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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2920_Библиотеки_им_академика_М_И_Перельмана
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PATIENT-TEACHING AID
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Improving circulation in your legs
Dear Patient:
To help stimulate circulation in your legs, perform these exercises (called Berger’s exercises) as
part of your regular exercise program. Do them
four times each day or as often as your physician
specifies.
Begin by lying flat on your back; then raise
your legs straight up at a 90-degree angle, and
hold this position for 2 minutes.
Now sit on the edge of a table or any flat surface
that’s high enough so that your legs don’t touch
the floor. Dangle your legs and swirl them in circles for 2 minutes.
INTERMITTENT CLAUDICATION 401
Finally, lie flat for 2 minutes; then repeat the sequence twice.
This patient-teaching aid may be reproduced by office copier for distribution to patients.
© 2011, Lippincott Williams & Wilkins.
402 INTERMITTENT CLAUDICATION
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M
EDICAL CAUSES
◆ Aortic arteriosclerotic occlusive disease.
With this disorder, intermittent claudication occurs in the buttock, hip, thigh, and calf, along
with absent or diminished femoral pulses. Bruits
can be auscultated over the femoral and iliac
arteries. Examination reveals pallor of the affected limb on elevation and profound limb
weakness. The leg may be cool to the touch.
◆ Arterial occlusion (acute). This disorder pro-
duces intense intermittent claudication. A saddle
embolus may affect both legs. Associated findings
include paresthesia, paresis, and a sensation of
cold in the affected limb. The limb is cool, pale,
and cyanotic (mottled) with absent pulses below
the occlusion. Capillary refill time is increased.
◆ Arteriosclerosis obliterans. This disorder
usually affects the femoral and popliteal arteries, causing intermittent claudication (the most
common symptom) in the calf. Typical associated findings include diminished or absent
popliteal and pedal pulses, coolness in the affected limb, pallor on elevation, and profound
limb weakness with continuing exercise. Other
possible findings include numbness, paresthesia
and, in severe disease, pain in the toes or foot
while at rest, ulceration, and gangrene.
◆ Buerger’s disease. This disorder typically
produces intermittent claudication of the instep.
Men are affected more than women; most of the
affected men smoke and are between ages 20
and 40. It’s common in the Orient, southeast
Asia, India, and the Middle East and is rare in
Blacks. Early signs include migratory superficial
nodules and erythema along extremity blood
vessels (nodular phlebitis) as well as migratory
venous phlebitis. With exposure to cold, the feet
initially become cold, cyanotic, and numb; later,
they redden, become hot, and tingle. Occasionally, Buerger’s disease also affects the hands and
can cause painful ulcerations on the fingertips.
Other characteristic findings include impaired
peripheral pulses, paresthesia of the hands and
feet, and migratory superficial thrombophlebitis.
◆ Cauda equina syndrome. Spinal stenosis
causes pressure on nerve roots resulting in
symptoms of claudication from the hip down as
with Leriche’s syndrome. Diagnosis can be determined by noninvasive exercise studies. With cauda equina syndrome, the pressure doesn’t drop
when the patient exercises on the treadmill.
◆ Leriche’s syndrome. Arterial occlusion
causes intermittent claudication of the hip,
thigh, buttocks, and calf as well as impotence in
men. Examination reveals bruits, global atrophy, absent or diminished pulses, and gangrene
of the toes. The leg becomes cool and pale
when elevated.
◆ Neurogenic claudication. Neurospinal dis-
ease causes pain from neurogenic intermittent
claudication that requires a longer rest time
than the 2 to 3 minutes needed in vascular claudication. Associated findings include paresthesia, weakness and clumsiness when walking,
and hypoactive deep tendon reflexes after walking. Pulses are unaffected.
◆ Thoracic outlet syndrome. Activity that re-
quires raising the hands above the shoulders,
lifting a weight, or abducting the arm can cause
intermittent pain along the ulnar distribution of
the arm and forearm along with paresthesia and
weakness. The pain isn’t true claudication pain
because it’s related to position, not exercise.
Signs and symptoms disappear when the arm is
lowered. Other features include asymmetrical
blood pressure and cool, pale skin.
S
PECIAL CONSIDERATIONS
Encourage the patient to exercise to improve
collateral circulation and increase venous return, and advise him to avoid prolonged sitting
or standing as well as crossing his legs at the
knees. (See Improving circulation in your legs,
page 401.) If intermittent claudication interferes
with the patient’s lifestyle, he may require diagnostic tests (Doppler flow studies, arteriography,
and digital subtraction angiography) to determine the location and degree of occlusion.
P
EDIATRIC POINTERS
Intermittent claudication rarely occurs in children. Although it sometimes develops in patients with coarctation of the aorta, extensive
compensatory collateral circulation typically prevents manifestation of this sign. Muscle cramps
from exercise and growing pains may be mistaken for intermittent claudication in children.
P
ATIENT COUNSELING
Counsel the patient with intermittent claudication about risk factors. Encourage him to stop
smoking, and refer him to a support group, if
appropriate. Teach him to inspect his legs and
feet for ulcers; to keep his extremities warm,
clean, and dry; and to avoid injury.
Urge the patient to immediately report skin
breakdown that doesn’t heal. Also urge him to
report any chest discomfort when circulation is
restored to his legs. Increased exercise tolerance may lead to angina if the patient has coronary artery disease that was previously asymptomatic because of exercise limitations.
J
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Janeway’s lesions
Slightly raised but usually flat, irregular, and
nontender, Janeway’s lesions are small (1 to
4 mm in diameter), erythematous lesions on the
palms and soles that disappear spontaneously.
They blanch with pressure or elevation of the
affected extremity; occasionally, they form a diffuse rash over the trunk and extremities.
Janeway’s lesions were once a common finding in those with infective endocarditis, possibly reflecting an immunologic reaction to the
infecting organisms (usually bacteria). These
lesions are rarely seen today because the disease is now detected and managed at an
earlier stage.
H
ISTORY AND PHYSICAL
EXAMINATION
If you observe Janeway’s lesions, obtain a medical history from the patient, noting especially
valvular or rheumatic heart disease. If the patient has had valvular or rheumatic heart disease, ask about recent dental procedures or invasive diagnostic tests. Does he have a
prosthetic replacement valve? Find out about
recent meningitis and any skin, bone, or respiratory tract infections. Does the patient have renal disease requiring an arteriovenous shunt?
Has he had recent long-term I.V. therapy such
as total parenteral nutrition? Ask him to describe how he feels. Does he report weakness,
fatigue, chills, anorexia, or night sweats, possibly indicating an infection? Does he have other
complaints?
Obtain a drug history. Find out if the patient
with valvular or rheumatic heart disease has
been taking a prophylactic antibiotic. Ask about
I.V. drug use. Note the use of any immunosuppressant.
Next, perform a physical examination. Inspect his skin for other lesions, such as petechiae on his trunk or mucous membranes, and
Osler’s nodes on his palms, soles, or finger or
toe pads. Inspect his fingers for clubbing and
splinter hemorrhages.
Take the patient’s vital signs, noting fever
and tachycardia (which may indicate heart failure if it persists after fever disappears). Inspect
and palpate his extremities for edema. Auscultate for gallops and murmurs. Assess other
body systems for embolic complications of infective endocarditis, such as acute abdominal
pain and hematuria. Examining his eyes with an
ophthalmoscope may reveal Roth’s spots, another sign of infective endocarditis.
M
EDICAL CAUSES
◆ Acute infective endocarditis. Janeway’s le-
sions are a late sign of this infectious disorder.
Early signs and symptoms include a sudden onset of shaking chills and fever, peripheral edema, dyspnea, petechiae, Osler’s nodes, Roth’s
spots, and hematuria.
◆ Subacute infective endocarditis. Janeway’s
lesions may appear late in this disorder, which
has an insidious onset. Early findings include
weakness, fatigue, weight loss, fever, night
sweats, anorexia, and arthralgia. Other signs
and symptoms include an elevated pulse, pale
403
404 JAUNDICE
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skin, Osler’s nodes, splinter hemorrhages under
the fingernails, petechiae, Roth’s spots, clubbing
of the fingers (in long-standing disease),
splenomegaly, and murmurs. Embolization may
produce acute signs and symptoms, such as
chest, abdominal, and extremity pain; paralysis;
hematuria; and blindness.
S
PECIAL CONSIDERATIONS
Tell the patient that Janeway’s lesions will disappear without damaging his skin. Treatment of
infective endocarditis includes an antibiotic
and—with complications such as heart failure—
a diuretic and cardiac glycoside. Monitor the patient’s intake, output, and cardiac status, and be
alert for embolic complications, acute chest
pain, abdominal pain, and paralysis. Prepare the
patient for diagnostic tests, such as blood cultures and an echocardiogram.
P
EDIATRIC POINTERS
In children, Janeway’s lesions result from infective endocarditis, which commonly stems from
congenital heart defects or rheumatic fever.
Jaundice
[Icterus]
A yellow discoloration of the skin, mucous
membranes, or sclera of the eyes, jaundice indicates excessive levels of conjugated or unconjugated bilirubin in the blood. In fair-skinned patients, it’s most noticeable on the face, trunk,
and sclera; in dark-skinned patients, on the
hard palate, sclera, and conjunctiva.
Jaundice is most apparent in natural sunlight.
In fact, it may be undetectable in artificial or
poor light. It’s commonly accompanied by pruritus (because bile pigment damages sensory
nerves), dark urine, and clay-colored stools.
Jaundice may result from any of three pathophysiologic processes. (See Jaundice: Impaired
bilirubin metabolism.) It may be the only warning sign of certain disorders such as pancreatic
cancer.
H
ISTORY AND PHYSICAL
EXAMINATION
Documenting a history of the patient’s jaundice
is critical in determining its cause. Begin by asking the patient when he first noticed the jaundice. Does he also have pruritus, clay-colored
stools, or dark urine? Ask about past episodes
or a family history of jaundice. Does he have
nonspecific signs or symptoms, such as fatigue,
fever, or chills; GI signs or symptoms, such as
anorexia, abdominal pain, nausea, weight loss,
or vomiting; or cardiopulmonary symptoms,
such as shortness of breath or palpitations? Ask
about alcohol use and a history of cancer or liver or gallbladder disease. Has the patient lost
weight recently? Also, obtain a drug history. Ask
about a history of hepatitis, gallstones, or liver
or pancreatic disease.
Perform the physical examination in a room
with natural light. Make sure that the orangeyellow hue is jaundice and not due to hypercarotenemia, which is more prominent on the
palms and soles and doesn’t affect the sclera.
Inspect the patient’s skin for texture and dryness and for hyperpigmentation and xanthomas. Look for spider angiomas or petechiae,
clubbed fingers, and gynecomastia. If the patient has heart failure, auscultate for arrhythmias, murmurs, and gallops. For all patients,
auscultate for crackles and abnormal bowel
sounds. Palpate the lymph nodes for swelling
and the abdomen for tenderness, pain, and
swelling. Palpate and percuss the liver and
spleen for enlargement, and test for ascites with
the shifting dullness and fluid wave techniques.
Obtain baseline data on the patient’s mental
status: Slight changes in sensorium may be an
early sign of deteriorating hepatic function. (See
Differential diagnosis: Jaundice, pages 406 and
407.)
M
EDICAL CAUSES
◆ Agnogenic myeloid metaplasia. This
myeloproliferative disorder of the bone marrow
may cause jaundice. Its typical effects, however,
are associated with anemia, including fatigue,
weakness, anorexia, massive splenomegaly, hepatomegaly, purpura, and bleeding tendencies.
◆ Carcinoma. Cancer of the ampulla of Vater
initially produces fluctuating jaundice, mild abdominal pain, recurrent fever, and chills. Occult
bleeding may be its first sign. Other findings include weight loss, pruritus, and back pain.
Hepatic cancer (primary liver cancer or another
cancer that has metastasized to the liver) may
cause jaundice by causing obstruction of the bile
duct. Even advanced cancer causes nonspecific
signs and symptoms, such as right-upperquadrant discomfort and tenderness, nausea,
weight loss, and slight fever. Examination may
reveal irregular, nodular, firm hepatomegaly, ascites, peripheral edema, a bruit heard over the
liver, and a right-upper-quadrant mass.
JAUNDICE 405
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Jaundice: Impaired bilirubin metabolism
Jaundice occurs in three forms: prehepatic, hepatic, and posthepatic. In all three, bilirubin levels
in the blood increase because of impaired metabolism.
With prehepatic jaundice, certain conditions
and disorders, such as transfusion reactions
and sickle cell anemia, cause massive hemolysis. Red blood cells rupture faster than the
liver can conjugate bilirubin, so large amounts
of unconjugated bilirubin pass into the blood,
causing increased intestinal conversion of this
bilirubin to water-soluble urobilinogen for excretion in urine and stools. (Unconjugated
bilirubin is insoluble in water, so it can’t be
directly excreted in urine.)
Hepatic jaundice results from the liver’s
inability to conjugate or excrete bilirubin,
leading to increased blood levels of conjugated and unconjugated bilirubin. This occurs
with such disorders as hepatitis, cirrhosis, and
metastatic cancer and during the prolonged
use of drugs metabolized by the liver.
With posthepatic jaundice, which occurs in pa-
tients with a biliary or pancreatic disorder,
bilirubin forms at its normal rate, but inflammation, scar tissue, a tumor, or gallstones
block the flow of bile into the intestine. This
causes an accumulation of conjugated bilirubin in the blood. Water-soluble, conjugated
bilirubin is excreted in the urine.
406 JAUNDICE
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Differential diagnosis: Jaundice
History of present illness
Focused physical examination: GI system
Common signs and symptoms
◆ Nausea and vomiting
◆ Dark urine
◆ Clay-colored stools
◆ Pruritus
Cholelithiasis
Additional signs and symptoms
◆ Biliary colic
◆ Severe, steady pain in right upper
quadrant (RUQ) or epigastrium that
radiates to the right scapula
◆ Positive Murphy’s sign
◆ Tachycardia
◆ Restlessness
◆ Dyspepsia after a fatty meal
Diagnosis: Laboratory tests (complete
blood count [CBC], liver function test,
electrolytes), imaging studies (ultrasound, computed tomography [CT]
scan, endoscopic retrograde cholangiopancreatography [ERCP], cholecystogram, hydroxy iminodiacetic acid
scan)
Treatment: Gallstone-solubilizing
agent, diet modification, surgery
Follow-up: Reevaluation every 3
months; referral to surgeon, if acute
With pancreatic cancer, progressive
jaundice—possibly with pruritus—may be the
only sign. Related early findings are nonspecific,
such as weight loss and back or abdominal
pain. Other signs and symptoms include
anorexia, nausea and vomiting, fever, steatorrhea, fatigue, weakness, diarrhea, pruritus, and
skin lesions (usually on the legs).
◆ Cholangitis. Obstruction and infection in the
common bile duct cause Charcot’s triad: jaun-
Acute hepatitis
Additional signs and symptoms
◆ Fatigue
◆ Malaise
◆ Arthralgia
◆ Myalgia
◆ Headache
◆ Anorexia
◆ Photophobia
◆ Cough
◆ Sore throat
◆ Liver and lymph node enlargement
Diagnosis: Hepatitis surface antigen or
antibody based testing (A, B, C, D)
Treatment: Based on symptoms, rest,
avoidance of alcohol and hepatotoxic
substances, safer sex practices
Follow-up: For hepatitis A and E,
reevaluation every 2 to 4 weeks; for hepatitis B, C, D, referral to hepatologist or
gastroenterologist
dice, right-upper-quadrant pain, and high fever
with chills.
◆ Cholecystitis. This disorder produces non-
obstructive jaundice in about 25% of patients.
Biliary colic typically peaks abruptly, persisting
for 2 to 4 hours. The pain then localizes to the
right upper quadrant and becomes constant. Local inflammation or passage of stones to the
common bile duct causes jaundice. Other findings include nausea, vomiting (usually indicating
Cholestasis
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Additional signs and symptoms
◆ Prolonged attacks of jaundice
◆ Fatigue
◆ Weight loss
◆ Anorexia
◆ RUQ pain
Diagnosis: History, liver function tests,
imaging studies (CT scan, magnetic
resonance imaging, cholangiography,
ultrasound, ERCP)
Treatment: Treatment of causative
factor (such as certain drugs), diet
modification, medication (antibacterial,
phenobarbital), surgery
Follow-up: Referral to gastroenterologist
JAUNDICE 407
Acute pancreatitis
Signs and symptoms
◆ Severe relentless epigastric pain
that radiates to the back
◆ Nausea
◆ Persistent vomiting
◆ Abdominal distention
◆ Turner’s or Cullen’s sign (possibly)
◆ Fever
◆ Tachycardia
◆ Hypoactive bowel sounds
◆ Abdominal rigidity and tenderness
◆ Shock (if severe)
Diagnosis: Laboratory tests (amylase, lipase, CBC, electrolytes, calcium, albumin, liver function test),
imaging studies (CT scan, ultrasound)
Treatment: Based on symptoms, I.V.
hydration, medication (analgesics,
electrolyte replacement, insulin therapy)
Follow-up: Referral to gastroenterologist
Additional differential diagnoses: agnogenic myeloid metaplasia ◆ cholangitis ◆ cholecystitis ◆ cirrhosis
◆ Dubin-Johnson syndrome ◆ glucose-6-phosphate dehydrogenase deficiency ◆ hemolytic anemia (acquired)
◆ hepatic abscess ◆ hepatic cancer ◆ leptospirosis ◆ pancreatic cancer ◆ sickle cell anemia ◆ Zieve
syndrome
Other causes: androgenic steroids
contraceptives
shunt
◆ isoniazid ◆ I.V. tetracycline ◆ mercaptopurine ◆ niacin ◆ phenothiazines ◆ portocaval
◆ sulfonamides ◆ troleandomycin ◆ upper abdominal surgery
the presence of a stone), fever, profuse diaphoresis, chills, tenderness on palpation, a
positive Murphy’s sign, and, possibly, abdominal
distention and rigidity.
◆ Cholelithiasis. This disorder commonly
causes jaundice and biliary colic. It’s characterized by severe, steady pain in the right upper
quadrant or epigastrium that radiates to the
right scapula or shoulder and intensifies over
several hours. Accompanying signs and symp-
◆ erythromycin estolate ◆ HMG-CoA reductase inhibitors ◆ hormonal
toms include nausea and vomiting, tachycardia,
and restlessness. Occlusion of the common bile
duct causes fever, chills, jaundice, clay-colored
stools, and abdominal tenderness. After consuming a fatty meal, the patient may experience
vague epigastric fullness and dyspepsia.
◆ Cholestasis. With benign, recurrent intra-
hepatic cholestasis, the patient experiences prolonged attacks of jaundice (sometimes spaced
several years apart) accompanied by pruritus.
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Other signs and symptoms are similar to those
of hepatitis—fatigue, nausea, weight loss,
anorexia, pale stools, and right-upper-quadrant
pain.
◆ Cirrhosis. With Laënnec’s cirrhosis, mild to
moderate jaundice with pruritus usually signals
hepatocellular necrosis or progressive hepatic
insufficiency. Common early findings include ascites, weakness, leg edema, nausea and vomiting, diarrhea or constipation, anorexia, weight
loss, and right-upper-quadrant pain. Massive
hematemesis and other bleeding tendencies
may also occur. Other findings include an enlarged liver and parotid gland, clubbed fingers,
Dupuytren’s contracture, mental changes, asterixis, fetor hepaticus, spider angiomas, and palmar erythema. Males may exhibit gynecomastia, scanty chest and axillary hair, and testicular
atrophy; females may experience menstrual irregularities.
With primary biliary cirrhosis, fluctuating
jaundice may appear years after the onset of
other signs and symptoms, such as pruritus that
worsens at bedtime (commonly the first sign),
weakness, fatigue, weight loss, and vague abdominal pain. Itching may lead to skin excoriation. Associated findings include hyperpigmentation; indications of malabsorption, such as
nocturnal diarrhea, steatorrhea, purpura, and
osteomalacia; hematemesis from esophageal
varices; ascites; edema; xanthelasmas; xanthomas on the palms, soles, and elbows; and
hepatomegaly.
◆ Dubin-Johnson syndrome. With this rare,
chronic inherited syndrome, fluctuating jaundice
that increases with stress is the major sign, appearing as late as age 40. Related findings include slight hepatic enlargement and tenderness, upper abdominal pain, nausea, and
vomiting.
◆ Glucose-6-phosphate dehydrogenase defi-
ciency. Acute intravascular hemolysis following
ingestion of such drugs as quinine or aspirin
causes jaundice, pallor, dyspnea, tachycardia,
and malaise. Palpation may reveal
splenomegaly and hepatomegaly.
◆ Heart failure. Jaundice due to liver dysfunc-
tion occurs in patients with severe right-sided
heart failure. Other effects include jugular vein
distention, cyanosis, dependent edema of the
legs and sacrum, steady weight gain, confusion,
hepatomegaly, nausea and vomiting, abdominal
discomfort, and anorexia due to visceral edema.
Ascites is a late sign. Oliguria, marked weakness, and anxiety may also occur. If left-sided
heart failure develops first, other findings may
include fatigue, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, tachypnea, arrhythmias,
and tachycardia.
◆ Hemolytic anemia (acquired). This disor-
der may produce prominent jaundice along with
dyspnea, fatigue, pallor, tachycardia, and palpitations. Rapid hemolysis causes chills, fever, irritability, headache, and abdominal pain; severe
hemolysis causes signs of shock.
◆ Hepatic abscess. Multiple abscesses may
cause jaundice, but the primary effects are persistent fever with chills and sweating. Other
findings include steady, severe pain in the right
upper quadrant or midepigastrium that may be
referred to the shoulder; nausea and vomiting;
anorexia; hepatomegaly; elevated right hemidiaphragm; and ascites.
◆ Hepatitis. Dark urine and clay-colored stools
usually develop before jaundice in the late
stages of acute viral hepatitis. Early systemic
signs and symptoms vary and include fatigue,
nausea, vomiting, malaise, arthralgias, myalgias, headache, anorexia, photophobia, pharyngitis, cough, diarrhea or constipation, and a
low-grade fever associated with liver and lymph
node enlargement. During the icteric phase
(which subsides within 2 to 3 weeks unless
complications occur), systemic signs subside,
but an enlarged, palpable liver may be present
along with weight loss, anorexia, and rightupper-quadrant pain and tenderness.
◆ Leptospirosis. Severe leptospirosis (Weil’s
disease) may cause jaundice. This disorder begins suddenly with a frontal headache, severe
muscle aches in the thighs and lumbar area, cutaneous hyperesthesia, abdominal pain, nausea,
conjunctival suffusion, and vomiting. Chills and
a rapidly rising fever follow. Signs and symptoms of meningeal irritation include drowsiness, decreased mentation, stiff neck, and
positive Kernig’s and Brudzinski’s signs.
Right-upper-quadrant tenderness, hepatomegaly, and jaundice indicate hepatic involvement; proteinuria, pyuria, and hematuria
indicate renal involvement. Epistaxis, hematemesis, melena, and hemoptysis may also
occur.
◆ Pancreatitis (acute). Edema of the head of
the pancreas and obstruction of the common
bile duct can cause jaundice; however, this disorder’s primary symptom is usually severe epigastric pain that commonly radiates to the back.
Lying with the knees flexed on the chest or sitting up and leaning forward brings relief. Early
JAW PAIN
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409
associated signs and symptoms include nausea,
persistent vomiting, abdominal distention, and
Turner’s or Cullen’s sign. Other findings include
fever, tachycardia, abdominal rigidity and tenderness, hypoactive bowel sounds, and crackles.
Severe pancreatitis produces extreme restlessness; mottled skin; cold, diaphoretic extremities; paresthesia; and tetany—the last two being symptoms of hypocalcemia. Fulminant
pancreatitis causes massive hemorrhage.
◆ Sickle cell anemia. Hemolysis produces
jaundice in patients with this disorder. Other
findings include impaired growth and development, increased susceptibility to infection, lifethreatening thrombotic complications and,
commonly, leg ulcers, (painful) swollen joints,
fever, and chills. Bone aches and chest pain
may also occur. Severe hemolysis may cause
hematuria and pallor, chronic fatigue, weakness, dyspnea (or dyspnea on exertion), and
tachycardia. The patient may also have
splenomegaly. During a sickle cell crisis, the patient may have severe bone, abdominal, thoracic, and muscular pain; low-grade fever; and
increased weakness, jaundice, and dyspnea.
◆ Zieve syndrome. Caused by alcohol abuse,
this relatively rare disorder produces abdominal
pain and a sudden onset of severe jaundice.
However, spider angiomas, ascites, and other
signs of advanced liver disease are absent.
O
THER CAUSES
◆ Drugs. Many drugs may cause hepatic injury
and resultant jaundice. Examples include acetaminophen, I.V. tetracycline, isoniazid, hormonal
contraceptives, sulfonamides, mercaptopurine,
erythromycin estolate, niacin, troleandomycin,
androgenic steroids, HMG-CoA reductase inhibitors, phenothiazines, ethanol, methyldopa,
rifampin, and phenytoin.
◆ Treatments. Upper abdominal surgery may
cause postoperative jaundice, which occurs secondary to hepatocellular damage from the manipulation of organs, leading to edema and obstructed bile flow; from the administration of
halothane; or from prolonged surgery resulting
in shock, blood loss, or blood transfusion.
A surgical shunt used to reduce portal hypertension (such as a portacaval shunt) may also
produce jaundice.
S
PECIAL CONSIDERATIONS
To help decrease pruritus, frequently bathe the
patient, apply an antipruritic lotion, such as
calamine, and administer diphenhydramine hydrochloride or hydroxyzine hydrochloride. Prepare the patient for diagnostic tests to evaluate
biliary and hepatic function. Laboratory studies
include urine and fecal urobilinogen, serum
bilirubin, hepatic enzyme, and cholesterol levels; prothrombin time; and a complete blood
count. Other tests include ultrasonography,
cholangiography, liver biopsy, and exploratory
laparotomy.
P
EDIATRIC POINTERS
Physiologic jaundice is common in neonates,
developing 3 to 5 days after birth. In infants, obstructive jaundice usually results from congenital biliary atresia. A choledochal cyst—a congenital cystic dilation of the common bile
duct—may also cause jaundice in children, particularly those of Japanese descent.
The list of other causes of jaundice is extensive and includes, but isn’t limited to,
Crigler-Najjar syndrome, Gilbert’s disease, Rotor’s syndrome, thalassemia major, hereditary
spherocytosis, erythroblastosis fetalis,
Hodgkin’s disease, infectious mononucleosis,
Wilson’s disease, amyloidosis, and Reye’s
syndrome.
G
ERIATRIC POINTERS
In patients older than age 60, jaundice is
usually caused by cholestasis resulting from
extrahepatic obstruction.
P
ATIENT COUNSELING
Encourage the patient with a hepatic disorder to
decrease his protein intake sharply and increase
his intake of carbohydrates. If he has obstructive jaundice, encourage a nutritious, balanced
diet (avoiding high-fat foods) and frequent small
meals.
Jaw pain
Jaw pain may arise from either of the two bones
that hold the teeth in the jaw—the maxilla (upper jaw) and the mandible (lower jaw). Jaw
pain also includes pain in the temporomandibular joint (TMJ), where the mandible meets the
temporal bone.
Jaw pain may develop gradually or abruptly
and may range from barely noticeable to excruciating, depending on its cause. It usually results from disorders of the teeth, soft tissue, or
glands of the mouth or throat or from local
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trauma or infection. Systemic causes include
musculoskeletal, neurologic, cardiovascular,
endocrine, immunologic, metabolic, and
infectious disorders. Life-threatening disorders,
such as myocardial infarction (MI) and tetany,
also produce jaw pain, as do certain drugs (especially phenothiazines) and dental or surgical
procedures.
Jaw pain is seldom a primary indicator of any
one disorder; however, some causes are medical emergencies.
EMERGENCY INTERVENTIONS Ask the
patient when the jaw pain began. Did it arise
suddenly or gradually? Is it more severe or frequent now than when it first occurred? Sudden severe jaw pain, especially when associated with
chest pain, shortness of breath, or arm pain, requires prompt evaluation because it may herald a
life-threatening disorder. Perform an electrocardiogram and obtain blood samples for cardiac
enzyme levels. Administer oxygen, morphine
sulfate, and a vasodilator as indicated.
H
ISTORY AND PHYSICAL
EXAMINATION
Begin the patient history by asking the patient
to describe the pain’s character, intensity, and
frequency. When did he first notice the jaw
pain? Where on the jaw does he feel pain? Does
the pain radiate to other areas? Sharp or burning pain arises from the skin or subcutaneous
tissues. Causalgia, an intense burning sensation, usually results from damage to the fifth
cranial, or trigeminal, nerve. This type of superficial pain is easily localized, unlike dull, aching,
boring, or throbbing pain, which originates in
muscle, bone, or joints. Also ask about aggravating or alleviating factors.
Ask about recent trauma, surgery, or procedures, especially dental work. Ask about associated signs and symptoms, such as joint or chest
pain, dyspnea, palpitations, fatigue, headache,
malaise, anorexia, weight loss, intermittent
claudication, diplopia, and hearing loss. (Keep
in mind that jaw pain may accompany more
characteristic signs and symptoms of lifethreatening disorders, such as chest pain in a
patient with an MI.)
Focus your physical examination on the jaw.
Inspect the painful area for redness, and palpate
for edema or warmth. Facing the patient directly,
look for facial asymmetry indicating swelling.
Check the TMJs by placing your fingertips just
anterior to the external auditory meatus and
asking the patient to open and close, and to
thrust out and retract his jaw. Note the presence
of crepitus, an abnormal scraping or grinding
sensation in the joint. (Clicks heard when the
jaw is widely spread apart are normal.) How
wide can the patient open his mouth? Less than
1
1
⁄8” (3 cm) or more than 23⁄8” (6 cm) between
upper and lower teeth is abnormal. Next, palpate the parotid area for pain and swelling, and
inspect and palpate the oral cavity for lesions,
elevation of the tongue, or masses.
M
EDICAL CAUSES
◆ Angina pectoris. Angina may produce jaw
pain (usually radiating from the substernal area)
and left arm pain. Angina is less severe than the
pain of an MI. It’s commonly triggered by exertion, emotional stress, or ingestion of a heavy
meal and usually subsides with rest and the administration of nitroglycerin. Other signs and
symptoms include shortness of breath, nausea
and vomiting, tachycardia, dizziness, diaphoresis, belching, and palpitations.
◆ Arthritis. With osteoarthritis, which usually
affects the small joints of the hand, aching jaw
pain increases with activity (talking, eating) and
subsides with rest. Other features are crepitus
heard and felt over the TMJ, enlarged joints with
a restricted range of motion, and stiffness on
awakening that improves with a few minutes
of activity. Redness and warmth are usually
absent.
Rheumatoid arthritis causes symmetrical
pain in all joints (commonly affecting proximal
finger joints first), including the jaw. The joints
display limited range of motion and are tender,
warm, swollen, and stiff after inactivity, especially in the morning. Myalgia is common.
Systemic signs and symptoms include fatigue,
weight loss, malaise, anorexia, lymphadenopathy, and mild fever. Painless, movable
rheumatoid nodules may appear on the
elbows, knees, and knuckles. Progressive
disease causes deformities, crepitation with
joint rotation, muscle weakness and atrophy
around the involved joint, and multiple
systemic complications.
GENDER CUE Rheumatoid arthritis usually
appears in early middle age, between ages
36 and 50, and most commonly in women.
◆ Head and neck cancer. Many types of head
and neck cancer, especially of the oral cavity
and nasopharynx, produce aching jaw pain of
insidious onset. Other findings include a history
of leukoplakia ulcers of the mucous membranes; palpable masses in the jaw, mouth, and
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