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D.
Prior GI infection-induced IBS.
E.
Genetics is considered a factor.
F.
Carbohydrate intolerance may produce signicant
11: GASTROINTESTINAL GUIDELINES
symptoms.
COMMON
A.
COMPLAINTS
Chronic relapsing stool pattern:
1.
Diarrhea: more than three loose stools per day. Or
2.
Alternation of diarrhea with constipation. Diarrhea is
typically small in volume, has visible mucus, and may follow a hard movement by a few hours. Or
3.
Constipation: fewer than three bowel movements
(BMs) per week.
B.
Feeling of incomplete evacuation.
C.
Abdominal distention and bloating.
D.
Straining with BMs.
E.
Aching or cramps in periumbilical or lower abdominal
region.
F.
Pain relief with BM.
OTHER
SIGNS AND SYMPTOMS
A.
Change in bowel function.
B.
Clear mucous stool.
C.
Pain may be precipitated by meals.
D.
Pain radiates to the left chest or arm, from gas in splenic
exure. Nocturnal pain is unusual and is considered a warning sign.
E.
Flatulence.
F.
Nausea.
G.
Anxiety.
H.
Depression.
I.
Preoccupation with bowel symptoms.
J.
Extraintestinal symptoms:
1.
Dysmenorrhea.
2.
Urinary frequency, urgency, and incomplete bladder
emptying.
3.
Impaired sexual function and dyspareunia.
4.
Fibromyalgia.
K.
Menses may exacerbate IBS symptoms.
L.
Red ag symptoms and differential diagnoses for IBS
(Table 11.16).
SUBJECTIVE
A.
Review the pattern of main symptoms, including the
DATA
onset, duration, and usual course.
B.
Ask the client about the predominant symptoms: abdomi-
nal pain, diarrhea, or constipation.
C.
Review the client’s history for stress factors and ask
whether recurrent symptoms occur in relation to them.
D.
Ask the client what other symptoms occur with the pain,
diarrhea, or constipation, such as bloating, blood in stool, or
nighttime BMs. Bleeding, weight loss, and nocturnal diar-
rhea are not characteristic of IBS. Symptoms of IBS disappear during sleep.
E.
Establish the client’s normal weight history, and deter-
mine the amount of weight loss, if any, and over what time
period.
F.
Review the client’s diet:
1.
Response to milk or lactose products.
2.
Articial sweeteners.
3.
Alcohol intake.
4.
Irregular or inadequate meals.
5.
Insufcient uid intake.
6.
Excessive ber intake.
7.
Obsession with dietary hygiene.
8.
Response to gluten (wheat, barley, rye) ingestion.
G.
Inquire about the client’s prescription, herbal, and
over-the-countermedications. Ask specically about the use
of laxatives.
H.
Review travel and food history for dominant history of
diarrhea.
I.
Ask the client if there is a family history of colon can-
cer, ulcerative colitis (UC), Crohn’s disease (CD), or
malabsorption.
J.
Is there any fever accompanying lower abdominal pain?
K.
What is the relation of symptoms to menstruation?
L.
Ask about celiac disease, inammatory bowel disease,
anemia, and alarm symptoms (unintentional weight loss,
TABLE
11.16 COMMON AND RED FLAG DIFFERENTIAL DIAGNOSES FOR IBS
Disorder Signs and Symptoms Diagnostic Tests
Ulcerative colitis Peaks at ages 15–35 years Sigmoidoscopy, colonoscopy, BE
Bloody diarrhea with mucus, fever, abdominal pain,
tenesmus, weight loss
Crohn’s disease Onset at ages 15–35 or 70–80 years Sigmoidoscopy, colonoscopy, BE
Fever, abdominal pain, diarrhea, fatigue, weight loss,
anorectal fissures, fistulae, abscesses
Infectious diarrhea Chronic diarrhea with cramps with or without blood and
Microscopy, stool studies, sigmoidoscopy
mucus
Diverticulitis Lower left abdominal pain, fever, altered bowel habits CBC, CT, BE
Colorectal malignancy Age 50 years or older Colonoscopy
Rectal bleeding, altered bowel habits, abdominal or back
pain, anemia, occult blood in stool, weight loss
Medication side effects Antacids, laxatives, SSRIs, thyroid hormones, metformin,
narcotics, calcium channel blockers, anticholinergics
History of concordance of symptoms with
medication initiation, trial of drug holiday or
reducing dosage, rechallenge
BE,
barium enema; CBC, complete blood count; IBS, irritable bowel syndrome; SSRI, selective serotonin reuptake inhibitor.
IRRITABLE BOWEL SYNDROME
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rectal bleeding, change in bowel habits to looser, more frequent stools in clients >60 years of age).
PHYSICAL
A.
Check temperature, pulse, respirations, blood pressure,
EXAMINATION
and weight. Note weight loss (alarm symptom).
B.
Inspect:
1.
Observe the client’s general appearance. Does the cli-
ent appear anxious or depressed?
2.
Inspect the abdominal contour for masses and bulges.
C.
Auscultate:
1.
All quadrants of the abdomen for bowel sounds; note
whether they are normal or mildly hyperactive.
D.
Percuss:
1.
Abdomen for tympany or dullness.
E.
Palpate:
1.
Abdomen for mild tenderness, rigidity, guarding, and
masses.
2.
Evaluate for hepatosplenomegaly.
3.
Evaluate for lymphadenopathy.
F.
Rectal examination:
1.
Check for masses and tenderness.
2.
Obtain stool for diagnostic tests.
3.
Rectal examination is normal with IBS.
DIAGNOSTIC
A.
The American Gastroenterological Association Task
TESTS
Force on IBS recommendations state that clients younger
than 50 years who do not have alarm features need not
undergo routine colonic imaging. Clients with IBS symptoms who have alarm features, such as anemia or weight
loss, or those who are older than 60 years, should undergo
colonic imaging to exclude organic disease.
B.
Diagnosis of IBS is usually suspected on the basis of the
client’s history and physical examination without additional
tests (Table 11.17).
C.
Diagnostic tests are performed to exclude organic disease
that may masquerade as IBS:
1.
Complete blood count.
2.
Sedimentation rate or C-reactive protein.
3.
Serum potassium if the client is on diuretics; hypokale-
mia may reduce bowel contractility and produce an ileus.
4.
Blood glucose if diarrhea predominates; rule out diabe-
tes mellitus, which may present as diarrhea resulting from
diabetic gastroenteropathy.
5.
Thyroid function study.
6.
Check fecal calprotectin, fecal lactoferrin and C-reactive
protein to rule out inammatory bowel disease.
7.
Stool specimen: Culture for leukocytes and fat, ova and
parasites, and occult blood; leukocyte-free mucus is a hallmark of IBS.
8.
Stool cultures for Clostridium difcile toxin assay if clini-
cally indicated.
9.
Barium enemaand/or proctosigmoidoscopy for severe
signs and symptoms, after consultation or referral.
10.
Celiac serology if IBS-D is predominate.
11.
A mucosal biopsy is appropriate if a colonoscopy or
sigmoidoscopy is performed.
12.
Esophagogastroduodenoscopy (EGD) and distal duo-
denal biopsy in clients with diarrhea should be considered
to rule out celiac disease, tropical sprue, and giardiasis,
and for clients in whom abdominal pain and discomfort
are located more in the upper abdomen.
13.
Hydrogen breath test to evaluate lactose intolerance
and small intestinal bacterial overgrowth (SIBO).
14.
Utilize the Bristol Stool Form Scale (BSFS) to categorize
clients based on IBS subtype.
a.
Assessment should focus on days when client expe-
riences abnormal BM symptoms.
b.
Utilize daily BM diary for 2 weeks while client is not
using treatments that may affect BM.
c.
Pattern of stool consistency leads to IBS subtype.
i.
IBS-C: 25% of stools with BSFS 1 or 2 AND BSFS
6 or 7 occurs less than 25%.
ii.
IBS-D: >25% of stools with BSFS 6 or 7 AND less
than 25% of stools with BSFS 1 or 2.
iii.
IBS-M: >25% of stools with BFSF 1 or 2 AND
>25% of stools with BSFS 6 or 7.
DIFFERENTIAL
A.
IBS.
B.
Inammatory bowel disease (CD/UC).
C.
Viral or bacterial gastroenteritis.
D.
GI neoplasm.
E.
Acute diarrhea caused by protozoa or bacteria.
F.
Lactose insufciency/deciency.
G.
Laxative abuse.
H.
Drug side effect.
I.
Diabetes.
J.
Celiac spruce/gluten etiology.
K.
Diverticulitis.
L.
Failure to thrive in children.
M.
Endometriosis/pelvic inammatory disease.
N.
Zollinger–Ellison syndrome.
O.
Diverticulitis.
P.
Microscopic colitis.
Q.
SIBO.
DIAGNOSES
TABLE
11.17 ROME IV DIAGNOSTIC CRITERIA
FOR IBS
Onset of symptoms at least 6 months before diagnosis
Recurrent abdominal pain or discomfort for more than 1 day per week
during the past 3 months
At least two of the following features:
•
Related to defecation
•
Association with a change in frequency of stool
•
Association with a change in stool form
IBS,
irritable bowel syndrome.
PLAN
A.
General interventions:
1.
Advise the client to keep a diary of events of BMs and
precipitating factors.
2.
Encourage the client to quit smoking: Nicotine may
aggravate symptoms.
3.
Recommend daily exercise to reduce stress.
4.
Stress management should be encouraged, including
counseling, tapes, meditation, and yoga.
5.
Limited trial of low fermentable oligosaccharides,
disaccharides, monosaccharides, and polyols (FODMAP)
diet.
B.
Client teaching: See Client Teaching Guide for this chapter,
“Irritable Bowel Syndrome.”
C.
Pharmaceutical therapy:
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1.
11: GASTROINTESTINAL GUIDELINES
Tell the client to stop all nonessential medications that
may affect bowel function, especially irritant laxatives.
Avoid narcotics, depressants, and other long-term drug
use if possible.
2.
Recommend eliminating sorbitol-containing candy
and restricting lactose-containing milk products.
3.
First line therapy: soluble, viscous, poorly fermentable
ber such as psyllium hydrophilic mucilloid (Metamucil)
1 tablespoon per day in 8 oz of juice or water, followed
with another 8 oz of liquid. This treats both diarrhea and
constipation.
4.
Pain relief:
a.
Opiates should be avoided due to the risk of depen-
dence and addiction in clients with chronic conditions.
b.
Nonsteroidal anti-inammatory drugs have an
undesirable side effect on the GI tract.
c.
Antispasmodics and anticholinergic agents are
not recommended by the American College of
Gastroenterology due to lack of data on efcacy and
potential side effects (especially in the elderly) due to
anticholinergic effects.
d.
Peppermint oil may alleviate global symptoms of
IBS.
e.
Tricyclic antidepressants for IBS-D predominant.
Tricyclics should be avoided for constipated clients:
i.
Amitriptyline (Elavil) 10mg at bedtime initially;
titrate up slowly to 75mg/d at bedtime as needed.
ii.
Desipramine (Norpramin) 10mg at bedtime ini-
tially; titrate up slowly up to 75mg/d.
iii.
Imipramine (Tofranil) 10 to 50 mg orally at
bedtime.
5.
Selective serotonin reuptake inhibitors (SSRIs):
a.
Paroxetine (Paxil) 10 to 60mg/d.
b.
Citalopram (Celexa) 5 to 60mg/d.
6.
Antidiarrheals:
a.
Opiate-derived medications are reserved for very
severe cases secondary to the potential for abuse.
b.
Loperamide (Imodium):
i.
Adults: 2 to 12 mg orally in divided BID/TID
doses; doses differ greatly among individuals.
ii.
Pediatrics older than 2 years: 0.08 to 0.24 mg/
kg/d orally divided in BID/TID doses; not to
exceed 2 mg/dose.
c.
Alosetron (Lotronex), a 5-HT
receptor antagonist, is
3
indicated only for females with severe IBS-D predominant. Starting dose is 0.5 mg BID; may increase to 1 mg
BID after 4 weeks of starting dose. Discontinue if no
relief after 4 weeks of 1 mg dosing.
7.
Laxatives and stool softeners (IBS-C predominant)
along with dietary measures and ber supplements:
a.
Mineral oil 15 to 45 mL orally daily or in divided
TID dosing.
b.
Stimulant laxatives may be necessary intermittently
for short periods, but prolonged use of stimulant laxatives should be avoided.
c.
Lactulose is a colonic acidier that promotes laxa-
tion. Transit time through the colon may be slow; 24 to
48 hours may be required to produce a BM. The usual
dose is 1 to 2 tablespoons daily. Lactulose contains
galactose and lactose and should be used with caution
in clients with diabetes. Safety in pediatric clients has
not been established.
d.
The American College of Gastroenterology recom-
mends against the use of polyethylene glycol products
alone to treat IBS-C.
8.
Lubiprostone (Amitiza), a selective C-2 chloride-
channel activator, is indicated for females 18 years and
over with IBS-C predominant; 8 mcg BID with food and
water.
9.
5-HT4 agonist tegaserod (Zelnorm) can be used in
females less than 65 years old with one of fewer risk factors for cardiovascular disease if other treatments have
failed.
10.
Linaclotide (Linzess), guanylate cyclase-C (GC-C) ago-
nist, is used for both IBS-C and CIC.
11.
Eluxadoline (Viberzi), a mu-opioid receptor agonist,
is indicated for IBS-D predominant. There are two recommended dosing regimens:
a.
Dosing is 100mg tablet BID taken with food.
b.
Alternative dosing is 75mg BID taken with food for
clients with the following conditions:
i.
Do not have a gallbladder.
ii.
Unable to tolerate 100mg BID.
iii.
Are receiving a concomitant OATP1B1 inhibi-
tor, such as the lipid-lowering drug gembrozil and
its metabolite gembrozil 1Ob.
iv.
Have mild or moderate hepatic impairment.
c.
If a dose is missed, clients should not compensate by
taking two doses at once.
12.
Antibiotic: Two-week trial of rifaximin may be used in
clients who fail to respond to other therapies.
13.
The American College of Gastroenterology recom-
mends against the use of probiotics.
D.
Dietary management:
1.
Increasing ber intake may improve symptoms.
However, some clients experience worsening of symptoms
with increased ber intake.
2.
Tell the client to avoid foods that aggravate the bowel,
including gas-producing foods, such as broccoli, beans,
onions, garlic, and so forth. Advise the client to follow a low
FODMAP diet. See Appendix B, “Diet Recommendations,”
for the FODMAP diet. When diarrhea predominates,
dietary review is essential for clues of intolerance to lactose or sorbitol.
FOLLOW-UP
A.
Reevaluate the effectiveness of treatment in 2 weeks.
Treatment may be challenging for symptom management;
numerous tests are inconclusive but rule out pathology.
B.
If symptoms persist without relief, have the client return
as needed.
C.
Return if diarrhea/constipation lasts more than 2 weeks
on medication therapy.
CONSULTATION/REFERRAL
A.
Refer to a gastroenterologist for red ag symptoms.
B.
Refer to a pediatric gastroenterologist if ndings from the
client’s history, physical examination, or screening laboratory
tests are suggestive of organic disease.
C.
Alosetron (Lotronex) is prescribed under a restricted dis-
tribution program through a gastroenterologist.
D.
Consult a physician if all treatment options fail.
E.
Consider a psychiatric consultation if indicated for anxi-
ety, depression, somatization, and symptom-related fears.
JAUNDICE
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INDIVIDUAL
A.
Pediatrics:
1.
CONSIDERATIONS
In children, IBS is recognized, and many clients trace
the onset of symptoms to childhood.
2.
Children who have a history of recurrent abdominal
pain are at increased risk of IBS during adolescence and
young adulthood.
3.
The recommended daily intake of ber (in grams) for
children is estimated by adding four to their age in years.
B.
Adults:
1.
Annual rectal examination and sigmoidoscopy are rec-
ommended after age 50 years.
2.
When constipation predominates, rule out malignancy,
particularly in clients older than age 40 years who have
weight loss or a family history of colon cancer.
RESOURCE
Rome
Foundation: https://theromefoundation.org
BIBLIOGRAPHY
Ford, A. C., Moayyedi, P., Lacy, B. E., Lembo, A. J., Saito, Y. A., Schiller, L.
R., Soffer, E. E., Spiegel, B. M. R., & Quigley, E. M. M. (2018). & Task
Force on the Management of Functional Bowel Disorders. >American
College of Gastroenterology monograph on management of irritable
bowel syndrome and chronic idiopathic constipation. American Journal
of Gastroenterology, 113(suppl 2), S1–S18. https://doi.org/ 10.1038/
s41395-018-0084-x
Lacey, B.E., Pemental, M., Brenner, D.M., Chey, W.D., keefer, L.A., Long,
M.D., & Moshiree, B. (2020). ACG clinical guideline: Management of
irritable bowel syndrome. American Journal of Gastroenterology, 116(1),
17–44. https://doi.org/10.14309/ajg.0000000000001036
Lehrer, J. K. (2022, April). Irritable bowel syndrome treatment and management.
UpToDate. https://emedicine.medscape.com/article/180389-treatmen
t#d10
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 prac-
tice 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. http://www.uphs.upenn.edu/bugdrug/antibiotic_manual/
C%20difcile%20guidelines%20IDSA2017.pdf
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health. (2019). Irritable bowel syndrome. https://
www.niddk.nih.gov/health-information/digestive-diseases/
irritable-bowel-syndrome
Wald, A. (2022, April). Patient education: Irritable bowel syndrome (beyond
the basics). UpToDate. https://www.uptodate.com/contents/
irritable-bowel-syndrome-beyond-the-basics
Wald, A. (2022, April). Treatment of irritable bowel syndrome in adults. UpToDate.
https://www.uptodate.com/contents/treatment-of-irritable-bowelsyndrome-in-adults#H2957204
JAUNDICE
PATHOGENESIS
A.
The mechanism responsible for jaundice includes excess
bilirubin production, decreased hepatic uptake, impaired conjugation, intrahepatic cholestasis, extrahepatic obstruction,
and hepatocellular injury (Table 11.18). However, it is important to recognize that more than one mechanism can be operating in a given case (e.g., sickle cell anemia and HIV).
1.
Excess bilirubin production results from accelerated
red cell destruction. The excessive amounts of hemoglobin and resultant bilirubin released into the bloodstream
overwhelm the liver’s normal capacity for uptake, and an
unconjugated hyperbilirubinemia ensues.
2.
With decreased uptake and conjugation, there is often a
concurrent, acquired illness such as infection, cardiac disease, or cancer. Hereditary conditions, such as Gilbert and
Crigler–Najjar syndromes, are responsible.
3.
Intrahepatic cholestasis may occur at a number of lev-
els: intracellularly (e.g., hepatitis), at the canalicular level
(when estrogen is induced), at the ductule (phenothiazine
exposure), at the septal ducts (primary biliary cirrhosis),
and at the intralobular ducts (cholangiocarcinoma).
4.
Extrahepatic obstruction occurs when a stone, stricture,
or tumor blocks the ow of bile within the extrahepatic biliary tree. A history of gallstones, biliary tract surgery, or
malignancy may be elicited.
PREDISPOSING
A.
Previous blood transfusion.
B.
Travel to an area endemic for hepatitis.
C.
Raw shellsh consumption.
D.
Intravenous drug abuse.
E.
High-risk sexual practices.
F.
Family history of episodic jaundice.
G.
History of gallstones.
H.
Biliary obstruction/previous biliary tract surgery.
I.
Alcoholism.
J.
Chemical exposure.
K.
Working in the healthcare profession.
L.
Sickle cell disease.
M.
Pregnancy (intrahepatic cholestasis).
N.
Liver, gallbladder, and biliary tract cancer.
O.
Sepsis and hypoperfusion states.
COMMON
A.
Pruritus.
B.
Dark, tea-colored urine, from conjugated bilirubinuria.
C.
Light, clay-colored stools, from absence of bile.
D.
Fatigue.
E.
Right upper quadrant (RUQ) pain.
FACTORS
COMPLAINTS
DEFINITION
A.
Jaundice is a yellow tinge to the skin or mucous mem-
branes. It is a symptom, not a disease. The diagnostic
approach begins with gathering a comprehensive history,
physical examination, and screening laboratory tests. The differential diagnosis is formulated, and further testing may be
warranted. The onset of jaundice usually prompts the client or
family to seek medical attention. Jaundice can reect a medical emergency secondary to massive hemolysis, ascending
cholangitis, unconjugated hyperbilirubinemia in the neonatal
period, and fulminant liver failure.
INCIDENCE
A.
Incidence is variable according to pathogenesis, age, and
population.
TABLE
11.18 CLASSIFICATION OF JAUNDICE
ACCORDING TO BILE PIGMENT AND BY
MECHANISM
Unconjugated
Hyperbilirubinemia
Increased/overproduction of
bilirubin
Impaired/decreased hepatic
uptake of bilirubin
Impaired/decreased conjugation Extrahepatic cholestasis (biliary
Conjugated
Hyperbilirubinemia
Hepatocellular injury/disease
Intrahepatic cholestasis
obstruction)
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OTHER
A.
Enlarged liver.
B.
Splenomegaly.
C.
Fever.
D.
Chills.
E.
Gastrointestinal: appetite loss, weight loss, abdominal
11: GASTROINTESTINAL GUIDELINES
SIGNS AND SYMPTOMS
pain, nausea, or vomiting.
F.
Ascites.
G.
Shortness of breath.
H.
Palpitations.
I.
Ecchymosis.
J.
Steatorrhea, severe.
K.
Asterixis (tremor).
L.
Myalgias.
M.
Malaise.
SUBJECTIVE
A.
Review the onset, duration, and course of symptoms.
B.
Review the client’s medication history for drugs/herbal
DATA
products that may induce jaundice (Table 11.19).
C.
Inquire about recent blood transfusions. Are there any
known blood disorders in the client’s family history?
D.
Ask about contact with a person who has an infection,
such as infectious hepatitis.
E.
Ask about unprotected sexual activity/HIV status.
F.
Review ingestion of potentially contaminated food or
water, including Amanita mushrooms, milk, or shellsh.
G.
Ask about the client’s exposure to any toxic chemicals,
such as carbon tetrachloride, chloroform, phosphorus, arsenic, ethanol, or halothane (Fluothane).
H.
Review the client’s history of nonsterile needle punctures.
I.
Review the client’s medical/surgical history for gall-
stones, hepatitis, tumor, pancreatitis, Wilson disease, Budd–
Chiari syndrome, liver surgery, or transplantation. Is there a
family history of gallstones?
J.
Ask how much alcohol the client has ingested over the
years.
K.
Ask about dark urine or white or clay-colored stool.
L.
Inquire about dyspepsia, anorexia, nausea, vomiting, RUQ
or epigastric pain, or pain radiating to the back or shoulder
blade. Ask about the relationship of pain to eating.
M.
Inquire about fever, fatigue, malaise, loss of vigor and
strength, easy bruising, and weight loss.
N.
Review travel history.
TABLE
11.19 DRUGS AND HERBAL PRODUCTS
ASSOCIATED WITH JAUNDICE
Angiotensin-converting enzyme inhibitors
Acetaminophen (Tylenol)
Alkylated steroids
Aminobenzoic acid
Antibiotics
Antidiabetic drugs
Arsenic
Chloramphenicol
Chlorpromazine
Ethinyl estradiol/oral contraceptives/hormone replacement
Herbal medications (e.g., Jamaican bush tea)
Isoniazid
Mercaptopurine (Purinethol)
Methyldopa (Aldomet)
Monoamine oxidase inhibitors
Nitrofurantoin
Perphenazine (Trilafon)
Phenothiazine derivatives
Probenecid
Propylthiouracil
Rifampin
Sulfonamides
Tamoxifen
Total parenteral nutrition
PHYSICAL
A.
Check temperature, pulse, respirations, blood pressure,
EXAMINATION
and weight. Marked weight loss accompanied by jaundice
suggests carcinoma of the head of the pancreas or metastatic
disease obstructing the common duct. Note breath odor for
fetor hepaticus (breath of the dead).
B.
Inspect:
1.
Skin, mouth, palms, and sclera for yellow tinge. Severe
jaundice may cause greenish tinge from oxidation of bilirubin to biliverdin.
a.
In fair-skinned people, discoloration is most evident
on the face, trunk, and sclera (sclera icterus).
b.
In dark-skinned people, discoloration is most evi-
dent in the sclera and the roof of the mouth.
c.
In newborns, jaundice rst appears over the face or
upper body, then progresses over larger areas; it can
also be seen in conjunctivae of the eyes.
d.
Jaundice is most noticeable in natural sunlight. In
articial or poor light, it may be hard to detect.
2.
Skin for spider angiomata, rashes or scratches from
severe itching due to pruritus, and bruising or petechiae.
3.
Palms for erythema or overt bleeding.
4.
Chest for gynecomastia.
C.
Auscultate:
1.
Heart.
2.
Lungs.
3.
Abdomen for bowel sounds.
D.
Percuss:
1.
Abdomen.
E.
Palpate:
1.
Abdomen for tenderness, masses, liver enlargement in
RUQ, and ascites.
a.
Extrahepatic obstruction and intrahepatic cholesta-
sis may be identical in presentation.
b.
Tenderness is minimal unless cholangitis or rapid
distention occur.
c.
Splenomegaly is unlikely except in primary biliary
cirrhosis.
d.
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Gallbladder may be palpable (Courvoisier sign). A
sudden onset of pain results from passage of a stone
that becomes wedged into a common duct; fever and
sepsis shortly thereafter indicate cholangitis.
e.
Malignancy usually presents as a rock-hard mass.
f.
Absence of abdominal pain does not rule out
obstruction, especially when it develops slowly from
tumor growth or primary biliary cirrhosis.
g.
Advanced hepatocellular disease is indicated by a
small liver, signs of portal hypertension (ascites, splenomegaly, prominent abdominal venous pattern),
asterixis, peripheral edema (from hypoalbuminemia),
spider angiomata, gynecomastia, palmar erythema,
and testicular atrophy.
h.
Palpate the liver for hepatomegaly.
F.
Neurologic examination:
1.
Note the client’s level of consciousness.
2.
The asterixis test can be used to test for peripheral neu-
ritis caused by impaired liver function. Screen for a apping tremor occurring with the wrist dorsiexed.
G.
Rectal examination:
1.
Check for masses and occult blood.
DIAGNOSTIC
A.
The diagnostic approach begins with a careful history,
TESTS
physical examination, and screening laboratory studies. A differential diagnosis is formulated, and appropriate further testing is performed to narrow the diagnosis.
B.
Initial laboratory tests:
1.
Serum bilirubin: direct, indirect (unconjugated), and
total; clinically, jaundice becomes noticeable when levels
reach 2.0 to 2.5 mg/dL:
a.
Intrahepatic cholestasis and extrahepatic obstruc-
tion: elevated conjugated bilirubin, elevated serum
alkaline phosphatase (ALP), mild to moderate rise in
transaminase.
b.
Gilbert syndrome is the most common cause of
decreased uptake and unconjugated hyperbilirubinemia. This benign disorder produces recurrent
self-limited episodes of mild jaundice. Typically, the
unconjugated fraction rises to no more than 1.5 to 3.0
mg/100 mL. In Gilbert syndrome, fasting and minor
illness can precipitate jaundice.
2.
ALP:
a.
Cholestatic cause may be indicated if ALP elevation
is disproportionate to aspartate transaminase (AST)/
alanine transaminase (ALT).
3.
AST/ALT:
a.
Elevation of ALT and AST may indicate liver cell
damage or may be caused by opiates and aspirin.
b.
Aspirin use may also decrease AST and ALT.
c.
Hepatocellular injury is indicated when there is a
disproportionate elevation of AST/ALT levels when
compared with ALP.
d.
Calculate R ratio: R = (ALT value/ALT upper limit
of normal) divided by ALP value/ALP upper limit of
normal. R ratio >5 suggests hepatocellular injury. R
ration <2 suggests cholestatic injury. R ratio of 2 to 5 is
a mixed pattern.
4.
International normalized ratio (INR):
a.
INR may be elevated due to malabsorption, but this
effect is reversible by vitamin K injection.
b.
Elevated INR unresponsive to parenteral vitamin K
strongly suggests hepatocellular failure.
JAUNDICE
c.
Cholestasis and obstruction may also produce pro-
403
longation of prothrombin time (PT) but can be reversed
by vitamin K.
d.
Phenazopyridine (Pyridium) may cause a
false-positive bilirubin result.
C.
Other laboratory testing as needed:
1.
Total serum protein.
2.
Serum albumin and globulin:
a.
Albumin decreases with cirrhosis and chronic
hepatitis.
b.
Globulin increases with cirrhosis, chronic obstruc-
tive jaundice, and viral hepatitis.
c.
To interpret the albumin level, consider the client’s
dietary intake and sources of possible protein loss.
3.
Cholesterol.
4.
Lactate dehydrogenase.
5.
Gamma-glutamyl transpeptidase.
6.
Serum ammonia.
7.
Bile acid radioimmunoassay: Elevated levels indicate
hepatic disease.
8.
Serologic tests for viral hepatitis.
9.
Serum iron, transferrin, and ferritin to evaluate
hemochromatosis.
10.
Serum ceruloplasmin levels to evaluate for Wilson
disease.
11.
Alpha-1 antitrypsin activity to evaluate for alpha-1
antitrypsin deciency.
12.
Urine for bilirubin: Bilirubinuria may be an early sign
of liver disease:
a.
Collect specimens over a 2-hour period after lunch.
b.
Place the specimen in a dark brown container
and send it to the laboratory immediately to prevent
decomposition.
D.
Abdominal ultrasound is considered the screening proce-
dure of choice. More selective imaging procedures are ordered
based on clinical evaluation.
E.
Other imaging procedures:
1.
Endoscopic ultrasound (EUS).
2.
Hepatobiliary iminodiacetic acid (HIDA) scan: uses
radioactive isotopes to create a picture of the liver, gallbladder, biliary tract, and small intestines.
3.
Oral cholecystography.
4.
Endoscopic retrograde cholangiopancreatography
(ERCP).
5.
Percutaneous transhepatic cholangiography (PTC).
6.
Helical CT.
7.
Magnetic resonance cholangiopancreatography is an
alternative to ERCP.
8.
Liver biopsy may be indicated for denitive diagnosis.
DIFFERENTIAL
A.
Jaundice is a symptom, not a diagnosis.
B.
Cancer of the pancreas.
C.
Obstruction of the biliary tract.
D.
Icteric phase of hepatitis.
E.
Cirrhosis.
F.
Right-sided heart failure.
G.
Chronic hemolysis from a prosthetic heart valve.
DIAGNOSES
PLAN
A.
General interventions:
1.
Management depends on the primary diagnosis. Most
clients can be managed on an ambulatory basis, unless
they are unable to maintain hydration or begin to show
evidence of severe hepatocellular failure.
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B.
Client teaching:
1.
11: GASTROINTESTINAL GUIDELINES
Explain that jaundice is secondary to the client’s dis-
order and that a multidisciplinary team will be managing treatment (primary care provider, gastroenterologist,
pathologist, general surgeon, and radiologist).
C.
Pharmaceutical therapy:
1.
Cholestyramine 2 to 8 g orally BID may be used to help
relieve itching. Cholestyramine is ineffective with complete biliary obstruction.
2.
Over-the-counterantihistamines could be used at bed-
time (not recommended for geriatric clients).
3.
Generally, collaborate with the gastroenterologist or
general surgeon regarding medications specic to the
underlying etiology.
FOLLOW-UP
A.
See the client 2 to 4 weeks after initial diagnosis and
referral.
B.
Subsequent routine evaluations are related to the primary
diagnosis.
CONSULTATION/REFERRAL
A.
Consult with a gastroenterologist or hepatologist when
hepatocellular disease is suspected; when there is evidence
of hepatic failure, portal hypertension, or encephalopathy; or
when jaundice persists longer than 3 months.
B.
Consultation with a gastroenterologist, surgeon, or radiol-
ogist experienced in evaluation of jaundice can be very useful
when there is clinical suspicion of extrahepatic obstruction.
C.
Admission is mandatory when jaundice is complicated by
a fever and peritoneal signs indicative of cholangitis. IV antibiotics and prompt surgical consultation are required.
INDIVIDUAL
A.
Pregnancy:
1.
CONSIDERATIONS
Viral hepatitis is the most frequent cause of jaundice in
pregnancy.
2.
Intrahepatic cholestasis in pregnancy is associated
with modest maternal risks, including increased risk of
peripartum bleeding and increased likelihood of subsequent cholelithiasis.
3.
Cholestyramine resin, generally 4 g every 4 to 6 hours,
has been reported to afford some relief of pruritus in 50%
of affected females, presumably by removing a portion of
the bile acids by irreversible binding in the gut.
4.
Pregnant individuals who take cholestyramine are
at increased risk for depletion of vitamin K-dependent
coagulation factors and should be followed with serial PT
times. Such clients should also receive prophylactic vitamin K supplementation. If PT becomes prolonged, medication should be discontinued.
5.
Liver dysfunction and jaundice are common in clients
with hyperemesis gravidarum.
B.
Pediatrics:
1.
Hepatitis predominates as a cause of jaundice.
2.
Neonatal jaundice is more common when the mother
has insulin-dependent diabetes, probably resulting from
a higher hematocrit developed in utero, especially if oxygen availability is decreased. Newborn jaundice due to
liver immaturity is common. It begins on day 2, peaks at
1 week, and disappears in 2 to 3 weeks. About half of all
full-term newborns and 90% of premature newborns have
some degree of jaundice. Jaundice is usually mild and can
be treated with hydration and UV lamp exposure.
3.
Intense, persistent jaundice suggests liver disease or
severe, overwhelming infection.
4.
In infants with Rh isoimmunization who do not receive
appropriate treatment (exchange transfusion), progressive
jaundice leads to brain damage (kernicterus), death, or
severe handicap (deafness, spasticity, and choreoathetosis).
5.
Acute jaundice in young, healthy individuals suggests
acute viral hepatitis.
6.
An overdose of acetaminophen is a common cause of
jaundice in the young adult.
C.
Geriatrics:
1.
The most frequent cause of jaundice in clients older
than 65 years is choledocholithiasis (the presence of one or
more gallstones in the common bile duct).
2.
The second most frequent cause of jaundice for clients
65 years and older is cancer, especially of the gallbladder.
3.
Painless jaundice in the elderly with weight loss and a
mass, but with minimal pruritus, suggests biliary obstruction caused by cancer.
BIBLIOGRAPHY
Herrine, S. K. (2016, May). Jaundice). Merck manual: Professional version.
http://www.merckmanuals.com/professional/hepatic-and-biliarydisorders/approach-to-the-patient-with-liver-disease/jaundice
Kwo, P. Y., Chohen, S. M., & Lim, J. K. (2017). ACG clinical guideline:
Evaluation of Abnormal Liver chemistries. American Journal of
Gastroenterology, 112(1), 18–35. https://doi.org/10.1038/ajg.2016.517
Zakko, S. F. (2020). Patient education: Gallstones (beyond the basics). UpToDate.
https://www.uptodate.com/contents/gallstones-beyond-the-basics
MALABSORPTION
DEFINITION
A.
Malabsorption syndrome is a group of signs and symp-
toms that occur as a result of digestive problems and problems with absorption of nutrients. There may be a resultant
decrease in absorption of fat-soluble vitamins A, D, E, and K.
Poor absorption of carbohydrates, minerals, and proteins may
also occur.
B.
The presentation of malabsorption varies from severe
overt symptoms with weight loss to discrete oligosymptomatic changes in hematologic/laboratory tests that are found
incidentally. Malabsorption can result from congenital defects
or from acquired defects, such as bariatric surgery, and may
be either global or partial. The degree of nutrient malabsorption from bariatric surgery depends on the type of bariatric
procedure.
INCIDENCE
A.
Incidence is unknown.
PATHOGENESIS
A.
Deciency of intestinal enzymes: lactase deciency.
B.
Inadequate digestion caused by disease of the pancreas
(such as cystic brosis), pancreatic cancer, gallbladder, or liver.
C.
Change in the bacteria that normally live in the intestinal
tract.
D.
Disease of the intestinal walls, such as helminths (worms)
or parasites, tropical sprue, or celiac disease.
E.
Surgery that reduces the intestinal tract, decreasing the
area for absorption, such as bariatric surgery.
F.
Intolerance to gluten or celiac sprue.
G.
Atrophic gastritis results in hypochlorhydria and achlor-
hydria. The body does not produce enough pepsin and
MALABSORPTION
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405
hydrochloric acid to release the food-bound vitamin B12 from
protein.
PREDISPOSING
A.
Lactase deciency:
1.
Incidence is increased in African Americans, Indians,
FACTORS
and Asians.
2.
Jewish descent typically have onset in adulthood.
B.
Family history of malabsorption or cystic brosis.
C.
Use of drugs, such as mineral oil or other laxatives.
D.
Excess alcohol consumption.
E.
Travel to foreign countries.
F.
Intestinal surgery:
1.
Partial or total gastrectomy.
2.
Small bowel resections (jejunum, ileum, ileocecal).
3.
Partial or total resection of the pancreas.
G.
Chronic pancreatitis.
H.
Advanced age (increased risk for malabsorption and
malnutrition).
I.
Long-term adherence to a strict vegetarian or vegan diet
(exclusion of all forms of animal protein, including eggs and
dairy products).
J.
HIV infection.
COMMON
A.
B.
C.
D.
E.
OTHER
A.
COMPLAINTS
Diarrheal stools that are pale, greasy, and copious.
Foul-smelling stools, frequently with mucus.
Weight loss despite adequate food intake.
Gas or vague abdominal discomfort.
Anorexia.
SIGNS AND SYMPTOMS
Early malabsorption:
1.
Minimal weight loss.
2.
Softer, more frequent stools.
3.
Steatorrhea; stools “oat” due to increased trapped
gas.
4.
Abdominal discomfort.
5.
Bloating.
B.
Later signs: aforementioned symptoms plus the following:
1.
Marked weight loss.
2.
Foul-smelling, bulky, greasy stools.
C.
Malabsorption of fats and carbohydrates: previous symp-
toms plus the following:
1.
Foul-smelling, bulky, greasy, “sticky” stools that may
be difcult to ush down the toilet.
2.
Ecchymosis.
3.
Bone pain.
4.
Glossitis.
5.
Muscle tenderness.
6.
Cramping in the lower abdomen after bowel move-
ments (BMs).
D.
Malabsorption of lactose:
1.
Nausea and bloating.
2.
Cramps.
3.
Diarrhea after ingesting more than customary intake of
milk products.
4.
Absent or mild weight loss and steatorrhea.
5.
Good appetite.
E.
Edema: With severe protein depletion.
F.
Ecchymosis and bleeding disorders secondary to vitamin
K malabsorption.
G.
Vitamin malabsorption:
1.
Generalized motor weakness (pantothenic acid, vita-
min D).
2.
Peripheral neuropathy (thiamine).
3.
Sense of loss for vibration and position, anemia
(cobalamin).
4.
Night blindness, follicular hyperkeratosis (vitamin A).
5.
Seizures (biotin).
6.
Hematoma, bleeding disorders (vitamin K).
H.
Malabsorption of calcium: tetany, paresthesia, pathologic
fractures.
SUBJECTIVE
A.
Review the onset, duration, and course of symptoms.
DATA
Are there any other family members with the same history/
symptoms?
B.
Ask the client about dietary intake history; note the client’s
tolerance of dairy, fruit and wheat products.
C.
Review any changes in BMs and stool characteristics.
Utilize the Bristol Stool Form Scale.
D.
Inquire about recent travel to areas known for giardiasis or
other parasites.
E.
Document weight loss, including how much and over
what period of time.
F.
Review previous gastrointestinal (GI) surgery, including
bariatric procedures and reversals, small bowel resections,
and partial or total resection of the pancreas.
G.
Ask the client about signs and symptoms of inammatory
bowel disease, such as easy bruising, paresthesia, and sore
tongue.
H.
I.
Review current medications.
J.
Review history of chronic illness (diabetes mellitus, hyper-
thyroid, systemic lupus erythematosus, connective tissue disorder, HIV infection, history of GI cancer).
PHYSICAL
A.
Check temperature, pulse, respirations, blood pressure
EXAMINATION
(may have orthostatic hypotension), and weight. Follow serial
weight loss and plot on growth charts.
B.
Inspect:
1.
Observe the client’s general appearance, noting wast-
ing and an apathetic appearance.
2.
If the client experiences a BM after the examination,
observe the stool for volume, appearance, and presence of
blood, mucus, and gross worms/parasites.
3.
Inspect the skin for ecchymosis, jaundice, pallor, sur-
gical scars, stigmata of hyperthyroidism or hepatocellular
failure, or signs of Kaposi sarcoma. Alopecia or seborrheic
dermatitis may be present.
4.
Inspect the ears, nose, and throat for glossitis, stomati-
tis, aphthous ulcers, poor dentition, and goiter.
C.
Auscultate:
1.
Heart for tachycardia.
2.
Abdomen in all four quadrants for bowel sounds, not-
ing borborygmi.
D.
Percuss:
1.
Abdomen.
E.
Palpate:
1.
All lymph nodes; look for lymphadenopathy.
2.
Abdomen for organomegaly, focal tenderness, masses,
distention, and ascites.
F.
Neurologic examination:
1.
Assess for signs of vitamin B
deciency, including
12
motor weakness, peripheral neuropathy, or ataxia.
G.
Rectal examination:
1.
Evaluate tenderness, discharge, blood, and stool.
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11: GASTROINTESTINAL GUIDELINES
DIAGNOSTIC
A.
Assessment of stool fat: qualitative assessment on a single
TESTS
specimen.
B.
Quantitative assessment of a 72-hour stool collection while
the client is following a 100 g fat/d diet.
C.
Increased fecal fat: test for celiac disease.
D.
Abdominal ultrasound.
E.
Colonoscopy to evaluate and obtain biopsies.
F.
Upper endoscopy to evaluate and obtain biopsies.
G.
Barium studies.
H.
Consider CT of the abdomen.
I.
Magnetic resonance cholangiopancreatography to evalu-
ate the pancreas and bile ducts.
J.
Breath tests for carbohydrate malabsorption.
K.
Complete blood count and electrolytes.
L.
Serum iron, vitamin B
M.
Prothrombin time: may be prolonged due to vitamin K
, and folate concentrations.
12
deciency.
N.
Vitamin levels: Vitamins A, D, E, and K may be decreased.
O.
Total protein: may be decreased.
P.
Albumin: may be decreased.
Q.
Serum amylase.
R.
Stool for ova and parasites; obtain on alternate days
for three or more specimens because parasites are passed
intermittently.
S.
Serum immunoglobulin A (IgA): used to rule out IgA
deciency.
T.
Three-stage Schilling test: vitamin B
U.
Endoscopic ultrasound to detect the cause of malabsorp-
deciency.
12
tion due to pancreatic diseases such as chronic pancreatitis or
pancreatic malignancy.
DIFFERENTIAL
A.
Malabsorption.
B.
AIDS.
C.
Alcoholism.
D.
Worms or parasites.
E.
Cystic brosis.
F.
Failure to thrive.
G.
Crohn’s disease.
H.
Tropical sprue.
I.
Side effect from bariatric surgery.
J.
Disaccharidase deciencies (lactase).
K.
Fructose intolerance.
L.
Milk or protein allergy.
M.
Whipple disease.
N.
Zollinger–Ellison syndrome.
O.
Chronic pancreatitis.
P.
Cirrhosis.
Q.
Pancreatic insufciency.
DIAGNOSES
PLAN
A.
General interventions:
1.
Treatment depends on the underlying cause.
B.
Client teaching: See Client Teaching Guide for this chapter,
“Lactose Intolerance and Malabsorption.”
C.
Pharmaceutical therapy:
1.
Antidiarrheal agents if unknown cause.
2.
Vitamin supplements: Fat-soluble vitamins A, D, and
K are most likely to be depleted. Supplements help prevent malnutrition, even though caloric intake may be
replenished:
a.
Vitamin A: 25,000 to 50,000 U/d orally.
b.
Vitamin D: 30,000 U/d orally.
c.
Vitamin K: 4 to 12mg/d orally.
d.
Vitamin B
3.
Enzyme replacements: These replace endogenous exo-
: 1,000 g/mo by intramuscular injection.
12
crine pancreatic enzymes and aid in digestion of starches,
fat, and proteins. Pancreatic supplements are typically
expressed in U.S. Pharmacopeia Convention (USP) units:
1 international unit (IU) is equivalent to approximately 2
to 3 USP units.
a.
Pancreatin, adults and children: Doses vary with the
condition being treated. Oral doses are given before
or with meals or each snack. They may also be given
in divided doses at 1- to 2-hour intervals throughout
the day. Use with extreme caution in clients with a
known hypersensitivity to pork products.
i.
Malabsorption syndrome: 8,000 to 24,000
USP units of lipase activity; occasionally up to
36,000 units of lipase activity may be required.
Considerable dosage variation exists, partly due to
the susceptibility of pancreatin to acid–peptic inactivity in the upper GI tract.
ii.
Functional indigestion: 1,200 to 2,400 USP of
lipase activity.
b.
Pancrelipase (Creon, Pancrease, Zenpep, Viokase):
This must be given with each meal or snack.
i.
Adults and children older than 4 years: Dosage
for pancreatic exocrine dysfunction or for cystic brosis (CF) is 400 to 2,500 units/kg with meals; titrate
dose to desired clinical response. Total daily dose
should not exceed 10,000 units/kg body weight/d.
ii.
Children aged 1 to 4 years: Dosages for pan-
creatic exocrine dysfunction or for CF: 1,000 U of
lipase/kg/meal orally; dosage should be individualized to the client’s response. Adjust dose according to stool fat and nitrogen content. Dosage range:
1,000 to 25,000 units/kg/meal.
4.
Antispasmodics:
a.
Anticholinergic agents are used to reduce the cho-
linergic stimulation of colonic activity that occurs in
response to a meal.
b.
Drug of choice: dicyclomine hydrochloride
(Antispas), 10 to 20mg orally before meals.
5.
Iron and folic acid supplementation is usually required
for celiac disease.
6.
Calcium and magnesium supplementation is required
after extensive small intestine resection.
7.
Antibiotic therapy is not recommended as nonspecic
therapy. Treat with antibiotics if high suspicion of infection.
8.
Corticosteroids and anti-inammatory agents to treat
regional enteritis.
D.
Dietary management:
1.
In most clients, diet modication, such as a gluten-free
diet for celiac disease, or dietary supplements will restore
health.
2.
A lactose-free diet is recommended for clients with lac-
tose intolerance.
3.
A low-fat diet is recommended for clients with malab-
sorption due to short bowel syndrome.
FOLLOW-UP
A.
If the examination is normal, observe the client for 1 month
and have the client keep a diary of food intake and weight.
B.
For persistent malabsorption, monitor for osteoporosis/
bone mass with a dual-energy x-ray absorptiometry (DEXA)
scan.
NAUSEA AND VOMITING
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CONSULTATION/REFERRAL
A.
Any client with weight loss of 15 kg is likely to have a
life-threatening condition and requires prompt consultation
and hospitalization.
B.
Consult a gastroenterologist when malabsorption is docu-
mented by a 72-hour stool fat assessment.
C.
Consider a dietary consultation.
D.
Refer the client back to the bariatric surgeon/center,
depending on surgical complications from bariatric surgery.
E.
Consider a referral for allergy testing for milk and proteins.
INDIVIDUAL
A.
Geriatrics:
1.
CONSIDERATIONS
To identify impediments to adequate food intake, ques-
tion the client about social isolation, depression, bereavement, physical impairment, poor dentition/edentulism,
inability to x meals, and poverty.
2.
Loss of taste is sometimes responsible for poor intake
and should be checked.
BIBLIOGRAPHY
DynaMed. Malabsorption-Approach to the Patient. EBSCO Information
Services. https://www-dynamed-com.frontier.idm.oclc.org/approachto/malabsorption-approach-to-the-patient
Hammami, M. B. (2019, January 24). Malabsorption work up. Medscape.
https://emedicine.medscape.com/article/180785-workup#c4
Harreiter, J., Schindler, K., Bancher-Todesca, D., Gobel, C., Langer, F.,
Prager, G., Gessl, A., Leutner, M., Ludvik, B., Luger, A., Kautzky-Willer,
A., & Krebs, M. (2018, June 2018). Management of pregnant women
after bariatric surgery. Journal of Obesity, 1–14. https://doi.org/ https:
//doi.org/10.1155/2018/4587064
Katkin, J. (2022, April). Cystic brosis: Clinical manifestations and diagnosis.
UpToDate. https://www-uptodate-com.ckmproxy.vumc.org/contents/
cystic-fibrosis-clinical-manifestations-and-diagnosis?search=cystic
%20fibrosis&source=search_result&selectedTitle=1~150&usage_type
=default&display_rank=1
Mason, J. B. (2022April). Approach to the adult patient with suspected malab-
sorption. UpToDate. https://www.uptodate.com/contents/approach-
to-the-adult-patient-with-suspected-malabsorption#H1338969811
Sharma, G. D. (2019, May 2). Cystic brosis. Medscape. http://emedicine.
medscape.com/article/1001602-overview
NAUSEA
AND VOMITING
DEFINITION
A. Nausea
and vomiting are common symptoms of many conditions and diseases, and several terms are used to describe
these symptoms (Table 11.20).
1.
Hyperemesis gravidarum is a condition of persistent,
uncontrollable vomiting that begins in the rst weeks of
pregnancy and improves by the end of the rst trimester;
however, it may persist throughout pregnancy.
2.
Chronic nausea and vomiting is dened as lasting at
least 1 month in duration.
3.
Complications of nausea and vomiting include uid
depletion, hypokalemia, and metabolic alkalosis.
4.
Vomiting is also considered a protective mechanism to
remove harmful ingested substances.
INCIDENCE
A.
Nausea and vomiting are very common, and the etiology
depends on the disease/condition.
B.
During pregnancy, 50% to 90% of individuals experience
nausea and/or vomiting; 50% have both nausea and vomiting. Onset after the initial 9 weeks of pregnancy should direct
TABLE
11.20 DEFINITIONS OF TERMS USED TO
DESCRIBE NAUSEA AND VOMITING
Term Definition
Vomiting Forceful oral expulsion of gastric contents
associated with contraction of the abdominal
and chest wall musculature
Nausea The unpleasant sensation of the imminent need
to vomit, usually referred to the throat or
epigastrium; a sensation that may or may not
ultimately lead to vomiting
Regurgitation The act by which food is brought back into
the mouth without the abdominal and
diaphragmatic muscular activity that
characterizes vomiting
Anorexia Loss of desire to eat; a true loss of appetite
Sitophobia Fear of eating because of subsequent or
associated discomfort
Early satiety Feeling full after eating an unusually small quantity
of food
Retching Spasmodic respiratory movements against a
closed glottis with contraction of the abdominal
musculature without expulsion of any gastric
contents, referred to as “dry heaves”
Rumination Chewing and swallowing of regurgitated food that
has come back into the mouth through voluntary
increase in abdominal pressure within minutes
of eating or during eating; rumination may be
accompanied by weight loss and bulimia
especially careful evaluation for another cause within the differential diagnoses of nausea and vomiting in nonpregnant clients.
C.
Hyperemesis gravidarum occurs in as much as 2% of all
pregnancies.
D.
Severe hyperemesis requires hospitalization in 0.3% to 2%
of pregnancies.
E.
Approximately one-third of surgical clients have nausea
and/or vomiting after general anesthesia.
F.
The incidence of nausea and/or vomiting subsequent to
cancer treatment is high.
PATHOGENESIS
A.
Protective mechanisms are activated by numerous gas-
trointestinal (GI) and non-GI causes. Normal function of the
upper GI tract involves an interaction between the gut and the
central nervous system (CNS).
B.
Nausea and vomiting in pregnancy are related to increased
hormones, including human chorionic gonadotropin, estrogen, and progesterone, as well as decreased gastric motility
and relative hypoglycemia that results from a night-long fast.
PREDISPOSING
A.
Acute nausea and vomiting:
1.
Medications: digitalis toxicity, opiate use, chemother-
FACTORS
apy agents, drug withdrawal, nicotine/nicotine patches,
antibiotics, hormones, and antivirals.
2.
Ketoacidosis.
3.
Pregnancy or hormones.
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