Wednesday, December 30, 2015
DIARRHEA
DIARRHEA
Definition. Diarrhea is either an increased
frequency or volume of stool per day; stool can also
be defined as diarrhea if the number of stools per day is few, but their consistency is watery.
Pathogenesis. The most common
causes of diarrhea
are of an infectious, antibiotic-associated, or
lactose-intolerance etiology or from irritable bowel or carcinoid syndrome.
Clinical Presentation. The patient
is often hypotensive, febrile, and experiencing abdominal pain.
Diagnosis. The first thing to do in the evaluation of diarrhea
in terms of direct patient care is to see if there is hypovolemia as defined as
hypotension or orthostasis. This is more important than determining the
specific etiology because of the chance that the patient may die while waiting
for the results to come back.
Treatment. No matter the etiology, if the patient
is hypotensive, febrile,
and having abdominal pain, he or she should be
admitted to the hospital and given intravenous fluids and antibiot- ics. The
presence of blood in the stool is especially serious and is probably the single
strongest indication for the use of antibiotics, such as ciprofloxacin.
INFLAMMATORY BOWEL DISEASE
INFLAMMATORY BOWEL DISEASE
Inflammatory bowel disease
(IBD) is a term comprising 2 disease entities: Crohn disease (CD) and ulcerative colitis (UC).
They can be discussed simultaneously because of the large degree of overlap in terms of
presentation, testing, and treatment. Both CD and UC are idiopathic disorders of the bowel associated with diarrhea, bleeding, weight loss, fever, and abdominal
pain. Both are most accurately diagnosed with endoscopy and sometimes with barium stud- ies, “string sign” on small bowel follow through after barium meal in CD, and both are treated with
anti-inflammatory medications, such as mesalamine, azathioprine, and
6-mercaptopu- rine (6MP). Steroids
are used for acute exacerbations of both diseases.
Clinical Presentation. IBD presents with fever, diarrhea, weight
loss, and, occasionally, abdomi- nal pain and bleeding. The extraintestinal manifestations of IBD are episcleritis, scleritis and iri- tis,
sclerosing cholangitis, joint pains, and skin manifestations, such as pyoderma gangrenosum or erythema nodosum.
Crohn disease is more likely
to be associated with a palpable abdominal mass because CD has
granulomas in the bowel wall that are transmural in nature. This
can lead to the different loops of bowel being
inflamed and sticking
together, forming a mass. The abdominal masses
of CD can be palpated and
cause pain. CD is not necessarily continuous, and one hallmark of the disorder is that there are “skip lesions,”
or areas
of normal tissue
in between
the areas
of disease.
UC is
limited exclusively to the large bowel. It is exclusively a mucosal disease,
and although it can cause bleeding, it does not result in fistula formation. UC
has no skip lesions, no fistula formation, and no oral or perianal involvement.
UC is more likely to cause bloody diarrhea.
Note
Sclerosing cholangitis does not correlate to disease
activity.
Both
forms of IBD can lead to colon cancer after 8 to 10 years of involvement of the
colon. If the CD does not result in colonic involvement, then it will not lead
to cancer. Complications of Crohn
disease are calcium oxalate kidney stones, diarrhea, and cholesterol gallstones.
Diagnosis. IBD is diagnosed with endoscopy
and sometimes with barium studies. (CD can
result in deficiency of vitamin B12, calcium, vitamin K,
and iron because of malabsorption.) Anti–Saccharomyces cerevisiae antibodies (ASCA)
are associated with CD, and antineutrophil
cytoplasmic antibody (ANCA) is associated
with UC. If a patient is ASCA positive
and ANCA
negative, then he
or she has a >90% chance of
having CD. If the patient is ASCA negative and
ANCA positive, there is a >90% chance of having UC.
Prothrombin time may be prolonged in CD because
of vitamin K malabsorption. Kidney
stones form more often in CD because the fat malabsorption results in a
low calcium level and an increased absorption of oxalate, which
forms kidney stones.
Treatment. Mesalamine derivatives are the mainstay of therapy
for IBD in all of its forms. Pentasa is a form of mesalamine released in both
the upper and lower bowel; hence, it is used in CD. Asacol
is a form of mesalamine released
in the large bowel, and it is most useful
for UC. Rowasa is used
exclusively for rectal disease. Sulfasalazine was used in the past for the same
effect. The difficulty with sulfasalazine is that the high load of sulfa
delivered causes a number of
adverse effects, such as rash, hemolysis, and allergic interstitial nephritis.
Sulfasalazine also causes reversible infertility in men and leukopenia by its
sulfapyridine group.
Acute exacerbations of
IBD are treated with high-dose steroids. Budesonide is a form of steroid that is ideal for IBD. It has a strong
local effect when used orally, but is largely
cleared by the liver in
a first-pass effect.
This limits the amount of systemic
toxicity. Azathioprine and 6-mercaptopu- rine are associated with drug-induced pancreatitis, but are still used on a long-term
basis to try to
keep patients off steroids. Ciprofloxacin and metronidazole are used for CD in those with perianal disease. Infliximab is used
for CD in those who
form fistulae or have disease refractory to the other
forms of therapy. There has
been re-activation of tuberculosis with infliximab, and
it is important to test for latent tuberculosis with a purified
protein derivative (PPD) prior to treatment. If the PPD
is positive, then patients should receive
isoniazid. The most
common side effect of infliximab
is arthralgias. Balsalazide and olsalazine are other
forms of mesalamine that are only active in the colon and are used occasionally.
Surgery is curative in UC; almost 60% of patients will require
surgery within
5 years after diagnosis due to refractory symptoms or severe disease.
Surgery is not very effective in CD and disease
tends to reoccur at the site of
anastomosis.
Nonulcer Dyspepsia
Nonulcer Dyspepsia
When all the causes
of epigastric pain have been excluded and there is still
pain, the diagnosis is functional or nonulcer dyspepsia. There is no specific
therapy for nonulcer dyspepsia known
to cure the
disorder. Antacids
of various types
from H2 blockers to liquid antacids to PPIs are tried
until something is found to relieve
the discomfort. The cause
of nonulcer dyspepsia
is unknown.
Treatment of Helicobacter pylori in nonulcer dyspepsia is of equivocal value.
If there is no response to anti-secretory therapy with a PPI, you can try to treat H. Pylori
by adding clarithromycin and amoxicillin. Treating H. Pylori will improve
symptoms in another
10–20% of patients.
Dumping Syndrome
Dumping Syndrome
Pathogenesis. This
is an increasingly rare disorder because of the rarity of the necessity for
surgery in the treatment of ulcer disease. It was far more common in the past,
when vagotomy and gastric resection were performed to treat severe ulcer disease.
Dumping
syndrome is caused by two phenomena. First, there is the rapid release of
hypertonic chyme into the duodenum, which acts as an osmotic
draw into the duodenum, causing
intravas- cular volume depletion. Next, there is a sudden peak in glucose
levels in the blood because
of the rapid release of food
into the small intestine. This is followed by the rapid release of insulin in
response to this high glucose
level, which then causes hypoglycemia to develop.
Clinical Presentation. Patients present with sweating, shaking,
palpitations, and lightheaded- ness shortly after a meal.
Treatment. There is no cure for dumping syndrome. The management is to eat multiple, small meals.
Gastroparesis
Gastroparesis
Pathogenesis. Gastroparesis literally means
the presence of a weak
stomach. The most
common association for gastroparesis is diabetes. Electrolyte problems
with potassium, magnesium, and calcium can also weaken the musculature of the
bowel wall.
Clinical Presentation. Patients present with early satiety,
postprandial nausea, and a general sense of increased abdominal
fullness. This is from decreased motility of the stomach and the accumulation
of food there. Gastroparesis generally occurs in those presenting with
abdominal pain and bloating and who have a long-standing history of diabetes, along
with retinopathy, neuropathy, nephropathy, and history of poor glycemic control.
Diagnosis. Although a gastric-emptying study can be done with the ingestion
of radioisotope- labeled food,
this is rarely necessary. The diagnosis of diabetic gastroparesis is generally obvious as the cause of bloating, vomiting,
and nausea in a long-term
diabetic after endoscopy
excludes other diseases.
Treatment. The treatment
of gastroparesis is with agents
that will increase
motility of the stomach,
such as erythromycin or metoclopramide. Erythromycin increases motilin levels.
Barrett Esophagus
Barrett Esophagus
Pathogenesis. Barrett esophagus is a complication of long-standing reflux disease. After sev-
eral years of GERD, the epithelium of the lower esophagus undergoes
histologic change from a
normal squamous epithelium to a columnar epithelium.
Diagnosis. Patients with Barrett
esophagus should have a repeat
endoscopy every 2 to 3 years
to see whether dysplasia or esophageal cancer has developed. Patients with
low-grade dyspla- sia should undergo repeat endoscopy in 3 to 6 months to see
if the lesion has progressed or resolved. Patients with high-grade dysplasia
should have a distal esophagectomy or an endo- scopic mucosal resection because
of its very high rate of progression to invasive esophageal carcinoma. The
usual rate of progression to cancer is about 0.5% per year.
Barium studies are typically normal. Endoscopy should be performed if the
patient has GERD and if there are alarm symptoms, such as dysphagia,
odynophagia, weight loss, anemia, or heme-positive stool. It is not clear
when endoscopy should
be done when there is a history
only of GERD.
Treatment. All patients with
Barrett esophagus should
receive PPIs.
Tuesday, December 29, 2015
Gastroesophageal Reflux Disease
Gastroesophageal Reflux Disease
A 32-year-old man comes to the emergency department for substernal chest pain of 2 hours’ duration.
He says that he sometimes
gets this pain while lying in bed at
night. He is otherwise free of symptoms, except for a nonproductive cough
that he has had for the past month or so. His physical
examination is unremarkable. His ECG is normal. He is
given sublingual nitroglycerin and notes that his chest discomfort is worsened.
Pathogenesis. Gastroesophageal reflux
disease, or GERD,
is caused by the abnormal flow of the acid gastric contents backward from
the stomach up into the esophagus. The lower esophageal sphincter
(LES) is not a true anatomic sphincter;
you can’t find it in a cadaver.
The LES is cre- ated by the different response of the smooth muscle
cells in the distal esophagus.
A number of factors can cause decreased tone
or loosening of this sphincter,
such as nicotine, alcohol,
caffeine, peppermint, chocolate, and
anticholinergics. We also
know that calcium-channel blocking agents and nitrates also lower the sphincter
pressure. When the tone of the LES decreases,
acid is more likely to reflux backward into the esophagus,
particularly when the patient is
lying flat. GERD can still occur in the absence of these precipitating factors and can often simply be idiopathic in origin.
Clinical Presentation. Dyspepsia or epigastric pain can be caused by GERD, ulcer disease, pan- creatitis, gastritis, and nonulcer dyspepsia. GERD can be
differentiated from the others by the presence
of a sore throat; a bad, metal-like taste in the mouth; hoarseness; and cough and wheez-
ing. In addition, GERD is the one most likely
to be associated with pain in the substernal area.
Diagnosis. Specific diagnostic testing is not necessary when the patient’s symptoms are those described in the clinical presentation. In clear cases of epigastric pain going under the sternum and associated with a respiratory complaint
or a bad taste in the mouth, therapy should be initiated immediately with antisecretory
medications, such as proton-pump inhibitors (PPIs). The most accurate diagnostic test is a 24-hour pH monitor, but this is only necessary when the patient’s presentation is equivocal in nature and the diagnosis is not clear. An electrode is placed several
centimeters above the gastroesophageal junction, and a determination is made of what the average
pH is in that area. Normal endoscopy does not exclude reflux disease.
Treatment. Therapy for GERD is primarily with PPIs, all of which
are essentially equal
in effi- cacy. Omeprazole, esomeprazole,
lansoprazole, pantoprazole, and rabeprazole will all reliably increase the pH of the gastric
contents to a level above
4.0. Do motility studies prior
to surgery to avoid
iatrogenic dysphagia.
A small number of persons, usually <5%, will
not respond to PPIs and will need to undergo surgery to tighten the sphincter. Traditionally, this has been a Nissen
fundoplication, which is done laparoscopically. Another method is simply
placing a circular purse-string suture in the LES to tighten it