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should be performed to identify the bleeding site.
Monitor blood pressure and pulse to detect hypotension and tachycardia, and draw an arterial
blood sample for laboratory analysis to monitor
respiratory status.
H
ISTORY AND PHYSICAL
EXAMINATION
If the hemoptysis is mild, ask the patient when it
began. Has he ever coughed up blood before?
How much blood is he coughing up now and
how often? Ask about a history of cardiac, pulmonary, or bleeding disorders. If he’s receiving
anticoagulant therapy, find out which drug, its
dosage and schedule, and the duration of therapy. Is he taking other prescription drugs? Does
he smoke? Ask the patient if he has recently had
any infections or been exposed to tuberculosis.
When was his last tine test and what were the
results?
Take the patient’s vital signs and examine his
nose, mouth, and pharynx for sources of bleeding. Inspect the configuration of his chest and
look for abnormal movement during breathing,
use of accessory muscles, and retractions. Observe his respiratory rate, depth, and rhythm.
Finally, examine his skin for lesions.
Next, palpate the patient’s chest for diaphragm level and for tenderness, respiratory
excursion, fremitus, and abnormal pulsations;
then percuss for flatness, dullness, resonance,
hyperresonance, and tympany. Finally, auscultate the lungs, noting especially the quality and
intensity of breath sounds. Also auscultate for
heart murmurs, bruits, and pleural friction rubs.
Obtain a sputum specimen and examine it for
overall quantity, for the amount of blood it contains, and for its color, odor, and consistency.
M
EDICAL CAUSES
◆ Aortic aneurysm (ruptured). Rarely, an aor-
tic aneurysm ruptures into the tracheobronchial
tree, causing hemoptysis and sudden death.
◆ Blast lung injury. Although individuals with
this type of injury may not have obvious external chest injuries, they sometimes show other
indications of internal damage, such as hemoptysis. Health care providers should evaluate survivors of explosive detonations for other classic
signs and symptoms of a blast lung injury, such
as chest pain, cyanosis, dyspnea, and wheezing.
Treatment includes careful administration of fluids and oxygen to ensure tissue perfusion.
◆ Bronchial adenoma. This insidious disorder
causes recurring hemoptysis in up to 30% of pa-
EXAMINATION TIP
Identifying
hemoptysis
These guidelines will help you distinguish
hemoptysis from epistaxis, hematemesis,
and brown, red, or pink sputum.
Hemoptysis
Often frothy because it’s mixed with air, hemoptysis typically produces bright red sputum with an alkaline pH (tested with nitrazine paper). It’s strongly suggested by
respiratory signs and symptoms, including a
cough, a tickling sensation in the throat,
and blood produced from repeated coughing episodes. (You can rule out epistaxis because the patient’s nasal passages and posterior pharynx are usually clear.)
Hematemesis
Hematemesis usually originates in the GI
tract; the patient vomits or regurgitates coffee-ground material that contains food particles, tests positive for occult blood, and has
an acid pH. However, he may vomit bright
red blood or swallowed blood from the oral
cavity and nasopharynx. After an episode of
hematemesis, the patient’s stools may have
with traces of blood. Many patients with hematemesis also complain of dyspepsia.
Brown, red, or pink sputum
Brown, red, or pink sputum can result from
oxidation of inhaled bronchodilators. Sputum
that looks like old blood may result from rupture of an amebic abscess into the bronchus.
Red or brown sputum may occur in a patient
with pneumonia caused by the enterobacterium Serratia marcescens. Currant-jelly sputum occurs with Klebsiella infections.
tients along with a chronic cough and local
wheezing.
◆ Bronchiectasis. Inflamed bronchial surfaces
and eroded bronchial blood vessels cause hemoptysis, which can vary from blood-tinged
sputum to blood (in about 20% of patients). The
patient typically has a chronic cough producing
copious amounts of foul-smelling, purulent sputum. He may also exhibit coarse crackles, clubbing (a late sign), fever, weight loss, fatigue,
weakness, malaise, and dyspnea on exertion.
◆ Bronchitis (chronic). The first sign of this
disorder is typically a productive cough that
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What happens in
hemoptysis
Hemoptysis results when bronchial or pulmonary vessels bleed into the respiratory
tract. Bleeding reflects alterations in the
vascular walls and in blood-clotting mechanisms. It can result from any of the following pathophysiologic processes:
◆ hemorrhage and diapedesis of red blood
cells from the pulmonary microvasculature
into the alveoli
◆ necrosis of lung tissue that causes inflam-
mation and rupture of blood vessels or hemorrhage into the alveolar spaces
◆ rupture of an aortic aneurysm into the tra-
cheobronchial tree
◆ rupture of distended endobronchial blood
vessels from pulmonary hypertension due
to mitral stenosis
◆ rupture of a pulmonary arteriovenous fis-
tula, of bronchial or pulmonary artery collateral channels, or of pulmonary venous
collateral channels
◆ sloughing of a caseous lesion into the tra-
cheobronchial tree
◆ ulceration and erosion of the bronchial
epithelium.
lasts at least 3 months. Eventually this leads to
production of blood-streaked sputum; massive
hemorrhage is unusual. Other respiratory effects include dyspnea, prolonged expirations,
wheezing, scattered rhonchi, accessory muscle
use, barrel chest, tachypnea, and clubbing (a
late sign).
◆ Coagulation disorders. Such disorders as
thrombocytopenia and disseminated intravascular coagulation can cause hemoptysis, multisystem hemorrhaging (for example, GI bleeding
or epistaxis), and purpuric lesions.
◆ Laryngeal cancer. Hemoptysis occurs in this
cancer, but hoarseness is usually the initial sign.
Other findings may include dysphagia, dyspnea,
stridor, cervical lymphadenopathy, and neck pain.
◆ Lung abscess. In about 50% of patients, this
disorder produces blood-streaked sputum resulting from bronchial ulceration, necrosis, and
granulation tissue. Common associated findings
include a cough producing large amounts of purulent, foul-smelling sputum; fever with chills;
diaphoresis; anorexia; weight loss; headache;
weakness; dyspnea; pleuritic or dull chest pain;
and clubbing. Auscultation reveals tubular or
cavernous breath sounds and crackles. Percussion reveals dullness on the affected side.
◆ Lung cancer. Ulceration of the bronchus
commonly causes recurring hemoptysis (an early sign), which can vary from blood-streaked
sputum to blood. Related findings include a productive cough, dyspnea, fever, anorexia, weight
loss, wheezing, and chest pain (a late symptom).
◆ Plague. The pneumonic form of this acute
bacterial infection, caused by Yersinia pestis, can
produce hemoptysis, a productive cough, chest
pain, tachypnea, dyspnea, increasing respiratory
distress, and cardiopulmonary insufficiency.
Pneumonic plague begins abruptly with chills,
fever, headache, and myalgia.
◆ Pneumonia. In up to 50% of patients, Kleb-
siella pneumonia produces dark brown or red
(currant-jelly) sputum, which is so tenacious
that the patient has difficulty expelling it from
his mouth. This type of pneumonia begins
abruptly with chills, fever, dyspnea, a productive
cough, and severe pleuritic chest pain. Associated findings may include cyanosis, prostration,
tachycardia, decreased breath sounds, and
crackles.
Pneumococcal pneumonia causes pinkish or
rusty mucoid sputum. It begins with sudden
shaking chills; a rapidly rising temperature; and,
in over 80% of patients, tachycardia and tachypnea. Within a few hours, the patient typically
experiences a productive cough along with severe, stabbing, pleuritic pain that leads to rapid,
shallow, grunting respirations with splinting.
Examination reveals respiratory distress with
dyspnea and accessory muscle use, crackles,
and dullness on percussion over the affected
lung. Malaise, weakness, myalgia, and prostration accompany a high fever.
◆ Pulmonary arteriovenous fistula. Occur-
ring in young adults, this genetic disorder causes intermittent hemoptysis along with cyanosis,
clubbing, mild dyspnea, fatigue, vertigo, syncope, confusion, and speech and visual impairments. The patient may bleed from the nose,
mouth, or lips. Ruby red patches appear on the
face, tongue, skin, mucous membranes, or nail
beds.
◆ Pulmonary contusion. Blunt chest trauma
commonly causes a cough with hemoptysis.
Other signs and symptoms that appear over
several hours include dyspnea, tachypnea, chest
pain, tachycardia, hypotension, crackles, and
decreased or absent breath sounds over the affected area. Severe respiratory distress—with
oppressive dyspnea, nasal flaring, use of
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accessory muscles, extreme anxiety, cyanosis,
and diaphoresis—may develop at any time.
◆ Pulmonary edema. Severe cardiogenic or
noncardiogenic pulmonary edema commonly
causes frothy, blood-tinged pink sputum, which
accompanies severe dyspnea, orthopnea, gasping, anxiety, cyanosis, diffuse crackles, a ventricular gallop, and cold, clammy skin. This lifethreatening condition may also cause
tachycardia, lethargy, cardiac arrhythmias,
tachypnea, hypotension, and a thready pulse.
◆ Pulmonary embolism with infarction. He-
moptysis is a common finding in this lifethreatening disorder, although massive hemoptysis is rare. Typical initial symptoms are
dyspnea and anginal or pleuritic chest pain.
Other common clinical features include tachycardia, tachypnea, low-grade fever, and diaphoresis. Less common features include
splinting of the chest, leg edema, and—with a
large embolus—cyanosis, syncope, and jugular
vein distention. Examination reveals decreased
breath sounds, pleural friction rub, crackles,
diffuse wheezing, dullness on percussion, and
signs of circulatory collapse (weak, rapid pulse
and hypotension), cerebral ischemia (transient
loss of consciousness and seizures), and hypoxemia (restlessness and, particularly in elderly patients, hemiplegia and other focal neurologic deficits).
◆ Pulmonary hypertension (primary). He-
moptysis, exertional dyspnea, and fatigue generally develop late in this disorder. Angina-like
pain usually occurs with exertion and may radiate to the neck but not to the arms. Other findings include arrhythmias, syncope, cough, and
hoarseness.
◆ Pulmonary tuberculosis. Blood-streaked or
blood-tinged sputum commonly occurs in this
disorder; massive hemoptysis may occur in advanced cavitary tuberculosis. Accompanying
respiratory findings include a chronic productive
cough, fine crackles after coughing, dyspnea,
dullness on percussion, increased tactile fremitus and, possibly, amphoric breath sounds. The
patient may also develop night sweats, malaise,
fatigue, fever, anorexia, weight loss, and pleuritic chest pain.
◆ Silicosis. This chronic disorder causes a pro-
ductive cough with mucopurulent sputum that
later becomes blood streaked. Occasionally,
massive hemoptysis may occur. Other findings
include fine end-inspiratory crackles at lung
bases, exertional dyspnea, tachypnea, weight
loss, fatigue, and weakness.
◆ Systemic lupus erythematosus. In 50% of
patients with this disorder, pleuritis and pneumonitis cause hemoptysis, a cough, dyspnea,
pleuritic chest pain, and crackles. Related findings are a butterfly rash in the acute phase, nondeforming joint pain and stiffness, photosensitivity, Raynaud’s phenomenon, seizures or
psychoses, anorexia with weight loss, and lymphadenopathy.
◆ Tracheal trauma. Torn tracheal mucosa
may cause hemoptysis, hoarseness, dysphagia,
neck pain, airway occlusion, and respiratory
distress.
◆ Wegener’s granulomatosis. Necrotizing,
granulomatous vasculitis characterizes this
multisystem disorder. Findings include hemoptysis, chest pain, cough, wheezing, dyspnea,
epistaxis, severe sinusitis, and hemorrhagic skin
lesions.
O
THER CAUSES
◆ Diagnostic tests. Lung or airway injury from
bronchoscopy, laryngoscopy, mediastinoscopy,
or lung biopsy can cause bleeding and hemoptysis.
S
PECIAL CONSIDERATIONS
Comfort and reassure the patient, who may react to this alarming sign with anxiety and apprehension. If necessary, to protect the nonbleeding lung, place him in the lateral decubitus
position, with the suspected bleeding lung facing down. Perform this maneuver with caution
because hypoxemia may worsen with the
healthy lung facing up.
Prepare the patient for diagnostic tests to determine the cause of bleeding. These may include a complete blood count, a sputum culture
and smear, chest X-rays, coagulation studies,
bronchoscopy, lung biopsy, pulmonary arteriography, and a lung scan.
P
EDIATRIC POINTERS
Hemoptysis in children may stem from Goodpasture’s syndrome, cystic fibrosis, or (rarely) idiopathic primary pulmonary hemosiderosis.
Sometimes no cause can be found for pulmonary hemorrhage occurring within the first
2 weeks of life; in such cases, the prognosis is
poor.
G
ERIATRIC POINTERS
If the patient is receiving anticoagulants, determine any changes that need to be made in his
diet or medications (including over-the-counter
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drugs and natural supplements) because these
factors may affect clotting.
P
ATIENT COUNSELING
Hemoptysis usually ceases gradually during treatment of the causative disorder. Many chronic disorders, however, cause recurrent hemoptysis. Instruct the patient to report recurring episodes and
to bring a sputum specimen containing blood if
he returns for treatment or reevaluation.
Hepatomegaly
Hepatomegaly, an enlarged liver, indicates potentially reversible primary or secondary liver
disease. This sign may stem from diverse pathophysiologic mechanisms, including dilated hepatic sinusoids (in heart failure), persistently
high venous pressure leading to liver congestion (in chronic constrictive pericarditis), dysfunction and engorgement of hepatocytes (in
hepatitis), fatty infiltration of parenchymal cells
causing fibrous tissue (in cirrhosis), distention of
liver cells with glycogen (in diabetes), and infiltration of amyloid (in amyloidosis).
Hepatomegaly may be confirmed by palpation, percussion, or radiologic tests. It may be
mistaken for displacement of the liver by the diaphragm (in a respiratory disorder), by an abdominal tumor, by a spinal deformity such as
kyphosis, by the gallbladder, or by fecal material
or a tumor in the colon.
H
ISTORY AND PHYSICAL
EXAMINATION
Hepatomegaly is seldom a patient’s reason for
seeking care. It usually comes to light during
palpation and percussion of the abdomen.
If you suspect hepatomegaly, ask the patient
about his use of alcohol and exposure to hepatitis. Also ask if he’s currently ill or taking any
prescribed drugs. If he complains of abdominal
pain, ask him to locate and describe it.
Inspect the patient’s skin and sclerae for
jaundice, dilated veins (suggesting generalized
congestion), scars from previous surgery, and
spider angiomas (common in cirrhosis). Next,
inspect the contour of his abdomen. Is it protuberant over the liver or distended (possibly from
ascites)? Measure his abdominal girth.
Percuss the liver, being careful to identify
structures and conditions that can obscure dull
percussion notes, such as the sternum, ribs,
breast tissue, pleural effusions, and gas in the
colon. (See Percussing for liver size and position.)
Next, palpate the liver’s edge during deep inspiration; it’s tender and rounded in hepatitis and
cardiac decompensation, rocklike in carcinoma,
and firm in cirrhosis.
Take the patient’s baseline vital signs, and
assess his nutritional status. An enlarged liver
that’s functioning poorly causes muscle wasting, exaggerated skeletal prominences, weight
loss, thin hair, and edema.
Evaluate the patient’s level of consciousness.
When an enlarged liver loses its ability to detoxify waste products, metabolic substances toxic
to brain cells accumulate. As a result, watch for
personality changes, irritability, agitation, memory loss, inability to concentrate, poor mentation, and—in a severely ill patient—a coma.
M
EDICAL CAUSES
◆ Amyloidosis. This rare disorder can cause
hepatomegaly and mild jaundice as well as renal, cardiac, and other GI effects.
◆ Cirrhosis. Late in this disorder, the liver be-
comes enlarged, nodular, and hard. Other late
signs and symptoms affect all body systems.
Respiratory findings include limited thoracic expansion due to abdominal ascites, leading to hypoxia. Central nervous system findings include
signs and symptoms of hepatic encephalopathy,
such as lethargy, slurred speech, asterixis, peripheral neuritis, paranoia, hallucinations, extreme obtundation, and coma. Hematologic
signs include epistaxis, easy bruising, and bleeding gums. Endocrine findings include testicular
atrophy, gynecomastia, loss of chest and axillary
hair, and menstrual irregularities. Integumentary
effects include abnormal pigmentation, jaundice,
severe pruritus and dryness, poor tissue turgor,
spider angiomas, and palmar erythema.
The patient may also develop fetor hepaticus,
enlarged superficial abdominal veins, muscle atrophy, right-upper-quadrant pain that worsens
when he sits up or leans forward, and a palpable spleen. Portal hypertension—elevated pressure in the portal vein—causes bleeding from
esophageal varices.
◆ Diabetes mellitus. Poorly controlled dia-
betes in overweight patients commonly produces fatty infiltration of the liver, hepatomegaly, and right-upper-quadrant
tenderness along with polydipsia, polyphagia,
and polyuria. These features are more common
in type 2 than in type 1 diabetes. A chronically
enlarged fatty liver typically produces no symptoms except for slight tenderness.
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◆ Granulomatous disorders. Sarcoidosis, histo-
plasmosis, and other granulomatous disorders
commonly produce a slightly enlarged, firm liver.
◆ Heart failure. This disorder produces he-
patomegaly along with jugular vein distention,
cyanosis, nocturia, dependent edema of the legs
and sacrum, steady weight gain, confusion and,
possibly, nausea, vomiting, abdominal discomfort, and anorexia due to visceral edema. Ascites is a late sign. Massive right-sided heart
failure may cause anasarca, oliguria, severe
weakness, and anxiety. If left-sided heart failure
precedes right-sided heart failure, the patient
exhibits dyspnea, paroxysmal nocturnal dyspnea, orthopnea, tachypnea, arrhythmias, tachycardia, and fatigue.
◆ Hemochromatosis. This rare disease of iron
metabolism causes hepatomegaly, altered skin
pigmentation and, possibly, cardiac failure.
◆ Hepatic abscess. Hepatomegaly may ac-
company fever (a primary sign), nausea, vomiting, chills, weakness, diarrhea, anorexia, elevated right hemidiaphragm, and
right-upper-quadrant pain and tenderness.
◆ Hepatitis. In viral hepatitis, early signs and
symptoms include nausea, anorexia, vomiting,
fatigue, malaise, photophobia, sore throat,
cough, and headache. Hepatomegaly occurs in
the icteric phase and continues during the recovery phase. Also, during the icteric phase, the
early signs and symptoms diminish and others
appear: liver tenderness, slight weight loss, dark
urine, clay-colored stools, jaundice, pruritus,
right-upper-quadrant pain, and splenomegaly.
◆ Leukemia and lymphomas. These prolifer-
ative blood cell disorders commonly cause
moderate to massive hepatomegaly and
splenomegaly as well as abdominal discomfort.
General signs and symptoms include malaise,
low-grade fever, fatigue, weakness, tachycardia,
anorexia, weight loss, and bleeding disorders.
◆ Liver cancer. Primary tumors commonly
cause an enlarged, irregular, nodular, firm liver
with pain or tenderness in the right upper quadrant and a friction rub or bruit over the liver.
Common related findings are anorexia, weight
loss, cachexia, nausea, and vomiting. Peripheral
edema, ascites, jaundice, and a palpable rightupper-quadrant mass may also develop. When
metastatic liver tumors cause hepatomegaly, the
patient’s signs and symptoms reflect his primary
cancer.
◆ Mononucleosis (infectious). Occasionally,
this disorder causes hepatomegaly. Prodromal
symptoms include headache, malaise, and
EXAMINATION TIP
Percussing for
liver size and
position
With your patient in a supine position, begin
percussing at the right iliac crest and proceed up the right midclavicular line (MCL),
as shown below. The percussion note becomes dull when you reach the liver’s inferior border—usually at the costal margin but
sometimes at a lower point in a patient with
liver disease. Mark this point and then percuss down from the right clavicle, again
along the right MCL. The liver’s superior
border usually lies between the fifth and
seventh intercostal spaces. Mark the superior border.
The distance between the two marked
points represents the approximate span of
the liver’s right lobe, which normally ranges
1
from 2
⁄4⬘⬘ to 43⁄4⬘⬘ (6 to 12 cm).
Next, assess the liver’s left lobe similarly,
percussing along the sternal midline. Again,
mark the points where you hear dull percussion notes. Also, measure the span of the
left lobe, which normally ranges from 1
1
3
⁄8⬘⬘ (4 to 8 cm). Record your findings for use
as a baseline.
fatigue. After 3 to 5 days, the patient typically
develops a sore throat, cervical lymphadenopathy, and temperature fluctuations. He may also
develop stomatitis, palatal petechiae, periorbital
edema, splenomegaly, exudative tonsillitis,
pharyngitis and, possibly, a maculopapular rash.
◆ Obesity. Hepatomegaly can result from fatty
infiltration of the liver. Weight loss reduces the
liver’s size.
◆ Pancreatic cancer. In this disease, he-
patomegaly accompanies such classic signs and
1
⁄2⬘⬘ to
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symptoms as anorexia, weight loss, abdominal
or back pain, and jaundice. Other findings include nausea, vomiting, fever, fatigue, weakness, pruritus, and skin lesions (usually on the
legs).
◆ Pericarditis. In chronic constrictive pericardi-
tis, an increase in systemic venous pressure produces marked congestive hepatomegaly. Distended jugular veins (more prominent on
inspiration) are a common finding. The usual
signs of heart disease typically are absent; other
features include peripheral edema, ascites, fatigue, and decreased muscle mass.
O
THER CAUSES
◆ Drugs. Hepatomegaly is a rare but serious
side effect of drugs used to treat HIV-positive
hepatitis, such as tenofovir and lamivudine.
S
PECIAL CONSIDERATIONS
Prepare the patient for hepatic enzyme, alkaline
phosphatase, bilirubin, albumin, and globulin
studies to evaluate liver function, and for
X-rays, liver scan, celiac arteriography, computed
tomography scan, and ultrasonography to confirm hepatomegaly.
Bed rest, relief from stress, and adequate nutrition are important for the patient with hepatomegaly to help protect liver cells from further damage and to allow the liver to regenerate
functioning cells. Dietary protein intake may
need to be monitored and possibly restricted.
Ammonia, a major cause of hepatic encephalopathy, is a byproduct of protein metabolism. Hepatotoxic drugs or drugs metabolized by
the liver should be given in very small doses, if
at all. Expalin these treatment measures to the
patient.
P
EDIATRIC POINTERS
Assess hepatomegaly in children the same way
you do in adults. Childhood hepatomegaly may
stem from Reye’s syndrome; biliary atresia; rare
disorders, such as Wilson’s disease, Gaucher’s
disease, and Niemann-Pick disease; or poorly
controlled type 1 diabetes mellitus.
Hiccups
[Singultus]
Hiccups occur as a two-stage process: an involuntary, spasmodic contraction of the diaphragm
followed by sudden closure of the glottis. Their
characteristic sound reflects the vibration of
closed vocal cords as air suddenly rushes into
the lungs. (See How hiccups occur.)
Usually benign and transient, hiccups are
common and usually subside spontaneously or
with simple treatment. However, in a patient
with a neurologic disorder, they may indicate
increasing intracranial pressure or extension of
a brain stem lesion. They may also occur after
ingestion of hot or cold liquids or other irritants,
after exposure to cold, or with irritation from a
drainage tube. Persistent hiccups cause considerable distress and may lead to vomiting. Increased serum levels of carbon dioxide may inhibit hiccups; decreased levels may accentuate
them.
H
ISTORY AND PHYSICAL
EXAMINATION
Find out when the patient’s hiccups began. If
he’s also vomiting and unconscious, turn him
on his side to prevent aspiration.
If the patient is conscious, find out if the hiccups are tiring him. Ask if he has had hiccups
before, what caused them, and what made them
stop. Also, note whether he has a history of abdominal or thoracic disorders.
M
EDICAL CAUSES
◆ Abdominal distention. The most common
cause of hiccups, abdominal distention also
causes a feeling of fullness and, depending on
the cause, abdominal pain, nausea, and vomiting.
◆ Brain stem lesion. Producing persistent hic-
cups, this type of lesion causes decreased level
of consciousness, dysphagia, dysarthria, an absent corneal reflex on the side opposite the lesion, altered respiratory pattern, abnormal
pupillary response, and ocular deviation.
◆ Gastric cancer. Persistent hiccups can be
the presenting sign of this disease, which may
be accompanied by dyspepsia, abdominal pain,
anorexia, early satiety, and weight loss.
◆ Gastric dilation. Besides hiccups, possible
signs and symptoms include a sense of fullness,
epigastric pain, and regurgitation or persistent
vomiting.
◆ Gastritis. This disorder can cause hiccups
along with mild epigastric discomfort (sometimes the only symptom). The patient may develop upper abdominal pain, eructation, fever,
malaise, nausea, vomiting, hematemesis, and
melena.
◆ Increased intracranial pressure. Early find-
ings may include hiccups, drowsiness, and
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How hiccups occur
Hiccups may result from irritations in the chest or abdomen that trigger transmission of impulses
through the vagus (afferent) and phrenic (efferent) nerves to the diaphragm. Upon completion of
this reflex arc, the diaphragm contracts. The resulting abrupt intake of air is promptly cut off as the
glottis snaps shut.
Glottis
Phrenic nerve
Vagus nerve
Irritation of vagus
nerve branches
Diaphragm
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headache. Classic later signs include changes in
pupillary reactions and respiratory pattern, increased systolic pressure, and bradycardia.
◆ Pancreatitis. Hiccups, vomiting, and sudden
and steady epigastric pain (often radiating to
the back) may occur in this disorder. A severe
attack may cause persistent vomiting, extreme
restlessness, fever, and abdominal tenderness
and rigidity.
◆ Pleural irritation. Besides hiccups, this con-
dition may cause cough, dyspnea, or chest pain.
◆ Renal failure. Hiccups may occur in the late
stages of both chronic and acute renal failure.
Associated signs and symptoms affect every
body system and include fatigue, oliguria or
anuria, nausea, vomiting, confusion, yellowbrown or bronze skin, uremic frost, ammonia
breath odor, bleeding tendencies, gum ulcerations, asterixis, and Kussmaul’s respirations.
O
THER CAUSES
◆ Surgery. Mild and transient attacks of hic-
cups occasionally follow abdominal surgery.
S
PECIAL CONSIDERATIONS
Teach the patient simple methods of relieving
hiccups, such as holding his breath repeatedly
or rebreathing into a paper bag (both of which
increase his serum carbon dioxide level). Other
treatments for hiccups include gastric lavage or
applying finger pressure on the eyeballs
(through closed lids). Hiccups may also be relieved by briefly applying ice cubes to both sides
of the neck at the level of the larynx. If hiccups
persist, a phenothiazine (especially chlorpromazine), metoclopramide, or nasogastric intubation may provide relief. (Caution: The tube
may cause vomiting.) If simpler methods fail,
treatment may include a phrenic nerve block.
P
EDIATRIC POINTERS
In an infant, hiccups usually result from rapid
ingestion of liquids without adequate burping.
Tell parents to hold the infant upright during
feedings.
nausea and vomiting, can indicate worsening or
acute decompensation of renal function.
Hirsutism
Hirsutism is the excessive growth of coarse
body hair in females. Excessive production of
androgens (male hormones) stimulates hair
growth on the pubic region, axillae, chin, upper
lip, cheeks, anterior neck, sternum, linea alba,
forearms, upper arms, abdomen, and back. This
condition may also occur in a patient with normal levels of androgens whose skin is more
sensitive to the hormones. In mild hirsutism,
fine and pigmented hair appears on the sides of
the face and the chin (but doesn’t form a complete beard) and on the extremities, chest, abdomen, and perineum. In moderate hirsutism,
coarse and pigmented hair appears on the same
areas. In severe hirsutism, coarse hair also covers the whole beard area, the proximal interphalangeal joints, and the ears and nose.
Depending on the degree of excess androgen
production, hirsutism may be associated with
acne and increased skin oiliness, increased libido, and menstrual irregularities (including
anovulation and amenorrhea). Extremely high
androgen levels cause further virilization, including such signs as breast atrophy, loss of female body contour, frontal balding, and deepening of the voice. (See Recognizing signs of
virilization.)
Hirsutism may result from endocrine abnormalities and idiopathic causes. It may also occur in pregnancy from transient androgen production by the placenta or corpus luteum, and
in menopause from increased androgen and decreased estrogen production. Some patients
have a strong familial predisposition to hirsutism, which may be considered normal for
their genetic background, culture, and race. Although hirsutism is a female characteristic, excessive hair growth may also be present in male
family members.
P
ATIENT COUNSELING
If abdominal distention is the probable cause of
hiccups, teach the patient lifestyle changes,
such as eating smaller, more frequent meals
and avoiding large meals before bedtime. Also,
advise the patient to increase fiber and fluid intake to avoid constipation.
Warn the patient with chronic renal failure
that persistent hiccups, usually accompanied by
H
ISTORY AND PHYSICAL
EXAMINATION
Begin by asking the patient where on her body
she first noticed excessive hair. How old was
she then? Where and how quickly did other hirsute areas develop? Does she use any hair removal technique? If so, how often does she use
it, and when did she use it last? Next, obtain a
menstrual history: the patient’s age at menar-
HIRSUTISM
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Recognizing signs of virilization
Excessive androgen levels produce severe hirsutism and other marked signs of virilization, as
shown in the figure below.
Temporal hair
recession
Acne
Deepening of the voice
Oily, malodorous
perspiration
Breast atrophy
Muscle hypertrophy
379
Clitoral enlargement
che, the duration of her periods, the usual
amount of blood flow, and the number of days
between periods.
Ask about medications, too. If the patient is
taking a drug containing an androgen or progestin compound, or another drug that can cause
hirsutism, find out its name, dosage, schedule,
and therapeutic aim. Does she sometimes miss
doses or take extra ones?
Next, examine the hirsute areas. Does excessive hair appear only on the upper lip or on
Loss of female body
contour
other body parts as well? Is the hair fine and
pigmented, or dense and coarse? Is the patient
obese? Observe her for other signs of virilization.
M
EDICAL CAUSES
◆ Acromegaly. About 15% of patients with this
chronic, progressive disorder display hirsutism.
Acromegaly also causes enlarged hands and feet,
coarsened facial features, prognathism, increased
diaphoresis and need for sleep, oily skin, fatigue,
weight gain, heat intolerance, and lethargy.
380 HOARSENESS
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◆ Adrenocortical carcinoma. This disorder
produces rapidly progressive hirsutism along
with truncal obesity, buffalo hump, moon face,
oligomenorrhea, amenorrhea, muscle wasting,
and thin skin with purple striae. The patient
also exhibits muscle weakness, excessive diaphoresis, poor wound healing, weakness, fatigue, hypertension, hyperpigmentation, and
personality changes.
◆ Androgen overproduction by ovaries. The
most common cause of hirsutism, this condition
is associated with anovulation that progresses
slowly over several years.
◆ Cushing’s syndrome (hypercortisolism).
This disorder commonly causes increased hair
growth on the face, abdomen, breasts, chest, or
upper thighs. Other findings include truncal
obesity, buffalo hump, moon face, thin skin with
purple striae, ecchymosis, petechiae, muscle
wasting and weakness, poor wound healing,
hypertension, weakness, fatigue, excessive diaphoresis, hyperpigmentation, menstrual irregularities, and personality changes.
◆ Hyperprolactinemia. This disorder produces
hirsutism, hypogonadism, galactorrhea, amenorrhea, and acne.
◆ Idiopathic hirsutism. In patients with nor-
mal-sized ovaries, normal menses, and no evidence of adrenal hyperplasia or adrenal or ovarian tumors, excess hair appears at puberty and
increases into early adulthood. It’s accompanied
by acne, obesity, infrequent menses or anovulation, and thick, oily skin. Idiopathic hirsutism with
regular ovulation and no menstrual abnormalities
may be hereditary or related to certain ethnic
groups who are hypersensitive to androgens.
◆ Ovarian tumor. An ovarian tumor may pro-
duce no symptoms, or it can cause rapidly progressing hirsutism (only if the tumor produces
androgens) as well as amenorrhea and rapidly
developing virilization.
◆ Polycystic ovary disease. Ovarian cysts,
particularly chronic ones, can cause hirsutism.
This hirsutism usually occurs after the onset of
menstrual irregularities, which may begin at puberty. The patient may also be obese and have
amenorrhea, oligomenorrhea, menometrorrhagia, infertility, insulin resistance and diabetes,
and acne.
O
THER CAUSES
◆ Drugs. Hirsutism can result from drugs con-
taining androgens or progestins or from
aminoglutethimide, glucocorticoids, metoclopramide, cyclosporine, and minoxidil.
S
PECIAL CONSIDERATIONS
Prepare the patient for tests to determine blood
levels of luteinizing hormone, folliclestimulating hormone, prolactin, and other hormones. Other tests may include computed tomography scan and ultrasonography.
At the patient’s request, provide information
on hair removal methods, such as bleaching,
tweezing, hot wax treatments, chemical depilatories, shaving, and electrolysis. Inform the patient that electrolysis should be done only by a
licensed professional.
P
EDIATRIC POINTERS
Childhood hirsutism can stem from congenital
adrenal hyperplasia. This disorder is usually detected at birth because affected infants have
ambiguous genitalia. Rarely, a mild form becomes apparent after puberty when hirsutism,
irregular bleeding or amenorrhea, and signs of
virilization appear. Hirsutism that occurs at or
after puberty often results from polycystic ovary
disease.
Give the parents as well as the child emotional support and clear explanations about the
cause of hirsutism. Allow the parents and child
to express their concerns separately.
G
ERIATRIC POINTERS
Hirsutism can occur after menopause if peripheral conversion of estrogen is poor.
P
ATIENT COUNSELING
Help relieve the patient’s anxiety by explaining
the cause of excessive hair growth and by encouraging her to talk about her self-image problems or fears. Involve the family in your discussions.
Tell the patient that hormonal treatment
stops further hair growth but doesn’t always reverse hair growth that has already occurred.
Treatment requires at least 6 to 24 months and
may be lifelong.
Hoarseness
Hoarseness—a rough or harsh sound to the
voice—can result from infections, inflammatory
lesions, or exudates of the larynx; from laryngeal edema; and from compression or disruption of the vocal cords or recurrent laryngeal
nerve. This common sign can also result from a
thoracic aortic aneurysm, vocal cord paralysis,
and systemic disorders, such as Sjögren’s syn-
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