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11: GASTROINTESTINAL GUIDELINES
cannot be contained by diapers or toilet use should be
excluded from day care until diarrhea stops.
4.
Breastfeeding can continue during diarrhea.
5.
Children should not attend day-care facilities until
24 hours or more after diarrhea ceases.
6.
In cases of Shigella, the health department may not per-
mit return to day-care facilities until the child has one or
more stool cultures negative for Shigella.
7.
Children should not go to water parks/swimming
pools for 1 week after symptoms resolve.
B.
Adults:
1.
Those with concomitant chronic debilitating disease
are at a higher risk of mortality.
C.
Geriatrics:
1.
Elderly clients are at a higher risk of mortality second-
ary to dehydration. Signs of dehydration include:
a.
Confusion.
b.
Muscle weakness.
c.
Fever.
d.
Dizziness.
e.
Poor skin turgor.
f.
Hypotension.
g.
Tachycardia.
2.
Diminished thirst mechanism and decreased body
water exacerbate dehydration.
3.
New residents to nursing/group homes should be iso-
lated from ill clients.
RESOURCE
Centers
for Disease Control and Prevention: www.cdc.gov
BIBLIOGRAPHY
Alexandraki, I., & Smetana, G. W. (2022, May). Acute viral gastro -enteritis
in adults. UpToDate. https://www.uptodate.com/contents/acute-viral
-gastroenteritis-in-adults?sectionName=DIFFERENTIAL%20DIAGN
OSIS&topicRef=2710&anchor=H752813318&source=see_link#H7528
13340
Centers for Disease Control and Prevention. (2018a, July 25). Rotavirus
vaccination. Celiac disease foundation. https://www.cdc.gov/vaccines/
vpd/rotavirus/index.html
Centers for Disease Control and Prevention. (2018b, September 20).
Rotavirus. Immunization action coalition. http://www.immunize.org/
askexperts/experts_rota.asp
Hammer, H., & Hogenauer, C. (2022). Lactose intolerance: Clinical mani-
festations, diagnosis, and management. UpToDate. https://www.upt
odate.com/contents/lactose-intolerance-clinical-manifestationsdiagnosis-and-management
Lee, R. M., Lessler, J., Lee, R. A., Rudolph, K. E., Reich, N. G., Perl, T. M., &
Cummings, D. A. T. (2013). Incubation periods of viral gastroenteritis:
a systematic review. BMC Infectious Diseases 13, 446(2013). https://doi.
org/10.1186/1471-2334-13-446
McDonald, L., Gerding, D., Johnson, S., Bakken, J., Carroll, K., Cofn, S.,
Dubberke, E. R., Garey, K. W., Gould, C. V., Kelly, C., Loo, V., Sammons,
J. S., Sandora, T. J., & Wilcox, M. (2018, December 2018). Clinical practice guidelines for Clostridium difcile infection in adults and children:
2017 update by the Infectious Diseases Society of America and Society
for Healthcare Epidemiology of America. IDSA Clinical Practice
Guidelines, 1–48. https://doi.org/10.1093/cid/ciy149 http://www.
uphs.upenn.edu/bugdrug/antibiotic_manual/C%20difcile%20guid
elines%20IDSA2017.pdf
GASTROESOPHAGEAL
REFLUX DISEASE
DEFINITION
A.
The American College of Gastroenterology (ACG) denes
gastroesophageal reux disease (GERD) as symptoms or complications resulting from the reux of gastric contents into the esophagus or beyond into the oral cavity (including larynx) or lung.
B.
Gastroesophageal reux is considered a normal physi-
ologic process in healthy infants, children, and adults. Most
episodes last less than 3 minutes, and they most often occur
30 to 60 minutes after meals and with reclining positions.
GERD is present when the symptoms occur more than twice
a week.
C.
Complications of GERD include erosive esophagitis (EE),
esophageal strictures, and Barrett esophagus.
D.
A very large population of clients will present after
self-medicating with antacids, bicarbonate soda, and over-thecounter (OTC) medications. Management of GERD should be
tailored to the frequency, severity, and duration of symptoms.
INCIDENCE
A.
Daily GERD (also known as heartburn) is very common;
it typically occurs postprandially and has been estimated
to affect 17% to 65% of the normal adult population. Reux
esophagitis affects 30% to 80% of females at some time during pregnancy. It is estimated that 30% to 90% of clients with
asthma have GERD. Barrett esophagus, which affects fewer
than 1% of adults, is commonly associated with GERD.
PATHOGENESIS
A.
Gastroesophageal reux is relaxation or incompetence of
the lower esophagus persisting beyond the newborn period.
Relaxation of the lower esophageal sphincter (LES) allows
reux of gastric acid and pepsin into the distal esophagus. Heartburn occurs when reverse peristaltic waves cause
regurgitation of acidic stomach contents into the esophagus.
Anatomic abnormalities, such as a hiatal hernia, predispose
persons to GERD. Improper diet and nervous tension are also
precipitating factors.
B.
As a trigger for asthma, GERD has been identied as possi-
bly activating vagal reexes and/or microaspiration. Asthma
may promote GERD, and GERD may provoke asthma. Some
asthma medications may reduce LES tone, further complicating the picture. Conversely, a client with GERD may experience pulmonary disease as a response to the esophageal acid
exposure.
PREDISPOSING
A.
Obesity.
B.
Consuming large meals.
C.
Pregnancy.
D.
Immature, weak sphincter in newborns.
E.
Emotional stress.
F.
Increased abdominal pressure from tight clothes, straining
FACTORS
to lift or defecate, or swallowing air.
G.
Ingesting drugs and foods that promote LES relaxation:
1.
Nonsteroidal anti-inammatory drugs (NSAIDs).
2.
Benzodiazepines.
3.
Calcium channel blockers.
4.
Theophylline.
5.
Nitrates.
6.
Anticholinergics.
7.
Alcohol.
8.
Chocolate and peppermint.
H.
Smoking: increases stomach acid and LES pressure.
I.
Ingestion of caustic agents such as lye.
J.
Infection by agents, such as Candida, herpes simplex, or
cytomegalovirus (CMV), which directly attack the esophageal
mucosa, causing esophagitis that leads to/aggravates GERD.
K.
Compromised immunity, from AIDS, diabetes, or
chemotherapy.
L.
Asthma.
GASTROESOPHAGEAL REFLUX DISEASE
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COMMON
A.
COMPLAINTS
Heartburn: most commonly experienced in the postpran-
dial period.
B.
Regurgitation of uid or food.
C.
Chest pain.
ALARM
SYMPTOMS
A.
Dysphagia (difculty swallowing).
B.
Unintentional weight loss.
C.
Predominant upper abdominal pain.
D.
Hematemesis (vomiting blood).
E.
Melena (black feces/blood stool).
F.
Odynophagia (painful swallowing).
G.
Severe symptoms.
OTHER
SIGNS AND SYMPTOMS
A.
Retrosternal aching or burning.
B.
Nocturnal aspiration, water or “acid” brash.
C.
Harsh taste in the mouth upon awakening.
D.
Chronic cough, especially at bedtime.
E.
Hoarseness.
F.
Globus sensation.
G.
Nausea.
H.
Dental erosion.
I.
Infants: failure to thrive, vomiting.
SUBJECTIVE
A.
Review the onset, duration, and course of heartburn or
DATA
other symptoms.
B.
Review the client’s medication history, including OTC
medications and herbals:
1.
Has the client been taking OTC antacids, H2 blockers,
or OTC proton pump inhibitors (PPIs)?
2.
How long has the client been using these OTC agents?
3.
Is the client taking drugs that induce esophagitis?
a.
Antibiotics.
b.
Alendronate.
c.
NSAIDs.
d.
Ascorbic acid.
e.
Potassium chloride.
f.
Quinidine.
g.
Iron.
C.
Ask the client about alleviating and aggravating factors.
D.
Review the client’s habits, including smoking and alcohol
intake.
E.
Inquire about other symptoms, such as weight loss, dys-
phagia, blood loss, regurgitation, and diarrhea.
F.
Establish the client’s usual weight to determine the extent
of the problem.
G.
Ask the client about any history of asthma and Crohn’s
disease.
H.
Rule out ingestion of caustic agents, especially in the pedi-
atric population.
I.
Review the client’s dietary history for bulimia.
PHYSICAL
A.
Check pulse, respirations, blood pressure, and weight.
B.
Inspect:
EXAMINATION
1.
Examine the throat and evaluate the mouth for dental
erosion.
2.
Assess swallowing ability.
C.
Auscultate:
1.
Evaluate the presence of wheezing in the lungs.
2.
General observation of respiratory distress, including
stridor.
3.
Auscultate the heart.
4.
Evaluate the abdomen in all four quadrants.
D.
Percuss:
1.
Abdomen.
E.
Palpate:
1.
Palpate the abdomen for presence of hepatospleno-
megaly and masses if there is any suspicion of hepatic
pathology.
2.
Assess the abdomen for tenderness or distention.
F.
Rectal examination:
1.
Perform this exam if indicated for any history of
hematemesis.
DIAGNOSTIC
A.
Clinical examination and history alone usually conrm the
TESTS
diagnosis in the vast majority of clients with reux.
B.
Rule out cardiac/noncardiac chest pain before institution
of therapy (see Chapter 10, “Cardiovascular Guidelines,” for
discussion on chest pain).
C.
Endoscopy is not required for the presence of typi-
cal GERD symptoms, but is recommended for the presence
of alarm symptoms or for screening clients at high risk for
complications.
D.
Endoscopy with biopsy is usually the rst diagnostic tool
in cases of caustic ingestion or suspected infectious etiology. The ACG does not recommend an endoscopy to establish the diagnosis of GERD-related asthma, chronic cough, or
laryngitis.
E.
Ambulatory 24-hour pH monitoring: Prolonged monitor-
ing is the best clinical tool for diagnosing GERD in clients with
asthma. However, it is very expensive and not universally
available.
F.
Upper gastrointestinal series or barium contrast radiog-
raphy is not used to diagnose GERD but rules out anatomic
abnormalities of the upper digestive tract.
G.
Esophageal manometry is not used for diagnosis of GERD,
but is used to evaluate clients who have failed to respond to
an empirical trial of PPIs.
H.
Guaiac test for occult blood: Bleeding may accompany
reux esophagitis and be slow and chronic, resulting in
iron-deciency anemia, or brisk, resulting in hematemesis.
GERD may not be obvious to the clinician when obtaining a
client history, especially in a client with asthma and confounding respiratory symptoms.
I.
Consider Helicobacter pylori testing.
DIFFERENTIAL
A.
GERD.
B.
Myocardial infarction/angina.
C.
Esophageal spasm.
D.
Gallbladder disease.
E.
Cancer: gastric or esophageal.
F.
Infections: CMV, herpes simplex virus, and Candida.
G.
Peptic ulcer.
H.
Ingestion of caustic substance.
I.
Self-induced vomiting/bulimia.
J.
Pyloric stenosis.
K.
Food allergy.
L.
Eosinophilic esophagitis.
M.
Autoimmune skin disorders affecting the esophagus.
N.
Esophageal motility disorder.
O.
Hiatal hernia.
P.
Esophagitis.
Q.
Achalasia.
DIAGNOSES
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11: GASTROINTESTINAL GUIDELINES
PLAN
A.
General interventions:
1.
Management depends on the cause and severity of
symptoms.
B.
Client teaching: See Client Teaching Guide for this chapter,
“Gastroesophageal Reux Disease (GERD).”
C.
Pharmaceutical therapy:
1.
The potentially adverse effects of acid suppression include
increased risk of community-acquired pneumonia and GI
infections, including Clostridium difcile- associated diarrhea.
2.
Long-term use of acid suppression therapy without a
diagnosis is not advised.
3.
The target of pharmaceutical therapy is improvement
in quality of life through reduction/relief of symptoms
and healing of EE.
4.
On-demand or self-directed therapy has been shown to
be effective; however, the client’s use and response should
be evaluated.
5.
Histamine-2 receptor antagonists (H2 blockers) are
effective in managing milder, infrequent GI symptoms.
Tolerance occurs with chronic use of H2 blockers. Several
H2 blockers are currently available by prescription or
OTC: nizatidine (Axid), famotidine (Pepcid), cimetidine
(Tagamet), and ranitidine (Zantac).
6.
PPIs are used for both GERD and EE and are consid-
ered the “gold standard” of treatment.
a.
Initially a PPI should be prescribed once a day, before
the rst meal of the day. For maximal pH control, the
traditional delayed-release PPI should be administered
30 to 60 minutes before a meal.
b.
Avoid the concomitant use of clopidogrel (Plavix) with
omeprazole or esomeprazole due to the signicant reduction in the antiplatelet activity of clopidogrel. This is a
Food and Drug Administration safety labeling change.
c.
Dosages are age- and weight-based.
d.
Long-term therapy should be titrated down to the
lowest effective dose based on symptom control.
e.
Clients may experience a relapse in their GERD
symptoms after discontinuance and therefore may
need to be tapered off or use a stepdown approach
with an antacid or an H2 blocker.
f.
No PPI is approved for use in infants younger than
1 year.
g.
PPIs are currently available by prescription and
OTC (Table 11.12).
h.
Clients with known osteoporosis can remain on PPI
therapy except for long-term use in clients with other
risks for hip fracture.
i.
PPI therapy can be a risk factor for C. difcile infec-
tion and should be used with care in clients at risk.
7.
Antacids: The role is limited and are used for relief of
mild GERD symptoms.
8.
Surface agents: Sucralfate adheres to mucosal surface
and promotes healing.
D.
Dietary and lifestyle management:
1.
Weight loss is advised for overweight or obese clients
with GERD symptoms.
2.
At present, there are no supporting data for special
dietary precautions; however, dietary elimination of foods
(fatty foods, caffeine, chocolate, spicy foods, food with
high fat content, carbonated beverages, and peppermint)
helps identify triggers.
3.
Elevation of the head of the bed for individuals with
nocturnal symptoms.
4.
Avoidance of tight-tting clothes.
E.
Surgical management:
1.
Nissen fundoplication is a surgical procedure used
to treat GERD in clients with asthma. It improves the
TABLE
11.12 PROTON PUMP INHIBITORS
PPI Available Dosages Over the Counter
Omeprazole (Prilosec, Losec,
Omesec)
Capsules: 10, 20, and 40mg Tablet 20mg
Capsules: 15 and 30mg Capsules: 15mg
Lansoprazole (Prevacid)
Oral suspension and SoluTab: 15 and 30mg
IV: 30mg
Rabeprazole (Aciphex) Capsules: 20mg Not available
Capsules: 20 and 40mg Not available
Pantoprazole (Protonix)
Oral suspension: 30mg
IV: 40mg
Capsules: 20 and 40mg Not available
Esomeprazole (Nexium)
Oral suspension: 20 and 40mg
IV: 20 and 40mg
Dexlansoprazole (Dexilant) Capsules: 30 and 60mg Not available
Omeprazole + sodium
bicarbonate (Zegerid)
IV,
intravenous; PPI, proton pump inhibitor.
Capsules: omeprazole 20 and 20mg plus 300mg Na
Oral suspension: omeprazole 20 and 40mg plus 460mg Na
+
+
Capsules: 20mg
GIARDIASIS INTESTINALIS
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371
antireux barrier and provides a lasting solution. Because
it is not always successful, it is reserved for severe cases.
The Nissen operation is often performed as a laparoscopic procedure. Achalasia or severe hypomotility
(scleroderma-like esophagus) are conditions that would
be contraindications to Nissen fundoplication.
2.
Surgical therapy is not recommended for clients who
do not respond to PPI therapy.
3.
The ACG guidelines note that surgical therapy is as
effective as medical therapy for carefully selected clients
with chronic GERD when performed by an experienced
surgeon.
4.
Clients on NSAIDs who experience upper gastric pain,
including reux, need to be referred for endoscopy as soon
as possible.
FOLLOW-UP
A.
Noncardiac chest pain due to GERD should have a diag-
nostic evaluation before institution of therapy.
B.
Empirical treatment with a PPI may be attempted for
a short period except for clients presenting with any alarm
symptoms. Schedule a return visit in 1 to 2 weeks to evaluate
the relief of symptoms.
C.
Some clients have frequent relapses; failure to adequately
respond or long-term OTC H2 blockers and PPI use warrants
an endoscopic evaluation.
D.
The need for prescribed long-term PPI treatment or the
presence of alarm symptoms requires a gastroenterology
consultation.
E.
Consider bone density studies for clients with long-term
PPI use.
CONSULTATION/REFERRAL
A.
A GERD diagnosis should not be made without a full eval-
uation in infants with vomiting or poor weight gain; refer the
client to a pediatric gastroenterologist for evaluation.
B.
Referral is necessary if the client fails to improve after try-
ing two different medications, or if the client has dysphagia,
recent weight loss, or blood loss.
C.
PPI nonresponders need to be referred for evaluation.
INDIVIDUAL
A.
Pregnancy:
1.
CONSIDERATIONS
The diagnosis of heartburn during pregnancy is usu-
ally made by taking a thorough history. Underlying causes
of GERD in pregnancy are diminished gastric motility and
displacement of the stomach by the enlarging uterus.
2.
Sodium bicarbonate-containing antacids should be
avoided as they may lead to metabolic alkalosis and uid
overload in both the fetus and the mother.
3.
To rule out pregnancy-induced hypertension, evaluate the
client immediately for signs and symptoms of sudden-onset
discomfort with no relief from antacids (PIH or hemolysis,
elevated liver enzymes, and low platelet count syndrome).
B.
Pediatrics:
1.
Some regurgitation is normal in neonates because the
cardiac sphincter is immature and weak. However, vomiting is an abnormal sign associated with overfeeding, sepsis, metabolic disorders such as galactosemia, increased
intracranial pressure (ICP), and intestinal atresia and stenosis. Regurgitation and vomiting must be differentiated.
Regurgitation most frequently occurs within the
a.
rst hour after feeding in conjunction with burping or
spontaneous eructation of air.
b.
Infants may exhibit refusal to eat, irritability, or
arching of their back during or immediately after
feeding.
c.
Vomiting, often projectile in nature, can occur at any
time and results in the loss of signicant amounts of
body uids and electrolytes.
2.
Milk protein sensitivity should be ruled out.
3.
There is no evidence on eliminating specic foods in
children and adolescents as a means to manage GERD.
4.
The major agents used in children are gastric acid buff-
ering agents, mucosal surface barriers, and gastric antisecretory agents.
C.
Geriatrics:
1.
GERD prevalence increases with age and may be asso-
ciated with a hiatal hernia.
2.
Prolonged reux results in esophagitis and may lead
to stricture development. Chronic recurrence may develop
into Barrett syndrome.
3.
Treatment of GERD in geriatric clients is the same as
that for general adults; however, diagnostic testing should
be performed in a short time sequence secondary to stricture and cancer in the elderly.
RESOURCES
American
Rome
2013
Gastroenterological Association: www.gastro.org
Foundation: https://theromefoundation.org
guidelines for the diagnosis and management of gastroesophageal
reux disease: https://journals.lww.com/ajg/Fulltext/2013/03000/
Guidelines_for_the_Diagnosis_and_Management_of.6.aspx
BIBLIOGRAPHY
Kahrilas, P. (2021, November 29). Medical management of gastroesophageal
reux disease in adults. UpToDate. https://www.uptodate.com/contents/
medical-management-of-gastroesophageal-reux-disease-in-adults
McDonald, L., Gerding, D., Johnson, S., Bakken, J., Carroll, K., Cofn, S.,
Dubberke, E. R., Garey, K. W., Gould, C. V., Kelly, C., Loo, V., Sammons,
J. S., Sandora, T. J., & Wilcox, M. (2018, December 2018). Clinical practice guidelines for Clostridium difcile infection in adults and children:
2017 update by the Infectious Diseases Society of America and Society
for Healthcare Epidemiology of America. IDSA Clinical Practice
Guidelines, 1–48. https://doi.org/10.1093/cid/ciy149. http://www.
uphs.upenn.edu/bugdrug/antibiotic_manual/C%20difficile%20
guidelines%20IDSA2017.pdf
Saad, R. J., & Chey, W. D. (2015, June 23). First-line treatment strategies for
Helicobacter pylori infection. Gastroenterology & Endoscopy News, 6, 1–8.
https://www.gastroendonews.com/Review-Articles/Article/06-15/
First-Line-Treatment-Strategies-for-Helicobacter-nbsp-pyloriInfection/32678/ses=ogst
GIARDIASIS
INTESTINALIS
DEFINITION
A.
Giardia intestinalis (formerly Giardia lamblia) is the leading
parasitic cause of diarrhea. Infestation can lead to malabsorption by coating large areas of the small bowel, particularly the
lower duodenum and upper jejunum. Most people infected
with G. intestinalis remain asymptomatic and most infections
are self-limited.
INCIDENCE
A.
Giardiasis has a worldwide distribution. It is common
in areas where water supplies are contaminated by human
sewage. The age-specic prevalence of giardiasis is highest
in children 1 to 9 years and adults 35 to 44 years of age. The
peak onset occurs annually during early summer through
early fall.
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11: GASTROINTESTINAL GUIDELINES
PATHOGENESIS
A.
G. intestinalis is a agellated protozoan. The infective form
is the cyst. Humans are the principal reservoir of infection, but
Giardia can also infect dogs, cats, beavers, and other animals,
which may then contaminate water with feces containing cysts.
B.
People become infected either directly, by hand-to-mouth
transfer of cysts from feces of an infected person (e.g., childcare), or indirectly, by ingestion of fecal-contaminated water
or food. Most community-wide epidemics result from contaminated water supplies.
C.
The incubation period is 1 to 3 weeks, with an average of
7 to 10 days. The infective form is the cyst, with infection limited to the small intestine and the biliary tract. Disease is communicable for as long as the infected person excretes cysts.
PREDISPOSING
A.
About 50% to 75% of outbreaks occur in childcare settings.
B.
Travel to endemic areas.
C.
Subjection to unsanitary food handling.
D.
Exposure to contaminated water supplies.
E.
Male homosexuality.
F.
Cystic brosis.
G.
Immunocompromised individuals are at high risk.
COMMON
A.
Asymptomatic infection: About half of all infected indi-
FACTORS
COMPLAINTS
viduals clear the infection in the absence of clinical symptoms,
and approximately 15% shed cysts asymptomatically.
B.
Acute complaints:
1.
Explosive, foul-smelling diarrhea.
2.
Mucus in stools, bulky stools.
3.
Upper abdominal pain or discomfort.
4.
Flatulence.
5.
Nausea.
6.
Anorexia.
7.
Weight loss.
8.
Fever.
OTHER
SIGNS AND SYMPTOMS
A.
Chronic complaints:
1.
Intermittent loose stools (but not diarrhea).
2.
Steatorrhea.
3.
Increased atulence or distention.
4.
Vague abdominal discomfort.
5.
Fatigue related to anemia.
6.
Profound weight loss (10%−20% of body weight).
7.
Malabsorption.
8.
Urticaria.
9.
Dehydration.
SUBJECTIVE
A.
Review the onset, duration, and course of symptoms. Is
DATA
diarrhea acute or chronic?
B.
Ask the client about travel to areas known for giardiasis.
C.
Review the client’s intake of medications and other sub-
stances that can cause diarrhea, especially antibiotics, laxatives, quinidine, magnesium-containing antacids, excess
alcohol, caffeine, herbal teas, digitalis, loop diuretics, antihypertensive agents, and sorbitol-containing (sugar-free) gums
and mints.
D.
Review the nature of the client’s bowel movements,
including frequency, consistency, volume, and presence of
blood, pus, or mucus.
E.
Does diarrhea have any relationship to meals? Onset of
diarrhea within hours of ingesting a potentially contaminated
food is suggestive of bacterial infection with a pathogen such
as Escherichia coli; this is conrmed by checking if others were
similarly affected.
F.
Ask the client about associated symptoms that need evalu-
ation, such as fever, abdominal pain, or rash.
G.
Ask the client if other family members or sexual contacts
are also ill.
H.
Establish the client’s normal weight, and, if any weight has
recently been lost, review the amount and over what period of
time.
PHYSICAL
A.
The physical examination may reveal no specic nding.
B.
Check temperature (if indicated), pulse, respirations,
EXAMINATION
blood pressure, and weight.
C.
Inspect:
1.
General appearance for signs of dehydration include
evaluation of mucous membranes and infants’ fontanelles.
D.
Auscultate:
1.
Abdomen for bowel sounds in all quadrants.
E.
Percuss:
1.
Abdomen for dullness or shifting dullness.
F.
Palpate:
1.
Abdomen for masses, tenderness, guarding, and
rebound. Clients with periumbilical or right lower quadrant pain and copious volumes of watery stool are likely
to have a small bowel etiology.
2.
Lymph nodes for enlargement.
G.
Rectal examination.
DIAGNOSTIC
A.
Enzyme immunoassay and direct uorescence antibody
TESTS
are becoming the standard for diagnosis of giardiasis in the
United States.
B.
Stool bacteria culture and sensitivity.
C.
Mucous stool for leukocytes: Mucus free of leukocytes is
the hallmark of irritable bowel syndrome (IBS); a large number of white blood cells suggests inammatory or invasive
diarrhea.
D.
Stool for ova and parasites; test three times on alternate
days. Parasites are passed intermittently, so examine stools on
alternating days.
E.
Stool for occult blood.
F.
Endoscopy to identify cysts in duodenal uid or small
bowel tissue.
DIFFERENTIAL
A.
Giardiasis.
B.
Malabsorption.
C.
E. coli infection.
D.
IBS.
E.
Viral diarrhea.
F.
Lactose intolerance.
G.
Other bacterial infections, such as Shigella, Salmonella, and
DIAGNOSES
Campylobacter.
H.
Crohn’s disease.
I.
Sprue.
PLAN
A.
General interventions:
1.
Advise children and adult workers with diarrhea
to stay away from day-care centers until they become
asymptomatic.
2.
Advise the client’s household and sexual contacts to
seek medical examination and treatment.
B.
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Client teaching: See Client Teaching Guide for this chapter,
“Diarrhea.”
1.
Discuss safe sexual practices. Avoiding oral–anal and
oral–genital sex can decrease venereal transmission.
2.
Recommend contact precautions for the duration of ill-
ness for diapered and/or incontinent children.
3.
People with diarrhea caused by Giardia should not use
recreational water venues, including swimming pools and
water slides, for 2 weeks after symptoms resolve.
C.
Pharmaceutical therapy:
1.
Treatment of asymptomatic carriers is not generally
recommended.
2.
Fluid and electrolyte management is critical in clients
with large-volume diarrheal losses.
3.
Treat children with acute or chronic diarrhea who man-
ifest failure to thrive, malabsorption, or other gastrointestinal tract symptoms when Giardia has been identied.
4.
Metronidazole, tinidazole, and nitazoxanide are the
drugs of choice for treatment.
a.
Metronidazole (Flagyl) is the principal agent used to
treat giardiasis in the United States.
i.
Adults: 250mg orally TID for 5 to 7 days.
ii.
Pediatrics: 5 mg/kg/d orally divided in TID
dosing for 5 to 7 days; not to exceed 750mg/d.
b.
Tinidazole (Tindamax) is a onetime dose for chil-
dren 3 years of age and older; it has fewer side effects
than metronidazole.
i.
Adults: 2 g single dose.
ii.
Pediatrics: 50mg/kg single dose (maximum 2 g).
c.
Nitazoxanide (Alinia) oral suspension has similar
efcacy to metronidazole and has the advantage of
treating other intestinal parasites; it has been approved
for children 1 year of age and older.
i.
Age 1 to 3 years: 5 mL (100mg) oral suspension
Q12H with food for 3 days.
ii.
Age 4 to 11 years: 10mL (200mg) oral suspen-
sion Q12H with food for 3 days.
iii.
Age 12 years and older: 500mg tablet Q12H or
25mL oral suspension Q12H with food for 3 days.
5.
Paromomycin (Humatin), a nonabsorbable amino-
glycoside, is recommended for treatment of symptomatic infection in pregnant females in the second and third
trimesters.
a.
Adults: 100mg TID for 5 to 7 days.
b.
Pediatrics: 20 mg/kg/d TID with meals for 5 to 7
days.
D.
Dietary management:
1.
Tell the client or caregiver to prevent dehydration from
diarrhea by increasing uids.
2.
Advise restricting milk products to rule out lactose
intolerance. Postgiardiasis lactose intolerance occurs in
20% to 40% of clients.
3.
Advise backpackers, campers, and people likely to be
exposed to contaminated water to avoid drinking directly
from streams. To make water for safe drinking, boil water
or use chemical disinfection or ltration. Boiling water is
the most reliable method to make water safe for drinking.
FOLLOW-UP
A.
Relapses after treatment are common, especially in immu-
nocompromised clients.
B.
Schedule follow-ups at 6 weeks and 6 months after treat-
ment, as indicated.
HEMORRHOIDS
C.
If diarrhea persists for 2 weeks or more, secondary evalu-
373
ation is indicated. Stools should be examined again for blood,
leukocytes, and parasites.
D.
Clients who remain undiagnosed after an extensive evalu-
ation and trial of metronidazole (Flagyl) often turn out to have
IBS or surreptitious laxative abuse.
CONSULTATION/REFERRAL
A.
Severely dehydrated or malnourished clients should be
admitted for further care.
B.
Consult a gastroenterologist if the client has no relief of
symptoms after completion of therapies.
C.
Consultations with a pediatric infectious disease specialist
and pediatric gastroenterologist are recommended.
INDIVIDUAL
A.
Pregnancy:
1.
CONSIDERATIONS
Treatment of clients during pregnancy is recom-
mended. Giardiasis in pregnancy is associated with dehydration, malabsorption, and severe symptoms.
2.
Malabsorptive symptoms may persist, as regeneration
of functioning intestinal mucosa requires time.
3.
Breastfeeding appears to protect infants from G.
intestinalis.
B.
Pediatrics:
1.
When an outbreak is suspected in a childcare set-
ting, the local health department should be notied to
investigate.
2.
Children who are carriers do not have to be excluded
from childcare; however, personal hygiene/universal precautions should be followed.
BIBLIOGRAPHY
Hammer, H., & Hogenauer, C. (2020). Lactose intolerance: Clinical mani-
festations, diagnosis, and management. UpToDate. https://www.upt
odate.com/contents/lactose-intolerance-clinical-manifestationsdiagnosis-and-management
Leder, K., & Weller, P. F. (2022, May). Giardiasis: Epidemiology, clinical mani-
festations and diagnosis. UpToDate. https://www.uptodate.com/conte
nts/giardiasis-epidemiology-clinical-manifestations-and-diagnosis#
H8
Sharma, G. D. (2019, May 2). Cystic brosis. Medscape. http://emedicine.
medscape.com/article/1001602-overview
HEMORRHOIDS
DEFINITION
A.
Hemorrhoids are clusters of vascular tissues, smooth mus-
cle, and connective tissue of the anal canal.
B.
Internal hemorrhoids are above the anorectal line, covered
by rectal mucosa, and can be found at any position in the rectum. Hemorrhoids can be found at any position of the rectum.
Internal hemorrhoids are graded by severity (Table 11.13).
C.
External hemorrhoids are below the anorectal line, cov-
ered by anal skin, and appear as painless, accid skin tags
(Figure 11.2).
D.
When blood within the hemorrhoid becomes clotted due
to obstruction, the hemorrhoids are referred to as thrombosed
and appear as blue, shiny masses.
E.
Although rectal bleeding is commonly associated with
hemorrhoids, it may be a symptom of other disease processes, such as colorectal cancer (CRC), inammatory bowel
disease (IBD), other conditions, diverticular disease, and
angiodysplasia.
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11: GASTROINTESTINAL GUIDELINES
TABLE
11.13 SEVERITY OF HEMORRHOIDS TO
GUIDE TREATMENT OPTIONS
Grade Severity
I The hemorrhoids bleed but do not prolapse.
II
III
IV
The hemorrhoids prolapse upon defecation but reduce
spontaneously.
The hemorrhoids prolapse upon defecation and must be
reduced manually.
The hemorrhoids are prolapsed and cannot be reduced
manually.
PREDISPOSING
A.
Increased abdominal pressure (constipation, pelvic con-
FACTORS
gestion, pregnancy, portal hypertension, cirrhosis).
B.
Altered bowel function (constipation, diarrhea).
C.
Poor muscle tone.
D.
Low-ber diet.
E.
Sedentary jobs, such as driving trucks and piloting planes.
F.
Loss of muscle tone due to advanced age.
G.
Anal intercourse.
H.
Obesity.
I.
Colon malignancy.
J.
Rectal surgery.
K.
IBD.
COMMON
A.
COMPLAINTS
Cardinal features:
1.
Bleeding: painless, bright red bleeding with defecation
(internal).
2.
Anal pruritus.
3.
Prolapse.
4.
Pain related to thrombosis.
OTHER
SIGNS AND SYMPTOMS
A.
Visible prolapsed mass.
B.
Incomplete defecation.
C.
Leakage of feces (internal hemorrhoids).
D.
Excessive moisture.
E.
Weakness or fatigue, with anemia.
F.
External hemorrhoid: Covered by skin, an external hemor-
rhoid protrudes from the rectum.
Internal
FIGURE
11.2 Internal and external
External
hemorrhoid
hemorrhoids. Internal hemorrhoid:
Covered by a thin sheet of tissue
called mucous membrane, an internal
hemorrhoid bulges into the rectal
opening and may sink a bit during
bowel movements. External hemorrhoid:
Covered by skin, an external hemorrhoid
protrudes from the rectum.
INCIDENCE
A.
In the United States, the self-reported incidence of hemor-
rhoids is 10 million per year, corresponding to a 4.4% prevalence. Clients tend to present after utilization and failure of
over-the-counter (OTC) treatments. Hemorrhoids are common in people older than 20 years of age. They are uncommon in people younger than 20 years of age except secondary
to pregnancy.
PATHOGENESIS
A.
The underlying mechanism is unknown. Prolapse may be
initiated by shearing force from passage of large rm stool, by
increased venous pressure from HF or pregnancy, or by straining that occurs with lifting or defecation.
SUBJECTIVE
A.
Review the onset and duration of symptoms, especially
DATA
history of rectal bleeding, prolapse, and issues of hygiene and
pain.
B.
Review the client’s history of hemorrhoids and treatments,
including surgery.
C.
Ask the client about recent pregnancy, liver disease, and
constipation.
D.
Inquire about the client’s job and level of daily activity.
E.
Review the client’s sexual practices for anal intercourse.
F.
Review the client’s dietary history for uid intake and
sources/amount of ber.
G.
Ask about bowel habits, including frequency, consistency,
and ease of evacuation.
H.
Review a detailed family history, with emphasis on intesti-
nal disease.
PHYSICAL
A.
Check temperature (if indicated), pulse, respirations,
EXAMINATION
blood pressure, and weight.
B.
Inspect:
1.
Observe the rectal area for skin tags, prolapse, irrita-
tion, ssures, and condyloma.
a.
Internal hemorrhoids are usually not visible unless
prolapsed.
b.
External hemorrhoids protrude with straining or
standing.
2.
Using anoscopy, visualize internal rectum for hemor-
rhoids, ssures, or masses.
C.
Palpate:
1.
Palpate abdomen for masses.
D.
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Rectal examination:
1.
Internal hemorrhoids are usually not palpable unless
thrombosed.
2.
Digital rectal evaluation.
DIAGNOSTIC
A.
Hematocrit and hemoglobin, if bleeding present.
B.
Anoscopy reveals internal hemorrhoids as bright red to
TESTS
purplish bulges. Digital rectal examination alone can neither diagnose nor exclude internal hemorrhoids; anoscopy is
required.
C.
Endoscopic evaluation: In clients older than 40 years, ex-
ible sigmoidoscopy or colonoscopy is performed if there are
risk factors for CRC.
D.
Stool for guaiac testing.
E.
Air-contrast barium enema for atypical bleeding.
DIFFERENTIAL
A.
Hemorrhoids.
B.
Condyloma acuminata.
C.
Rectal prolapse.
D.
Rectal bleeding due to one of the following:
1.
CRC.
2.
Polyps.
3.
Anal ssure.
4.
Fistula.
5.
Perianal abscess.
6.
IBD, including ulcerative colitis and Crohn’s disease.
7.
Diverticulitis.
8.
Pelvic tumor.
E.
Proctitis.
DIAGNOSES
PLAN
A.
General interventions:
1.
No treatment is necessary if the client is asymptomatic
except for maintaining regular bowel habits and performing comfort measures.
B.
Client teaching: See Client Teaching Guide for this chapter,
“Hemorrhoids.”
C.
Pharmaceutical therapy:
1.
Drug of choice: bulk-forming agents such as psyllium
seed (Metamucil), methylcellulose (Citrucel), or calcium
polycarbophil (Fibercon), 1 to 3 teaspoons in 8 oz of liquid
TID. Maintenance dose is 1 to 3 teaspoons after dinner.
2.
Stool softener: docusate sodium (Colace) or docusate
calcium (Doxidan) 100mg TID.
3.
For irritation and pruritus, topical creams and anesthet-
ics are found in OTC products such as Anusol, pramoxine
HCl (Tronolane Cream), Preparation H, and topical hydrocortisone preparations.
4.
Nonsteroidal anti-inammatory drugs supplemented
with narcotics: An oral analgesic such as codeine may
be prescribed for thrombosed hemorrhoids. However,
codeine causes constipation.
D.
Dietary management:
1.
High-ber diet and an adequate uid intake should be
continued indenitely to maintain a soft bulky stool that
can be passed without straining (see Appendix B, Table B.6).
E.
Medical management:
1.
Use warm sitz baths up to three times a day for irrita-
tion and pruritus.
2.
Conservative treatment for thrombosed hemorrhoids
includes lying prone and applying an ice pack to the area.
HEMORRHOIDS
3.
Incision and evacuation of thrombosis or clot may
375
be performed under local anesthesia. Other treatments
for thrombosed hemorrhoids noted in clinical trials have
included the following:
a.
Topical nitroglycerin 0.2% topical ointment for tem-
porary analgesia. The most common side effect was
headache.
b.
Topical nifedipine.
c.
In a small study, one intrasphincter injection of bot-
ulinum toxin relieved pain within 24 hours.
F.
Surgical management:
1.
Symptomatic grade I, grade II, and some grade III
hemorrhoids may be treated by the following:
a.
Rubber band ligation is the treatment of choice for
grades I and II hemorrhoids. Rubber band ligation is
the most widely used procedure and is associated with
fewer complications than surgery.
b.
Bipolar, infrared, and laser coagulation (may require
more than one treatment).
c.
Sclerotherapy.
d.
Stapled hemorrhoidopexy can be performed in cli-
ents with grade III hemorrhoids.
2.
External hemorrhoids usually do not require surgi-
cal therapy except in cases of thrombosis. For selective
grade III and grade IV internal and strangulated hemorrhoids that fail to respond to medical and nonoperative
therapies, surgical treatment is required. Stapled hemor-
rhoidopexy has a faster recovery but a higher recurrence
rate. Hemorrhoidectomy is the treatment of last choice
because it requires hospitalization and an extended
recovery period, and it risks compromising competence
of the anal sphincter. Hemorrhoidectomy complications
include:
a.
Urinary retention.
b.
Urinary tract infection.
c.
Fecal impaction.
d.
Pain.
e.
Hemorrhage.
f.
Stricture formation (1%) or sphincter damage (rare).
g.
Nonhealing wound.
h.
Fistula formation.
i.
Anal leakage.
FOLLOW-UP
A.
None necessary if resolution occurs and the client is
asymptomatic.
B.
Reevaluate the client in 2 weeks for further treatment if
symptoms persist.
C.
Evaluate the client with an intervention in 7 to 10 days.
CONSULTATION/REFERRAL
A.
The onset of urinary retention and fever immediately after
an ofce-based procedure may be the initial sign of perianal
sepsis and mandates emergent client evaluation.
B.
Clients with family history of CRC, familial polypo-
sis, constitutional symptoms such as anemia, weight loss,
and changes in the consistency of stools that are suggestive
of malignancy should be referred to a gastroenterologist for
endoscopic evaluation.
C.
Refer the client with an acute thrombosed external hemor-
rhoid to a gastrointestinal specialist if the client is experiencing severe pain, or if the pain does not resolve after 48 hours
with conservative measures.
376
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D.
Refer the client to a surgeon if hemorrhoids bleed repeat-
11: GASTROINTESTINAL GUIDELINES
edly, prolapse, produce intractable pain, or are thrombosed,
and if 3 to 5 consecutive days of treatment do not provide
relief.
INDIVIDUAL
A.
Pregnancy:
1.
CONSIDERATIONS
Labor, which results in pressure on the pelvic oor by
the presenting part of the fetus and the expulsive efforts of
the client, may aggravate hemorrhoids, causing protrusion
and inammation during the puerperium. Hemorrhoids
may be pushed back after delivery to prevent them from
becoming swollen and painful.
2.
Surgical treatment is contraindicated in pregnancy due
to the risk of inducing labor.
3.
Conservative treatment is recommended, with excision
of thrombosed external hemorrhoids if necessary.
B.
Pediatrics:
1.
Rectal prolapse in children is associated with cystic
brosis.
Prolapse
looks like a pink doughnut or rosette; complete prolapse involv-
ing the muscular wall is larger and red, and has circular folds.
C.
Geriatrics:
1.
Prolapse of the rectal mucosa is more common in the
elderly.
2.
Colonoscopy is recommended in the geriatric popula-
tion to exclude malignancy or other underlying disease.
BIBLIOGRAPHY
Bleday, R., & Breen, E. (2019, April 3). Hemorrhoids: Clinical manifesta-
tions and diagnosis. UpToDate. https://www.uptodate.com/contents/
hemorrhoids-clinical-manifestations-and-diagnosis#H909159015
Sharma, G. D. (2019, May 2). Cystic brosis. Medscape. http://emedicine.
medscape.com/article/1001602-overview
Sun, Z., & Miglay, J. (2016). Review of hemorrhoid disease: Presentation
and management. Clinics in Colon and Rectal Surgery, 29(1), 22–29.
https://doi.org/10.1055/s-0035-1568144
HEPATITIS
A
DEFINITION
A.
Hepatitis A is an acute self-limited illness characterized by
inammation of the liver and jaundice caused by the hepatitis A virus (HAV). Infection rates have increased in recent
years due to community outbreaks in susceptible individuals. All cases of hepatitis A are reportable to the public health
department.
TRANSMISSION
A.
Hepatitis A is usually transmitted by the fecal–oral route
AND RISK FACTORS
through direct contact with an infected host or consumption
of contaminated food or water. Risk factors for transmission
include:
1.
Person-to-person contact:
a.
Household.
b.
Sexual.
c.
Residential institution.
d.
Day care.
e.
Military.
2.
Contact with contaminated water/food:
a.
Undercooked shellsh, produce.
b.
Infected food handlers.
B.
Transmission occurs through the fecal–oral route. Ingested
stool molecules are ingested and absorbed in the stomach and
intestines and travel to the hepatocytes by portal circulation.
Viral shedding may be noted 1 to 2 weeks before the onset of
illness (jaundice or elevation of liver enzymes), during which
time clients are most likely to transmit infection. Transmission
subsequently diminishes and is minimal in the week after the
onset of jaundice. Few children younger than 6 years have
concomitant jaundice, whereas up to 70% of older children
and adults will have jaundice. Fulminant hepatitis is rare, and
chronic infectious and carrier states do not occur.
C.
Duration of HAV infection is typically 8 weeks, but pro-
longed disease, as long as 6 months, can occur in 10% to 15% of
symptomatic clients, especially in neonates and young children.
D.
Fulminant hepatic failure occurs in less than 1% of cases.
E.
The major methods of prevention include improved sanita-
tion of water sources, improved hygiene practice prior to food
preparation and diaper changes, immunization with the hepatitis A vaccine, and administration of immune globulin (IG).
INCIDENCE
A.
Approximately 30% to 35% of acute hepatitis cases in the
United States are due to HAV. In developing countries, where
infection is endemic, most people are infected during the rst
decade of life. In the United States, the incidence of HAV has
declined since 1995 due to the administration of the HAV
vaccine.
B.
HAV has been increasing since 2016 as a result of large
person-to-person outbreaks. The Centers for Disease Control
and Prevention (CDC) has recognized the following groups
as high risk for developing serious consequences from HAV:
people who use drugs, unstable housing, homeless, men who
have sex with men, current or recent incarceration, and people
with chronic liver disease.
C.
Mortality from HAV ranges from 0% to 1%. The single most
important determinant of illness severity is age; increasing age
directly correlates with the likelihood of adverse events.
PATHOGENESIS
A.
HAV is a small RNA enterovirus classied as a member of
the picornavirus group. Viral replication depends on hepatocyte uptake and synthesis, and assembly occurs exclusively
in liver cells. Transmission of HAV is person-to-person, primarily by the fecal–oral route and parenterally. The incubation period is 15 to 50 days, with an average of 25 to 30 days.
HAV does not cause chronic infection.
B.
Common-source, foodborne, and waterborne epidem-
ics have occurred, including several caused by shellsh contaminated with human sewage. Nosocomial outbreaks have
occurred as a result of shedding of HAV from infected asymptomatic neonates, children, or adults.
PREDISPOSING
A.
Ingestion of infected water, food, and shellsh:
1.
Undercooked HAV-contaminated foods are a source of
FACTORS
outbreaks.
2.
Cooked foods also can transmit HAV if the temperature
during food preparation is inadequate to kill the virus.
3.
Food contaminated after cooking is associated with
infected food handlers.
B.
Close personal contact with an HAV-infected person:
1.
Contact with a child who attends a childcare center
(especially with children in diapers).
2.
Men who have sex with men.
3.
Vertical transmission from mother to fetus (limited).
4.
Personal contact with a newly arriving international
adoptee.
5.
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Congregate living settings.
6.
Occupational risk.
C.
Poor sanitation or personal hygiene.
D.
Crowded living conditions.
E.
International travel.
F.
Drug abuse.
G.
Persons with clotting factor disorders.
H.
Persons working with nonhuman primates.
COMMON
A.
B.
C.
D.
E.
F.
G.
H.
OTHER
A.
COMPLAINTS
Asymptomatic, particularly in children under 6.
Malaise.
Anorexia.
Nausea with/without vomiting.
Low-grade fever.
Jaundice: icteric phase (70% of children over 6 and adults).
Abdominal pain.
Enlarged liver.
SIGNS AND SYMPTOMS
Infants and children under 6: mild, nonspecic, ulike
symptoms without jaundice.
B.
Adults: severe, prolonged course with fatigue, headache,
vomiting, and symptoms noted earlier. Symptoms may persist for 2 to 8 weeks.
C.
Relapsing hepatitis A is more common in the elderly. This
variant generally involves a protracted course of symptoms,
then a relapse of symptoms following an apparent resolution.
D.
Less common complaints include chills, cough, pruritus,
urticaria, skin rash, diarrhea, constipation, and joint pain.
HEPATITIS A
D.
Percuss:
1.
Abdomen.
E.
Palpate:
1.
Palpate all quadrants of the abdomen for masses, liver
377
tenderness, hepatomegaly (80% of cases), and splenomegaly (less common).
2.
Neck for lymphadenopathy.
DIAGNOSTIC
A.
Consider diagnosis based on clinical presentation: jaun-
TESTS
dice, dark urine, abdominal pain, fever, malaise, nausea, vomiting, or diarrhea.
B.
CDC clinical criteria: acute illness consistent with presen-
tation of HAV AND (1) jaundice or elevated bilirubin level
or (2) elevated serum alanine aminotransferase (ALT) levels
AND absence of a more likely diagnosis.
C.
Diagnosis conrmed with viral serology for typing HAV,
immunoglobulin G (IgG), and immunoglobulin M (IgM).
Serum IgM presents 5 to 10 days prior to symptoms, peaks
within 1 month, and may persist for up to 6 months. Presence
of IgG anti-HAV antibodies without virus-specic IgM indicates past infection and lifelong immunity.
D.
Liver function studies, including ALT, aspartate transami-
nase, lactate dehydrogenase, and alkaline phosphatase.
E.
Bilirubin, direct and indirect.
F.
Prothrombin time.
G.
Urinalysis reveals proteinuria and bilirubinuria.
H.
Imaging studies are usually not indicated for hepati-
tis A infection. An ultrasound may be used to exclude other
pathology.
SUBJECTIVE
A.
Review the duration, onset, and severity of symptoms,
DATA
including specics about urine or stool color changes. Look
for abrupt onset and symptoms that may have been present
up to 8 weeks.
B.
Include social history. Ask the client about family mem-
bers and sexual contacts with similar symptoms or infection
with HAV, child attending day care, congregate living, and
recent incarceration.
C.
Review the client’s history of blood transfusions, intrave-
nous drug use, and alcohol abuse.
D.
Inquire about occupational exposure.
E.
Ask the client about recent international travel or exposure
to newly arrived international adoptees.
F.
Review the client’s immunization status.
G.
Review the client’s medications for a possible Tylenol
overdose or Ecstasy use as a cause of acute drug-induced liver
injury.
H.
Ask about other liver disorders such as cirrhosis, hepatitis
B and hepatitis C.
PHYSICAL
A.
Check temperature (acute illness), pulse, respirations,
EXAMINATION
blood pressure, and weight.
B.
Inspect:
1.
Note general appearance.
2.
Inspect the skin for slight jaundice or rash.
3.
Inspect the mucous membranes and nail beds.
4.
Inspect the eyes for yellow sclera.
C.
Auscultate:
1.
Lung elds.
2.
All quadrants of the abdomen.
3.
Heart.
DIFFERENTIAL
A.
Other viral infections:
1.
Hepatitis A, B, C, D, E.
2.
Epstein–Barr virus.
3.
Cytomegalovirus.
4.
Herpes simplex virus.
5.
Acute HIV infection.
B.
Bacterial infections:
1.
Secondary syphilis.
2.
Sepsis.
3.
Typhoid fever.
C.
Autoimmune disease:
1.
Autoimmune hepatitis.
2.
Systemic lupus erythematosus (SLE).
D.
Obstructive jaundice.
E.
Alcoholic hepatitis or cirrhosis.
F.
Hepatotoxic drug use:
1.
Drug-induced liver injury (e.g., Tylenol, Ecstasy).
2.
Drug-induced hypersensitivity reaction (e.g., sulfasala-
DIAGNOSES
zine hypersensitivity).
G.
Food poisoning.
H.
Budd–Chiari syndrome, Wilson disease.
PLAN
A.
General interventions:
1.
Contact precautions are recommended for diapered
and/or incontinent clients for 2 weeks after the onset of
symptoms.
2.
Children and adults with acute HAV infection should
be excluded from school, work, and childcare centers for
2 weeks after the onset of illness.
3.
Hepatitis is self-limiting and does not require therapy.
Treatment is supportive.
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