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258 EDEMA, GENERALIZED
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Understanding fluid balance
Normally, fluid moves freely between the interstitial and intravascular spaces to maintain
homeostasis. Four basic types of pressure control fluid shifts across the capillary membrane
that separates these spaces:
◆ capillary hydrostatic pressure (the internal
fluid pressure on the capillary membrane)
◆ interstitial fluid pressure (the external fluid
pressure on the capillary membrane)
◆ osmotic pressure (the fluid-attracting pres-
sure from protein concentration within the
capillary)
◆ interstitial osmotic pressure (the fluid-attract-
ing pressure from protein concentration outside the capillary).
INTERSTITIAL FLUID
Capillary
Artery
Arteriole
Here’s how these pressures maintain homeostasis. Normally, capillary hydrostatic pressure
is greater than plasma osmotic pressure at the
capillary’s arterial end, forcing fluid out of the
capillary. At the capillary’s venous end, the reverse is true: The plasma osmotic pressure is
greater than the capillary hydrostatic pressure,
drawing fluid into the capillary. Normally, the
lymphatic system transports excess interstitial
fluid back to the intravascular space.
Edema results when this balance is upset by
increased capillary permeability, lymphatic obstruction, persistently increased capillary hydrostatic pressure, decreased plasma osmotic
or interstitial fluid pressure, or dilation of precapillary sphincters.
Venule
Vein
Fluid leaves Fluid enters
capillary Capillary membrane capillary
loss or coarsening, and psychomotor slowing.
Associated findings include hoarseness, weight
gain, fatigue, cold intolerance, bradycardia, hypoventilation, constipation, abdominal distention, menorrhagia, impotence, and infertility.
◆ Nephrotic syndrome. Although nephrotic
syndrome is characterized by generalized pitting
edema, the edema is initially localized around
the eyes. Anasarca develops in severe cases, increasing body weight by up to 50%. Other common signs and symptoms are ascites, anorexia,
fatigue, malaise, depression, and pallor.
◆ Pericardial effusion. In pericardial effusion,
generalized pitting edema may be most promi-
INTERSTITIAL FLUID
nent in the arms and legs. It may be accompanied by chest pain, dyspnea, orthopnea, a nonproductive cough, pericardial friction rub, jugular vein distention, dysphagia, and fever.
◆ Pericarditis (chronic constructive). Like
right-sided heart failure, this disorder usually
begins with pitting edema of the arms and legs
that may progress to generalized edema. Other
signs and symptoms include ascites, Kussmaul’s
sign, dyspnea, fatigue, weakness, abdominal
distention, and hepatomegaly.
◆ Protein-losing enteropathy. Increased albu-
min levels lead to progressive generalized pitting edema in this disorder. The patient may
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EXAMINATION TIP
Edema: Pitting or nonpitting?
To differentiate pitting from nonpitting edema, press your finger against a swollen area for 5 seconds, and then quickly remove it.
In pitting edema, pressure forces
fluid into the underlying tissues,
causing an indentation that fills
slowly. To determine the severity
of pitting edema, estimate the indentation’s depth in centimeters:
1+ (1 cm), 2+ (2 cm),
3+ (3 cm), or 4+ (4 cm).
In nonpitting edema, pressure
leaves no indentation because fluid has coagulated in the tissues.
Typically, the skin feels unusually
tight and firm.
TESTING FOR PITTING EDEMA PITTING EDEMA
also have a mild fever and abdominal pain with
bloody diarrhea and steatorrhea.
◆ Renal failure. Generalized pitting edema is
a late sign of acute renal failure. In chronic failure, edema is less likely to become generalized;
its severity depends on the degree of fluid overload. Both forms of renal failure cause oliguria,
anorexia, nausea and vomiting, drowsiness,
confusion, hypertension, dyspnea, crackles,
dizziness, and pallor.
◆ Septic shock. A late sign of this life-
threatening disorder, generalized edema typically develops rapidly. The edema is pitting and
moderately severe. Accompanying it may be cool
skin, hypotension, oliguria, tachycardia, cyanosis,
thirst, anxiety, and signs of respiratory failure.
O
THER CAUSES
◆ Drugs. Any drug that causes sodium reten-
tion may aggravate or cause generalized edema. Examples include antihypertensives, corticosteroids, androgenic and anabolic steroids,
estrogens, and nonsteroidal anti-inflammatory
drugs, such as ibuprofen and naproxen.
◆ Treatments. I.V. saline solution infusions and
internal feedings may cause sodium and fluid
overload, resulting in generalized edema, especially in patients with cardiac or renal disease.
S
PECIAL CONSIDERATIONS
Position the patient with his limbs above heart
level to promote drainage. Periodically reposition him to avoid pressure ulcers. If the patient
develops dyspnea, lower his limbs, elevate the
head of the bed, and administer oxygen. Massage areas where dependent edema has formed
(for example, the back, sacrum, hips, and buttocks). Prevent skin breakdown in these areas
by placing a pressure mattress on the patient’s
bed. Restrict fluids and sodium, and administer
a diuretic.
Monitor intake and output and daily weight.
Also monitor serum electrolyte levels, especially
sodium and albumin. Prepare the patient for
blood and urine tests, X-rays, echocardiography,
or an electrocardiogram.
P
EDIATRIC POINTERS
Renal failure in children commonly causes generalized edema. Monitor fluid balance closely.
Remember that fever or diaphoresis can lead to
fluid loss, so promote fluid intake.
Kwashiorkor (protein-deficiency malnutrition)
is more common in children than in adults and
causes anasarca.
G
ERIATRIC POINTERS
Elderly patients are more likely to develop edema for several reasons, including decreased
cardiac and renal function and, in some cases,
poor nutritional status. Use caution when giving
older patients I.V. fluids or medications that can
raise sodium levels and thereby increase fluid
retention.
P
ATIENT COUNSELING
Teach patients with known heart failure or renal
failure to watch for edema; explain that it’s an
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important sign of decompensation that indicates
the need for immediate adjustment of therapy.
Also teach patients to weigh themselves every
day at the same time with the same clothes on
to track if they have an increase in weight, which
may correspond to increased fluid retention.
Edema of the arm
The result of excess interstitial fluid in the arm,
this type of edema may be unilateral or bilateral
and may develop gradually or abruptly. It may
be aggravated by immobility and alleviated by
arm elevation and exercise.
Arm edema signals a localized fluid imbal-
ance between the vascular and interstitial
spaces. (See Understanding fluid balance, page
258.) It commonly results from trauma, venous
disorders, toxins, or certain treatments.
EMERGENCY INTERVENTIONS Remove
rings, bracelets, and watches from the
patient’s affected arm because they may act as a
tourniquet. Make sure the patient’s sleeves don’t
inhibit drainage of fluid or blood flow.
H
ISTORY AND PHYSICAL
EXAMINATION
When taking the patient’s history, one of the first
questions to ask is “How long has your arm
been swollen?” Then find out if the patient also
has arm pain, numbness, or tingling. Does exercise or arm elevation decrease the edema? Ask
about recent arm injury, such as burns or insect
stings. Also, note recent I.V. therapy, surgery, or
radiation therapy for breast cancer.
Determine the edema’s severity by comparing
the size and symmetry of both arms. Use a tape
measure to determine the exact girth. Be sure to
note whether the edema is unilateral or bilateral, and test for pitting. (See Edema: Pitting or
nonpitting? page 259.) Next, examine and compare the color and temperature of both arms.
Look for erythema and ecchymoses and for
wounds that suggest injury. Palpate and compare the radial and brachial pulses. Finally, look
for arm tenderness and decreased sensation or
mobility. If you detect signs of neurovascular
compromise, elevate the arm.
M
EDICAL CAUSES
◆ Angioneurotic edema. Angioneurotic ede-
ma is a common reaction that’s characterized
by sudden onset of painless, nonpruritic edema
in the hands, feet, eyelids, lips, face, neck, geni-
talia, or viscera. Although these swellings usually don’t itch, they may burn and tingle. If edema spreads to the larynx, signs of respiratory
distress may occur.
◆ Arm trauma. Shortly after a crush injury, se-
vere edema may affect the entire arm. It may be
accompanied by ecchymoses or superficial
bleeding, pain or numbness, and paralysis.
◆ Burns. Mild to severe edema, pain, and tis-
sue damage may occur up to 2 days after an
arm burn.
◆ Superior vena cava syndrome. Bilateral
arm edema usually progresses slowly in this
disorder and is accompanied by facial and neck
edema. Dilated veins mark these edematous areas. The patient also complains of headache,
vertigo, and vision disturbances.
◆ Thrombophlebitis. Thrombophlebitis, which
can result from peripherally inserted central
catheters or arm portacaths, may cause arm
edema, pain, and warmth. Deep vein thrombophlebitis can also produce cyanosis, fever,
chills, and malaise; superficial thrombophlebitis
also causes redness, tenderness, and induration
along the vein.
O
THER CAUSES
◆ Envenomation. Envenomation by snakes,
aquatic animals, or insects initially may cause
edema around the bite or sting that quickly
spreads to the entire arm. Pain, erythema, and
pruritus at the site are common; paresthesia
occurs occasionally. Later, the patient may develop generalized signs and symptoms, such
as nausea, vomiting, weakness, muscle
cramps, fever, chills, hypotension, headache
and, in severe cases, dyspnea, seizures, and
paralysis.
◆ Treatments. Localized arm edema may re-
sult from infiltration of I.V. fluid into the interstitial tissue. A radical or modified radical mastectomy that disrupts lymphatic drainage may
cause edema of the entire arm, as can axillary
lymph node dissection. Also, radiation therapy
for breast cancer may produce arm edema immediately after treatment or months later.
S
PECIAL CONSIDERATIONS
Treatment of the patient with arm edema varies
according to the underlying cause. General care
measures include elevation of the arm, frequent
repositioning, and appropriate use of bandages
and dressings to promote drainage and circulation. Provide meticulous skin care to prevent
breakdown and formation of pressure ulcers.
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261
Also, administer an analgesic and anticoagulant
as needed.
P
EDIATRIC POINTERS
Arm edema rarely occurs in children, except as
part of generalized edema, but it may result from
arm trauma, such as burns and crush injuries.
P
ATIENT COUNSELING
Warn the patient who has undergone a mastectomy or axillary lymph node dissection of the
possibility of arm edema, and advise her not to
have blood pressure measurements taken or
phlebotomies performed on the affected arm.
Teach the patient how to perform arm exercises
after surgery to prevent lymphedema.
Edema of the face
Facial edema refers to either localized
swelling—around the eyes, for example—or
more generalized facial swelling that may extend to the neck and upper arms. Occasionally
painful, this sign may develop gradually or
abruptly. Sometimes it precedes onset of peripheral or generalized edema. Mild facial edema
may be difficult to detect; the patient or someone
who’s familiar with his appearance may report it
before it’s noticed during assessment.
Facial edema results from disruption of the
hydrostatic and osmotic pressures that govern
fluid movement between the arteries, veins, and
lymphatics. (See Understanding fluid balance,
page 258.) It may result from venous, inflammatory, and certain systemic disorders; trauma; allergy; malnutrition; or the effects of certain
drugs, tests, and treatments.
EMERGENCY INTERVENTIONS If the
patient has facial edema associated with
burns or if he reports recent exposure to an
allergen, quickly evaluate his respiratory status:
Edema may also affect his upper airway, causing
a life-threatening obstruction. If you detect audible wheezing, inspiratory stridor, or other signs of
respiratory distress, administer epinephrine. For
patients in severe distress—with absent breath
sounds and cyanosis—tracheal intubation,
cricothyroidotomy, or tracheotomy may be
required. Always administer oxygen.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t in severe distress, take his
health history. Ask if facial edema developed
suddenly or gradually. Is it more prominent in
early morning, or does it worsen throughout the
day? Has the patient gained weight? If so, how
much and over what length of time? Has he noticed a change in his urine color or output? In
his appetite? Take a drug history and ask about
recent facial trauma.
Begin the physical examination by characterizing the edema. Is it localized to one part of the
face, or does it affect the entire face or other
parts of the body? Determine if the edema is pitting or nonpitting, and grade its severity. (See
Edema: Pitting or nonpitting? page 259.) Next,
take vital signs and assess neurologic status.
Examine the oral cavity to evaluate dental hygiene and look for signs of infection. Visualize
the oropharynx and look for any soft-tissue
swelling.
M
EDICAL CAUSES
◆ Abscess, periodontal. This type of abscess,
which usually results from poor oral hygiene, is
commonly caused by anaerobic organisms. It
can cause edema of the side of the face, pain,
warmth, erythema, and a purulent discharge
around the affected tooth.
◆ Abscess, peritonsillar. This complication of
tonsillitis may cause unilateral facial edema.
Other key signs and symptoms include severe
throat pain, neck swelling, drooling, cervical
adenopathy, fever, chills, and malaise.
◆ Allergic reaction. Facial edema may charac-
terize both a local allergic reaction and anaphylaxis. A local reaction produces facial edema,
erythema, and urticaria. In life-threatening anaphylaxis, angioneurotic facial edema may occur
with urticaria and flushing. (See Recognizing an-
gioneurotic edema, page 262.) Airway edema
causes hoarseness, stridor, and bronchospasm
with dyspnea and tachypnea. Signs of shock,
such as hypotension and cool, clammy skin,
may also occur.
◆ Cavernous sinus thrombosis. Cavernous si-
nus thrombosis is a rare but serious disorder
that may begin with unilateral edema that
quickly progresses to bilateral edema of the
forehead, base of the nose, and eyelids. It may
also produce chills, fever, headache, nausea,
lethargy, exophthalmos, and eye pain.
◆ Chalazion. A chalazion causes localized
swelling and tenderness of the affected eyelid,
accompanied by a small red lump on the conjunctival surface.
◆ Conjunctivitis. Conjunctivitis is an inflam-
mation that causes eyelid edema, excessive
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Recognizing
angioneurotic edema
Most dramatic in the lips, eyelids, and
tongue, angioneurotic edema commonly results from an allergic reaction. It’s characterized by rapid onset of painless, nonpitting, subcutaneous swelling that usually
resolves in 1 to 2 days. This type of edema
may also involve the hands, feet, genitalia,
and viscera; laryngeal edema may cause
life-threatening airway obstruction.
tearing, and itchy, burning eyes. Inspection reveals a thick purulent discharge, crusty eyelids,
and conjunctival injection. Corneal involvement
causes photophobia and pain.
◆ Corneal ulcers, fungal. Accompanying red,
edematous eyelids in this disorder are conjunctival injection, intense pain, photophobia, and severely impaired visual acuity. Copious amounts
of a purulent eye discharge make the eyelids
sticky and crusted. The characteristic dense,
central ulcer grows slowly, is whitish gray, and is
surrounded by progressively clearer rings.
◆ Dacryoadenitis. Severe periorbital swelling
characterizes dacryoadenitis, which may also
cause conjunctival injection, a purulent discharge, and temporal pain.
◆ Dacryocystitis. Lacrimal sac inflammation
causes prominent eyelid edema and constant
tearing. In acute cases, pain and tenderness near
the tear sac accompany a purulent discharge.
◆ Dermatomyositis. Periorbital edema and a
heliotropic rash develop gradually in this rare
disease. An itchy, lilac-colored rash appears on
the bridge of the nose, cheeks, and forehead.
Localized or diffuse erythema, eye pain, and
fever may also occur.
◆ Facial burns. Burns may cause extensive
edema that impairs respiration. Additional findings include singed nasal hairs, red mucosa,
sooty sputum, and signs of respiratory distress
such as inspiratory stridor.
◆ Facial trauma. The extent of edema varies
with the type of injury. For example, a contusion
may cause localized edema, whereas a nasal or
maxillary fracture causes more generalized edema. Associated features also depend on the
type of injury.
◆ Frontal sinus cancer. This rare form of can-
cer causes cheek edema on the affected side,
reddened skin over the sinus, unilateral nasal
bleeding or discharge, and exophthalmos. Pain
over the forehead and unilateral hypoesthesia
or anesthesia may occur later.
◆ Herpes zoster ophthalmicus (shingles). In
herpes zoster ophthalmicus, edematous and red
eyelids are usually accompanied by excessive
tearing and a serous discharge. Severe unilateral facial pain may occur several days before
vesicles erupt.
◆ Hordeolum (stye). Typically, a hordeolum
produces localized eyelid edema, erythema, and
pain.
◆ Malnutrition. Severe malnutrition causes fa-
cial edema followed by swelling of the feet and
legs. Associated signs and symptoms include
muscle atrophy and weakness; anorexia; diarrhea; lethargy; dry, wrinkled skin; sparse, brittle,
easily plucked hair; and decreased pulse and
respiratory rates.
◆ Melkersson’s syndrome. Facial edema (es-
pecially of the lips), facial paralysis, and folds in
the tongue are the three characteristic signs of
this rare disorder.
◆ Myxedema. Myxedema eventually causes
generalized facial edema, waxy dry skin, hair
loss or coarsening, and other signs of hypothyroidism.
◆ Nephrotic syndrome. Commonly the first
sign of nephrotic syndrome, periorbital edema
precedes dependent and abdominal edema. Associated findings include weight gain, nausea,
anorexia, lethargy, fatigue, and pallor.
◆ Orbital cellulitis. Sudden onset of perior-
bital edema marks this inflammatory disorder. It
may be accompanied by a unilateral purulent
discharge, hyperemia, exophthalmos, conjunctival injection, impaired extraocular movements,
fever, and extreme orbital pain.
◆ Osteomyelitis. When osteomyelitis affects
the frontal bone, it may cause forehead edema
as well as fever, chills, headache, and cool, pallid skin.
◆ Preeclampsia. Edema of the face, hands,
and ankles is an early sign of this disorder of
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pregnancy. Other characteristics include excessive weight gain, severe headache, blurred vision, hypertension, and midepigastric pain.
◆ Rhinitis, allergic. In allergic rhinitis, red and
edematous eyelids are accompanied by paroxysmal sneezing, itchy nose and eyes, and profuse, watery rhinorrhea. The patient may also
develop nasal congestion, excessive tearing,
headache, sinus pain, and sometimes malaise
and fever.
◆ Sinusitis. Frontal sinusitis causes edema of
the forehead and eyelids. Maxillary sinusitis
produces edema in the maxillary area as well as
malaise, gingival swelling, and trismus. Both
types are also accompanied by facial pain,
fever, nasal congestion, a purulent nasal discharge, and red, swollen nasal mucosa.
◆ Superior vena cava syndrome. Superior
vena cava syndrome gradually produces facial
and neck edema accompanied by thoracic or
jugular vein distention. It also causes central
nervous system symptoms, such as headache,
vision disturbances, and vertigo.
◆ Trachoma. In trachoma, edema affects the
eyelid and conjunctiva and is accompanied by eye
pain, excessive tearing, photophobia, and eye discharge. Examination reveals an inflamed preauricular node and visible conjunctival follicles.
◆ Trichinosis. This relatively rare infectious
disorder causes sudden onset of eyelid edema
with fever (102⬚ F to l04⬚ F [38.9⬚ C to 40⬚ C]),
conjunctivitis, muscle pain, itching and burning
skin, sweating, skin lesions, and delirium.
O
THER CAUSES
◆ Diagnostic tests. An allergic reaction to
contrast media used in radiologic tests may produce facial edema.
◆ Drugs. Long-term use of glucocorticoids
may produce facial edema. Any drug that causes an allergic reaction (aspirin, antipyretics,
penicillin, and sulfa preparations, for example)
may have the same effect.
HERB ALERT Ingestion of the fruit pulp
of ginkgo biloba can cause severe erythema
and edema and the rapid formation of vesicles.
Feverfew and chrysanthemum parthenium can
cause swelling of the lips, irritation of the tongue,
and mouth ulcers. Licorice may cause facial edema and water retention or bloating, especially if
used before menses.
◆ Surgery and transfusion. Facial edema may
result from cranial, nasal, or jaw surgery or
from a blood transfusion that causes an allergic
reaction.
S
PECIAL CONSIDERATIONS
Administer an analgesic for pain, and apply
cream to reduce itching. Unless contraindicated,
apply cold compresses to the patient’s eyes to
decrease edema. Elevate the head of the bed to
help drain the accumulated fluid. Urine and
blood tests are commonly ordered to help diagnose the cause of facial edema.
P
EDIATRIC POINTERS
Normally, periorbital tissue pressure is lower in
a child than in an adult. As a result, children
are more likely to develop periorbital edema.
In fact, periorbital edema is more common
than peripheral edema in children with such
disorders as heart failure and acute glomerulonephritis. Pertussis may also cause periorbital edema.
Edema of the leg
Leg edema is a common sign that results when
excess interstitial fluid accumulates in one or
both legs. It may affect just the foot and ankle or
extend to the thigh, and may be slight or dramatic and pitting or nonpitting.
Leg edema may result from venous disorders,
trauma, and certain bone and cardiac disorders
that disturb normal fluid balance. (See Under-
standing fluid balance, page 258.) It may result
from nephrotic syndrome, cirrhosis, acute or
chronic thrombophlebitis, chronic venous insufficiency (most common), cellulitis, lymphedema,
and the use of certain drugs. However, several
nonpathologic mechanisms may also cause leg
edema. For example, prolonged sitting, standing, or immobility may cause bilateral orthostatic edema. This pitting edema usually affects the
foot and disappears with rest and leg elevation.
Increased venous pressure late in pregnancy
may cause ankle edema. Constricting garters or
pantyhose may mechanically cause lowerextremity edema.
H
ISTORY AND PHYSICAL
EXAMINATION
To evaluate the patient, first ask how long he
has had the edema. Did it develop suddenly or
gradually? Does it decrease if he elevates his
legs? Is it painful when touched or when he
walks? Is it worse in the morning, or does it get
progressively worse during the day? Ask about
a recent leg injury or any recent surgery or illness that may have immobilized the patient.
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Does he have a history of cardiovascular disease? Finally, obtain a drug history.
Begin the physical examination by examining
each leg for pitting edema. (See Edema: Pitting or
nonpitting? page 259.) Because leg edema may
compromise arterial blood flow, palpate or use a
handheld Doppler device to auscultate peripheral pulses to detect any insufficiency. Observe leg
color and look for unusual vein patterns. Then
palpate for warmth, tenderness, and cords, and
gently squeeze the calf muscle against the tibia
to check for deep pain. If leg edema is unilateral,
dorsiflex the foot to look for Homans’ sign,
which is indicated by calf pain. Finally, note skin
thickening or ulceration in the edematous areas.
M
EDICAL CAUSES
◆ Burns. Mild to severe edema, pain, and tis-
sue damage may occur up to 2 days after a leg
burn.
◆ Cellulitis. Caused by a streptococcal or
staphylococcal infection that usually affects the
legs, cellulitis produces pitting edema and orange peel skin along with erythema, warmth,
and tenderness in the infected area.
◆ Cirrhosis. Cirrhosis commonly causes bilat-
eral edema, which is associated with ascites,
jaundice, and abdominal swelling.
◆ Heart failure. Bilateral leg edema is an early
sign of right-sided heart failure. Other signs and
symptoms include weight gain despite anorexia,
nausea, chest tightness, hypotension, pallor,
tachypnea, exertional dyspnea, orthopnea,
paroxysmal nocturnal dyspnea, palpitations, a
ventricular gallop, and inspiratory crackles. Pitting ankle edema, hepatomegaly, hemoptysis,
and cyanosis signal more advanced heart
failure.
◆ Hypoproteinemia. Malnourished patients
may develop bilateral leg edema secondary to
decreased protein and osmotic pressures.
◆ Leg trauma. Mild to severe localized edema
may form around the trauma site.
◆ Nephrotic syndrome. Nephrotic syndrome is
commonly seen in children and results in bilateral leg edema. It’s associated with polyuria and
eyelid swelling.
◆ Osteomyelitis. When this bone infection af-
fects the lower leg, it usually produces localized, mild to moderate edema, which may
spread to the adjacent joint. Edema typically follows fever, localized tenderness, and pain that
increases with leg movement.
◆ Phlegmasia cerulea dolens. Severe unilat-
eral leg edema and cyanosis may spread to the
abdomen and flank in this rare form of venous
thrombosis. Other signs and symptoms include
pain, cold skin, absent pulse in the affected leg,
and signs of shock, such as hypotension and
tachycardia.
◆ Rupture of the gastrocnemius muscle.
Ruptured gastrocnemius muscle can cause leg
edema and often occurs in runners. Pain is usually sudden, and ecchymosis is evident on the
ankles.
◆ Rupture of a popliteal (Baker’s) cyst. A
ruptured popliteal cyst can cause sudden onset
of unilateral calf pain and edema, usually after
walking or exercising. This type of cyst is common in patients with arthritis. It can compress
vascular structures and cause severe edema
and thrombophlebitis.
◆ Thrombophlebitis. Both deep and superfi-
cial vein thrombosis may cause unilateral mild
to moderate edema. Deep vein thrombophlebitis
may be asymptomatic or may cause mild to severe pain, warmth, and cyanosis in the affected
leg as well as fever, chills, and malaise. Superficial vein thrombophlebitis typically causes pain,
warmth, redness, tenderness, and induration
along the affected vein.
◆ Venous insufficiency (chronic). Moderate
to severe unilateral or bilateral leg edema occurs in patients with this disorder, which generally affects females. Initially soft and pitting,
the edema later becomes hard as tissues
thicken. Other signs include darkened skin and
painless, easily infected stasis ulcers around
the ankle.
O
THER CAUSES
◆ Coronary artery bypass surgery. Unilateral
venous insufficiency may follow saphenous vein
retrieval. Edema often occurs in the affected leg
or ankle and usually resolves after 6 to 8 weeks.
◆ Diagnostic tests. Venography is a rare cause
of leg edema.
◆ Drugs. Estrogen, hormonal contraceptives,
lithium, nonsteroidal anti-inflammatory drugs,
vasodilators, and drugs that cause sodium retention can cause bilateral leg edema.
◆ Envenomation. Mild to severe localized ede-
ma may develop suddenly at the site of a bite or
sting along with erythema, pain, urticaria, pruritus, and a burning sensation.
S
PECIAL CONSIDERATIONS
Provide an analgesic and an antibiotic as needed. Have the patient avoid prolonged sitting or
standing, and elevate his legs as necessary. A
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265
compression boot (Unna’s boot) may be used to
help reduce edema. Monitor the patient’s intake
and output, and check his weight and leg circumference daily to detect any change in the
edema. Prepare him for diagnostic tests, such as
blood and urine studies and X-rays. Determine
the need for dietary modifications, such as water and sodium restrictions. Monitor the affected
extremity for skin breakdown.
P
EDIATRIC POINTERS
Uncommon in children, leg edema may result
from osteomyelitis, leg trauma or, rarely, heart
failure.
P
ATIENT COUNSELING
Show the patient with leg edema how to apply
antiembolism stockings or bandages to promote
venous return. Encourage him to perform leg
exercises.
Enophthalmos
Enophthalmos is the backward displacement of
the eye into the orbit. This sign may develop suddenly or gradually and may be severe or mild.
Enophthalmos usually results from trauma, but it
may also be due to severe dehydration and eye
disorders. In elderly people, senile atrophy of orbital fat may produce physiologic enophthalmos.
Because enophthalmos allows the upper lid
to droop over the sunken eye, this sign is commonly mistaken for ptosis. However, exophthalmometry can differentiate these two signs. (See
Differentiating enophthalmos from ptosis, page
266.)
H
ISTORY AND PHYSICAL
EXAMINATION
Begin by asking the patient how long he has had
enophthalmos. Is it accompanied by headache
or eye pain? If so, ask him to describe its severity
and location. Next, ask about a history of trauma, cancer, or other eye disorders.
If you suspect an orbital fracture, don’t open
the patient’s eye or place any pressure on the
eyeball; this risks ocular laceration. Apply a
metal or plastic eye shield until the ophthalmologist can perform a complete examination.
Otherwise, perform a visual acuity test, with
and without correction. Then evaluate extraocular movements, and determine intraocular
pressure with a Schiøtz tonometer. Using a direct ophthalmoscope, check for papilledema
and other abnormalities. Check pupil response
to light, and note eyelid drooping.
Assess the patient for signs and symptoms of
dehydration, such as dry mucous membranes,
poor skin turgor, and hypotension.
M
EDICAL CAUSES
◆ Crouzon’s disease (craniofacial dysosto-
sis). Typically, enophthalmos occurs along with
an abnormally wide distance between the
pupils in this disorder. Other findings include
mental deficiency, astigmatism, epicanthal folds,
skull deformity and, occasionally, ocular deviation.
◆ Dehydration. Mild to severe enophthalmos
may accompany severe dehydration. Typically,
the patient also displays poor skin turgor, dry
mucous membranes, extreme thirst, weight
loss, fatigue, tachycardia, hypotension, nausea,
vomiting, and diarrhea.
◆ Duane’s syndrome. In this congenital syn-
drome, transient enophthalmos occurs when the
patient looks to the side. Visual acuity is usually
normal, but horizontal eye movement is impaired.
◆ Orbital fracture. In this type of fracture,
enophthalmos may not be apparent until edema subsides. The affected eyeball is displaced
downward and inward and is surrounded by
ecchymosis. Other findings include diplopia in
the affected eye, eye or head pain, subconjunctival hemorrhage, and a dilated or unreactive
pupil.
◆ Pancoast’s syndrome. This syndrome pro-
duces enophthalmos, ptosis, miosis, shoulder
pain, and paresthesia of the hand and arm of
the same side.
◆ Parinaud’s syndrome. In patients with this
disorder, enophthalmos occurs with nystagmus when the patient tries to look up. Ocular
muscles show absent voluntary movement but
normal conjugate movement. Other signs include lid retraction, ptosis, dilated pupils with
poor or absent light response, and papilledema.
◆ Parry-Romberg syndrome. This syndrome
produces enophthalmos and may cause irises of
different color, facial hemiatrophy, miotic pupils
with a sluggish response to dim light, nystagmus, ocular muscle paralysis, and ptosis.
S
PECIAL CONSIDERATIONS
Regularly monitor vital signs and evaluate
pupillary response to light. Prepare the trauma
patient for skull X-rays and an eye examination.
266 ENURESIS
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EXAMINATION TIP
Differentiating enophthalmos from ptosis
In patients with enophthalmos, the eye is displaced backward in its socket, causing the upper eyelid to droop. In those with ptosis, eyelid
drooping is also characteristic, but it results
from muscle weakness or cranial nerve paralysis.
To differentiate enophthalmos from ptosis,
use an exophthalmometer to measure the distance between the orbital rim and the tip of
the cornea. Have the patient stand against the
wall and look into your eyes. Place the device
on the patient’s face like a pair of glasses, ad-
just it to fit snugly at the orbital rims, and note
the bar reading. Then look into the 45-degreeangle mirrors, and measure the corneal apex
by lining it up visually against the millimeter
scale.
Normally, the corneal apex is 12 to 24 mm in
front of the orbital rim, and the difference between the eyes is less than 2 mm. In patients
with enophthalmos, the reading in one or both
eyes may be less than 12 mm; in those with
ptosis, the readings are within the normal
range.
P
EDIATRIC POINTERS
In neonates, enophthalmos usually results
from microphthalmos (abnormally small eyes).
Later, its causes are the same as those for
adults.
Enuresis
Enuresis usually refers to nighttime urinary incontinence in girls age 5 and older and boys age
6 and older. This sign rarely continues into
adulthood but may occur in some adults with
sleep apnea. It’s most common in boys and may
be classified as primary or secondary. In primary
enuresis, a child has never achieved bladder
control; in secondary enuresis, a child who
achieved bladder control for at least 3 months
has lost it.
Factors that may contribute to enuresis are
delayed development of detrusor muscle control, unusually deep or sound sleep, organic
disorders (such as a urinary tract infection
[UTI] or obstruction), and psychological
stress. Psychological stress, probably the
most important factor, commonly results from
the birth of a sibling, the death of a parent or
loved one, divorce, or premature, rigorous
PATIENT-TEACHING AID
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Helping your child have dry nights
ENURESIS 267
Dear Parent:
Although no single treatment for bed-wetting
is always effective, by following these recommendations you can help your child achieve
bladder control:
◆ Restrict your child’s intake of fluids—
especially colas—after supper.
◆ Make sure your child urinates before bed-
time. In addition, wake him once during the
night to go to the bathroom.
◆ Reward your child after each dry night with
praise and encouragement. Keep a progress
chart, marking each dry night with a sticker.
This patient-teaching aid may be reproduced by office copier for distribution to patients. © 2011, Lippincott Williams
& Wilkins.
toilet training. The child may be too embarrassed or ashamed to discuss his bed-wetting,
which intensifies psychological stress and
makes enuresis more likely—thus creating a
vicious circle.
H
ISTORY AND PHYSICAL
EXAMINATION
When taking a history, include the parents as
well as the child. First, determine the number of
nights each week or month that the child wets
the bed. Is there a family history of enuresis?
Ask about the child’s daily fluid intake. Does he
drink much after supper? What are his typical
sleep and voiding patterns? Find out if the child
has ever had control of his bladder. If so, try to
pinpoint what may have precipitated enuresis,
such as an organic disorder or psychological
stress. Does the bed-wetting occur both at
home and away from home? Ask the parents
how they have tried to manage the problem,
and have them describe the child’s toilet training. Observe the child’s and parents’ attitudes
toward bed-wetting. Finally, ask the child if it
hurts when he urinates.
Next, perform a physical examination to detect
signs of neurologic or urinary tract disorders. Observe the child’s gait to check for motor dysfunction, and test sensory function in the legs. Inspect
the urethral meatus for erythema, and obtain a
urine specimen. A rectal examination to evaluate
sphincter control may be required.
◆ Reward your child with a book, a small toy,
or a special activity for a certain number of
consecutive dry nights.
◆ Always give your child emotional support.
Never punish him if he wets the bed; instead
reassure him that he’ll learn to achieve bladder
control. Remember that most children simply
outgrow bed-wetting. However, wet and dry
nights will alternate before your child develops
a constant pattern of dryness.
M
EDICAL CAUSES
◆ Detrusor muscle hyperactivity. Involuntary
detrusor muscle contractions may cause primary or secondary enuresis associated with urinary urgency, frequency, and incontinence.
Signs and symptoms of UTI are also common.
◆ Urinary tract obstruction. Although it usually
causes daytime incontinence, this disorder may
also produce primary or secondary enuresis as
well as flank and lower back pain; upper abdominal distention; urinary frequency, urgency, hesitancy, and dribbling; dysuria; diminished urine
stream; hematuria; and variable urine output.
◆ UTI. In children, most UTIs produce sec-
ondary enuresis. Associated features include urinary frequency and urgency, dysuria, straining to
urinate, and hematuria. Low back pain, fatigue,
and suprapubic discomfort may also occur.
S
PECIAL CONSIDERATIONS
Provide emotional support to the child and his
family. Encourage the parents to accept and
support the child. Tell them how to manage
enuresis at home. (See Helping your child have
dry nights.)
Bladder training may help control enuresis
caused by detrusor muscle hyperactivity. An
alarm device may be useful for children ages 8
and older. This moisture-sensitive device fits in
his mattress and triggers an alarm when
moistened, waking the child. The alarm conditions him to avoid bed-wetting and should be
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