
 (Rarely) As a complication of collagenous colitis  [28, 29]
 Behçet syndrome: Rarely, affected patients can develop toxic megacolon as
a complication [30, 31]
 Kaposi sarcoma [1]
 Methotrexate therapy [32]
Often, triggering or predisposing factors can be identified. Signs and symptoms of acute
colitis may be present for as long as 1 week before dilatation develops. Although the
risk of toxic megacolon increases with the severity of the colitis, rapid tapering or abrupt
discontinuation of medications such as steroids, sulfasalazine, and 5-aminosalicylic acid
may precipitate toxemia and dilatation.
Medications that negatively impact bowel motility are also implicated in the development
of toxic megacolon. These include, but are not limited to, anticholinergics,
antidepressants, loperamide, atropine, [5] and opioids. Procedures such as barium
enema or colonoscopy may cause distention, impair blood supply, or exacerbate a
microperforation and cause subsequent toxemia.  [12]
A retrospective study by Tschudin-Sutter et al indicated that the incidence of toxic
megacolon is higher in pediatric patients with community–associated, rather than
healthcare facility–associated, C difficile infection. [33] The study involved 202 pediatric
patients with C difficile infection, including 38 with community–associated infection, 144
with healthcare facility–associated infection, and 20 with an indeterminate source of
infection. Compared with the healthcare facility–associated group, children with a
community–associated infection had a higher rate not only of toxic megacolon but also
of toxic shock and recurrence. (They were less likely, however, to have comorbidities
than were children with healthcare facility–associated infection.)  [33]

Epidemiology
There is a lack in literature regarding accurate reporting of toxic megacolon prevalence.
The incidence rates can change based on the main etiology. The risk of developing
toxic megacolon can increase with older age and/or the presence of other risk factors
such as hypertension, neurologic disorders, coagulopathy, anemia, chronic pulmonary
disease, congestive heart failure, and renal failure.  [34, 35]
Doshi et al reported the results of an analysis of data collected from the Nationwide
Inpatient Sample database from January 2010 through December 2014: The most
common cause of hospital admissions was inflammatory bowel disease (IBD) (51.6%),
followed by septicemia (10.2%) and intestinal infections (4.1%).  [34, 36]
Three decades ago, the incidence of toxic megacolon in IBD patients was
approximately 1-5%. [14] However, this rate has diminished due to early recognition and
intensive medical management of severe colitis. Unfortunately, the data on the
incidence of toxic megacolon in ulcerative colitis versus Crohn disease are
contradicting; some studies show a higher incidence in patients with Crohn disease
compared to those with ulcerative colitis (1-2.5% ulcerative colitis; 4.4-6.3% Crohn
disease), [14] whereas others report the opposite.  [4, 37]
The incidence of toxic megacolon in patients with C difficile colitis rapidly increased from
0.4% to 3% before 1990 to 4.3% after 1990, due to the rising use of broad spectrum
antibiotics and the development of a hypervirulent Crohn disease strain.  [4, 35, 37]

Prognosis
Toxic megacolon mortality is variable depending on the treatment modality. One study
revealed that before 1976, there was a 27% mortality of toxic megacolon among
patients treated medically and a 19% mortality in patients treated surgically.  [38] In-
hospital mortality for patients with toxic megacolon fell from 9.2% to 6.5%, according to
an observational study for the period between 2010 and 2014.  [35] Older age,
hypertension, neurologic disorders, coagulopathy, anemia, chronic lung disease, heart
failure, and renal failure were the main predictors of increased mortality.  [35]
Colon perforation is associated with higher surgical mortality relative to undergoing
surgery before colonic perforation. [34, 38]  Similarly, postoperative mortality in patients
with C difficile infection and toxicity is lower when they undergo surgery before the
development of septic shock compared to septic patients who have surgery.  [39]
Fecal microbiota transplantation has shown promise as a salvage therapy for critically ill
patients with C difficile infection and toxic megacolon in whom maximum medical
therapy failed and who are not a surgical candidates.  [40]
Mortality in patients with inflammatory bowel disease (IBD) and toxic megacolon have
fallen in the last 3 decades due to multiple factors, including early recognition of toxic
megacolon, early escalation from steroid treatment to biologics such as infliximab or
cyclosporine, improved care in the intensive care unit (ICU), earlier surgical intervention,
and optimal postoperative care. [41]
Note that C difficile infection in patients with IBD are associated with higher rates of
colectomy and longer hospital stays compared to IBD patients without C
difficile infection. [42]

Patient Education

Educating patients about toxic megacolon, is crucial. First, educate the patient about the
causes of the disease, of which the most common is inflammatory bowel disease (IBD).
However, with the rising incidence of C difficile infections, pseudomembranous colitis
must always be considered, even in patients with IBD. Educate patients about ulcerative
colitis, Crohn disease, and indeterminate colitis.
Also discuss with patients that medications such as corticosteroids,
immunosuppressants, and/or immunomodulators may be administered to control the
disease severity and that antibiotics may be used to prevent or treat infection. Inform
patients of the potential risks and benefits of these agents as well as those that can
exacerbate their condition (eg, opioids, antidepressants, nonsteroidal anti-
inflammatories, antidiarrheals, anticholinergics.)
Secondly, clearly inform patients that if an operation is required for this acute problem,
an ostomy likely will be the necessary procedure, regardless of the cause. Patients
require at least a temporary and, possibly, a permanent ostomy. Provide a thoughtful,
compassionate discussion regarding this aspect of their treatment: The psychological
aspects of dealing with an ostomy can be extremely difficult.
Finally, educate patients so that they understand that this disease may require several
months to overcome if an operation is needed and that a two- or three-stage procedure
is usually required.
.
Toxic Megacolon Clinical Presentation
History
Patients with inflammatory bowel disease (IBD) are at a higher risk of developing toxic
megacolon during the early stages of their disease; in some cases, it can be the first
manifestation of the disease. [43, 44] Patients with Crohn colitis are more vulnerable than
those with ulcerative colitis for developing toxic megacolon.  [14]
Findings of ileus may indicate the severity of colitis in patients with C
difficile infection. [45]
Patients with toxic megacolon typically have signs and symptoms of acute colitis that
may be refractory to treatment. Common complaints include diarrhea, abdominal pain,
rectal bleeding, tenesmus, vomiting, and fever. In a paper that studied the clinical
presentation of pseudomembranous enterocolitis complicated with toxic megacolon, the
presenting symptoms and signs included diarrhea (100%), malaise (91%), abdominal
pain (82%), abdominal distention (82%), and abdominal tenderness (72%).  [46] However,
another study revealed that absence of diarrhea does not rule out the severity of the C
difficile infections and the risk of developing toxic megacolon.  [47]
A careful history may reveal recent travel, antibiotic use, chemotherapy, occupational
exposure, or immunosuppression. Patients are usually very ill, and they can present
with signs of fever, tachycardia, hypotension, and/or abdominal distention and
tenderness.

Physical Examination
The vital signs in a patient with toxic megacolon generally reveal tachycardia and fever.
If the condition is severe, the patient may be hypotensive or tachypneic; patients may
be obtunded.
In inflammatory colitides (ie, ulcerative colitis, Crohn colitis), physical findings may be
minimal, because high-dose steroids are routinely administered; however, the abdomen
may be distended, and the bowel sounds are usually hypoactive. Signs of perforation
may also be masked by high-dose steroids.
Peritoneal signs may indicate perforation. They include the following:
 Rebound
 Rigidity
 Peritoneal irritation

Diagnostic Considerations
As noted earlier, it is important to differentiate toxic megacolon from other conditions
that present with colon dilatation without systemic toxicity (eg, Hirschsprung
disease, [6] idiopathic megacolon/chronic constipation, chronic long-standing constipation
of any etiology, and intestinal pseudo-obstruction [Ogilvie syndrome]). [1]  Patients with
these conditions do not develop signs of systemic toxicity and, therefore, do not fall into
the category of having toxic megacolon.
Differential Diagnoses
 Acute Colonic Pseudoobstruction (Acute Megacolon, Ogilvie Syndrome)
 Appendicitis
  Chagas Disease (American Trypanosomiasis)
 Chronic Megacolon
 Colitis
Including ischemic, infectious, pseudomembranous, ulcerative, etc.
 Crohn Disease
 Cytomegalovirus (CMV)
 Cytomegalovirus Colitis
 Diverticulitis
 Hirschsprung Disease
 Idiopathic or acquired megacolon due to chronic constipation
 Intestinal Pseudo-Obstruction
 Ischemic Colitis
 Large-Bowel Obstruction
Due to luminal obstructing mass or any mass causing external pressure
 Sigmoid and Cecal Volvulus
 Small-Bowel Obstruction
 Ulcerative Colitis

Approach Considerations
In general, toxic megacolon should be suspected in patients presenting with abdominal
pain with distention and acute-onset chronic diarrhea. The diagnosis is made based on
the clinical picture of systemic toxicity along with evidence of colon dilatation more than
6 cm. [4]
The most common criteria used to diagnose toxic megacolon are the ones proposed by
Jalan et al in 1969, [43] as follows:
 Radiographic evidence of colonic dilatation: The classic finding is a more than 6-
cm dilatation in the transverse colon
 Any three of the following: Fever (>101.5°F [>38°C]), tachycardia (>120
beats/min), neutrophilic leukocytosis (>10.5 x 103/µL), or anemia
 Any of the following: Dehydration, altered mental status, electrolyte abnormality,
or hypotension
Complete blood cell (CBC) count 
Patients with toxic megacolon may develop leukocytosis with a left shift. Patients can
also present with leukemoid reaction. Additionally, bloody diarrhea results in anemia.
Although the presence of an increased white blood cell (WBC) count contributes to the
diagnosis of toxic megacolon—and most investigators believe that the absence of a
high WBC count makes defining a disease as toxic megacolon difficult—an abnormally
low count, or even a WBC count that is within normal limits, does not rule out toxic
megacolon. This is because in immunosuppressed or extremely toxic patients, the WBC
count actually may be normal or low.
Chemistry panel
Electrolyte disturbances are very common in toxic megacolon secondary to
inflammatory diarrhea, steroid use, and ongoing gastrointestinal losses. The inflamed
colon is unable to reabsorb salt and water. Acid-base disorders have been described
(eg, metabolic alkalosis) with the large volume loss.  [48] Metabolic acidosis can occur with
advanced disease and the development of bowel ischemia.
Nutrition and coagulation panels
A coagulation panel should be ordered in the event that surgery is required. A nutrition
panel, in accordance with the physician's practice, is helpful in assessing the patient's
nutritional status. Hypoalbuminemia is common at the later stages of the disease due to
protein wasting, decreased hepatic production, and severe inflammation.
ESR and CRP
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are usually
elevated. Although these findings are not specific to toxic megacolon, they may support
the diagnosis.
Histology
Pathology in cases of toxic megacolon demonstrates acute inflammation involving all
layers of the colon. Variable amounts of necrosis and degeneration are present.
Infiltration by inflammatory cells (neutrophils, macrophages, and lymphocytes) is noted.
The myenteric and submucosal plexuses are usually preserved.
Stool studies
Stool cultures, examination for ova and parasites (O&P), and as well as testing for C
difficile toxin should be obtained.

Radiography
Plain abdominal radiographs are essential for the diagnosis and management of toxic
megacolon. Repeated serial abdominal plain films are necessary to monitor the
progress of the disease and the efficacy of treatment.
Radiographic findings include the following:
 Air-fluid levels in the colon with an absent or abnormal haustral pattern
 Deep mucosal ulcerations and possible pseudopolyp projections into the colon
lumen
 The presence of air in the small bowel on x-ray: Can be predictive of toxic
megacolon [49]
 Segmental parietal thinning: Pathognomic for toxic megacolon  [3]
Comparison with old baseline films, if available, is helpful. Avoid barium enema studies
in a patient who is severely toxic; the potential for perforation is considerable.
The following image depicts a dilated (>6 cm) transverse colon.
 Toxic Megacolon. A 22-year-old
man presented with abdominal pain, passage of blood and mucus per rectum,
abdominal distention, fever, and disorientation. Findings from sigmoidoscopy confirmed
ulcerative colitis. Abdominal radiographs obtained 2 days apart show mucosal edema
and worsening of the distention in the transverse colon. The patient's clinical condition
deteriorated over the next 36 hours despite steroid and antibiotic therapy, and the
patient had to undergo a total colectomy and ileostomy.

Loss of colonic haustrations, possible "thumbprinting," is shown below

Toxic Megacolon. Plain abdominal radiograph from a patient with known ulcerative
colitis who presented with an acute exacerbation of his symptoms. This image shows
thumbprinting in the region of the splenic flexure of the colon.

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Severe dilatation and a featureless transverse and sigmoid colon are demonstrated in

the following image.

Toxic Megacolon. A 45-year-old woman presented with acute pain and colitis of
uncertain etiology. The radiograph shows an increase in gaseous distention of the distal
transverse colon, now measuring up to 80 mm in diameter (it was 60 mm 2 days
previous). The transverse colon and sigmoid colon are both featureless, consistent with
severe colitis. There is fecal loading in the right side of colon. No evidence of free gas or
pneumatosis intestinalis is noted. The appearance is concerning for toxic megacolon.
Courtesy of Craig Hacking, MBBS, Associate Professor, Royal Brisbane and Women’s
Hospital (Radiopaedia.org, rID: 79194).

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