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JAW PAIN
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411
neck; dysphagia; bloody discharge; drooling;
lymphadenopathy; and trismus.
◆ Hypocalcemic tetany. Besides painful mus-
cle contractions of the jaw and mouth, this lifethreatening disorder produces paresthesia and
carpopedal spasms. The patient may complain
of weakness, fatigue, and palpitations. Examination reveals hyperreflexia and positive
Chvostek’s and Trousseau’s signs. Muscle
twitching, choreiform movements, and muscle
cramps may also occur. With severe hypocalcemia, laryngeal spasm may occur with stridor,
cyanosis, seizures, and cardiac arrhythmias.
◆ Ludwig’s angina. An acute streptococcal in-
fection of the sublingual and submandibular
spaces that produces severe jaw pain in the
mandibular area with tongue elevation, sublingual edema, and drooling. Fever is a common
sign. Progressive disease produces dysphagia,
dysphonia, and stridor and dyspnea due to
laryngeal edema and obstruction by an elevated
tongue.
◆ Myocardial infarction. Initially, this life-
threatening disorder causes intense, crushing
substernal pain that’s unrelieved by rest or nitroglycerin. The pain may radiate to the lower
jaw, left arm, neck, back, or shoulder blades.
(Rarely, jaw pain occurs without chest pain.)
Other findings include pallor, clammy skin, dyspnea, excessive diaphoresis, nausea and vomiting, anxiety, restlessness, a feeling of impending
doom, low-grade fever, decreased or increased
blood pressure, arrhythmias, an atrial gallop,
new murmurs (in many cases from mitral insufficiency), and crackles.
◆ Osteomyelitis. Bone infection after trauma,
sinus infection, dental injury, or surgery (dental
or facial) may produce diffuse, aching jaw pain
along with warmth, swelling, tenderness, erythema, and restricted jaw movement. Acute
osteomyelitis may also cause tachycardia, sudden fever, nausea, and malaise. Chronic osteomyelitis may recur after minor trauma.
◆ Sialolithiasis. With this disorder, stones
form in the salivary glands, causing painful
swelling that makes chewing uncomfortable.
Jaw pain occurs in the lower jaw, floor of the
mouth, and TMJ. It may also radiate to the ear
or neck.
◆ Sinusitis. Maxillary sinusitis produces in-
tense boring pain in the maxilla and cheek that
may radiate to the eye. This type of sinusitis
also causes a feeling of fullness, increased pain
on percussion of the first and second molars
and, in those with nasal obstruction, the loss of
the sense of smell. Sphenoid sinusitis causes
scanty nasal discharge and chronic pain at the
mandibular ramus and vertex of the head and in
the temporal area. Other signs and symptoms of
both types of sinusitis include fever, halitosis,
headache, malaise, cough, sore throat, and
fever.
◆ Suppurative parotitis. Bacterial infection of
the parotid gland by Staphylococcus aureus
tends to develop in debilitated patients with dry
mouth or poor oral hygiene. Besides the abrupt
onset of jaw pain, high fever, and chills, findings
include erythema and edema of the overlying
skin; a tender, swollen gland; and pus at the
second top molar (Stensen’s ducts). Infection
may lead to disorientation; shock and death are
common.
◆ Temporal arteritis. Most common in
women older than age 60, this disorder produces sharp jaw pain after chewing or talking.
Nonspecific signs and symptoms include lowgrade fever, generalized muscle pain, malaise,
fatigue, anorexia, and weight loss. Vascular lesions produce jaw pain; throbbing, unilateral
headache in the frontotemporal region; swollen,
nodular, tender and, possibly, pulseless temporal arteries; and, at times, erythema of the overlying skin.
◆ Temporomandibular joint syndrome. This
common syndrome produces jaw pain at the
TMJ; spasm and pain of the masticating muscle;
clicking, popping, or crepitus of the TMJ; and restricted jaw movement. Unilateral, localized
pain may radiate to other head and neck areas.
The patient typically reports teeth clenching,
bruxism, and emotional stress. He may also experience ear pain, headache, deviation of the
jaw to the affected side upon opening the
mouth, and jaw subluxation or dislocation, especially after yawning.
◆ Tetanus. A rare life-threatening disorder
caused by a bacterial toxin, tetanus produces
stiffness and pain in the jaw and difficulty opening the mouth. Early nonspecific signs and
symptoms (commonly unnoticed or mistaken
for influenza) include headache, irritability, restlessness, low-grade fever, and chills. Examination reveals tachycardia, profuse diaphoresis,
and hyperreflexia. Progressive disease leads to
painful, involuntary muscle spasms that spread
to the abdomen, back, or face. The slightest
stimulus may produce reflex spasms of any
muscle group. Ultimately, laryngospasm, respiratory distress, and seizures may occur.
412 JUGULAR VEIN DISTENTION
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◆ Trauma. Injury to the face, head, or neck—
particularly fracture of the maxilla or
mandible—may produce jaw pain and swelling
and decreased jaw mobility. Associated findings
include hypotension and tachycardia (indicating
shock), lacerations, ecchymoses, and
hematomas. Rhinorrhea or otorrhea indicates
the leakage of cerebrospinal fluid; blurred vision
indicates orbital involvement.
◆ Trigeminal neuralgia. This disorder is
marked by paroxysmal attacks of intense unilateral jaw pain (stopping at the facial midline) or
rapid-fire shooting sensations in one division of
the trigeminal nerve (usually the mandibular or
maxillary division). This superficial pain, felt
mainly over the lips and chin and in the teeth,
lasts from 1 to 15 minutes. Mouth and nose areas
may be hypersensitive. Involvement of the ophthalmic branch of the trigeminal nerve causes a
diminished or absent corneal reflex on the same
side. Attacks can be triggered by mild stimulation
of the nerve (for example, lightly touching the
cheeks), exposure to heat or cold, or consumption of hot or cold foods or beverages.
O
THER CAUSES
◆ Drugs. Some drugs, such as phenothiazines,
affect the extrapyramidal tract, causing dyskinesias; others cause tetany of the jaw secondary
to hypocalcemia.
S
PECIAL CONSIDERATIONS
If the patient is in severe pain, withhold food,
liquids, and oral medications until the diagnosis
is confirmed. Administer an analgesic. Prepare
the patient for diagnostic tests such as jaw
X-rays. Apply an ice pack if the jaw is swollen,
and discourage the patient from talking or
moving his jaw.
P
EDIATRIC POINTERS
Be alert for nonverbal signs of jaw pain, such as
rubbing the affected area or wincing while talking or swallowing. In infants, initial signs of
tetany from hypocalcemia include episodes of
apnea and generalized jitteriness progressing to
facial grimaces and generalized rigidity. Finally,
seizures may occur.
Jaw pain in children sometimes stems from
disorders uncommon in adults. Mumps, for example, causes unilateral or bilateral swelling
from the lower mandible to the zygomatic arch.
Parotiditis due to cystic fibrosis also causes jaw
pain. When trauma causes jaw pain in children,
always consider the possibility of abuse.
Jugular vein distention
Jugular vein distention is the abnormal fullness
and height of the pulse waves in the internal or
external jugular veins. For a patient in a supine
position with his head elevated 45 degrees, a
pulse wave height greater than 1
to 4 cm) above the angle of Louis indicates distention. Engorged, distended veins reflect increased venous pressure in the right side of the
heart, which in turn, indicates an increased central venous pressure. This common sign characteristically occurs in heart failure and other cardiovascular disorders, such as constrictive
pericarditis, tricuspid stenosis, and obstruction
of the superior vena cava.
EMERGENCY INTERVENTIONS Evaluat-
ing jugular vein distention involves visualizing and assessing venous pulsations. (See
Evaluating jugular vein distention.) If you detect
jugular vein distention in a patient with pale,
clammy skin who suddenly appears anxious and
dyspneic, take his blood pressure. If you note hypotension and paradoxical pulse, suspect cardiac
tamponade. Elevate the foot of the bed 20 to
30 degrees, give supplemental oxygen, and
monitor cardiac status and rhythm, oxygen saturation, and mental status. Start an I.V. catheter
for medication administration, and keep cardiopulmonary resuscitation equipment close by.
Assemble the needed equipment for emergency
pericardiocentesis (to relieve pressure on the
heart.) Throughout the procedure, monitor the
patient’s blood pressure, heart rhythm, and
respirations.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t in severe distress, obtain a
personal history. Has he recently gained
weight? Does he have difficulty putting on
shoes? Are his ankles swollen? Ask about chest
pain, shortness of breath, paroxysmal nocturnal dyspnea, anorexia, nausea or vomiting, and
a history of cancer or cardiac, pulmonary, hepatic, or renal disease. Obtain a drug history
noting diuretic use and dosage. Is the patient
taking drugs as prescribed? Ask the patient
about his regular diet patterns, noting a high
sodium intake.
Next, perform a physical examination, beginning with vital signs. Tachycardia, tachypnea,
and increased blood pressure indicate fluid
overload that’s stressing the heart. Inspect and
palpate the patient’s extremities and face for
1
⁄4” to 11⁄2” (3
JUGULAR VEIN DISTENTION
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EXAMINATION TIP
Evaluating jugular vein distention
413
With the patient in a supine position, position
him so that you can visualize jugular vein pulsations reflected from the right atrium. Elevate
the head of the bed 45 to 90 degrees. (In the
normal patient, veins distend only when the
patient lies flat.)
Next, locate the angle of Louis (sternal
notch)—the reference point for measuring venous pressure. To do so, palpate the clavicles
where they join the sternum (the suprasternal
notch). Place your first two fingers on the
suprasternal notch. Then, without lifting them
from the skin, slide them down the sternum
until you feel a bony protuberance—this is the
angle of Louis.
Find the internal jugular vein (which indicates venous pressure more reliably than the
external jugular vein). Shine a flashlight across
Common
carotid artery
Sternocleidomastoid
muscle
Internal jugular vein
External jugular vein
the patient’s neck to create shadows that highlight his venous pulse. Be sure to distinguish
jugular vein pulsations from carotid artery pulsations. One way to do this is to palpate the
vessel: Arterial pulsations continue, whereas
venous pulsations disappear with light finger
pressure. Also, venous pulsations increase or
decrease with changes in body position; arterial pulsations remain constant.
Next, locate the highest point along the vein
where you can see pulsations. Using a centimeter ruler, measure the distance between
that high point and the sternal notch. Record
this finding as well as the angle at which the
patient was lying. A finding greater than 1
1
to 1
⁄2” (3 to 4 cm) above the sternal notch,
with the head of the bed at a 45-degree angle,
indicates jugular vein distention.
Highest level
Jugular vein
distention
of visible
pulsation
Angle of Louis
(sternal notch)
1
⁄4”
Head of bed elevated 45 to 90 degrees
edema. Then weigh the patient and compare
that weight to his baseline.
Auscultate his lungs for crackles and his
heart for gallops, a pericardial friction rub, and
muffled heart sounds. Inspect his abdomen for
distention, and palpate and percuss for an enlarged liver. Finally monitor urine output and
note any decrease.
M
EDICAL CAUSES
◆ Cardiac tamponade. This life-threatening
condition produces jugular vein distention
along with anxiety, restlessness, cyanosis, chest
pain, dyspnea, hypotension, and clammy skin. It
also causes tachycardia, tachypnea, muffled
heart sounds, a pericardial friction rub, weak or
absent peripheral pulses or pulses that decrease
414 JUGULAR VEIN DISTENTION
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during inspiration (pulsus paradoxus), and hepatomegaly. The patient may sit upright or lean
forward to ease breathing.
◆ Heart failure. Sudden or gradual develop-
ment of right-sided heart failure commonly
causes jugular vein distention, along with
weakness and anxiety, cyanosis, dependent
edema of the legs and sacrum, steady weight
gain, confusion, and hepatomegaly. Other findings include nausea and vomiting, abdominal
discomfort, and anorexia due to visceral edema.
Ascites is a late sign. Massive right-sided heart
failure may produce anasarca and oliguria.
If left-sided heart failure precedes right-sided
heart failure, jugular vein distention is a late
sign. Other signs and symptoms include fatigue,
dyspnea, orthopnea, paroxysmal nocturnal dyspnea, tachypnea, tachycardia, and arrhythmias.
Auscultation reveals crackles and a ventricular
gallop.
◆ Hypervolemia. Markedly increased intravas-
cular fluid volume causes jugular vein distention, along with rapid weight gain, elevated
blood pressure, bounding pulse, peripheral
edema, dyspnea, and crackles.
◆ Pericarditis (chronic constrictive). Progres-
sive signs and symptoms of restricted heart filling include jugular vein distention that’s more
prominent on inspiration (Kussmaul’s sign). The
patient usually complains of chest pain. Other
signs and symptoms include fluid retention with
dependent edema, hepatomegaly, ascites, and
pericardial friction rub.
◆ Superior vena cava obstruction. A tumor
or, rarely, thrombosis may gradually lead to
jugular vein distention when the veins of the
head, neck, and arms fail to empty effectively,
causing facial, neck, and upper arm edema.
Metastasis of a malignant tumor to the mediastinum may cause dyspnea, cough, substernal
chest pain, and hoarseness.
P
EDIATRIC POINTERS
Jugular vein distention is difficult (sometimes
impossible) to evaluate in most infants and toddlers because of their short, thick necks. Even in
school-age children, measurement of jugular
vein distention can be unreliable because the
sternal angle may not be the same distance
3
(2” to 2
⁄4⬙ [5 to 7 cm]) above the right atrium as
it is in adults.
P
ATIENT COUNSELING
Teach the patient with heart failure about appropriate treatments, including dietary restrictions (such as a low-sodium diet).
S
PECIAL CONSIDERATIONS
If the patient has cardiac tamponade, prepare
him for pericardiocentesis. If he doesn’t have
cardiac tamponade, restrict fluids and monitor
his intake and output. Insert an indwelling urinary catheter if necessary. If the patient has
heart failure, administer a diuretic. Routinely
change his position to avoid skin breakdown
from peripheral edema. Prepare the patient for a
central venous or Swan-Ganz catheter insertion
in order to measure right- and left-sided heart
pressure.
K
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Kehr’s sign
A cardinal sign of hemorrhage within the peritoneal cavity, Kehr’s sign is referred left shoulder pain due to diaphragmatic irritation by intraperitoneal blood. The pain usually arises
when the patient assumes the supine position
or lowers his head. Such positioning increases
the contact of free blood or clots with the left diaphragm, involving the phrenic nerve.
Kehr’s sign usually develops right after the
hemorrhage; however, its onset is sometimes
delayed up to 48 hours. A classic symptom of a
ruptured spleen, Kehr’s sign also occurs in ruptured ectopic pregnancy.
EMERGENCY INTERVENTIONS After you
detect Kehr’s sign, quickly take the patient’s
vital signs. If the patient shows signs of hypovolemia, elevate his feet 30 degrees. In addition, insert a large-bore I.V. catheter for fluid and blood
replacement and an indwelling urinary catheter.
Begin monitoring intake and output. Draw blood
to determine hematocrit, and provide supplemental oxygen.
Inspect the patient’s abdomen for bruises and
distention, and palpate for tenderness. Percuss for
Ballance’s sign—an indicator of massive
perisplenic clotting and free blood in the peritoneal cavity from a ruptured spleen.
M
EDICAL CAUSES
◆ Intra-abdominal hemorrhage. Kehr’s sign
usually accompanies intense abdominal pain,
abdominal rigidity, and muscle spasm. Other
findings vary with the cause of bleeding. Many
patients have a history of blunt or penetrating
abdominal injuries.
S
PECIAL CONSIDERATIONS
In anticipation of surgery, withhold oral intake,
and prepare the patient for abdominal X-rays, a
computed tomography scan, an ultrasound and,
possibly, paracentesis, peritoneal lavage, and
culdocentesis. Give an analgesic, if needed.
P
EDIATRIC POINTERS
Because a child may have difficulty describing
pain, watch for nonverbal clues such as rubbing
of the shoulder.
Kernig’s sign
A reliable early indicator and tool used to diagnose meningeal irritation, Kernig’s sign elicits
both resistance and hamstring muscle pain
when the examiner attempts to extend the knee
while the hip and knee are both flexed 90 degrees. However, when the patient’s thigh isn’t
flexed on the abdomen, he’s usually able to
completely extend his leg. (See Eliciting Kernig’s
sign, page 416.) This sign is usually elicited in
meningitis or subarachnoid hemorrhage. With
these potentially life-threatening disorders,
hamstring muscle resistance results from
stretching the blood- or exudate-irritated
meninges surrounding spinal nerve roots.
Kernig’s sign can also indicate a herniated
disk or spinal tumor. With these disorders,
415
416 KERNIG’S SIGN
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EXAMINATION TIP
Eliciting Kernig’s sign
To elicit Kernig’s sign, place the patient in a supine position. Flex his leg at the hip and knee, as
shown here. Then try to extend the leg while you keep the hip flexed. If the patient experiences
pain and possibly spasm in the hamstring muscle and resists further extension, you can assume
that meningeal irritation has occurred.
sciatic pain results from disk or tumor pressure
on spinal nerve roots.
H
ISTORY AND PHYSICAL
EXAMINATION
If you elicit a positive Kernig’s sign and suspect
life-threatening meningitis or subarachnoid hemorrhage, immediately prepare for emergency
intervention. (See When Kernig’s sign signals
CNS crisis.)
If you don’t suspect meningeal irritation, ask
the patient if he feels any back pain that radiates down one or both legs. Does he also feel
leg numbness, tingling, or weakness? Ask about
other signs and symptoms, and find out if he
has a history of cancer or back injury. Then perform a physical examination, concentrating on
motor and sensory function.
M
EDICAL CAUSES
◆ Lumbosacral herniated disk. A positive
Kernig’s sign may be elicited in patients with
this disorder, but the cardinal and earliest feature is sciatic pain on the affected side or on
both sides. Associated findings include postural
deformity (lumbar lordosis or scoliosis), paresthesia, hypoactive deep tendon reflexes in the
involved leg, and dorsiflexor muscle weakness.
◆ Meningitis. A positive Kernig’s sign usually
occurs early with meningitis, along with fever
and, possibly, chills. Other signs and symptoms
of meningeal irritation include nuchal rigidity,
hyperreflexia, Brudzinski’s sign, and
opisthotonos. As intracranial pressure (ICP) increases, headache and vomiting may occur. In
severe meningitis, the patient may experience
stupor, coma, and seizures. Cranial nerve involvement may produce ocular palsies, facial
weakness, deafness, and photophobia. An erythematous maculopapular rash may occur in
viral meningitis; a purpuric rash may be seen in
those with meningococcal meningitis.
◆ Spinal cord tumor. Kernig’s sign can be
elicited occasionally, but the earliest symptom is
typically pain felt locally or along the spinal
nerve, commonly in the leg. Associated findings
include weakness or paralysis distal to the tumor, paresthesia, urine retention, urinary or fecal incontinence, and sexual dysfunction.
◆ Subarachnoid hemorrhage. Kernig’s sign
and Brudzinski’s sign can both be elicited within
minutes after the initial bleed. The patient experiences a sudden onset of severe headache that
begins in a localized area and then spreads,
pupillary inequality, nuchal rigidity, and decreased level of consciousness. Photophobia,
fever, nausea and vomiting, dizziness, and
seizures are possible. Focal signs include hemiparesis or hemiplegia, aphasia, and sensory or
visual disturbances. Increasing ICP may produce
bradycardia, increased blood pressure, respiratory pattern change, and rapid progression to
coma.
KERNIG’S SIGN
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EMERGENCY INTERVENTION
When Kernig’s sign signals CNS crisis
417
Because Kernig’s sign may signal meningitis
or subarachnoid hemorrhage—both lifethreatening central nervous system (CNS) disorders—take the patient’s vital signs at once
to obtain baseline information. Then test for
Brudzinski’s sign to obtain further evidence of
meningeal irritation. (See Testing for Brudzins-
ki’s sign, page 125.) Next, ask the patient or
his family to describe the onset of illness. Typically, the progressive onset of headache,
fever, nuchal rigidity, and confusion suggests
meningitis. Conversely, the sudden onset of a
severe headache, nuchal rigidity, photophobia, and, possibly, loss of consciousness usually indicates subarachnoid hemorrhage.
Meningitis
If a diagnosis of meningitis is suspected, ask
about recent infections, especially tooth abscesses. Ask about exposure to infected persons or places where meningitis is endemic.
Meningitis is usually a complication of
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, such as
a computed tomography scan, magnetic resonance imaging, spinal X-ray, myelography, and
lumbar puncture. Closely monitor his vital
signs, ICP, and cardiopulmonary and neurologic status. Ensure bed rest, quiet, and minimal
stress.
If the patient has a subarachnoid hemorrhage, darken the room and elevate the head of
the bed at least 30 degrees to reduce ICP. If he
has a herniated disk or spinal tumor, he may require pelvic traction.
another bacterial infection, so draw blood for
culture studies to determine the causative organism. Prepare the patient for a lumbar
puncture (if a tumor or abscess can be ruled
out). Also, find out if the patient has a history
of I.V. drug abuse, an open-head injury, or endocarditis. Insert an I.V. catheter, and immediately begin administering an antibiotic.
Subarachnoid hemorrhage
If subarachnoid hemorrhage is the suspected
diagnosis, ask about a history of hypertension, cerebral aneurysm, head trauma, or arteriovenous malformation. Also ask about
sudden withdrawal of an antihypertensive.
Check the patient’s pupils for dilation, and
assess him for signs of increasing intracranial
pressure, such as bradycardia, increased systolic blood pressure, and widened pulse pressure. Insert an I.V. line, and administer supplemental oxygen.
P
EDIATRIC POINTERS
Kernig’s sign is considered ominous in children
because of their greater potential for rapid deterioration.
L
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Leg pain
Although leg pain commonly signifies a musculoskeletal disorder, it can also result from a
more serious vascular or neurologic disorder.
The pain may arise suddenly or gradually and
may be localized or affect the entire leg. Constant or intermittent, it may feel dull, burning,
sharp, shooting, or tingling. Leg pain may affect
locomotion, limiting weight bearing. Severe leg
pain that follows cast application for a fracture
may signal limb-threatening compartment syndrome. Sudden onset of severe leg pain in a patient with underlying vascular insufficiency may
signal acute deterioration, possibly requiring an
arterial graft or amputation. (See Highlighting
causes of local leg pain.)
EMERGENCY INTERVENTIONS If the pa-
tient has acute leg pain and a history of trauma, quickly take his vital signs and determine the
leg’s neurovascular status. Observe the patient’s
leg position and check for swelling, gross deformities, or abnormal rotation. Also, be sure to check
distal pulses and note skin color and temperature.
A pale, cool, and pulseless leg may indicate impaired circulation, which may require emergency
surgery.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient’s condition permits, ask him when
the pain began and have him describe its intensity, character, and pattern. Is the pain worse in
the morning, at night, or with movement? If it
doesn’t prevent him from walking, must he rely
on a crutch or other assistive device? Also ask
him about the presence of other signs and
symptoms.
Find out if the patient has a history of leg injury or surgery and if he or a family member has
a history of joint, vascular, or back problems.
Also ask what medications he’s taking and
whether they have helped to relieve his leg
pain.
Begin the physical examination by watching
the patient walk, if his condition permits. Observe how he holds his leg while standing and
sitting. Palpate the legs, buttocks, and lower
back to determine the extent of pain and tenderness. If a fracture has been ruled out, test the
patient’s range of motion in the hip and knee.
Also, check reflexes with the patient’s leg
straightened and raised, noting any action that
causes pain. Then compare both legs for symmetry, movement, and active range of motion.
Additionally, assess sensation and strength. If
the patient wears a leg cast, splint, or restrictive
dressing, carefully check distal circulation, sensation, and mobility, and stretch his toes to elicit
any associated pain.
M
EDICAL CAUSES
◆ Bone cancer. Continuous deep or boring
pain, commonly worse at night, may be the first
symptom. Later, skin breakdown and impaired
circulation may occur, along with cachexia,
fever, and impaired mobility.
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LEG PAIN
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Highlighting causes of local leg pain
Various disorders cause hip, knee, ankle, or foot pain, which may radiate to surrounding tissues
and be reported as leg pain. Local pain is commonly accompanied by tenderness, swelling, and
deformity in the affected area.
419
Hip pain
Arthritis
Avascular necrosis
Bursitis
Dislocation
Fracture
Sepsis
Tumor
Knee pain
Arthritis
Bursitis
Chondromalacia
Contusion
Cruciate ligament injury
Dislocation
Fracture
Meniscal injury
Osteochondritis dissecans
Phlebitis
Popliteal cyst
Radiculopathy
Ruptured extensor
mechanism
Sprain
Ankle pain
Achilles tendon contracture
Arthritis
Dislocation
Fracture
Sprain
Tenosynovitis
Foot pain
Arthritis
Bunion
Callus or corn
Dislocation
Flatfoot
Fracture
Gout
Hallux rigidus
Hammer toe
Ingrown toenail
Köhler’s disease
Morton’s neuroma
Occlusive vascular disease
Plantar fasciitis
Plantar wart
Radiculopathy
Tabes dorsalis
Tarsal tunnel syndrome
◆ Compartment syndrome. Progressive, in-
tense lower leg pain that increases with passive
muscle stretching is a cardinal sign of this limbthreatening disorder. Restrictive dressings or
traction may aggravate the pain, which typically
worsens despite analgesic administration. Other
findings include muscle weakness and paresthesia, but apparently normal distal circulation.
With irreversible muscle ischemia, paralysis and
absent pulse also occur.
◆ Fracture. Severe, acute pain accompanies
swelling and ecchymosis in the affected leg.
Movement produces extreme pain, and the leg
may be unable to bear weight. Neurovascular
status distal to the fracture may be impaired,
causing paresthesia, absent pulse, mottled
cyanosis, and cool skin. Deformity, muscle
spasms, and bony crepitation may also occur.
◆ Infection. Local leg pain, erythema, swelling,
streaking, and warmth characterize soft-tissue
and bone infections. Fever and tachycardia may
be present with other systemic signs.
◆ Multiple myeloma. Pain that begins in the
ribs or lower back and progresses to the hips
and legs may be a symptom of advanced multiple myeloma. Other signs and symptoms may
include kidney problems, fatigue, and recurrent
infections.
420 LEVEL OF CONSCIOUSNESS, DECREASED
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◆ Occlusive vascular disease. Continuous
cramping pain in the legs and feet may worsen
with walking, inducing claudication. The patient
may report increased pain at night, cold feet,
cold intolerance, numbness, and tingling. Examination may reveal ankle and lower leg edema, decreased or absent pulses, and increased
capillary refill time. (Normal time is less than
3 seconds.)
◆ Sciatica. Pain, described as shooting, aching,
or tingling that radiates down the back of the
leg along the sciatic nerve. Typically, activity exacerbates the pain and rest relieves it. The patient may limp to avoid exacerbating the pain
and may have difficulty moving from a sitting to
a standing position.
◆ Strain or sprain. Acute strain causes sharp,
transient pain and rapid swelling, followed by
leg tenderness and ecchymosis. Chronic strain
produces stiffness, soreness, and generalized
leg tenderness several hours after the injury; active and passive motion may be painful or impossible. A sprain causes local pain, especially
during joint movement; ecchymosis and, possibly, local swelling and loss of mobility develop.
◆ Thrombophlebitis. Discomfort may range
from calf tenderness to severe pain accompanied by swelling, warmth, and a feeling of heaviness in the affected leg. The patient may also
develop fever, chills, malaise, muscle cramps,
and a positive Homans’ sign. Assessment may
reveal superficial veins that are visibly engorged; palpable, hard, thready, and cordlike;
and sensitive to pressure.
◆ Varicose veins. Mild to severe leg symptoms
may develop, including nocturnal cramping; a
feeling of heaviness; diffuse, dull aching after
prolonged standing or walking; and aching during menses. Assessment may reveal palpable
nodules, orthostatic edema, and stasis pigmentation of the calves and ankles.
GENDER CUE Primary varicose veins origi-
nate in the superficial system and are more
common in women.
◆ Venous stasis ulcers. Localized pain and
bleeding arise from infected ulcerations on the
lower extremities. Mottled, bluish pigmentation
is characteristic, and local edema may occur.
S
PECIAL CONSIDERATIONS
If the patient has acute leg pain, closely monitor
his neurovascular status by frequently checking
distal pulses and evaluating both legs for temperature, color and sensation. Also monitor his
thigh and calf circumference to evaluate bleed-
ing into tissues from a possible fracture site.
Prepare him for X-rays. Use sandbags to immobilize his leg; apply ice and, if needed, skeletal
traction. If a fracture isn’t suspected, prepare
the patient for laboratory tests to detect an infectious agent or for venography, Doppler ultrasonography, plethysmography, or angiography
to determine vascular competency. Withhold
food and fluids until the need for surgery has
been ruled out, and withhold analgesics until a
preliminary diagnosis is made. Administer an
anticoagulant and antibiotic as needed.
P
EDIATRIC POINTERS
Common pediatric causes of leg pain include
fracture, growing pains, osteomyelitis, and bone
cancer. If parents fail to give an adequate explanation for a leg fracture, consider the possibility
of child abuse.
P
ATIENT COUNSELING
If the patient has chronic leg pain, instruct him
to take an anti-inflammatory and teach him to
perform range-of-motion exercises and, if necessary, to use a cane, walker, or other assistive
device. Discuss with the patient and his family
any lifestyle changes that may be necessary until leg pain resolves. If physical therapy is necessary, stress the importance of establishing a daily exercise regimen. Based on the cause of the
leg pain, discuss the appropriate positioning of
the lower extremity to enhance blood flow and
venous return.
Level of consciousness,
decreased
A decrease in level of consciousness (LOC),
from lethargy to stupor to coma, usually results
from a neurologic disorder and may signal a
life-threatening complication, such as hemorrhage, trauma, or cerebral edema. However,
this sign can also result from a metabolic, GI,
musculoskeletal, urologic, or cardiopulmonary
disorder; severe nutritional deficiency; the effects of toxins; or drug use. LOC can deteriorate
suddenly or gradually and can remain altered
temporarily or permanently.
Consciousness is affected by the reticular
activating system (RAS), an intricate network
of neurons with axons extending from the
brain stem, thalamus, and hypothalamus to the
cerebral cortex. A disturbance in any part of
this integrated system prevents the intercom-
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