Amputation-pain management

-Psychiatric/ Mental Hlth

-Postoperative Management
General postoperative care for the patient who has had an amputation depends largely on the patient's
general state of health, the reason for the amputation, and the patient's age. Nursing care must be
individualized on the basis of these factors. For example, an older adult patient needs particularly careful
monitoring of respiratory status. A victim of a motor vehicle accident may need careful neurologic
monitoring. Individuals who undergo amputation as a result of a traumatic injury need to be monitored for
posttraumatic stress disorder because they had no time to prepare or perhaps even participate in the
decision to have a limb amputated.
Prevention and detection of complications are important nursing responsibilities during the postoperative
period. Careful monitoring of the patient's vital signs and dressing can alert the nurse to hemorrhage in
the operative area. Careful attention to sterile technique during dressing changes reduces the potential for
wound infection and subsequent interruption of rehabilitation.
If an immediate postoperative prosthesis has been applied, the nurse must monitor vital signs carefully
because the surgical site is heavily covered and may not be visible. A surgical tourniquet must always be
available for emergency use. If hemorrhage occurs, the surgeon should be notified immediately, and
efforts to control the hemorrhage should begin at once.
The orthopedic surgeon will decide the type of prosthetic fitting that will be used after surgery. An
immediate prosthetic fitting, often called the immediate postsurgical fitting or the immediate postoperative
fitting, is done in the operating room after the amputation. A rigid, castlike bandage is applied around the
closed residual limb with a prosthetic pylon and an ankle-foot assembly. While the patient is still
anesthetized, the prosthetic pylon and ankle-foot assembly are aligned and adjusted to provide a smooth
gait and to avoid excessive pressure on the residual limb area. A strap is placed on the proximal anterior
surface of the rigid plaster bandage and attached to a waistband to prevent slippage. The main
advantages of this device are reduction of edema and the psychologic benefit of early ambulation. A
disadvantage is the inability to directly visualize the surgical site.
The delayed prosthetic fitting may be the best choice for certain patients. Patients who have had
amputations above the knee or below the elbow, older adults, debilitated individuals, and those with
infection usually have delayed prosthetic fittings (Fig. 61-17). The appropriate time for use of a prosthesis
depends on satisfactory healing of the residual limb, as well as on the general condition of the patient. A
temporary prosthesis may be used for partial weight bearing once the sutures are removed. Barring any
problems, patients can bear full weight on permanent prostheses by approximately 3 months after
amputation.

FIG. 61-17 Two types of prosthesis. A, Traditional fiberglass. B, New materials and techniques have
made possible fabrication of prosthetic sockets that are light, soft, flexible, and secure.

Not all patients are candidates for a prosthesis. It is important that the surgeon discuss ambulation
possibilities frankly with the patient and family. The seriously ill or debilitated patient may not have the
energy required to use a prosthesis. Mobility with a wheelchair may be the most realistic goal for this type
of patient.
Collaborative care also includes the direction and coordination of the rehabilitation program for the
amputee. Success depends on the physical and emotional health of the patient. Chronic illness and
debilitation complicate aggressive rehabilitation efforts. Both physical and occupational therapy must be
an integral component of the patient's overall plan of care.

Flexion contractures may delay the rehabilitation process. The most common and debilitating contracture
is hip flexion. Hip adduction contracture is rare. Patients should avoid sitting in a chair for more than 1
hour with hips flexed or having pillows under the surgical extremity to prevent flexion contractures. Unless
specifically contraindicated, patients should lie on their abdomen for 30 minutes three to four times each
day and position the hip in extension while prone.
Proper residual limb bandaging fosters shaping and molding for eventual prosthesis fitting (Fig. 61-18).
The physician usually orders a compression bandage to be applied immediately after surgery to support
the soft tissues, reduce edema, hasten healing, minimize pain, and promote residual limb shrinkage and
maturation. This bandage may be an elastic roll applied to the residual limb or a residual limb shrinker,
which is an elastic stocking that fits tightly over the residual limb and lower trunk area. [38]

FIG. 61-18 Bandaging for the above-the-knee amputation residual limb. Figure-of-eight style covers
progressive areas of the residual limb. Two elastic wraps are required.
The compression bandage is initially worn at all times except during physical therapy and bathing. The
bandage is taken off and reapplied several times daily, and care is taken so that it is applied snugly but
not so tight as to interfere with circulation. Shrinker bandages should be washed and changed daily. It is
recommended that the patient have two residual limb shrinker bandages so that one can be worn while
the other is being washed. After healing has occurred, the residual limb is bandaged only when the patient
is not wearing the prosthesis. The patient should be instructed to avoid dangling the residual limb over the
bedside to minimize edema formation.
As the patient's overall condition improves, the nurse begins instruction in the principles and techniques of
transferring from bed to chair and back. Active exercises and conditioning are essential in developing
ambulation skills. The exercise regimen is normally started under the supervision of the physician and the
physical therapist. The nurse must have a clear understanding of the exercise regimen to reinforce it and
ensure that the exercises are performed correctly. Active ROM exercises of all joints should be started as
soon after surgery as the patient's pain level and medical status permit. In preparation for mobility, the
patient should increase triceps and shoulder strength and lower limb support and learn balance of the
altered body. The loss of the weight of a limb requires adaptation of the patient's proprioceptive
mechanisms to prevent falls and frustration.
Crutch walking is started as soon as patients are physically able. If they have had immediate postsurgical
fitting, orders related to weight bearing must be carefully followed to avoid disruption of the skin flap and
delay of the healing process. Initial periods of ambulation should not exceed 5 minutes to prevent
dependent edema.
Before discharge, the patient and family need careful instruction related to residual limb care, ambulation,
prevention of contractures, recognition of complications, exercise, and follow-up care. Table 61-15 outlines
patient and family teaching following an amputation.
TABLE 61-15
Patient & Family Teaching Guide Following an Amputation
0

1. Inspect the residual limb daily for signs of skin irritation, especially redness and abrasion. Pay
particular attention to areas prone to pressure.
2. Discontinue use of the prosthesis if an irritation develops. Have the area checked
before resuming use of the prosthesis.
3. Wash residual limb thoroughly each night with warm water and a bacteriostatic soap.
Rinse thoroughly and dry gently. Expose the residual limb to air for 20 minutes.
4. Do not use any substance such as lotions, alcohol, powders, or oil unless prescribed by
the health care provider.
5. Wear only a residual limb sock that is in good condition and supplied by the prosthetist.
6. Change residual limb sock daily. Launder in a mild soap, squeeze, and lay flat to dry.
7. Use prescribed pain management techniques.

8. Perform ROM to all joints daily. Perform general strengthening exercises including the
upper extremities daily.
9. Do not elevate the residual limb on a pillow.
10. Lay prone with hip extension for 30 minutes three to four times daily.

Anticoagulants
Clinical Concepts: Med-Surg/Pedi/Geri
Anticoagulant therapy-effect
The use of anticoagulants and antiplatelet agents to treat stroke is controversial and depends on the
health care provider's preference. The principal drugs used are aspirin, heparin, lowmolecular weight
heparin (enoxaparin [Lovenox]), and warfarin (Coumadin). If the client received thrombolytic therapy, an
IV anticoagulant is usually prescribed as a follow-up treatment.
The provider typically prescribes sodium heparin (Hepalean) subcutaneously or via a continuous IV
infusion to prevent the progression of transient ischemic attacks (TIAs) or evolving strokes. This drug is
also effective in prevention of deep vein thrombosis (DVT), a hazard of immobility. Baseline prothrombin
time (PT) and partial thromboplastin time (PTT) values are usually obtained before initiating of heparin
therapy, 6 to 8 hours after the start of the infusion, and every morning while the client is receiving heparin
therapy. The therapeutic goal is to achieve 1.5 to 2 times the client's normal baseline PT and PTT values.
PT is used to monitor oral anticoagulant therapy, whereas PTT is used to monitor heparin therapy. The
World Health Organization advocates use of the International Normalized Ratio (INR) to monitor warfarin
therapy. The target INR value for most clients with strokes is 2.0 to 3.0; for strokes of cardiac origin, the
goal is usually 3.0 to 4.5.
Sodium heparin and other anticoagulants, such as warfarin (Coumadin, Warfilone), can cause bleeding.
Observe for signs of blood in the urine or stool, epistaxis, bleeding gums, and easy bruising. Anticoagulant
therapy is contraindicated in clients who have ulcers, uremia, or hepatic failure.
Enteric-coated or other forms of aspirin (Ecotrin, Ancasal) have proved useful primarily in the prevention
of recurrent stroke or embolic stroke. These drugs prevent blood clotting by reducing platelet
adhesiveness. Other commonly used antiplatelet medications include ticlopidine hydrochloride (Ticlid),
clopidogrel (Plavix), and dipyridamole (Persantine, Apo-Dipyridamole). These agents can cause bruising,
hemorrhage, and liver disease. Always teach the client to report any unusual bruising or bleeding to the
health care provider. Liver function and coagulation studies are carefully monitored during the course of
drug therapy. Clopidogrel should be taken with food to prevent gastric distress.
Monitor Anticoagulant Therapy
Most physicians use an algorithm to adjust the dose of heparin based on the client's PTT levels. Blood is
sampled every 4 to 8 hours for PTT or INR and the dose is adjusted accordingly. Warfarin therapy requires
the PT or INR be drawn on a regular basis. Low-molecular-weight heparin requires no testing. When
invasive studies are necessary (e.g., arterial blood gas analyses), apply pressure for 30 minutes to the
puncture site.
Bleeding can occur in any client receiving anticoagulation. The client should also be observed for frank
bleeding in the urine, tarry or frank blood in the stool, bleeding with brushing the teeth, easy
subcutaneous bruising, and flank pain.
INTEGRATING PHARMACOLOGY
Anticoagulant Therapy for the Prevention and Treatment of Deep Vein Thrombosis
LMWH has been available for the past decade. LMWHs are longer acting, homogeneous molecules,
with a reliable dose-response curve requiring little or no monitoring, but they are much more expensive
than heparin. The action of heparin and the LMWHs are similar. Both bind to antithrombin III, increasing
its activity and inhibiting thrombin and other factors. Whereas the anticoagulant function of heparin can be
measured through PTT, no such blood test is available for LMWH. This may seem like a drawback for
LMWHs, but the reason that standard heparin therapy must be monitored is because heparin has an

unpredictable bioavailability and pharmacokinetics, particularly when administered subcutaneously.

LMWHs, however, have extremely high bioavailability. The same bleeding precautions and drug-drug
interactions apply with LMWH.
Coumadin (warfarin or coumarin) is an oral anticoagulant. It is often used as a long-term anticoagulant
after the acute DVT has been treated with injectable forms of heparin. Coumadin has a long half-life (3 to
5 days). Therefore the drug must be stopped for 3 days before any invasive procedure is done. Coumadin
is prescribed based on International Normalized Ratio (INR) levels, the recommended therapeutic range is
2 to 2.5. Coumadin can also be prescribed based on prothrombin (ProTime) levels, but there is variation
from one laboratory to another, so INR levels are becoming more common, especially with long-term use
of warfarin (Coumadin). For hospitalized clients, warfarin (Coumadin) is administered in the afternoon or
early evening. This schedule allows for dose adjustments based on daily INR or ProTime results. Warfarin
(Coumadin) can be reversed with injections of vitamin K (phytonadione). The therapeutic effect of warfarin
(Coumadin) is altered by a host of medications and foods, and in clients with liver disease. Potential drugdrug and drug-food interactions should be reviewed by a pharmacist if the intended response (e.g.,
changes in INR) is not seen as predicted.
Prevention of Deep Vein Thrombosis
Several medications can be used to prevent DVT. Standard heparin is increased by adjusting the dose to
maintain the aPTT ratio in the upper normal range. An average dose is 5000 units given subcutaneously in
the abdomen twice daily. LMWH is also given subcutaneously. Subcutaneous injection of anticoagulants
can lead to bruising at the injection sites. Clients and families should be taught that this is an expected
response and does not indicate active bleeding. The development of painful masses in the abdomen should
be reported and may indicate more active bleeding.
The use of antiplatelet drugs, aspirin, and nonsteroidal anti-inflammatory drugs may have a place in the
prevention of DVT postoperatively or once conventional anticoagulant therapy for DVT has been
concluded, although there is still debate on this topic.
Anticoagulation prevents the extension of the original thrombus and the development of new thrombi
while the existing thrombus is lysed naturally by fibrinolysis. Oral warfarin (Coumadin) and parenterally
administered heparin have been the mainstays of anticoagulant therapy since the 1940s. Even though it is
well known that these medications are effective, they have several undesirable characteristics, such as
unpredictability in dosage required for therapeutic effect, the need for careful laboratory monitoring, and
the potential for life-threatening toxicity.
Evaluation
The client will undergo a successful PTCA without any evidence of bleeding or thrombocytopenia, or
allergic response. With eptifibatide and tirofiban, the client will remain free of ACS-related thrombosis
without adverse effects.
Anticoagulant therapy is directed toward preventing intravascular thrombosis by decreasing blood
coagulability. This therapy has no direct effect on a blood clot that has already formed or on ischemic
tissue injured by an inadequate blood supply because of the clot. Anticoagulant drug therapy is primarily
prophylactic because these agents act by preventing (1) fibrin deposits, (2) extension of a thrombus, and
(3) thromboembolic complications. Although long-term anticoagulant therapy remains controversial, there
is evidence that such therapy reduces the incidence of thrombosis and therefore prolongs life in clients at
high risk for thromboembolic events. Clients at high risk for short-term thromboembolic events include
postsurgical clients (particularly with procedures that limit lower extremity movement, such as hip and
knee surgery). Clients with atrial fibrillation, pregnancy, cardiac valve replacement, and a history of
hypercoagulability (e.g., observed with some cancers) or thrombotic events are also at higher risk for
developing thrombosis and/or thromboembolic events. Clients with existing thrombosis, such as a DVT,
pose a grave risk for life-threatening embolic events (e.g., PE) and are also typically treated with higher
doses of anticoagulants. Clients with unstable angina, MI, or thromboembolic CVA are also candidates for
higher dose anticoagulant therapy.

How are the anticoagulants differentiated?

The two main groups of anticoagulant drugs are (1) parenteral anticoagulant drugs, and (2) oral
anticoagulant drugs.
The parenteral anticoagulants include heparin and the low molecular weight (LMW) heparins. These agents
consist of long chains of monosaccharides and proteins and have a large molecular weight. The LMW
agents are isolated from standard heparin and possess shorter monosaccharide/protein chains. These
LMW heparins (dalteparin, enoxaparin, tinzaparin) have longer durations of action and are typically dosed
once or twice daily via (subcutaneous) injection. All heparins (including the LMW agents) are derived
primarily from the mucosal lining of pig intestine (porcine source) but occasionally obtained from bovine
lung (beef source). The heparins potentiate antithrombin III action leading to decreased fibrin formation.
Heparin effect is measured with the activated partial thromboplastin time (aPTT).
Other parenteral anticoagulants include antithrombin III (ATnativ, Thrombate III), argatroban, bivalirudin
(Angiomax), fondaparinux (Arixtra), lepirudin (Refludan) and danaparoid (Orgaran). Antithrombin III binds
covalently to thrombin and its use is limited to clients with documented antithrombin III deficiencies.
Argatroban is a thrombin inhibitor used to treat thromboembolic events in clients with heparin-induced
thrombocytopenia. Bivalirudin, also known as Hirulog, is a reversible polypeptide thrombin inhibitor
indicated for use with aspirin for clients with unstable angina undergoing cardiac catheter procedures.
Fondaparinux is a synthetic pentasaccharide that selectively inhibits factor Xa. It was released on the
market in 2002, and its role in the prevention and treatment of thromboembolic events is evolving.
Lepirudin is derived from the medicinal leech and is used for clients who cannot tolerate heparin (typically
because of heparin-induced thrombocytopenia). Effect of lepirudin is monitored with the aPTT. Danaparoid
is a heparin-like derivative from porcine intestinal mucosa and has a low cross-reactivity with heparin.
Danaparoid, like the LMW heparins, is more specific for factor Xa.
The oral anticoagulant most commonly used is warfarin (Coumadin). Warfarin interferes with the
production of vitamin Kdependent clotting factors. Other similar agents include dicumarol and anisindione
(Miradon), but are infrequently used. The safety and efficacy of warfarin is evaluated with the PT and the
INR (see Box 30-3). The lag time between warfarin administration and decay of the vitamin Kdependent
clotting factors is typically 36 to 72 hours, making warfarin dosing more complicated than heparin.
Interactions with other drugs and foods also confound therapy. The antidotes for warfarin include vitamin
K and fresh frozen plasma. Warfarin is often used when longer term anticoagulation is required.
For effective anticoagulation, the manner of use for both parenteral and oral anticoagulants is important.
They have been used to complement each other, and often the administration of both a rapidly acting
parenteral anticoagulant (heparin) and one of the oral anticoagulants is started shortly thereafter. Heparin
is usually discontinued as soon as the PT/INR has been sufficiently increased and the oral compound is
producing a full therapeutic effect.
Lumbar Puncture
Lumbar puncture is the most common method of obtaining CSF for analysis. It is contraindicated in the
presence of increased intracranial pressure or infection at the site of puncture.
Nurses often assist in this procedure because it is usually performed in the patient's room. Before the
procedure, the nurse should have the patient empty the bladder. The patient should lie in the lateral
recumbent position, with the back as near as possible to the edge of the bed. The nurse should assist the
patient to draw up the knees to the abdomen and flex the head to the chest. This helps separate the
vertebrae so that the needle can be inserted more easily.
Using strict sterile technique, the physician inserts a long needle below the third lumbar vertebra. This
may cause some local discomfort. There is no danger of injuring the spinal cord because the cord
terminates between the first and second lumbar vertebrae. However, the patient may have some pain
radiating down the leg or muscle twitching if the needle irritates the spinal root. The nurse can assure the
patient that this is temporary and that the patient is not in danger of being paralyzed.

A manometer is attached to the needle, and CSF pressure is determined after the patient is asked to relax
and extend the legs. If this is not done, the pressure appears abnormally high. CSF is withdrawn in a
series of tubes and sent for analysis. Some examiners believe that the patient should be kept lying flat for
at least a few hours after the procedure to avoid a spinal headache, which is presumably caused by loss of
the cushioning effect of CSF as a result of leakage of CSF at the puncture site. The prone position may be
effective in preventing CSF leakage. Others do not believe that the lying position is necessary because
headache seems to develop in some patients despite precautions. Meningeal irritation (nuchal rigidity) or
signs and symptoms of local trauma (e.g., hematoma, pain) may develop in some patients.
FOLLOW-UP CARE.
After a lumbar puncture (LP), the client is generally restricted to bedrest in a flat position for 4 to 8 hours
as prescribed by the physician or as determined by hospital policy. This prevents CSF leakage from the
puncture site. However, a report by the Therapeutics and Assessment Subcommittee of the American
Academy of Neurology found that the duration of bedrest does not influence the occurrence of post-LP
headache (Evans et al., 2000). Instruct the client to increase fluid intake (to 3000 mL unless
contraindicated) for 24 to 48 hours to facilitate CSF production, although research has not supported or
refuted this practice.
A decrease in CSF may cause a severe, throbbing headache (also called a spinal headache). Administer
analgesics as prescribed for headache if it occurs. If the lumbar puncture was done to reduce intracranial
pressure, perform a rapid neurologic assessment (especially level of consciousness) more frequently until
stability is ensured. Complications of lumbar puncture, although uncommon, include infection, CSF
leakage, and hematoma formation.
Postprocedure Care.
Record vital signs after the LP. Lying flat for several hours is sometimes prescribed. The client can eat and
drink as before the test. Drinking extra fluids will help restore CSF volume. If the CSF pressure
measurement indicated a high ICP, assess the client for decreasing LOC, which would indicate rising ICP.
Post-LP headache (spinal puncture headache, spinal headache) is typically throbbing, bifrontal, and
suboccipital and may develop within a few hours to several days after an LP. Post-LP headache occurs in
10% to 25% of clients. The incidence has decreased in recent years as a result of the use of smaller
gauge spinal needles. The headache probably occurs because CSF continues to leak through the opening
in the dura made by the needle. As a result of the leak, the CSF circulating around the cranium is
depleted. The fluid loss allows abnormal movement of the brain inside the skull. When the brain moves,
tension is placed on the meninges and venous sinuses, causing pain. The headache is usually relieved
when the client lies down and is made worse with sitting up or with a sudden jolt of the head. Such
headaches usually disappear within 24 hours but may last for several days.
To reduce the risk of post-LP headache, have the client remain in bed after the examination. Although
physician's orders may differ, an average time in bed is 3 hours. Encourage fluids to replace the CSF
withdrawn during the test. Once a headache begins, treatment may be bed rest in a dark, quiet room and
the administration of analgesics and fluids.
If the headache continues, an epidural blood patch may be required. Blood is withdrawn from the client's
vein and injected into the epidural space, usually at the LP site. The blood acts as a fibrin patch to seal the
hole in the dura and prevents further CSF leakage. Blood patches cannot be performed in a client who has
bleeding tendencies or infection at the puncture site.
Myelography
A myelogram is an x-ray study in which contrast material is injected into the subarachnoid space to
examine the spinal canal. A LP is performed and some CSF is removed. Myelography is used to visualize
intradural nerve roots in selected clients in whom MRI cannot be performed.

Cerebral Angiography
A cerebral angiogram consists of injection of contrast material into an artery to visualize intracranial
circulation (Figure 69-8). Angiography is the procedure used most often to visualize aneurysms, AVMs,
major vessel displacement, vascular occlusion, and thrombi. Cerebral angiography is not only invasive, but
it is also a procedure in which small errors can result in permanent disability or death. Meticulous attention
must be given to the client before, during, and after angiography. Risks associated with the procedure are
lessened when the test is performed by an experienced interventional radiologist using newer, very small
catheters.

FIGURE 69-8 Cerebral angiography allows x-ray visualization of the brain's vascular system when a
contrast dye is injected arterially. A, Insertion of dye through a catheter in the common carotid artery,
subsequently outlining vessels of the brain. B, An angiogram using the subtraction technique. 1, Internal
carotid artery. 2, Middle cerebral artery. 3, Middle meningeal artery.
The technique for lumbar puncture (LP) in infants and children is similar to that in the adult, although
modifications are suggested in neonates, who have less distress in a side-lying position with modified neck
extension than in flexion or a sitting position. Pediatric lumbar puncture sets contain smaller spinal
needles, but sometimes the practitioner will specify a particular size or type of needle that the nurse
should make certain is placed on the tray.
Children are usually controlled best in the side-lying position, with the head flexed and the knees drawn up
toward the chest. Even cooperative children need to be held gently to prevent possible trauma from
unexpected, involuntary movement. They can be reassured that, although they are trusted, holding will
serve as a reminder to maintain the desired position. It also provides a measure of support and
reassurance to them.
The child is placed on the side with the back close to the edge of the examining table on the side from
which the practitioner is working. The nurse maintains the child's spine in a flexed position by holding the
child with one arm behind the neck and the other behind the thighs. The flexed position enlarges the
spaces between the lumbar vertebral spines, which facilitates access to the spinal fluid space. It is helpful
to wrap the legs before positioning to decrease leg movement.
An alternate position used with small infants and some older children is the sitting position. The child is
placed with the buttocks at the edge of the table and with the neck flexed so that the chin rests on the
chest or on the nurse's arm. Before starting the procedure, ensure that the infant's airway is not
compromised by the position chosen for restraint. The infant's arms and legs are immobilized by the
nurse's hands (Fig. 27-15, C).

NURSING ALERT

The sitting position may interfere with chest expansion and diaphragm excursion, and in infants the soft, pliable tra
Therefore observe the child for difficulty with breathing.

Another position that employs close and comforting contact for the child involves holding the child upright
against the nurse's (or parent's) chest with the child's legs wrapped around the adult's waist. The adult's
arms are used to hug and restrain the child. For ease of the examiner, the adult should be standing. A
small pillow is placed between the child's abdomen and the adult to help arch the child's back. If the pillow
proves unsuccessful, a third person can place an arm in this space to achieve the desired position. Care
should be taken that excessive pressure does not compromise circulation or breathing and that the nose
and mouth are not covered by the restrainer's body.
ATRAUMATIC CARE
Lumbar Puncture and Bone Marrow Test

Apply EMLA to the puncture site at least 60 minutes before the procedure. To identify the LP site, draw an imaginar
iliac crest across the spine to the opposite iliac crest. The puncture site is intersected by the line at approximately L
anesthesia, buffered lidocaine with a 30-gauge needle can be used. Unconscious sedation with agents such as prop
is recommended for bone marrow biopsy and aspiration. Conscious or unconscious sedation is recommended for LP

Fig. 27-16 EMLA, a local anesthetic cream, is placed under an occlusive dressing to decrease pain of lumbar punc
drawing an imaginery line from the top of the iliac crest to cross the spine at the approximate needle insertion site.

Specimens and spinal fluid pressure are obtained, measured, and sent for analysis in the same manner as
for the adult patient. Vital signs are taken as ordered, and the child is observed for any changes in level of
consciousness, motor activity, or other neurologic signs. Postlumbar puncture headache may occur and is
related to postural changes; this is less severe when the child lies flat. Headache is seen much less
frequently in young children than in adolescents.
Bone Scans
In bone scanning, images of the skeleton are obtained after a radioisotope, usually technetium 99m
(99mTc), is injected intravenously and allowed to migrate to bone. The whole body is usually scanned,
although just a limb may be scanned (pinhole scan) if a stress fracture is suspected. Bone scanning is
used to detect malignancies, osteomyelitis, osteoporosis, and some fractures, especially pathologic ones.
The radioisotope concentrates in these areas, indicating abnormal bone metabolism. The radioisotope does
not accumulate in poorly perfused bone.
Explain the procedure to the client and family, an-swer their questions, and obtain consent. The procedure
takes about an hour, during which time the client lies supine. Reassure the client that the procedure is not
painful and that there are no harmful effects from the isotopes. Suggest that the client void before the

procedure.
After the scan, no special precautions are required except that the client should drink large amounts of
water for 24 to 48 hours to help eliminate the radioisotope. Because the radioisotope carries minimal
radioactivity, there is no hazard to others.
Radioisotope Bone Scans
Radioisotope bone scans are performed primarily to demonstrate the presence of metastatic disease,
tumors, infection (osteomyelitis), and other conditions with increased bone activity. This nuclear scanning
test can also be used to diagnose the cause of undetermined bone pain and assess the healing of
fractures. Intravenously injected sodium pertechnetate technetium 99m (99mTc) is the isotope most
commonly used in this study. The 99mTc concentrates in areas of osteoblastic activity involved in the
exchange of calcium.
Technetium, a bone-seeking radioisotope, is taken up by the bone in areas of adequate blood supply and
metabolic activity. Hot spots on the scan indicate areas of increased bone turnover, as in fractures, bone
healing, and inflammatory responses. Cold spots, or areas of decalcified bone, indicate no bone activity,
as in lytic lesions. Lesions may be visualized on bone scans as early as 3 to 6 months before they are
evident on routine x-ray films. Bone scans are commonly used to rule out bony metastases from the
prostate, breast, and lung.
Technetium scans are also of some use in determining the degree of parotid gland involvement in
Sjgren's syndrome. The uptake, concentration, and excretion of the isotope by the major salivary glands
are measured by a technique known as sequential scintigraphy.
Persons being prepared for these procedures should know that the procedures are not painful and the
isotopes will not harm them. However, the patient may have to remain quietly in one position for an hour
or more. The nurse assesses the patient for iodine or seafood allergies and encourages the patient to drink
fluids before the examination. The bladder should be emptied just before the scan to avoid interference
with visualization of the pelvis. The radioisotope is injected intravenously about 2 hours before scanning.
Procedures using barium or iodine are not scheduled before the bone scan, since these substances
interfere with scanning. The kidneys excrete the radioisotope in the urine within 6 to 24 hours. Fluids are
encouraged after the scan to aid in excretion of the isotope.
Assessment- Hyperparathyroidism- Calculi
Ask the client about any bone fractures, recent weight loss, arthritis, or psychological distress. Determine
whether the client has received radiation treatment to the head or neck. The client with long-standing
disease may have a waxy pallor of the skin and bone deformities in the extremities and back.
Manifestations of hyperparathyroidism may be related either to the effects of excessive PTH or to the
effects of the accompanying hypercalcemia.
High levels of PTH cause renal calculi (kidney stones) and deposits of calcium in the soft tissue of the
kidney. Bone lesions are due to an increased rate of bone destruction and may result in pathologic
fractures, bone cysts, and osteoporosis.
Gastrointestinal manifestations (e.g., anorexia, nausea, vomiting, epigastric pain, constipation, weight
loss) are common, particularly when serum calcium levels are high. Elevated serum gastrin levels are
caused by hypercalcemia and lead to peptic ulcer disease. Fatigue and lethargy may be present and
become more severe as the serum calcium levels increase. When serum calcium levels are greater than 12
mg/dL, the client may have psychosis with mental confusion, which leads to coma and death if left
untreated. (See Chapter 16 for more information about hypercalcemia.)
Serum PTH, calcium, and phosphate levels and urine cyclic adenosine monophosphate (cAMP) are the
most commonly used laboratory tests to detect hyperparathyroidism. X-rays may show kidney stones,
calcium deposits, and bone lesions, such as cysts or fractures. Loss of bone density occurs in the client

with chronic hyperparathyroidism. Other diagnostic tests include arteriography, computed tomography
(CT), venous catheterization of the thyroid veins with sampling of the blood for PTH levels, and
ultrasonography. Explain the procedures and care for the client undergoing diagnostic tests.

Clinical Manifestations
Some clients with hyperparathyroidism may be asymptomatic. Others have myriad manifestations arising
from the skeletal disease, renal involvement, gastrointestinal tract disorders, and neurologic
abnormalities, as outlined in the Critical Monitoring feature on Hyperparathyroidism and
Hypoparathyroidism in Figure 45-3.

FIGURE 45-3 Clinical manifestations of primary hyperparathyroidism.

Manifestations of bone disease range from backache, joint pain, and bone pain to pathologic fractures of
the spine, ribs, and long bones. In long-standing cases, assessment reveals deformity and bending of the
bones. Osteitis fibrosa with superperiosteal resorption or bone cysts, arthritis, or radiologic osteoporosis
may be diagnosed.
Manifestations of renal involvement include polyuria and polydipsia; the appearance of sand, gravel, or
stones (calculi) in the urine; azotemia; and hypertension resulting from renal damage. Without
intervention, renal insufficiency may progress to fatal renal hypertension and uremia.
Hypercalcemia produces mainly gastrointestinal manifestations such as thirst, nausea, anorexia,
constipation, ileus, and abdominal pain. Decreased neuromuscular irritability is also common. Often,
clients have a history of peptic ulcer or gastrointestinal bleeding. Assessment may also reveal psychiatric
manifestations. Listlessness, depression, and paranoia are sometimes associated with high levels of serum
calcium. Finally, calcification may form in the eyes, impairing vision.
Major complications include the manifestations associated with hypercalcemia and those associated with
treatment, such as dehydration, hypocalcemia, and gastrointestinal problems.
The diagnosis of hyperparathyroidism mainly rests on laboratory and x-ray findings. Serum calcium levels
are elevated, serum phosphate levels are depressed, and both urine calcium and phosphorus levels are
high. In addition, alkaline phosphatase is elevated in the 25% of clients who have associated bone
disease. Clients with skeletal damage have the following characteristic x-ray findings: diffuse
demineralization of bones, bone cysts, subperiosteal bone resorption, and loss of the lamina dura around
the teeth. Ultrasonography or magnetic resonance imaging (MRI) may be used for preoperative
localization of the parathyroid glands.

Hypersecretion: Hyperparathyroidism
Hyperparathyroidism refers to elevated PTH levels caused by excessive release of PTH from the
parathyroid glands. Primary hyperparathyroidism and hypercalcemia of malignancy are the most common
causes of elevated serum calcium, accounting for approximately 90% of cases. Secondary
hyperparathyroidism results from malabsorption syndrome or a defect in mineral homeostasis, such as
renal failure, with a resultant increase in PTH secretion from the parathyroid glands. The serum calcium
level is not elevated in secondary hyperparathyroidism.
Primary Hyperparathyroidism
Etiology and Epidemiology
The most frequent cause of primary hyperparathyroidism is a solitary adenoma (85%) involving one of the
four parathyroid glands. The remaining 15% of patients usually have hyperparathyroidism of all four
glands or, in rare instances, primary parathyroid cancer.
It is postulated that the set point for negative feedback on PTH secretion by ambient ionized calcium
levels is elevated. In essence, this means that PTH secretion is not switched off in the adenoma or
hyperplastic cells when serum calcium levels are at the upper limit of normal. Parathyroid adenomas are
thought to represent clonal expression of mutant cells, in turn related to loss of function of tumor
suppressor genes.[11]
Primary hyperparathyroidism may also be part of a MEN syndrome. The type I syndrome, or MEN I,
consists of pituitary adenoma, pancreatic islet cell tumor, and primary hyperparathyroidism. The type II
syndrome, or MEN IIA, consists of pheochromocytoma, medullary thyroid cancer, and primary
hyperparathyroidism. An appropriate workup for these entities is prompted by family history, relevant
symptomatology, and physical findings.
The incidence of primary hyperparathyroidism is approximately 1 in 500 to 1000 individuals, with women
being affected more often than men by 3:1. The majority of patients are postmenopausal, in the sixth
decade of life, and asymptomatic. They are frequently incidentally diagnosed via a routine serum
chemistry panel that includes measurement of calcium levels. Some patients may be diagnosed after a
workup for suspected secondary causes of osteoporosis or osteopenia. [1214]
Pathophysiology
Elevation in PTH levels raises serum calcium via several mechanisms: (1) increased bone resorption; (2)
enhanced activation of vitamin D to 1,25-hydroxycholecalciferol, with resultant enhanced calcium
resorption from the gastrointestinal tract; and (3) enhanced renal tubular resorption of calcium from the
glomerular filtrate.
In addition, PTH enhances the renal excretion of phosphate with resultant decrease in the serum
phosphate level. Primary hyperparathyroidism is characterized by hypercalcemia with low to subnormal
serum phosphate. Excess bone resorption results in declining bone mass, especially in cortical bone. This
is best assessed with bone density measurements in the forearm. Although rare, cysts may form in the
bone in severe cases of hyperparathyroidism, giving rise to osteitis fibrosa cystica.
Most patients with mild hyperparathyroidism are asymptomatic. In contrast, patients with more advanced
disease are seen with renal calculi; bone pain; and vague, generalized arthralgias (Box 38-9
Box 38-9
Hypersecretion of Parathyroid Hormone: Pathophysiologic Alterations
and Clinical Manifestations

Increase in calcium resorption from bone resulting

in hypercalcemia, decreased bone mass, bone cysts, and
fractures that can be characterized by bone pain and
arthralgias
Alteration in urinary calcium excretion during
course of the disease

Early: hypocalciuria
Later: hypercalciuria with polyuria, polydipsia,
nephrolithiasis, and kidney failure
Decreased renal bicarbonate and phosphate
resorption
Hyperchloremic acidosis
Increased gastrin secretion causing peptic ulcer
disease
Increased renal activation of vitamin D producing
calcitriol (1,25-dihydroxycholecalciferol), increasing
gastrointestinal calcium absorption, thereby adding to the
hypercalcemia
Depression of nerve and muscle activity from
hypercalcemia
Cardiac muscle signs and symptoms, including
hypertension and electrocardiographic changes such as
shortened Q-T intervals and dysrhythmias
Neuromuscular signs and symptoms, including
impaired mentation, apathy, lethargy, somnolence, hypoactive
deep tendon reflexes, fasciculation of the tongue, muscle
weakness, and myalgias (lower limbs more than upper limbs)
Gastrointestinal signs and symptoms, including
anorexia, nausea, vomiting, and constipation
Hypercalcemia causing pancreatitis

).
Collaborative Care Management
Diagnostic Tests
The initial diagnostic tests for primary hyperparathyroidism are serum calcium, phosphorus, and PTH
levels. Various PTH assays are available, including C-terminal, N-terminal, midmolecule, and intact PTH.
The most reliable and clinically useful assay is the intact PTH assay. The combination of an elevated serum
calcium, low normal to subnormal serum phosphate, and elevated intact PTH level generally confirms the
diagnosis (see Chapter 37).
Results of tests indicative of primary hyperparathyroidism include elevated serum calcium, decreased
serum phosphate, and elevated PTH levels; elevated 24-hour urinary calcium excretion; and reduced bone
mineral density and renal calculi on radiographic examination.
When the results do not meet these criteria, an alternative explanation for hypercalcemia must be sought
(Box 38-10
Box 38-10
Causes of Hypercalcemia (Other Than Hyperparathyroidism)

Malignancy
Leukemia, lymphoma, multiple myeloma
Vitamin D intoxication
Granulomatous diseases (sarcoidosis)
Other endocrine disorders: thyrotoxicosis, adrenal
insufficiency
Milk-alkali syndrome
Immobilization

Medications (thiazides, lithium, aminophylline,

gonadal steroids)

). Malignancy is the most common alternative explanation for hypercalcemia when primary
hyperparathyroidism is not present. In general, patients with hypercalcemia of malignancy usually have
obvious features of malignancy such as cachexia and weight loss; many have a previously diagnosed
malignancy. Malignant cells can produce a PTH-like compound, parathyroid hormonerelated protein,
which can bind to and stimulate PTH receptors with resultant hypercalcemia. This so-called humoral
hypercalcemia of malignancy is usually seen in patients with a large tumor burden, and patients generally
have a poor prognosis related to the underlying malignancy.
Medications and Treatments
Acute medical intervention to lower serum calcium is reserved for patients who are symptomatic from the
hypercalcemia (anorexia, nausea, vomiting) and generally have serum calcium levels greater than 13
mg/dl. Long-term medical management is rarely undertaken except when patients are poor surgical
candidates.
The immediate treatment is to correct any dehydration and promote fluid intake of at least 2 L/day unless
contraindicated. Activity is encouraged to promote resorption of calcium by the bone. Thiazide diuretics
promote renal calcium retention and are contraindicated in this setting. Loop diuretics such as furosemide
reduce renal calcium resorption, but should be used cautiously because of the long-term risk of worsening
bone disease. If given to a patient with dehydration, furosemide may exacerbate prerenal kidney failure.
Diuresis results in significant lowering of serum calcium and symptomatic patient improvement. Effects are
temporary and cease when treatment is discontinued. Bisphosphonates (intravenous pamidronate or oral
alendronate) have been used to control the hypercalcemia of primary hyperparathyroidism. Effects are
also transient. Oral and intravenous phosphate is seldom used because of concerns about ectopic
calcifications in soft tissues. Phosphate can interfere with the absorption of calcium, renal hydroxylation of
vitamin D, and bone resorption.
Patients who are not surgical candidates are checked regularly to monitor disease progress. The nurse
evaluates the patient's serum calcium and electrolytes, albumin, creatinine, and alkaline phosphatase
levels at regular intervals. Bone densitometry and renal ultrasound are done every 1 to 2 years. [14]
Diet
Dietary calcium intake for the patient with hyperparathyroidism should be moderate, with high intake
being clearly undesirable. Low calcium intake may also be undesirable, since this could further stimulate
PTH secretion and exacerbate bone disease.
The patient with significant hypercalcemia that is being managed medically needs careful monitoring to
ensure adequate hydration, normal electrolytes, normal blood urea nitrogen and serum creatinine, and
normal serum phosphorus with optimal control of the serum calcium. Patients need a fluid intake of at
least 2 L/day, assuming the absence of limiting cardiac or renal processes, and must further increase their
fluid intake when outside temperatures are high because of increased insensible fluid losses via sweat.
Surgical Management
Surgery is the definitive therapy for primary hyperparathyroidism and is usually curative. Surgical
intervention prevents progression of preexisting complications of the disease (renal calculi, overt bone
disease, fracture, life-threatening hypercalcemia) and prevents development of complications in high-risk
patients. High risk is defined as[14]:

Serum calcium more than 1 mg/dl above the upper limit of normal

Age greater than 50 years

Marked hypercalciuria (more than 400 mg/24 hr)

Creatinine clearance reduced by more than 30% compared with age-matched

individuals

Bone mineral density at the distal radius more than 2.5 standard deviations below peak
bone mass (a T-score of less than 2.5)

Patients in whom medical surveillance is not desirable or possible

In most cases the procedure is removal of a solitary adenoma. In the case of four-gland hyperplasia, the
approach is to remove three and a half glands, leaving the half-gland remnant in the neck or
autotransplanting it in the nondominant forearm. The half-gland is left to prevent permanent
hypoparathyroidism. Operative success can be readily confirmed by intraoperative PTH assay; results are

available within 15 minutes. This intraoperative assay has assisted in reducing the need for repeat surgery
for hyperparathyroidism.[60]
In some centers parathyroidectomy is performed as an ambulatory procedure with local anesthesia, and
results are comparable to those with the patient under general anesthesia. Minimally invasive surgery with
or without perioperative radioisotope localization of abnormal parathyroid tissue is being carried out in
several centers. Persons with parathyroid hyperplasia, multiglandular disease, and abnormal neck
anatomy are generally not suited for the minimally invasive approach.
Preoperative Localization Testing
In the patient with no prior neck surgery, an experienced parathyroid surgeon finds the abnormal
parathyroid gland(s) in more than 90% of instances without any prior localization procedure. In the
patient who has had prior neck surgery with resultant distortion of anatomic landmarks, however, most
physicians support the use of preoperative localization to reduce the length of surgery and increase
operative success. Several preoperative localization tests have been used, including ultrasonography, CT,
MRI, and radioisotope (technetium-sestamibi) scintigraphy. This latter dual-isotopic method is currently
the preferred method in clinical practice. It is not uncommon for studies to be falsely positive, and two
different studies are frequently ordered to increase confidence in the localization.
Nursing Management- Hyperparathyroidism
Nursing management of the patient with hyperparathyroidism is somewhat dependent on the collaborative
treatment strategy. Nursing care for the patient following a parathyroidectomy is similar to that for a
patient after thyroidectomy. The major postoperative complications are associated with hemorrhage and
fluid and electrolyte disturbances. Tetany, a condition of neuromuscular hyperexcitability associated with
sudden decrease in calcium levels, is another concern. It is usually apparent early in the postoperative
period but may develop over several days. Mild tetany, characterized by unpleasant tingling of the hands
and around the mouth, may be present but should abate without problems. If tetany becomes more
severe (e.g., muscular spasms or laryngospasms develop), IV calcium may be given. IV calcium gluconate
should be readily available for patients following parathyroidectomy in the event that acute tetany occurs.
Strict monitoring of intake and output is necessary to evaluate fluid status. Calcium, potassium,
phosphate, and magnesium levels are assessed frequently, as well as Chvostek's and Trousseau's signs.
Mobility is encouraged to promote bone calcification.
If surgery is not performed, treatment to relieve symptoms and prevent complications is initiated. The
nurse can assist the patient with hyperparathyroidism to adapt the meal plan to his or her lifestyle. A
referral to a dietitian may be useful. Because immobility can aggravate the bone loss, the nurse can assist
the patient to implement an exercise program and identify resources, such as shopping malls and YMCAs
as places to exercise safely. The patient should be encouraged to keep the regular appointments, and the
tests being performed should be explained. The patient should also be instructed in the symptoms of
hypocalcemia or hypercalcemia and to report these should they occur.
DIVERTICULOSIS AND DIVERTICULITIS
A diverticulum is a saccular dilation or outpouching of the mucosa through the circular smooth muscle of
the intestinal wall. Clinically, diverticular disease occurs in two forms: diverticulosis and diverticulitis.
Multiple noninflamed diverticula are present with diverticulosis. The patient is most often free of symptoms
but may have some abdominal discomfort. In diverticulitis, inflammation of the diverticula occurs (Fig. 4114). Diverticula may occur at any point within the GI tract but are most commonly found in the sigmoid
colon.

FIG. 41-14 Diverticula are outpouchings of the colon. When they become inflamed, the
condition is diverticulitis. The inflammatory process can spread to the surrounding area in the
intestine.
Etiology and Pathophysiology
Diverticular disease is a common GI disorder that affects 5% of the population by the age of 40 years and
50% by the age of 80 years.[31] It affects men and women equally, but men seem to have a higher
complication rate. Although it affects almost 30 million Americans, most are asymptomatic.
There is no known cause of diverticular disease, but deficiency in dietary fiber has been associated with it.
The disease is more prevalent in Western populations that consume diets low in fiber and high in refined
carbohydrates, and it is virtually unknown in areas of the world, such as rural Africa, where high-fiber
diets are consumed.
When diverticula form, the smooth muscle of the colon wall becomes thickened (Fig. 41-15). Lack of
dietary fiber slows transit time, and more water is absorbed from the stool, making it more difficult to
pass through the lumen. Decreased bulk of the stool, combined with a more narrowed lumen in the
sigmoid colon, causes high intraluminal pressures. These factors are believed to contribute to the
formation of diverticula.

FIG. 41-15 In diverticular disease, the outpouches (arrows) of mucosa appear as slitlike
openings from the mucosal surface of the open bowel.
The cause of diverticulitis is related to the retention of stool and bacteria in the diverticulum, forming a
hardened mass called a fecalith. This causes inflammation and usually small perforations. Inflammation of
the diverticulum spreads to the surrounding area in the intestines (Fig. 41-16), causing the tissue to
become edematous. Abscesses may form, or complete perforation with peritonitis may occur.

FIG. 41-16 Complications of diverticulitis.

Clinical Manifestations
The majority of patients with diverticulosis have no symptoms. Those with symptoms typically have
crampy abdominal pain located in the left lower quadrant that is usually relieved by passage of flatus or
bowel movement. Alternating constipation and diarrhea may be present.
Approximately 15% of patients with diverticulosis progress to acute diverticulitis. In patients with
diverticulitis, abdominal pain is localized over the involved area of the colon. A tender, left lower quadrant
mass may be felt on palpation of the abdomen. Fever, chills, nausea, anorexia, and elevated WBC may be
present. Elderly patients with diverticulitis are frequently afebrile, with a normal WBC, and little, if any,
abdominal tenderness.
Complications of diverticulitis include perforation with peritonitis, abscess and fistula formation, bowel
obstruction, ureteral obstruction, and bleeding. Bleeding is a common complication of diverticulitis and is
manifested by hematochezia (maroon stools). Bleeding usually stops spontaneously.
Diagnostic Studies
A CT scan with oral contrast is the test of choice for diverticulitis.[31] A CBC, urinalysis, and fecal occult
blood test should be performed (Table 41-37). A barium enema is used to determine narrowing or
obstruction of the colonic lumen. A colonoscopy may be performed to rule out possible hidden polyps or
lesions. A patient with acute diverticulitis should not have a barium enema or colonoscopy because of the
possibility of perforation and peritonitis.
TABLE 41-37
Collaborative Care Diverticulosis and Diverticulitis
Diagnostic
History and physical examination
Testing of stool for occult blood
Barium enema
Sigmoidoscopy
Colonoscopy
CBC

Urinalysis
Blood culture
Collaborative Therapy
Ambulatory and Home Care
High-residue diet
Dietary fiber supplements
Stool softeners
Anticholinergics
Mineral oil
Bed rest
Clear liquid diet
Oral antibiotics
Bulk laxatives
Acute Care: Diverticulitis
Antibiotics
NPO status
IV fluids
Possible colon resection for obstruction or hemorrhage
Bed rest
NG suction

NURSING and COLLABORATIVE MANAGEMENT DIVERTICULOSIS AND DIVERTICULITIS

Uncomplicated diverticular disease is treated with a high-fiber diet (see Table 41-9) and bulk laxatives,
such as psyllium hydrophilic mucilloid (Metamucil). Anticholinergic drugs such as dicyclomine (Bentyl) and
Donnatal may be used to relieve discomfort from spasm of the bowel (see Table 41-37).
Fluids should be increased because fibers retain water, thus decreasing the amount absorbed by the body.
If the patient is obese, a reduction in weight is needed. Increased intraabdominal pressure should be
avoided because it may precipitate an attack. Factors that increase intraabdominal pressure are straining
at stool, vomiting, bending, lifting, and tight, restrictive clothing.
In acute diverticulitis, the goal of treatment is to allow the colon to rest and the inflammation to subside.
The patient is kept on NPO status and bed rest and is given parenteral fluids. An NG tube may be
necessary. The patient should be observed for signs of possible peritonitis. In acute diverticulitis, broadspectrum antibiotic therapy is required. The WBC count is monitored.
When the acute attack subsides, oral fluids progressing to a semisolid diet are allowed. Ambulation is also

permitted. At this stage the patient should be observed for a recurrent attack. If the patient has a bowel
resection or colostomy, the nursing care is the same as for these procedures.
Approximately 30% of patients with acute diverticulitis require surgical intervention. Patients with
complicated diverticular disease often require surgery. Surgical intervention is necessary to drain
abscesses or to resect an obstructing inflammatory mass. The usual surgical procedures involve resection
of the involved colon with a temporary diverting colostomy. The colostomy is reanastomosed after the
colon is healed.
The patient should be provided with a full explanation of the condition. The better the patient understands
the disease process and adheres to the prescribed regimen, the less likely the exacerbation of the disease
and the onset of complications.
HISTORY
Clients with diverticulosis are usually asymptomatic, and unless pain or bleeding develops, the condition
may go undiagnosed or found incidentally on routine colonoscopy. Occasionally diverticulosis causes
symptoms. For clients with uncomplicated diverticulosis, the nurse asks about a history of intermittent
pain in the left lower quadrant and a history of constipation. If diverticulitis is suspected, the client is
asked about a history of fever and abdominal pain. Inquire about recent bowel elimination patterns
because constipation may develop as a result of intestinal inflammation. The client is also questioned
about the presence of bleeding from the rectum.
DIVERTICULAR DISEASE
Diverticular disease refers to two disorders: diverticulosis and diverticulitis. A diverticulum is a blind outpouching or herniation of intestinal mucosa through the muscular coat of the large intestine, usually the
sigmoid colon. Diverticulosis is the presence of noninflamed diverticula. Diverticulitis is inflammation of a
diverticulum. Diverticulitis is common in obese clients and affects 5% to 10% of men and women over 45
years of age and 80% of those over 85 years of age. It is estimated, however, that only 20% of those with
diverticulitis will develop manifestations of disease. Although diverticula may be found all through the
bowel, 85% of diverticulitis arises in the sigmoid and descending colon.
Etiology and Risk Factors
Low-fiber diets have been implicated in the development of diverticula because such diets decrease bulk in
the stool and predispose to constipation. The etiology of diverticular disease is related mainly to two
factors: weakening of the bowel wall and increased intraluminal pressure. In the presence of muscle
weakness in the bowel, this increase in intraluminal pressure can lead to the formation of diverticula.
Diverticulitis occurs when undigested food blocks the diverticulum, leading to a decrease in blood supply to
the area and predisposing the bowel to invasion of bacteria into the diverticulum.
Pathophysiology
Diverticula have a narrow neck like that of a flask that communicates with the bowel lumen. Weak points
in the bowel musculature exist where branches of the blood vessels penetrate the colonic wall. These weak
points create areas for bowel protrusion when there is increased intraluminal pressure. Diverticula
frequently develop in the sigmoid colon because of the high pressures required in this area to move the
stool into the rectum.
Diverticulitis may be acute or chronic. If the diverticulum is not infected, it causes few problems. When
fecaliths do not liquefy and drain from the diverticulum, however, they may become trapped, causing
irritation and inflammation (diverticulitis). The inflamed area becomes congested with blood and may
bleed or perforate. Chronic diverticulitis results in increased scarring and eventual narrowing of the bowel
lumen, potentially causing obstruction.
Diagnosis of acute diverticulitis can be confirmed by computed tomography (CT). Sigmoidoscopy is of little
diagnostic value since the disease is usually extraluminal.
Clinical Manifestations
The manifestations of diverticulitis depend on the extent of the inflammation and the site of occurrence.
Discomfort consists of dull, episodic, or steady left quadrant or midabdominal pain. Assessment also
reveals alteration in bowel habits (constipation, diarrhea, or both), increased flatus, anorexia, and lowgrade fever. Localized tenderness may occur in the left lower quadrant. The inflammatory process usually
subsides within several weeks. If the infection penetrates the pelvic floor or retroperitoneal tissues,

abscesses may result. Extension of the inflammation to adjacent organs can lead to fistulas of the bladder
or vagina and peritonitis. Repeated inflammation can result in narrowing and obstruction of the bowel.
Trace blood may be found in the stools, but profuse bleeding is uncommon. Stools also may contain
mucus. Urinary frequency can occur if the inflammation is in the proximity of the bladder. Straining,
coughing, or lifting causes an increase in intra-abdominal pressure and manifestations such as diarrhea,
constipation, pain, mucus, and flatus. The clinician may palpate a tender mass on digital rectal
examinations.
Outcome Management
Medical Management
Asymptomatic diverticular disease requires no specific therapy other than diet modification. Mild disease
can be treated by adherence to a high-fiber diet and prevention of constipation with bran and bulk
laxatives (hydrophilic colloids). Advise clients to notify the physician of any change in bowel movement
pattern (constipation or diarrhea) or character (the presence of mucus or blood) or if fever, abdominal
pain, or urinary manifestations develop.
Diverticulitis may be treated conservatively with medical intervention by allowing the colon to rest. Clients
with acute diverticulitis are assigned to NPO status, may have an NG tube, and receive parenteral fluids
and antibiotics until pain, inflammation, and temperature decrease. If opioids are required for pain
management, meperidine is the drug of choice. Morphine sulfate should be avoided because it has been
shown to cause spasm of the colon. When the acute episode subsides, oral liquids and, later, a
progressively more inclusive diet can be added. Nursing care involves the preceding interventions and
teaching the client about diet changes.
Surgical Management
About 20% of clients with diverticulitis will require surgery. Surgery is indicated for diverticular disease
with complications such as hemorrhage, obstruction, abscesses, and perforation. Surgical procedures
usually involve ligation and removal of the sac or resection of involved bowel if complications develop.
With abscess or obstruction, the surgeon performs a colon resection with a temporary colostomy, which is
left in place until the client's condition improves. For some clients, the temporary colostomy alone allows
the bowel to rest and heal. For nursing care, see the earlier discussion of bowel resection.
Hematologic Status
Hematologic assessment of the patient is essential, especially in procedures with an expected blood loss.
The nurse should question patients regarding a history of anemia, bleeding disorders, and hematologic
malignancies. The nurse should elicit a history of blood transfusions and any adverse reactions to blood or
blood products. It is also important to ask whether the patient has donated his or her own blood
(autologous donation) for the surgical procedure. A thorough medication history is important, with
particular attention to medications that inhibit platelet function, such as anticoagulants, nonsteroidal
antiinflammatory drugs, aspirin, tricyclic antidepressants, alcohol, and beta-blockers. The nurse should
consult with the anesthesiologist or surgeon to determine if and when these medications need to be
discontinued before surgery.
Persons with a history of atrial fibrillation, venous thromboses, and mechanical heart valves are often
treated with the oral anticoagulant warfarin. Warfarin therapy increases the patient's risk for bleeding and
hemorrhage. Preoperative management of these patients is a challenge, since discontinuing anticoagulant
therapy increases the risk for thromboembolism. The literature has no evidence to support the best
practice for managing patients on long-term anticoagulant therapy. The nurse needs to consult with the
surgeon and anesthesiologist regarding perioperative management of anticoagulation therapy.
Another cornerstone of the preoperative assessment is questioning the patient about a history of deep
venous thrombosis (DVT) and pulmonary embolism. Persons with polycythemia, thrombocytosis, and other
conditions that increase blood viscosity are at risk for hemorrhage and thromboembolism. Risk factors for
DVT include age over 40 years, prior history of DVT, decreased mobility, pelvic or cardiovascular surgery,
total hip and total knee surgery, fracture or trauma, history of smoking, use of estrogen, and obesity.
Refer to Chapter 31 for a full discussion of DVT.

Rheumatoid arthritis-elevated RF
Autoantibody Tests
Abnormal antibodies that the body produces against itself are termed autoantibodies. Autoantibodies
injure self-tissues and produce the symptoms associated with autoimmune conditions. Several tests are
useful in confirming the presence of autoantibodies. Rheumatoid factor (RF) is an abnormal protein
consisting of IgM antibodies found in the serum of persons with rheumatoid arthritis and other
autoimmune diseases. Antinuclear antibodies (ANAs) or antideoxyribonucleic acid (DNA) antibodies are
gamma globulins formed against properties of the cell nucleus. Tests for ANAs are positive in a large
number of patients with autoimmune disorders such as SLE or systemic sclerosis. Healthy older adults
have increased antibodies (ANAs and RF), but the clinical relevance of these increases is unclear.
SERUM DIAGNOSTICS
Rheumatoid Factor (Latex Fixation): Used to determine presence of autoantibodies (rheumatoid
factor) found in clients with connective tissue disease; if antibody is present, it is suggestive of rheumatoid
arthritis; the higher the antibody titer, the greater the degree of inflammation.
Antinuclear Antibody (ANA): Measures the presence of antibodies that destroy the nucleus of body
tissue cells (i.e., those seen in connective tissue diseases); a positive test result is associated with
systemic lupus erythematosus.
Arthroscopy: Involves the use of an arthroscope inserted into a joint for visualization of the joint
structure; preferably, procedure is conducted in the operating room with strict asepsis and performed with
either local or general anesthesia; frequently used to diagnose structural abnormalities of the knee.
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a chronic inflammatory disease that usually affects the synovial (hinged) joints.
Although the cause is unknown, an autoimmune mechanism is suspected. It is strongly associated with
rheumatoid factor, an autoantibody present in 75% to 80% of patients with inflammatory rheumatoid
arthritis. It occurs in 1% to 2% of the population and affects females two to four times more frequently
than males.
Marked improvement in symptoms of rheumatoid arthritis often occurs during pregnancy. The exact
reason is unclear, but improvement is reported to parallel the rise in pregnancy-specific protein, which
suppresses inflammatory reactions. Hormonal factors also have been suggested. For instance, increased
levels of cortisol, estrogen, and progesterone may be beneficial in suppressing the immune response.
Unfortunately, a relapse (postpartum flare) occurs within 6 weeks to 6 months after birth.
In contrast to SLE, the risk of abortion does not increase in women with rheumatoid arthritis. Usually,
obstetric problems do not occur at delivery unless the hips or cervical spine are significantly deteriorated.
Rheumatoid Arthritis
*Rheumatoid arthritis is a systemic autoimmune disease that affects all areas of the body;
inflammatory responses occur in all connective tissue. Early symptoms include inflammation of
the synovial joints.

0
1

A. Joint involvement progresses in stages; if disease is diagnosed early, permanent joint

deterioration may be prevented.
1. The synovium becomes thickened and inflamed, and fluid accumulates in the
joint space; this causes a pannus to form.
2. The pannus tissue erodes the cartilage and destroys the joint.
B. Exacerbations and remissions occur. Condition tends to be progressive with each
exacerbation.
C. Condition is a problem of the connective tissue; inflammatory response may occur in
organs throughout the body (heart, lungs, blood vessels, muscles).

Assessment

0
1

0
0
1
2
3
1
2
0
1
3
4
0
1
2
3
5
6
7

0
1
2
3

A.

Risk factors/etiology.
1. Significantly increased incidence in women.
2. May occur at any age; peak incidence occurs between 20 and 45 years of age.

B.

Clinical manifestations.
1. Symmetrical joint involvement (hands and feet).
a. Warm, tender, red, painful joints.
b. Decrease in ROM.
c. Decrease in strength.
d. Stiffness and pain are worse in the morning and decrease during the day
with moderate activity.
2.

Subcutaneous nodules over bony prominences.

a. Painless, frequently occur on the elbows.
b. May be present for weeks to months.

3.

Systemic effects.
a. Vasculitis.
b. Pulmonary fibrosis.
c. Pericarditis.
d. Ocular problems.

4.
5.

Chronic deformities develop, most often in the hands.

Exacerbation of symptoms may be associated with physical or emotional stress.

C.

Diagnostics.
1. Positive serum rheumatoid arthritis factor.
2. Increased erythrocyte sedimentation rate.
3. Increased C-reactive protein level.
4. Aspiration of synovial joint fluid.

A.
B.

Disease-modifying antirheumatic drugs (DMARDs) (see Appendix 21-2).

NSAIDs.
1. Salicylate (aspirin) is primary drug.
2. Ibuprofen, naproxen.

C.
D.
E.
F.
G.
H.
I.

Corticosteroids (see Appendix 6-7).

Methotrexate (see Appendix 8-1).
Tumor necrosis factor inhibitors.
Heat and/or cold applications.
Assistive devices to preserve joints and prevent deformity.
Physical and rehabilitative therapy.
Surgery: joint replacements.

Treatment

0
1

Complications

A.
1.

Musculoskeletal.
Severe joint deformity, flexion contracture.

2.
3.

Diffuse skeletal demineralization.

Stress fractures.

B.

Systemic involvement.

Nursing Intervention
Goal: To relieve pain and preserve joint mobility and muscle strength (see Box 21-4).

A. Use warm, moist compresses to relieve pain and stiffness of muscle spasms.
B. If heat increases pain, cold compresses may be beneficial during an acute episode.
C. Acutely inflamed joints should be immobilized in a device that maintains a functional
position.
D. Position client to maintain correct body alignment and prevent contractures, especially
flexion contractures

Assess client for complications of immobility.

ALERT:

E. Immobility can increase the pain; ROM exercises and weight bearing may help
decrease pain.
F. Antiinflammatory medications should be taken before activity and with meals or food to
decrease gastric upset.
G. If client is taking steroids, he or she should wear an identification tag.

Goal: To assist client to prevent joint deformity, preserve joint function, and reduce inflammation and
pain.

A. Regularly scheduled rest periods (excessive fatigue is a problem); balance activities

with rest.
B. Protect joints.
1. Maintain functional joint alignment; avoid positions that precipitate joint contraction
(sitting too long with knees bent).
2. Warm moist or cold compresses to relieve pain and muscle spasms.
3. Acutely inflamed joints may be splinted; splint should be removed periodically and
gentle ROM exercises performed.
4. Use large muscle groups; avoid repetitive movement of smaller joints.
C. Demonstrate ability to carry out individual exercise program.
D. Identify medications that are effective in relieving pain.
E. Discuss with client importance of identifying false advertising regarding claims of cure
and relief of chronic pain.
F. Encourage client to be independent in activities of daily living (ADLs) as long as
possible.

Self-Care

A.

Encourage client to ventilate feelings regarding chronic progression of the disease

B.
C.
D.

Evaluate family support system; help family to identify measures to assist client.
Modify home routine to decrease stress on joints: ADLs, dressing, etc.
Identify measures to assist client to maintain self-esteem: What activities can client

state.

continue to participate in? Focus on what client can do.

E. Assist client to set realistic goals.
F. Identify available community resources.

ALERT:
Determine client's ability to perform self-care; assist family to manage care of client with long-term care needs.

Pathophysiology
Rheumatoid arthritis (RA) is one of the most common connective tissue diseases and is the most
destructive to the joints. It is a chronic, progressive, systemic inflammatory autoimmune disease process
that primarily affects the synovial joints. Systemic means this disease affects the body system, affecting
many joints and other tissues.
In RA, autoantibodies (rheumatoid factors [RFs]) are formed that attack healthy tissue, especially
synovium, causing inflammation. RFs consist mainly of immunoglobulin M and G, and they bind with
antigens forming immune complexes. Phagocytes attempt to engulf these complexes and, as a result,
release powerful enzymes, such as cytokines. The B- and T-lymphocytes of the immune system are also
stimulated and increase the inflammatory response.
Inflammation occurs first in the synovial membrane, which lines the joint cavity. It then begins to involve
the articular cartilage, joint capsule, and surrounding ligaments and tendons. Three processes cause
cartilage damage in clients with RA (McCance & Huether, 2002):

1. Neutrophils and other cells in synovial fluid are activated and break down the joint
cartilage
2. Cytokines, especially interleukin-1 (IL-1) and tumor necrosis factoralpha (TNFA),
cause chondrocytes to attack cartilage. TNF has effects on lipid metabolism, coagulation, insulin
resistance, and endothelial function.
3. Synovium digests cartilage, releasing inflammatory substances, such as IL-1 and TNFA.
(See Chapter 23 for a complete discussion of the inflammatory response.)

The synovium then thickens and becomes hyperemic, fluid accumulates in the joint space, and a pannus
forms. The pannus is vascular granulation tissue composed of inflammatory cells; it erodes articular
cartilage and eventually destroys bone. As a result, fibrous adhesions, bony ankylosis, and calcifications
occur; bone loses density and secondary osteoporosis occurs.
Permanent joint changes can be avoided if RA is diagnosed early. Early, aggressive treatment to suppress
synovitis may cause a remission. RA is a disease characterized by natural remissions and exacerbations.
Medical treatment helps control the disease to decrease the intensity and number of exacerbations.
Preventing RA flares helps prevent joint erosion and permanent joint damage. Advancement of knowledge
regarding the disease process and immune system provides many newer treatment options that better
control this disease.
Rheumatoid arthritis is a systemic disease; that is, areas of the body besides the synovial joints can be
affected. Inflammatory responses similar to those occurring in synovial tissue may be seen in any organ or
body system in which connective tissue is prevalent. If blood vessel involvement (vasculitis) occurs, the
organ supplied by that vessel can be affected. The result is malfunction and eventual failure of the organ
or system. These pathologic changes may occur late in the disease process and cause life-threatening
problems.
The etiology of RA remains unclear, but research suggests a combination of environmental and genetic
factors.

Genetic Considerations

Rheumatoid arthritis shows some familial clustering, suggesting either a genetic predisposition or gene-environmen
mutations are associated with RA, especially if they are present in a person with varieties of the tissue type human
DRB, HLA-DR4, or HLA-DP (McCance & Huether, 2002). For example, the risk for developing the disease in a perso
who is homozygous for mutations in any one of three susceptibility genes is 30% to 40% for men and 45% to 55%
Mendelian Inheritance in Man, 2004).

Some researchers suspect that female reproductive hormones influence the development of RA because it
affects women more often than menusually young- to middle-aged women. Others suspect that
infectious organisms may play a role, particularly the Epstein-Barr virus (McCance & Huether, 2002).
Physical and emotional stresses have been linked to exacerbations of the disorder and may be contributing
factors in its development.
CULTURAL CONSIDERATIONS

Despite the common lay belief that warm, dry climates can be beneficial to people with RA, there are no significant
among geographic locations. The incidence of RA in China is somewhat lower than elsewhere in the world (about 0
higher among the Pima Indians in North America (about 5%) (Harris, 2001). The cause for these differences is not

Collaborative Management
Assessment
The onset of rheumatoid arthritis (RA) may be acute and severe or slow and insidious; clients may have
vague complaints that last for several months before diagnosis. The onset of the disease is more common
in the winter months than in the warmer months. The manifestations of RA can be categorized as early or
late disease and as articular (joint) or extra-articular (Chart 24-7).
CHART 24-7
Key features of
The Client with Rheumatoid Arthritis

Early Manifestations
Joint

Inflammation

Low-grade fever
Fatigue
Weakness
Anorexia

Systemic

Paresthesias

Late Manifestations
Joint

Deformities (e.g., swan neck or ulnar deviation)

Moderate to severe pain and morning stiffness

Osteoporosis
Severe fatigue
Anemia
Weight loss
Subcutaneous nodules
Peripheral neuropathy
Vasculitis
Pericarditis
Fibrotic lung disease
Sjgren's syndrome
Renal disease

Systemic

Physical Assessment/Clinical Manifestations

EARLY DISEASE MANIFESTATIONS.
The client with RA typically complains of joint stiffness, swelling, pain, fatigue, and may complain of
generalized weakness and morning stiffness. Anorexia and a weight loss of about 2 or 3 pounds (1 kg)
may occur early in the disease process. Persistent low-grade fever may accompany these complaints. In
clients with early disease, the upper-extremity joints are often involved initially, typically the proximal
interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the hands. These joints may be slightly
reddened, warm, stiff, swollen, and tender or painful, particularly on palpation (synovitis). The typical
pattern of joint involvement in RA is bilateral and symmetric (e.g., both wrists), and the number of joints
involved usually increases as the disease progresses. In early disease, the client may complain of
migrating symptoms known as migratory arthritis. The presence of only one hot, swollen, painful joint
(out of proportion to the other joints) may mean the joint is infected. Refer the client to the health care
provider (generally the rheumatologist) immediately. Single hot, swollen joints are considered infected
until proven otherwise and require immediate long-term antibiotic treatment.
LATE DISEASE MANIFESTATIONS.
As the disease worsens, the joints become progressively inflamed and quite painful. The client complains
of morning stiffness (also called the gel phenomenon), which lasts between 45 minutes and several
hours after awakening. On palpation, the joints feel soft and look puffy because of synovitis and effusions
(joint swelling with fluid, especially the knees). The fingers often appear spindle-like. Note any muscle
atrophy (which can result from disuse secondary to joint pain) and a decreased range of motion in the
affected joints.
Most or all synovial joints are eventually affected. The temporomandibular joint (TMJ) may be involved in
severe disease, but such involvement is uncommon. When the TMJ is affected, the client typically
complains of pain when chewing or opening the mouth.

When the spinal column is involved, the cervical joints are most likely to be affected. During clinical
examination, gently palpate the posterior cervical spine and identify it as cervical pain, tenderness, or loss
of motion. Cervical disease may result in subluxation, especially with the first and second vertebrae. This
complication may be life threatening because branches of the phrenic nerve that supply the diaphragm can
be compressed, and respiratory function may be subsequently compromised. The client is also in danger
of becoming quadriparetic or quadriplegic. If you identify cervical pain or loss of range of motion in the
cervical spine of a person with RA, report this information to the client's physician, generally the
rheumatologist. Collaboration of such information will assist the physician or other provider to obtain the
necessary cervical spine x-ray and may save that client's life. Surgical stabilization is sometimes
necessary.
JOINT INVOLVEMENT.
Joint deformity occurs as a late, articular manifestation, and secondary osteoporosis can cause bone
fractures. Observe common deformities, especially in the hands and feet (Figure 24-4). Extensive wrist
involvement can result in carpal tunnel syndrome (see Chapter 54 for assessment and management of
carpal tunnel syndrome).

Palpate the tissues around the joints to elicit pain or tenderness associated with other rheumatoid
complications. For example, Baker's cysts (enlarged popliteal bursae) may occur and cause tissue
compression and pain. Tendon rupture is also possible, particularly rupture of the Achilles tendon.
SYSTEMIC COMPLICATIONS.
Numerous extra-articular clinical manifestations are associated with advanced disease. Assess other body
systems to ascertain systemic involvement. In addition to increased joint swelling and tenderness,
moderate to severe weight loss, fever, and extreme fatigue are common in late disease exacerbations,
often called flares. Approximately 25% of clients have the characteristic round, movable, nontender
subcutaneous nodules, which most often appear on the ulnar surface of the arm, on the fingers, or
along the Achilles tendon. These nodules can disappear and reappear at any time and are associated with
severe, destructive disease. Rheumatoid nodules are not generally a problem themselves; however, they
occasionally open and become infected, and they may interfere with activities of daily living (ADLs).
Bumping nodules may cause discomfort or pain. Occasionally nodules are identified within the lungs.
Inflammation of the blood vessels results in vasculitis, particularly of small- to medium-sized vessels.
When arte-rial involvement occurs, major organs and body systems become ischemic and malfunction.
Ischemic skin lesions appear in groups as small, brownish spots, most commonly around the nail bed
(periungual lesions). Monitor the number of lesions, note their location each day, and report vascular
changes to the health care provider. An increased number of lesions indicates increased vasculitis, and a
decreased number indicates decreased vasculitis. Also carefully assess any larger lesions that appear on
the lower extremities; such lesions often lead to ulceration, which heal slowly as a result of decreased
circulation. Peripheral neuropathy associated with decreased circulation can cause foot drop and
paresthesias (burning and tingling sensations), most often in older adults.
Respiratory complications manifest as pleurisy, pneumonitis, diffuse interstitial fibrosis, and pulmonary
hypertension. Cardiac complications include pericarditis and myocarditis. Assess for ocular involvement,
which typically manifests as iritis and scleritis. If either of these complications is present, the sclera of one
or both eyes is reddened and the pupils have an irregular shape.
ASSOCIATED SYNDROMES.
Several syndromes are seen in clients with advanced RA. The most common is Sjgren's syndrome,
which includes a triad of the following:

Dry eyes (keratoconjunctivitis sicca [KCS], or the sicca syndrome)

Dry mouth (xerostomia)

Dry vagina (in some cases)

In Sjgren's syndrome, immune complexes and inflammatory cells are thought to obstruct secretory
glands and ducts. The syndrome is usually associated with connective tissue diseases such as RA but may
occur alone. Note the client's complaint of dry mouth or dry eyes. Some clients state that their eyes feel
gritty, as if sand is in their eyes. Inspect the mouth for dry, sticky membranes and the eyes for redness

and lack of tearing.

Less commonly observed is Felty's syndrome, which is characterized by RA, hepatosplenomegaly
(enlarged liver and spleen), and leukopenia. Caplan's syndrome is characterized by the presence of
rheumatoid nodules in the lungs and pneumoconiosis, which is noted primarily in coal miners and asbestos
workers. The health care provider diagnoses these syndromes by physical examination and diagnostic
testing.
Psychosocial Assessment
Rheumatoid arthritis (RA) and other inflammatory types of arthritis are chronic diseases that can be
crippling if not well controlled. Fear of becoming disabled and dependent, uncertainty about the disease
process, altered body image, devaluation of self, frustration, and depression are common psychosocial
problems (Smedstad & Liang, 2001). Physical limitations caused by disease may limit activities of daily
living (ADLs). These physical limitations result in role changes in the family and society. For example, the
person may not be able to cook for the family or be an active sexual partner. In addition, extreme fatigue
often causes clients to desire an early bedtime and may result in a reluctance to socialize.
Body changes may also cause poor self-esteem and body image. Because many societies value people
with physically fit, attractive bodies, the client with RA may be embarrassed to be seen in public places.
The client may grieve or experience degrees of depression. The potential exists for the client to experience
a feeling of helplessness accompanied by a loss of control over a disease that can consume the body.
Fortunately, newer medications have significantly improved the treatment of RA and provide the client
with hope and better control of the disease.
Living with a chronic disease and the pain that results may be difficult for the client, family, and significant
others. The client may experience a loss of control and independence, especially if he or she is over 65
years of age (Ignatavicius, 2001). Chronic suffering affects quality of life. Assess the client's emotional
and mental status in relation to the disease and its problems and evaluate the client's support systems
and resources. Help each client gain control of his or her disease. Clients who are knowledgeable about
their disease and treatment options will feel emotionally stronger to cope with their disease and better
able to discuss treatment options with their physician.
RHEUMATOID FACTOR.
The test for rheumatoid factor (RF) measures the presence of unusual antibodies of the immunoglobulin
G (IgG) and IgM type that develop in a number of connective tissue diseases. Two methods may be used
to ascertain the degree to which these antibodies are present in the body: Rose-Waaler and latex
agglutination. In both procedures, values are reported as titers.
The Rose-Waaler test is more specific for a diagnosis of RA than the latex agglutination test, but it is not
as sensitive. A client with a positive Rose-Waaler result probably has RA and is seropositive; a client with a
negative test result may or may not have the disease or has seronegative inflammatory polyarthritis.
Approximately 60% of individuals with RA are seropositive and have a positive titer.
ANTINUCLEAR ANTIBODY TITER.
The antinuclear antibody (ANA) test measures the titer of unusual antibodies that destroy the nuclei of
cells and cause tissue death. The fluorescent method is sometimes referred to as FANA. If this test result
is positive (a value higher than 1:8), various subtypes of this antibody are identified and measured. ANA is
often negative until later in the disease process. ANA does not have to be positive to diagnosis RA. ANA
can be positive in other rheumatic diseases, such as systemic lupus erythematosus. It is also positive in a
small percentage of the population without any underlying disease.
ERYTHROCYTE SEDIMENTATION RATE.
The erythrocyte sedimentation rate (ESR) or sed rate, when it is elevated, can confirm inflammation or
infection anywhere in the body. An elevation in the ESR helps point to a diagnosis of an inflammatory
connective tissue disease; however, a high ESR does not always relate to severity of inflammatory disease.
The high-sensitivity C-reactive protein, or hsCRP, is another useful test to measure inflammation and may
be done along with or instead of the ESR.
Because several laboratory procedures are used to measure ESR, normal values will vary; women have
higher normal values than men. In general, a value of 20 to 40 mm/hr indicates mild inflammation; 40 to
70 mm/hr, moderate inflammation; and 70 to 150 mm/hr, severe inflammation.

The ESR is not always a reliable indicator but may sometimes be used to monitor a client's response to
anti-inflammatory drug therapy. This value should decrease if the drug dosage is effective. The ESR may
also be elevated with infection and in older adults.
OTHER LABORATORY TESTS.
Serum complement attaches to immune complexes in an attempt to destroy them. If a large amount of
complement is used in this lytic process, the concentration of free-floating complement in the blood
diminishes. Normal values vary considerably, depending on the laboratory technique used. An abnormal
finding is indicated by a decrease in serum complement and is seen primarily in clients with vasculitis.
In serum protein electrophoresis, the protein fractions of the plasma are measured, and an electrical
current is used to separate them. The level of alpha globulin is raised in acute inflammation; in chronic
inflammatory conditions such as RA, the level of gamma globulin is increased because of the increase in
immunoglobulins.
The serum immunoglobulins can be separated into subtypes. In chronic inflammation, IgG is needed to
combine with RF. Thus in RA the IgG value is typically elevated.
The presence of most chronic diseases usually causes mild to moderate anemia, which contributes to the
client's fatigue. Therefore the client's complete blood count (CBC) is monitored for a low hemoglobin,
hematocrit, and red blood cell (RBC) count. An increase in white blood cell (WBC) count is consistent with
an inflammatory response. A decrease in the WBC count may indicate Felty's syndrome. Thrombocytosis
(increased platelets) is common in clients with RA. Additional laboratory tests may be performed
depending on the body systems and organs that may be affected by the disease. For example, if heart
involvement is suspected, the health care provider may order cardiac enzymes.
OTHER DIAGNOSTIC ASSESSMENTS
A standard x-ray is used to visualize the joint changes and deformities typical of RA. A computed
tomography (CT) scan may help to determine the presence and degree of cervical spine involvement.
An arthrocentesis is a diagnostic procedure that may be used for clients with joint involvement. It may
be performed at the bedside or in a physician's office or clinic. After administering a local anesthetic, the
physician inserts a large-gauge needle into the joint (usually the knee) to aspirate a sample of synovial
fluid; this procedure may also relieve pressure. The fluid is analyzed for inflammatory cells and immune
complexes, including RF. Fluid from clients with RA shows increased WBCs, turbidity, and volume. After the
procedure, monitor the insertion site for bleeding or leakage of synovial fluid. Notify the physician if either
of these problems occurs. Teach the client to use ice and rest the affected joint for 24 hours. Often the
health care provider will recommend acetaminophen as needed for pain. If increased pain or swelling
occurs, have the client notify the health care provider.
A bone scan or joint scan can also assess the extent of joint involvement. Magnetic resonance imaging
(MRI) may be performed to assess spinal column disease.
Because RA can affect multiple body systems, tests to diagnose specific systemic manifestations are
performed as necessary. For example, electromyography helps to confirm peripheral neuropathy.
Pulmonary function tests help to determine the presence of lung involvement.
Interventions
As in other types of arthritis, the health care team manages pain by using a combination of pharmacologic
and nonpharmacologic measures. Total joint arthroplasty may be indicated when these measures are no
longer effective (see earlier discussion of this surgery in the section on Osteoarthritis, p. 385). The Plan of
Care on pp. 398 to 402 highlights the most important interdisciplinary interventions for the client with
rheumatoid arthritis (RA).
Drug Therapy.
Some medications prescribed for RA have analgesic, antipyretic, and anti-inflammatory actions. Other
drugs are immunosuppressive and disease modifying, which may cause remission of the illness and
prevent erosive joint changes. Biological response modifiers are the newest class of disease-modifying
drugs that help reduce signals for the immune system to cause inflammation and thereby reduce the
amount of inflammation that the joint receives (see Chart 24-9 on pp. 403-404). These medications have
demonstrated superior performance, giving clients additional benefits never before imagined. Clients with
inflammatory diseases other than RA are also using various biological response modifying medications
successfully. Future genetic research will further advance these medications to give even better control of
autoimmune diseases. Although RA is a chronic disease and no cure is yet available, medications now used
are better able to control the disease and prevent further deterioration.

Management of Mild Disease.

The health care provider, usually a rheumatologist, makes decisions about appropriate drug therapy for
clients with rheumatoid disease based on the severity of the disease. Mild disease is usually managed with
nonsteroidal anti-inflammatory drugs (NSAIDs) or disease-modifying agents.
Nonsteroidal Anti-Inflammatory Drugs. The NSAIDs are often an initial drug category of choice for
inflammatory arthritis to relieve pain and inflammation (see Chart 24-9). The choice of which one to
administer depends on the client's needs and the physician's preference. To minimize gastrointestinal (GI)
problems, the NSAID may be given with an H2-blocking agent, such as ranitidine (Zantac) or misoprostol
(Cytotec). If there is no clinical change after 6 to 8 weeks, the health care provider may discontinue the
current NSAID and try another one. This process may be repeated until an effective drug is found for that
client. Celecoxib (Celebrex), and valdecoxib (Bextra) are COX-2 inhibiting NSAIDs that are usually
preferred over older NSAIDs. COX-2 inhibitors have a decreased incidence of GI side effects associated
with older NSAIDs (for further information, see Analgesic Administration [Osteoarthritis], p. 384).
However, all COX-2 inhibiting drugs have recently been associated with cardiovascular disease, such as
myocardial infarction, and may soon be unavailable on the market.
Salicylates are an older type of NSAID and were previously the drug of choice for pain and inflammation.
Within the United States, they are no longer the drug of choice to treat RA because of toxicities, mainly GI
bleeding. Salicylates are excellent anti-inflammatory drugs and relatively inexpensive, and therefore they
are still used within some countries or when a client has specific needs or restrictions. Salicylates must be
taken with food and are sometimes given with GI-acid lowering agents providing GI protection such as
proton pump inhibitors. Monitor the client for heartburn, indigestion, stomach discomfort, or black, tarry
bowel movements (signs and symptoms of ulceration or GI bleeding). Report such symptoms to the health
care provider.
Disease-Modifying Anti-Rheumatic Drugs. Disease-modifying antirheumatic drugs (DMARDs), such as
hydroxychloroquine (Plaquenil), sulfasalazine, or minocycline, may be prescribed to slow the progression
of mild rheumatoid disease before it worsens (see Chart 24-9).
Hydroxychloroquine (Plaquenil) is an antimalarial drug that helps decrease joint and muscle pain and
often helps clients with early RA or other inflammatory autoimmune diseases such as systemic lupus
erythematosus (SLE), described later in this chapter. Some health care providers may use Plaquenil as one
of the initial treatments for mild disease. The client usually takes 400 mg each evening with a light snack.
Occasionally the dose is divided into 200 mg twice daily with food.
Clients generally tolerate Plaquenil quite well. In a few cases, mild stomach discomfort, light-headedness
or headache have been reported. The most serious adverse effect of the drug is retinal damage. Teach
clients to report blurred vision or headache. Remind clients to have an eye examination every 6 to 12
months to detect changes in the cornea, lens, or retina. If this complication occurs, the health care
provider discontinues the drug. Eye complications are rare, but prevention safety is the reason for the
recommendation.
Sulfasalazine (Azulfidine) is a medication that may be prescribed for mild to moderate inflammatory
arthritis conditions such as RA or psoriatic arthritis (an inflammatory arthritis variant described later). The
usual dosage is 1000 mg twice daily taken with breakfast and supper. Starting doses may be less, such as
500 mg once or twice daily, gradually building up to the standard adult dose. Minimization of such GI side
effects as sulfa taste, bloating, stomach discomfort, and gas occurs by gradually increasing drug dosing.
Monitor the complete blood count (CBC), paying special attention for a decrease in white blood cells
(WBCs) or platelet count. Changes in blood counts are rare but severe potential side effects for which the
medication must be discontinued. Clients with an allergy to sulfa drugs or aspirin should not take
sulfasalazine.
Minocycline (Minocin, a form of the antibiotic tetracycline) is sometimes used to treat mild RA symptoms.
Although its mechanism of action is not known, it has both antimicrobial and anti-inflammatory effects. It
is also an immune modifier, inhibiting certain chemicals that cause bone and cartilage damage.
Minocycline differs from other agents used for RA in that it has a low incidence of adverse effects. In

addition, the client does not develop a resistance to the drug after prolonged use (Sears & Ganger, 2000).
Management of Moderate to Severe Disease.
The health care provider selects medications that can slow progression of moderate to severe rheumatoid
arthritis (RA). The client may take several of these drugs together, but not in the same drug class. For
example, the provider may prescribe methotrexate and infliximab at the same time, along with a NSAID to
help relieve pain and inflammation (see Chart 24-9).
Methotrexate (Rheumatrex). Methotrexate, an immunosuppressive medication, in a low, once-a-week
dosage (generally 25 mg or less per week), has become the mainstay of therapy for advancing and
sustaining RA because it is effective and relatively inexpensive. It is a slow-acting drug, taking 4 to 6
weeks to begin to control inflammatory joint symptoms. Observe for desired drug effects, such as a
decrease in joint pain and swelling.
Monitor the client for potential side effects of decreasing WBCs and platelets (as a result of bone marrow
suppression) or elevations in liver enzymes or serum creatinine. Remind clients to avoid alcoholic
beverages while taking methotrexate to prevent liver toxicity. Teach the client to observe and report other
side and toxic effects, which include mouth sores and acute dyspnea from pneumonitis. Rarely, lymph
node tumor (lymphoma) has been associated in people who have RA and are taking methotrexate. Folic
acid, one of the B vitamins, is often given to clients who are taking methotrexate to help decrease some of
the drug's side effects.
Pregnancy is not recommended while taking methotrexate because birth defects are possible. Strict birth
control is recommended for childbearing women who are in need of methotrexate to control their RA. If
pregnancy is ever desired, the client is informed to consult the rheumatologist as well as their OB/GYN
health care provider. Generally, the physician will discontinue the drug at least 3 months before planned
pregnancy. Methotrexate may be restarted after birth if the client does not breast feed.
Leflunomide (Arava). Leflunomide is a slow-acting immune-modulating medication that helps diminish
inflammatory arthritis symptoms of joint swelling, stiffness, and improves mobility. It is generally
prescribed as follows: a loading dose of 100 mg daily for 3 days followed by 20 mg daily thereafter. Inform
the client that the drug generally takes 4 to 6 weeks and sometimes up to 3 months before maximum
benefit is realized.
Arava is a potent medication that is generally tolerated, but side effects of hair loss, diarrhea, decreased
WBCs and platelets, or increased liver enzymes have been reported. Teach clients to report these changes
and monitor laboratory results carefully. Remind them to avoid alcohol. Inform them that Arava can cause
birth defects, and therefore recommend strict birth control to women of childbearing age. Tell clients to
contact the health care provider immediately if pregnancy occurs while taking the drug. Cholestyramine
(Questran) is available to help block the drug's action.
Biological Response Modifiers. As a group, biological response modifiers (BRMs) are classified as the
newest antiarthritic drugs that neutralize the biologic activity of tumor necrosis factor (TNF) by inhibiting
its binding with TNF receptors. Any one of the BRMs may be tried. If one drug is not effective, the health
care provider prescribes another drug in the same class. All these medications are extremely expensive at
this time, and insurance companies may not completely pay for their use.
Clients with multiple sclerosis or tuberculosis are not given TNF inhibitors. Determine whether the client
has had a recent negative purified protein derivative (PPD) test. If not, a PPD skin test is typically
administered, and the selected BRM is not started until the results are known to be negative. Collaborate
with the client's health care provider to ensure that this process is complete.
Etanercept (Enbrel) is given subcutaneously by injection either as 50 mg once weekly or as 25 mg twice
weekly. Immunosuppression with medications such as methotrexate is generally tried before using Enbrel
or other biological response modifiers. Methotrexate may also be continued in combination with biologic
therapies because the combination may be more effective than either drug alone. Most clients tolerate
Enbrel or Enbrel and methotrexate together; however, laboratory monitoring is important. Combination
therapy requires complete blood count (CBC), serum creat-inine, and a liver panel to be drawn regularly,

generally every 4 to 8 weeks. In general, clinical outcomes with Enbrel have been excellent.
Teach the client or family member how to self-administer Enbrel injections. Injection site reactions and
infections (especially respiratory) are possible adverse effects. Ice and hydrocortisone 1% cream can be
used if the client develops a red itchy rash at the site of an injection. The drug manufacturer cannot yet
predict long-term potential side effects regarding severity of infection or cancer risk. To date what has
been seen is mild increase in upper respiratory infections with occasional serious infections. The health
care provider should be notified if infection or a delay in wound healing occurs.
Infliximab (Remicade), first approved to treat Crohn's disease, is given in a single IV infusion over
several hours. The initial dose generally used for RA is 3 mg/kg of body weight. Following the first few
weeks of therapy, the drug is repeated at intervals between 2 and 8 weeks, depending on the response of
the client. Clients typically take methotrexate before starting Remicade and continue on combination
therapy.
Teach the client to report symptoms of infusion reaction: chest discomfort, tachycardia, shortness of
breath, or lightheadedness. If any of these symptoms are reported, decrease the IV rate or discontinue it.
These symptoms generally subside, but the physician must be notified in case medical assistance is
needed. Dose, rate, and interval changes may be needed. Acetaminophen and Benadryl are medications
often given to each client before the start of Remicade, and are often used at the time of reported infusion
reaction. Clients who experience serious adverse effects, such as hypertension or anaphylaxis, may
require permanent discontinuation of the drug.
Adalimumab (Humira) is the first fully human TNF inhibitor and was approved by the federal Food and
Drug Association (FDA) in January 2003. Humira is a 40-mg once every 2 weeks subcutaneous injection.
Symptoms of inflammatory arthritis tend to decrease with the use of Humira, including less joint swelling,
less stiffness, and better movement.
Injection site reactions and adverse effects similar to the other TNF inhibitors have been reported. Careful
monitoring, especially with combination therapy of Humira and methotrexate or other immunosuppressive
medication, is important and similar to combination therapy with other BRMs.
Anakinra (Kineret) is another biological response modifier. Instead of affecting tumor necrosis factor
(TNF), however, it works to inhibit a different protein signal of the immune system called interleukin-1 (IL1). IL-1 is also a pro-inflammatory protein that signals the immune system to increase inflammation. It is
thought that IL-1 is a weaker protein than TNF, but having an alternative medication that targets a
different receptor site is helpful when a client is unable to take other biologics. Clients who have multiple
sclerosis or tuberculosis can not take TNF inhibitors, but Kineret can be used with this population.
Injection site reactions occur more often with Kineret compared with other BRMs. Ice and hydrocortisone
1% cream are recommended. Remind clients to rotate injection sites. Kineret is administered with a
simple jet that the client can use for self-administration. The client has the option to eliminate the simple
jet or administer the subcutaneous injection traditionally.
Adjunctive Treatment. Some drugs are given as adjuncts to the previously described medications. It is not
unusual for a client to be taking several disease-modifying drugs, such as methotrexate, a BRM, and an
adjunct medication. Each drug works differently to relieve symptoms and slow the progression of the
disease.
Glucocorticoids (steroids)usually Prednisone (Deltasone, Medrol)are given for their fast-acting antiinflammatory and immunosuppressive effects. Prednisone may be given in high dose for short duration
(pulse therapy) or as a low chronic dose. Moderate-dose, short-term tapering bridge therapy is
commonly used when inflammation is symptomatic and other RA medications are insufficient or have not
yet had an effect.
Chronic steroid therapy can result in numerous complications, such as diabetes mellitus, infection, fluid
and electrolyte imbalances, hypertension, osteoporosis, and glaucoma. Some drug effects are dose
related, whereas others are not. Observe the client for complications associated with chronic steroid

therapy and report them to the health care provider. For example, if blood pressure becomes elevated or
significant laboratory values change, notify the physician.
Instruct clients taking chronic steroids to take calcium 1200 to 1500 mg daily plus vitamin D 800 mg daily
to help prevent osteoporosis. Bisphosphonate medications such as Fosamax or Actonel are often
prescribed as well. Bone density measurements are recommended.
Clients with RA may experience one or a few joints that have more pain and inflammation than the others.
Cortisone injections in single joints may be used to relieve local pain and inflammation. Have the client ice
and rest the joint for 24 hours following the procedure. Oral analgesia is sometimes also needed during
that time.
Other Drugs.
Other immunosuppressive agents that may be used are azathioprine (Imuran) and cyclophosphamide
(Cytoxan). Cyclophosphamide is sometimes given specifically to control RA vasculitis. Such
immunosuppressive medications may cause bone marrow suppression and occasionally leukemia or
lymphoma. White blood cells are expected to decrease 7 to 14 days following the administration of IV
cyclophosphamide; therefore laboratory results are closely monitored to ensure safe limits. Hemorrhagic
cystitis is a concern more with oral cyclophosphamide. Instruct the client to drink water and void
frequently (about every 2 hours while awake), which dilutes the urine and empties the bladder, thus
decreasing opportunity for bladder irritation from residual drug. Hair thinning or loss can be seen with
immunosuppressive medications. Cyclophosphamide may also cause sterility; strict birth control is
recommended.
Clients should be well informed of each medication's desired and specific potential side effects, the method
for taking the medication correctly, and recommended monitoring methods. When taken correctly and
monitored, these immunosuppressive medications help control severe autoimmune inflammatory diseases.
Gold therapy is less frequently used to treat RA now that methotrexate and the newer biologic
medications are available; however, gold may still sometimes be used to modify RA disease and reduce
pain and inflammation. Some clients take gold if they are unable to use other immunosuppressive or
biologic medications. The most commonly used parenteral preparation is gold sodium thiomalate
(Myochrysine). For intramuscularly administered gold, a test dose of 10 mg is given to detect an allergy to
the drug, and weekly gold injections are given thereafter. The dosage increases from 25 to 50 mg weekly.
Blood tests must be monitored before each injection. The client's urine is tested for protein level and a
CBC is taken. Report any laboratory results outside the normal range to the physician, and hold the gold
injection.
If the client responds to gold without having toxic effects (e.g., rash, blood dyscrasias, renal involvement),
the injections are slowly tapered to every 2 weeks, then every 3 weeks, and then once a month. If
remission does not occur after a total of 1000 mg has been given, the drug is usually discontinued.
Auranofin (Ridaura) is different from IM gold in that it is a form of oral gold that is occasionally used to
treat mild RA. Three milligrams twice-daily dosing is generally prescribed. Its major side effects are GI
symptoms, especially diarrhea, nausea, and vomiting. Teach the client to report any GI problems to the
health care provider.
Analgesic drugs may be prescribed to supplement the pain relief property in anti-inflammatory drugs
specific for RA. Some analgesics include acetaminophen (Tylenol), propoxyphene (Darvon), and
propoxyphene napsylate (Darvocet-N). Propoxyphene and its associated products can cause headache,
dizziness, and drowsiness. In clients with decreased metabolic rates, this slowly excreted drug may
accumulate in the body over a long period and can cause death, especially in older adults. Teach the client
about the side effects and toxic effects of these drugs and advise the client to report any unusual
symptoms or complaints to the physician.
Nonpharmacologic Modalities.
Adequate rest, proper positioning, and ice and heat applications are important in pain management (see
Pain Management [Osteoarthritis], p. 384). If acute inflammation is present, the physical therapist (PT) or

assistive nursing personnel applies ice to the hot joints for pain relief until the inflammation lessens. The
ice pack should not be too heavy. Heated paraffin (wax) dips may help decrease pain and increase comfort
of arthritic hands. Finger and hand exercises are often done more easily following paraffin treatment.
To relieve morning stiffness or the pain of late-stage disease, recommend a hot shower rather than a
sponge bath or a tub bath. It is often difficult for the client with RA to get into and out of a bathtub,
although special hydraulic lifts and tub chairs may be available. Grab bars and nonskid tread in the tub
floor are important safety features to discuss with all clients.
Hot packs applied directly to involved joints may be beneficial. Most physical therapy departments have
machines that keep hot packs ready anytime they are needed. At home, the client may use the microwave
or stove-top heating instructions to warm the heat pack. Teach the client to follow the instructions given
with each heating device used.
Complementary and Alternative Therapies.
Some clients may have pain relief from hypnosis, acupuncture, magnet therapy, imagery, or music
therapy. Stress management is also popular as a pain relief intervention. Chapters 4 and 7 discuss these
therapies in detail.
Good nutrition is an important part of the management of RA. The inflammatory state may place a greater
burden on the metabolism of some essential nutrients. This catabolic state may be related to increased
cytokine production, specifically tumor necrosis factor (Kremer, 2001). Further research will contribute to
future nutritional recommendations. Some attention has been given to specific foods:

Omega-3 fatty acids (found in coldwater fish such as salmon, sea bass, and tuna) may
help decrease inflammation; however, the amount needed may be impractical for human
consumption.

Fish oil capsules containing omega-3 fatty acids at 2.5 to 5 g daily (should not be taken
if the client is taking anticoagulant therapy) may be recommended in areas in which coldwater fish
are not available.

Antioxidant vitamins (A, C, E) may help maintain the normal function of the immune
system.

Trace elements such as zinc, selenium, copper, and iron may be needed in sufficient
amounts for joint health.

According to the Arthritis Foundation, there is no one food that causes or cures RA; however, healthy
nutrition in general is supported. Refer the client to the Arthritis Foundation's pamphlet regarding diet and
arthritis. Refer the client to the health care provider or dietitian for vitamin- and nutrition-specific
questions or recommendations.
Promotion of Self-Care.
Although the physical appearance of a client with severe RA may create the image that independence in
activities of daily living (ADLs) is not possible, a number of alternative methods can be used to perform
these activities. Do not automatically perform these activities for the client; clients with RA do not want to
be dependent. For example, hand deformities often prevent a client from opening packages of food, such
as a box of crackers; however, he or she may prefer to use his or her teeth to open the crackers rather
than depend on someone else.
In the hospital or long-term care facility, a client may not eat because of the barriers of heavy plate
covers, milk cartons, small packages of condiments, and heavy containers. Styrofoam or paper cups may
bend and collapse as the client attempts to hold them. A china or heavy plastic cup with handles may be
easier to manipulate. Collaborate with the dietitian to allow access to food and total independence in
eating.
When fine motor activities (e.g., squeezing a tube of toothpaste) become impossible, larger joints or body
surfaces can substitute for smaller ones. For example, teach the client to use the palm of the hand to
press the paste onto the brush. Devices such as long-handled brushes can allow clients to brush their hair;
dressing sticks can facilitate putting on pants. These examples illustrate the need to assess the problem
area, suggest alternative methods, and refer the client to an occupational or physical therapist for special
assistive and adaptive devices if necessary.
Management of Fatigue.

Nursing interventions depend in part on identifying the factors contributing to fatigue. For example,
increases in pain, sleep disturbances, and weakness are positively associated with increased fatigue.
Anemia may also be a contributing factor and may be treated with iron (if an iron deficiency anemia is
present), folic acid, or vitamin supplements prescribed by the health care provider. Chronic normochromic
or chronic hypochromic anemia often occurs in most chronic, systemic diseases. Assess for drug-related
blood loss, such as that caused by salicylate therapy or other NSAIDs, by checking the stool for gross or
occult blood. Older white women are the most likely clients to experience GI bleeding as a result of taking
these medications.
When fatigue results from muscle atrophy, the physician prescribes an aggressive physical therapy
program to strengthen muscles and prevent further atrophy. Clients experience increased fatigue when
pain prevents them from getting adequate rest and sleep. Measures to facilitate sleep include promoting a
quiet environment, giving warm beverages, and administering hypnotics or relaxants as prescribed, if
necessary.
In addition to identifying and managing specific reasons for fatigue, determine the client's usual daily
activities and teach principles of energy conservation, including the following:

Pacing activities

Allowing rest periods

Setting priorities

Obtaining assistance when needed

Chart 24-10 lists specific suggestions for conserving energy and thus increasing activity tolerance.
CHART 24-10
Client Education Guide
Energy Conservation for the Client with Arthritis

Balance activity with rest. Take one or two naps each day.
Pace yourself; do not plan too much for one day.
Set priorities. Determine which activities are most important, and do them first.
Delegate responsibility and tasks to your family and friends.
Plan ahead to prevent last-minute rushing and stress.
Learn your own activity tolerance and do not exceed it.

Enhancement of Body Image.

Body image may be affected by both the disease process and drug therapy. Steroids can cause a moonfaced appearance, acne, striae, buffalo humps, and weight gain. Determine the client's perception of
these changes and the impact of the reactions of family and significant others. The most important
intervention is communicating acceptance of the client. When a trusting relationship is established,
encourage the client to express his or her feelings.
Another way to improve body image while in the hospital or nursing home is to use personal items. A
hospital gown reinforces the sick role. Encourage clients to wear their own clothes, to brush their hair, and
to use makeup if desired. Assist the client as needed. The use of colored hair accessories, nail polish, and
perfume may improve a female client's image and self-concept.
As a reaction to body image disturbance and the presence of a chronic, painful disease, clients may

display behaviors indicative of loss. They may use coping strategies that range from denial or fear to
anger or depression. In an attempt to regain control over the effects of the disease process, they may
appear to be manipulative and demanding and sometimes may be referred to as having an arthritis
personality. This personality, which has negative connotations, is a myth. Clients are trying to cope with
the effects of their illness and should be treated with patience and understanding. Continually assess and
accept these behaviors, but remain realistic in discussing goals to improve self-esteem. Emphasize clients'
strengths and help them identify previously successful coping strategies.
Community-Based Care
Clients with rheumatoid arthritis (RA) are usually managed at home but may be institutionalized in a longterm care setting if they become restricted to bed or a wheelchair. Some clients may be discharged to a
rehabilitation facility for several weeks to aid in developing strategies, techniques, and skills for
independent living at home.
HOME CARE MANAGEMENT
The amount of home care preparation depends on the severity of the disease. Structural changes may be
necessary if there are deficits in activities of daily living (ADLs) or mobility. Doors must be wide enough to
accommodate a wheelchair or walker if one is used. Ramps are needed to prevent the client in a
wheelchair from becoming homebound. If the client cannot negotiate stairs, he or she must have access to
facilities for all ADLs on one floor. Handrails should be available in the bathroom and halls.
To promote continued homemaking functions, countertops and appliances may require structural changes.
The client may also require handrails and elevated chairs and toilet seats, which facilitate transfers.
HEALTH TEACHING
Health teaching is a vital role for nurses in the diagnosis and management of arthritis. Many people have
signs and symptoms of joint inflammation but do not seek medical attention. Teach clients to seek
professional health care to reduce pain and disability (see the Meeting Healthy People 2010 Objectives box
below).

Meeting Healthy People 2010 Objectives

ARTHRITIS AND OTHER RHEUMATIC CONDITIONS

Objective 2.7: Increase the proportion of adults who have seen a health care provider for their chronic joint sympt

Teach clients with suspected arthritis the importance of seeing a health care provider for initial ev
Educate clients that maintaining functional ability and managing pain can reduce arthritis pain an
Remind older adults that arthritis is not a normal part of the aging process.
Assist the client in locating local health care providers who specialize in arthritis management (e.
internists).
Teach clients about the availability of community support groups for people with arthritis.

Objective 2.8: Increase the proportion of persons with arthritis who have had effective evidence-based arthritis ed
of the management of their condition.

Self-Help

Teach clients about community education programs at local hospitals or through the Arthritis Fou
course.
Educate clients about the value of evidence-based education programs (reduces pain and visits to
Provide client and family education about arthritis and its management, as needed.

Health teaching is also important for promoting compliance with a treatment plan. A client who
understands the disease process and the treatment rationale can better follow and ask questions about
the treatment plan.
Teach clients to discuss any questions with their health care provider before trying any over-the-counter or
home remedies. Some remedies may be harmful. Check with the Arthritis Foundation for the latest
information on arthritis myths and quackery.
Information about drug therapy, joint protection, energy conservation, rest, and exercise should be taught
to client, family, and significant others. This information is summarized in Charts 24-5, 24-6, 24-9, and
24-10.
The client with RA often complains of being on an emotional roller coaster from coping with a chronic
illness every day. Control over one's life is an important human need. The client with an unpredictable
chronic disease may lose this control, and this lowers self-esteem. Health care providers must allow the
client to make decisions about care. Families and significant others must also include the client in decisionmaking. Although the client's behavior may be perceived as demanding or manipulative, his or her selfesteem cannot be improved without this important aspect of interpersonal relationships.
Increased dependency also affects a sense of control and self-esteem. Some clients ignore their health
needs and portray a tough image for others by insisting that they need no assistance. Emphasize to the
client and family that asking for help may be the best decision at times to prevent further joint damage
and disease progression.
Rheumatoid arthritis (RA) may also affect work and social roles. The client may have physical difficulty
doing tasks that require lifting, climbing, grasp, gross or fine motor activities. The severity of RA disease
may cause difficulty with total number of hours worked. Some people with RA are able to do their jobs
well without problem; others may have varying degrees of difficulty. Clients who are no longer able to do
their job at work may need to discuss having a lighter workload with their employer, but some may need
to file for disability with their company and social security.
Arthritis support groups and self-help courses provide the education and the support that clients, families,
and friends need; however, refer the client to a psychological counselor or religious or spiritual leader for
emotional support and guidance during times of crisis or as needed. Identify and recommend other
support systems within the family and community when necessary.
HEALTH CARE RESOURCES
The need for health care resources for the client with RA is similar to that for the client with osteoarthritis.
A home care nurse or aide, physical therapist, or occupational therapist may be needed. In collaboration
with the discharge planner, the nurse in the hospital or nursing home identifies these resources and makes
sure they are available before discharge.
Pheochromocytoma
Pheochromocytoma is a rare tumor characterized by secretion of catecholamines. The tumor most
commonly arises from the chromaffin cells of the adrenal medulla but may occur wherever these cells are
found, such as along the paraganglia of the aorta or thoracolumbar sympathetic chain. Approximately
10% of these tumors are located in extraadrenal sites. In children they are frequently bilateral or multiple
and are generally benign. Often there is a familial transmission of the condition as an autosomal dominant
trait (Behrman, Kliegman, and Jenson, 2000).
Clinical Manifestations

The clinical manifestations of pheochromocytoma are caused by an increased production of

catecholamines, producing hypertension, tachycardia, headache, decreased gastrointestinal activity with
resultant constipation, increased metabolism with anorexia, weight loss, hyperglycemia, polyuria,
polydipsia, hyperventilation, nervousness, heat intolerance, and diaphoresis. In severe cases, signs of
congestive heart failure are evident.
Diagnostic Evaluation
The clinical manifestations mimic those of other disorders, such as hyperthyroidism or diabetes mellitus.
Tests specific to these conditions may be performed as part of the differential diagnosis. In a small number
of instances a palpable tumor suggests the diagnosis. Usually the tumor is identified by a CT scan or MRI.
Definitive tests include 24-hour measurement of urinary levels of the catecholamine metabolites;
histamine stimulation, which will provoke a hypertensive attack from sudden release of large amounts of
catecholamines; and alpha-blocking agents, which will produce a hypotensive episode by inhibiting the
action of circulating catecholamines.
Therapeutic Management
Definitive treatment consists of surgical removal of the tumor. In children the tumors may be bilateral,
requiring a bilateral adrenalectomy and lifelong glucocorticoid and mineralocorticoid therapy. The major
complications that can occur during surgery are severe hypertension, tachyarrhythmias, and hypotension.
The first two are caused by excessive release of catecholamines during manipulation of the tumor, and the
latter results from catecholamine withdrawal and hypovolemic shock.
Preoperative medication to inhibit the effects of catecholamines is begun 1 to 3 weeks before surgery to
prevent these complications. The major group of drugs used is the -adrenergic blocking agents with or
without -adrenergic blocking agents. The most commonly used -adrenergic blocker is
phenoxybenzamine (Dibenzyline), a longer-acting medication given orally every 12 hours. The shorteracting phentolamine (Regitine) is equally effective but less satisfactory for long-term use, although it is
useful for acute hypertension. To control catecholamine release when -adrenergic blocking agents are
inadequate, the child is given -adrenergic blocking agents.
Success of therapy is judged by lowering of blood pressure to normal, absence of hypertensive attacks
(flushing or blanching, fainting, headache, palpitations, tachycardia, nausea and vomiting, profuse
sweating), heat tolerance, decrease in perspiration, and disappearance of hyperglycemia. A disadvantage
of these drugs is their inability to block the effects of catecholamines on beta receptors.
Nursing Considerations
An initial nursing objective is identification of children with this disorder. Outstanding clues are
hypertension and hypertensive attacks. Because of behavioral changes (nervousness, excitability,
overactivity, even psychosis), increased cardiac and respiratory activity may appear to be related to an
acute anxiety attack. Therefore a careful history of the onset of symptoms and association with stressful
events is helpful in distinguishing between an organic and a psychologic cause for the symptoms.
Preoperative nursing care involves frequent monitoring of vital signs and observing for evidence of
hypertensive attacks and congestive heart failure. Therapeutic effects are evidenced by normal vital signs
and absence of glycosuria. Daily blood glucose levels, urine acetone, and any signs of hyperglycemia are
noted and reported immediately.

NURSING ALERT
Do not palpate the mass. Preoperative palpation of the mass releases catecholamines, which can stimulate severe
tachyarrhythmias.

The environment is made conducive to rest and free of emotional stress. This requires adequate
preparation during hospital admission and before surgery. Parents are encouraged to room-in with their

child and to participate in the care. Play activities need to be tailored to the child's energy level but not be
overly strenuous or challenging because these can increase metabolic rate and promote frustration and
anxiety.
After surgery the child is observed for signs of shock from removal of excess catecholamines. If a bilateral
adrenalectomy was performed, the nursing interventions are those discussed for chronic adrenocortical
insufficiency.

PHEOCHROMOCYTOMA
Pheochromocytoma is an adrenal tumor characterized by secretion of catecholamines. The tumor most
commonly arises from the chromaffin cells of the adrenal medulla but may occur wherever these cells are
found, such as along the paraganglia of the aorta or thoracolumbar sympathetic chain. In children this
type of tumor is most frequently bilateral or multiple and is generally benign. Often there is a familial
transmission of the condition as an autosomal-dominant trait that tends to favor males. The clinical
manifestations of pheochromocytoma are caused by an increased production of catecholamines, and they
mimic those of other disorders, such as hyperthyroidism, diabetes mellitus, or functional hyperventilation
(Box 29-12).
BOX 29-12
Hypertension
Tachycardia
Headache
Decreased gastrointestinal activity;resultant constipation
Anorexia
Weight loss
Hyperglycemia
Polyuria
Polydipsia
Hyperventilation
Nervousness
Heat intolerance
Diaphoresis
Signs of congestive heart failure in severe cases

Therapeutic Management
Definitive treatment consists of surgical removal of the tumor. In children the tumors may be bilateral,
requiring a bilateral adrenalectomy and lifelong glucocorticoid and mineralocorticoid therapy.
Nursing Considerations
An initial nursing objective is identification of children with this disorder. Outstanding clues are
hypertension and hypertensive attacks. Preoperative nursing care involves frequent monitoring of vital
signs and observing for evidence of hypertensive attacks and congestive heart failure. Urine should be
tested at least daily for glucose and ketones. Any signs of hyperglycemia are noted and reported
immediately.

NURSING ALERT

DO NOT PALPATE MASS. Preoperative palpation may facilitate release of catecholamines, which can stimulate sever
tachyarrhythmias.

The environment should be conducive to rest and free of emotional stress. This requires adequate
preparation during hospital admission and before surgery. Parents are encouraged to room-in with their
child and to participate in the care. Play activities need to be tailored to the child's energy level but should
not be overly strenuous or challenging, because these can increase the metabolic rate and promote
frustration and anxiety.
After surgery the child is observed for signs of shock from removal of excess catecholamines. If a bilateral
adrenalectomy was performed, the nursing interventions are those discussed for chronic adrenocortical
insufficiency.
Interventions
Surgery is the main treatment for a pheochromocytoma. One or both adrenal glands are removed
(depending on whether the tumor is bilateral). After surgery, focus on promoting adequate tissue
perfusion, nutritional needs, and comfort measures.
Hypertension is the hallmark of the disease. Monitor the blood pressure regularly and place the cuff
consistently on the same arm, with the client in lying and standing positions. Identify stressors that may
lead to a hypertensive crisis and attempt to reduce them. Instruct the client not to smoke, drink caffeinecontaining beverages, or change position suddenly. Do not palpate the abdomen because this action could
cause a sudden release of catecholamines and severe hypertension. Provide a diet rich in calories,
vitamins, and minerals.
The client often benefits from hydration before surgery because decreased blood volume increases the risk
for hypotension during and after surgery. Assess the client's hydration status and report manifestations of
dehydration or fluid overload.
Provide a calm, restful environment for the client who has a severe headache. Instruct the client to limit
activity. A private, darkened room helps promote rest. If the client is sleeping, avoid interruptions if
possible.
The client's blood pressure is stabilized with alpha-adrenergic blocking agents before surgery because of
the increased risk for severe hypertension during surgery. Anesthetic agents and touching of the tumor
during surgery can cause a catecholamine release. Short-acting alpha-adrenergic blockers are given by IV
bolus or drip for a hypertensive crisis. Phenoxybenzamine (Dibenzyline) produces long-acting alphaadrenergic blockade and is often used for management of hypertension before surgery. It is also used for
management of the client who is not a candidate for surgery.
The drug dosages are adjusted for 2 to 3 weeks before surgery until blood pressure is controlled and
hypertensive attacks do not occur. The blood volume expands, and blood pressure in the supine position
returns to normal.
Beta-adrenergic blocking agents are avoided in clients with a pheochromocytoma until after alphaadrenergic blockade is in effect, because these drugs may cause a rebound rise in blood pressure. After
alpha-adrenergic blockade, low doses of propranolol (Inderal, Detensol) or labetalol (Trandate) may be
used to treat tachycardia and dysrhythmias. Other drugs used for blood pressure control before surgery

include calcium channel blockers, such as nicardipine (Cardene) and agents that suppress catecholamine
synthesis such as metyrosine (Demser).
Nursing care after surgery is similar to that for the client who has undergone an adrenalectomy (see
Hypercortisolism [Cushing's Syndrome]). Closely monitor the client for hypotension (from the sudden
decrease in catecholamine levels) and for hypovolemia. Hemorrhage and shock are possible, and plasma
expanders or fluids may be needed. Monitor vital signs, as well as fluid intake and output. If opioids are
given, check for their effect on blood pressure.
Tumors may be inoperable because of the client's other medical conditions. Treatment then is medical,
with alpha-adrenergic and beta-adrenergic blocking agents, because the tumors do not respond well to
chemotherapy or radiation therapy. For clients who are medically managed, self-measurement of blood
pressure with home monitoring equipment is essential.
OR-banana allergy
-ANAPHYLAXIS, INSECT STING ALLERGY, AND LATEX ALLERGY
The most common causes of anaphylaxis are drugs, foods, latex exposure, and insect bites and stings.
Common food offenders in adults are peanuts, tree nuts, and shellfish (Table 78-3). Insect stings cause
many deaths in the United States every year. The incidence of anaphylaxis related to latex exposure,
especially in health care workers, has dramatically increased since the 1990s with the increased use of
latex gloves.
TABLE 78-3
Drugs
Penicillins (most common)

Vancomycin

Cephalosporins

Amphotericin B

Tetracyclines

Polymyxin

Streptomycin

Bacitracin

Kanamycin

Aspirin, other antiinflammatory agents

Neomycin

Colchicine

Heparin

Tranquilizers

Protamine
Foods
Peanuts

Milk

Seafood

Citrus fruits

Eggs

Strawberries

Nuts

Legumes

Insect Venoms
Hymenoptera (honeybees, wasps, yellow jackets, hornets, fire ants)
Biologicals
Heterologous antisera (especially equine)
Enzymes
Hormones
Vaccines (especially egg-cultured types)
Blood Products
Plasma

Whole blood

Cryoprecipitate

Gamma globulin

Allergen Extracts
Skin-testing agents
Desensitization
Diagnostic Agents
Sulfobromophthalein
Iodinated contrast media
Anaphylactic events commonly present with hives and angioedema and often with dyspnea, wheezing,
syncope, hypotension, nausea, vomiting, diarrhea, abdominal pain, flushing, headache, rhinitis, substernal
pain, and itching. Cardiovascular collapse, shock, and respiratory obstruction, which can occur
immediately and without other manifestations, are the primary cause of death from anaphylaxis. Although
manifestations usually begin 5 to 30 minutes after the offending trigger has been encountered, there can
be a delay of an hour or more. The more rapid the onset, the more severe the episode.
The incidence of anaphylaxis related to insect stings ranges from 0.3% to 3% in the general population.
The sting insects are members of the order Hymenoptera. People may be allergic to one or all of the
stinging insects, but the sting of the yellow jacket is the most common cause of allergy. Common
reactions to an insect sting include pain, swelling, and redness that may be localized or may extend over a
large area. The swelling usually peaks in 24 to 48 hours and may last for 7 to 10 days. There are no
factors that identify those at potential risk for anaphylaxis from an insect sting other than a prior history.
Those who have had severe anaphylaxis have an 80% chance of another reaction.
Health care workers are at particular risk for latex allergy. About 700,000 health care workers are
affected. Workers with allergies to latex also have a high incidence of reactions to certain foods, such as
chestnuts, bananas, kiwi, avocado, apricot, and papaya. Manifestations range from simple dermatitis to
generalized itching, urticaria, sneezing, coughing, wheezing, hypotension, and shock on exposure. The
diagnosis of type 1 hypersensitivity to latex is confirmed by in vivo skin testing with raw latex extracts or
in vitro blood assays that measure specific IgE responses to latex.
Medical Management
Anaphylaxis is treated by (1) subcutaneous epinephrine injection, (2) removing or discontinuing the
causative agent, (3) administering emergency oxygen, (4) maintaining an open airway, (5) placing the
client in the Trendelenburg position, and (6) giving supportive IV fluids, such as 0.9% normal saline or
lactated Ringer's solution as necessary.
Nursing Management of the Medical Client
Nursing Diagnoses Risk for Latex Allergy and Latex Allergy Response are more specific nursing diagnoses
for latex allergy reactions. Most of the interventions for these diagnoses have been described under the
nursing diagnosis Health-Seeking Behaviors. In addition, the incidence and severity of anaphylactic
reactions are decreased by both general and specific measures. Take a thorough history for drug, food,
insect, pollen, and animal allergies from every client. Counsel all clients with a history of anaphylaxis or
anaphylactic-like reactions to carry epinephrine with them at all times in the form of an Epi-Pen or Ana-Kit
for self-injection. Recommend that they carry a medical-alert bracelet or necklace and an identification
card in their wallet or purse and that they register with the proper authorities.
Nursing Management of the Medical Client
Nursing Diagnoses Risk for Latex Allergy and Latex Allergy Response are more specific nursing diagnoses
for latex allergy reactions. Most of the interventions for these diagnoses have been described under the
nursing diagnosis Health-Seeking Behaviors. In addition, the incidence and severity of anaphylactic
reactions are decreased by both general and specific measures. Take a thorough history for drug, food,
insect, pollen, and animal allergies from every client. Counsel all clients with a history of anaphylaxis or
anaphylactic-like reactions to carry epinephrine with them at all times in the form of an Epi-Pen or Ana-Kit
for self-injection. Recommend that they carry a medical-alert bracelet or necklace and an identification
card in their wallet or purse and that they register with the proper authorities.

SKILL 9-3 Sterile Gloving

Gloves help prevent the transmission of pathogens by direct and indirect contact. Nurses apply sterile
gloves before performing sterile procedures such as inserting urinary catheters, changing dressings on
central IV catheters, or applying sterile dressings. It is important to select the proper-size glove. The
gloves should not stretch so tightly over the fingers that they can easily tear, yet they should be tight
enough that objects can be picked up easily. Sterile gloves are available in sizes, such as sizes 6, 6, and
7. However, in most clinical areas sterile gloves in one size fits all are available.
It is important to choose not only the right size of glove but also the correct material. Many clients and
health care workers have known allergies to latex, the natural rubber used in most gloves and other
medical products (DeCastro, 2002). Box 9-2 lists individuals who are at risk for latex allergy. Latex
proteins enter the body in various waysthrough skin or mucous membranes, intravascularly, or via
inhalation. The cornstarch powder used to make latex gloves slip on easily over the hands is a carrier of
the latex proteins (Burt, 1998). When gloves are applied or removed, the cornstarch particles become
airborne and can remain so for hours. The latex can then be inhaled or settle on clothing, skin, or mucous
membranes. Reactions to latex can be mild to severe (Box 9-3). For individuals at high risk or with
suspected sensitivity to latex, it is important to choose latex-free or synthetic gloves. More health care
institutions are implementing latex-safe environments for workers (Kim and others, 1998).
BOX 9-2
Individuals at Risk for Latex Allergy

Spina bifida
Congenital or urogenital defects
History of indwelling catheters or repeated catheterizations
History of using condom catheters
High latex exposure (e.g., health care workers, housekeepers, food handlers, tire manufacturers
History of multiple childhood surgeries
History of food allergies

BOX 9-2
Levels of Latex Reactions
There are three types of common latex reactions which, in order of severity, include:

1. Irritant dermatitisa nonallergic response characterized by skin redness and itching.

2. Type IV hypersensitivitycell-mediated allergic reaction to chemicals used in latex processin
itching, and hives. Localized swelling, red and itchy or runny eyes and nose, and coughing may develop.
3. Type I allergic reactiona true latex allergy that can be life-threatening. Reactions vary base
including local and systemic. Symptoms include hives, generalized edema, itching, rash, wheezing, broncho
hypotension, tachycardia, and respiratory or cardiac arrest.

Once gloves are applied, the nurse should always be conscious of the position of the hands during
procedures. If a sterile glove touches a clean, a contaminated, or a questionably contaminated object, it
becomes unsterile and a new sterile glove must be applied. It is helpful to interlock the fingers and hold
the hands together in front of the body and above waist level while waiting to handle sterile items. If a
tear develops in a sterile glove, the nurse applies a new glove immediately.
DELEGATION CONSIDERATIONS
The skill of applying and removing sterile gloves can be delegated to assistive personnel. However, many
procedures that require the use of sterile gloves cannot be delegated to assistive personnel. (Refer to
specific skill for recommendations.)

EQUIPMENT
Package of proper-size sterile gloves; latex or synthetic nonlatex (NOTE: Hypoallergenic, low-powder,
and low-protein latex gloves may still contain enough latex protein to cause an allergic reaction.
Recording and Reporting

It is not necessary to record application of gloves. Record specific procedure performed

and client's response and status.
In the event of a latex allergy reaction, record client's response in nurses' notes and
vital sign flow sheet. Note type of response and client's reaction to emergency treatment.

Teaching Considerations
Nurse or client with a known latex allergy should wear a medical alert bracelet or tag
and carry a wallet card stating latex allergy.
Individuals with known latex allergies should carry a quick-acting oral antihistamine and an
epinephrine auto-injector at all times.

Latex Allergy
Latex allergy was identified as being a serious health hazard when a report linked intraoperative
anaphylaxis with latex in children with SB. One study suggests that the allergy is disease related in that
SB patients have a disease-associated propensity for latex sensitization (Zsolt and others, 1999). These
children are at high risk for developing latex allergy because of repeated exposure to latex products during
surgery and from numerous procedures (Mazon and others, 2000). Allergic reactions range from urticaria,
wheezing, watery eyes, and rashes to anaphylactic shock. More severe reactions tend to occur when latex
comes in contact with mucous membranes, wet skin, the bloodstream, or an airway. There also can be
cross-reactions to a number of foods (e.g., banana, avocado, kiwi, chestnut) (Kellet, 1997; Landwehr and
Boguniewicz, 1996; Sussman and Beezhold, 1997). In addition to patients with SB, high-risk populations
include patients with urogenital anomalies or multiple surgeries as well as health care workers (Poley and
Slater, 2000). See Box 11-3 for medical conditions associated with SB. The incidence of latex allergy in
children with SB ranges from an estimated 18% to 67% (Kellett, 1997).

Box 11-3
Medical Conditions Associated with Risk of Latex Allergy
Spina bifida
Urogenital anomalies
Imperforate anus
Tracheoesophageal fistula

VATER association (vertebral defects, imperforate anus, tracheoesophageal fistula, and r adial and renal dysplasia)
Preterm infants
Ventriculoperitoneal shunt
Mental retardation

Cerebral palsy
Quadriplegia
Multiple surgeries
Atopy

GUIDELINES
Identifying Latex Allergy

Does your child have any symptoms, such as sneezing, coughing, rashes, or wheezing, when handling rubber produc
Koosh balls, adhesive bandage strips) or when in contact with rubber hospital products, such as gloves or catheters?
Has your child ever had an allergic reaction during surgery?

Does your child have a history of rashes, asthma, or allergic reactions to medication or foods, especially milk, kiwi, b
How would you identify or recognize an allergic reaction in your child?
What would you do if an allergic reaction occurred?
Has anyone ever discussed latex or rubber allergy or sensitivity with you?
Has the child had any allergy testing?
When did the child last come in contact with any type of rubber product? Were you present?

The most important goals are prevention of latex allergy and identification of children with a known
hypersensitivity. (See Guidelines box.) High-risk and latex-allergic individuals must be managed in a
latex-safe environment. Care must be taken so that they do not come in direct or secondary contact with
products or equipment containing latex at any time during medical treatment. Allergy testing has been
used to identify latex allergy with varying success. Skin prick testing and provocation testing carry the risk
of allergic reaction or anaphylaxis. Several commercially available assays can be very useful in confirming
latex allergy. To date, none of these tests demonstrates complete diagnostic reliability and should not be
the sole determinent of the presence or absence of an allergic response to latex.

Nursing Care Plan

The Infant with Myelomeningocele

Nursing Diagnosis: Risk for infection related to presence of infective organisms, nonepithelialized meningeal sac,
Patient Goal 1: Will experience minimized risk of central nervous system infection

nursing interventions RationalesPosition infant to prevent contamination from urine and stoolCl
carefully with sterile normal saline if it becomes soiled or contaminatedApply sterile dressings and moisten w
ordered (normal saline, antibiotic) to prevent drying of sacAdminister antibiotics as prescribedMonitor closel
(elevated temperature, irritability, lethargy, nuchal rigidity) to prevent delay in treatmentAdminister similar
postoperatively
Expected OutcomeMeningeal sac remains clean, intact, and exhibits no evidence of infection

Patient Goal 2: Will experience minimized risk of urinary tract infection

nursing interventions/RationalesAvoid urethral contamination with stool to prevent introduction

urinary tractCarry out meticulous perineal hygiene to remove infective organismsMonitor urinary output for
infection due to stasis of urineAdminister antibiotics as prescribedAdminister urinary tract antiseptics if pres
intake to increase urination and prevent bacterial growth
Expected OutcomeInfant exhibits no evidence of urinary tract infection

Patient Goal 1: Will not experience trauma to spinal lesion or surgical site

nursing interventions/RationalesHandle infant carefully to prevent damage to meningeal sac or

prone position, or side-lying position if permitted, to minimize tension on the meningeal sac or surgical siteA
around sac (e.g., a surgical plastic drape, cut to fit and taped below the sac by the sacrum and loosely drap
a protective shieldModify routine nursing activities (e.g., feeding, making bed, comforting activities) to prev
Expected OutcomesMeningeal sac remains intactSurgical site heals without trauma

Patient Goal 1: Will not experience skin irritation

nursing interventions/RationalesChange diapers as soon as soiled, if diapered, to keep skin clea

Keep perianal area clean and dryPlace infant on pressure-reducing surface to reduce pressure on knees and
positioningGently massage healthy skin during cleansing and application of lotion to increase circulation
Expected OutcomeSkin remains clean and dry with no evidence of irritation

Patient Goal 1: Will not experience adverse effects of increased intracranial pressure (ICP)

nursing interventions/RationalesMeasure occipitofrontal circumference daily to detect increased

hydrocephalusObserve for signs of increased ICP, which might indicate developing hydrocephalus:Irritability
picked up or handled; quiets when lies stillIncreased occipitofrontal circumferenceSeparated suturesChange
ChildHeadache (especially in morning)ApathyConfusionMinimize stressful events (e.g., pain) because stress
main determinant of ICP(see Pain Assessment and Pain Management, Chapter 26)
Expected OutcomeEvidence of increased ICP and hydrocephalus is detected early, and appropria
implemented

Patient Goal 1: Will experience minimal exposure to latex

nursing interventions/RationalesIdentify children with latex allergy (see Guidelines box on p. 43

environment to reduce exposureEducate family members and other caregivers (i.e., daycare workers, teach
allergy and items to avoid to reduce exposureSigns of allergy (from hives, rash, and wheezing to anaphylax
quicklyEmergency treatment, including use of anaphylaxis kit and summoning emergency medical services,
treatment
Expected OutcomeChild does not develop allergic reactions to latex

Patient Goal 1: Will experience no or minimized risk of hip and lower extremity deformity

nursing interventions/RationalesCarry out passive range-of-motion exercises to prevent contrac

point of resistance to prevent traumaCarry out muscle stretching when indicated to prevent contracturesMa
moderate abduction to prevent dislocation; maintain feet in neutral position to prevent contracturesUse diap
animals, or specially designed appliances to maintain desired position
Expected OutcomesLower extremities maintain flexibilityHips and lower extremities are maintain
alignmentSee also:Nursing Care Plan: The Child with Chronic Illness or Disability, Chapter 22Nursing Care P
Hospital, Chapter 26Nursing Care Plan: The Family of the Child Who Is Ill or Hospitalized, Chapter 26

The radioallergosorbent test (RAST) has been used to measure the serum level of latex-specific
immunoglobulin E (IgE). The RAST has been shown to be 90% to 95% sensitive (Kellett, 1997).
Pretreatment with antihistamines and steroids (dexamethasone) before and after surgery to reduce the
possibility of a serious reaction remains controversial because it may interfere with healing.
Because children who have SB are prone to develop an allergy to latex, reducing exposure, from birth on,
hopefully will decrease the chance of allergy development. Latex, a natural product derived from the
rubber tree, is used in combination with other chemicals to give elasticity, strength, and durability to many
products.
Avoiding contact with latex is the most important intervention. The establishment of a latex-safe
environment is being accomplished in many health care facilities where patients and health care workers
are at risk. In addition, there are published lists of products, such as vinyl gloves, that may be substituted
for latex (see footnote to Box 11-4). In the health care arena it is important to use products with the
lowest potential risk of sensitizing patients and staff members. User labeling for latex-containing devices
that come into contact directly or indirectly with live human tissue has been proposed by the FDA (1996).
[*]
* Additional information regarding latex allergy may be found at the following web sites:
www.latexallergyhelp.com, www.latex-allergy.org, latexallergylinks.tripod.com, and. See additional sites in
Mitchell NA: Innovative informations: latex allergy: accessing information on the Internet, J Emerg Nurs
32(1):51-52, 1997.

Box 11-4

Selected Items Possibly Containing Latex[*]* It is very difficult to obtain full and accurate information on the latex
and product series. Double-checking with suppliers before use with latex-allergic individuals is strongly recomm
community) and alternative products call (800) 621-3141 or to download a list access www.sbaa.org, Spina Bifid
Washington, DC 20007-4226.
Medical Items
Adhesive bandage strips
Airways, masks (oxygen)
Anesthesia vent circuits, bags
Blood pressure cuffs and tubing
Bulb syringe
Catheters (indwelling, condom)
Cardiopulmonary resuscitation (CPR) manikins

Chux (washable rubber)

Crutches (axillary, hand pads)
Dressings and wraps (various)
Elastic bandages
Electrode pads, bulbs
Endotracheal tubes
Finger cots
Gloves (sterile and examining, surgical and medical)
Heparin lock adapter
Intravenous tubing, injection ports, bags, burets
Medication vials
Nasogastric tubes
Penrose drains
Pulse oximeters
Spacer (metered dose inhaler)
Stethoscope tubing
Suction tubing
Syringes (disposable)
Tape (cloth adhesive, paper)
Tourniquet
Urodynamics rectal pressure catheters
Wheelchair cushions, tires

Home and Community Items[] Latex-free products for home and community may be ordered from: Alternativ
618-3129 or (630) 587-2705, and Cetra Latex-Free Supplies (888) LATEX-NO.
Art supplies (paint, markers, glue)
Balloons (not Mylar)
Balls (Koosh, tennis, bowling)
Chewing gum

Cleaning/kitchen gloves
Condoms, contraceptive sponges, diaphragms
Dental dams and equipment
Rubber pants
Diaphragms
Elastic exercisers
Elastic on legs, waist of clothing, some disposable diapers
Feeding nipples
Foam rubber lining on splints, braces
Infant toothbrush-massager
Pacifier
Racquet handles
Rubberbands
Water toys, swim and scuba equipment
Wheelchair cushions, tires
Zippered plastic storage bags

The American Nurses' Association (ANA) (1997) has issued a position statement on latex allergies
emphasizing that all health care institutions abandon the unnecessary use of latex gloves and provide lowallergen, powder-free latex gloves in other settings. Procedures for the identification and treatment of
latex-sensitive patients, provision of latex-free medical products, and reporting of allergic events related to
latex medical devices to the Food and Drug Administration MedWatch Program are also strongly advocated
by the ANA. In addition, the ANA recommends that each health care facility have a multidisciplinary task
force to develop occupational health guidelines to ensure a safe environment for health care workers to
minimize latex exposure, identify those at risk for reaction to latex, and accommodate the needs of latexsensitive employees.

NURSING ALERT

Ask all patients about allergic reactions to latex, not only those at risk, during the health interview with the parent
a routine part of all preoperative and preprocedural histories. Stress the importance of the allergy history to all per
phlebotomists).

The identification of those sensitive to latex is best accomplished through careful screening of all patients.
(See Guidelines box, p. 433, for questions related to latex allergy.)
Children with latex allergy should carry some form of allergy identification, such as a Medic-Alert bracelet.
Education programs regarding latex allergy are aimed at those who care for high-risk groups, such as
children with SB, and may include relatives, school nurses, teachers, child care workers, and baby-sitters.
In addition to educating caregivers about the child's exposure to medical products that contain latex,
nurses need to inform them of common nonmedical latex objects (Box 11-4). Items brought to the
hospital, such as floral bouquets, are also screened for latex toys or balloons. Parents should also be given
literature explaining signs and symptoms of latex hypersensitivity and appropriate emergency treatment.
(See Anaphylaxis, Chapter 29.)
OR-malignant hyperthermia
Hyperthermia
Hyperthermia occurs less frequently than hypothermia in the surgical patient. MH generally occurs in
response to certain anesthetics. Other risk factors for hyperthermia include dehydration, fever,
vasoconstriction from medication, endocrine disorders such as thyroid disease, and intracranial infection or
injury to the hypothalamus.
During surgery nursing interventions for cooling include removing excessive drapes, applying alcohol or
cool water to the patient's skin, assisting with monitoring vital signs, using an automatic cooling blanket,
and assisting with the preparation and administration of cool intravenous fluids and emergency
medications. The nurse should record the patient's preoperative baseline temperature and monitor core
body temperature throughout the procedure.
As with all nursing interventions, documentation includes all measures taken, equipment used (including
serial numbers and temperature settings), and patient responses to treatment. Communication with the
postoperative receiving unit is imperative for the continuity of patient care. This is especially important in
cases in which an alteration in normothermia resulted in an emergent situation.
Malignant hyperthermia is a potentially lethal complication of a rare inherited muscle disorder. The
condition is precipitated by the administration of volatile anesthetics and neuromuscular blocking agents.
About 1 in 200 individuals may be at risk for the muscle disorder. Malignant hyperthermia is caused by
either increased calcium release or decreased calcium uptake with muscle contraction. This allows
intracellular calcium levels to rise, producing sustained, uncoordinated muscle contractions, which in turn
increase muscle work, oxygen consumption, and lactic acid production. As a result of these contractions,
acidosis develops and temperature rises (body temperature may rise 1 C [1.8 F] every 5 minutes);
approximately 20% of those who develop malignant hyperthermia do not survive. Malignant hyperthermia
occurs most often in children and young adults immediately after the induction of anesthesia.
Sympathetic responses and acidosis produce tachycardia and cardiac dysrhythmias, followed by
hypotension, decreased cardiac output, and eventually, cardiac arrest. Increasing temperature, acidosis,
hyperkalemia, and hypoxia produce comalike symptoms in the CNS (including unconsciousness, absent
reflexes, fixed pupils, apnea, and sometimes a flat electroencephalogram [EEG]). Oliguria and anuria are
common, probably resulting from shock, ischemia, and low cardiac output.[98]
Treatment includes withdrawal of the provoking agents and administration of dantrolene sodium (a
skeletal relaxant that inhibits calcium release during muscle contraction). Procainamide (Pronestyl) is used
to treat cardiac dysrhythmias. Sodium bicarbonate also may be used. Body temperature can be decreased
through use of ice bags, a cooling blanket, and iced saline lavage.
EVALUATION AND TREATMENT
Careful and thorough preoperative assessment should alert the anesthesiologist to the possibility of a

susceptible individual. A family history of anesthetic problems and previous untoward anesthetic
experiences (muscle cramping, unexplained fevers, dark urine) are criteria that require further clarification
before administration of a volatile anesthetic.
Priorities in treatment of myoglobinuria include identifying and treating the underlying disorder and
preventing life-threatening renal failure. Malignant hyperthermia and myoglobinuria caused by
succinylcholine or volatile anesthetic agents can be treated by halting the anesthetic administration and
infusing dantrolene sodium (Dantrium). Diluting myoglobin using intravenous fluids and administration of
mannitol, sodium bicarbonate, and furosemide (Lasix) to flush the kidney have been advocated to
prevent renal failure. Other secondary problems include electrolyte imbalance, volume depletion, acidosis,
hyperuricemia, hyperkalemia, and calcium imbalance. These require specific treatment. Short-term
dialysis also may be necessary.
Compartment syndromes may require emergency treatment when blood flow to the affected extremity is
compromised because of increased venous pressure, leading to decreased arterial inflow, ischemia, and
edema.[14] When clinical evaluation is inconclusive, the rising compartment pressure can be directly
measured by inserting a wick catheter, needle, or slit catheter into the muscle. Immediate fasciotomy and
debridement have been advocated for pressures of more than 30 mmHg. [15] Compartments frequently
affected are the anterior tibial, deep posterior tibial, volar, hand, and gluteal.
IMPLEMENTATION
Regardless of the type of anesthesia used, one of the most important nursing considerations during the
preanesthesia, intraanesthesia, and postanesthesia periods is close and frequent observation of all body
systems, with specific attention to the ABCs of nursing care (vital signs) and arterial oxygen saturation by
pulse oximetry (Spo2). These observations and interventions should be performed as frequently as needed
depending on the patient's status and in keeping with the standard of care for anesthesia. Sudden
elevation in the patient's body temperature (e.g., higher than 40 C [104 F]) while the patient is
receiving general anesthesia may indicate malignant hyperthermia, and immediate intervention is needed
to protect the patient from injury and possible death. Other nursing interventions include monitoring all
body systems, implementing safety measures, and carrying out the physician's orders.
Oxygen is often administered after a patient has received general anesthesia to compensate for the
respiratory depression that occurred during surgery as well as to elevate oxygen levels. Because oxygen is
a drug, a doctor's order is needed for its administration. Continuous monitoring of SpO 2 is usually
performed. In addition, hypotension and orthostatic hypotension are possible problems after anesthesia,
so postural blood pressure measurements (supine and standing) are needed. Should the patient require
pain management once the anesthesia has been terminated, the nurse must remember that the
anesthetic and any adjuvant drugs used continue to have an effect on the patient. Therefore,
administration of sedatives-hypnotics, narcotics, nonnarcotic analgesics, and other CNS depressants for
pain relief should be done cautiously and only with close monitoring of vital signs. If the patient has
received other medications (such as narcotics or CNS depressants) in a recovery area, dosages of drugs
used in the postanesthesia period and on the general nursing unit may be decreased by one half or one
fourth as ordered. This reduction will help to prevent any further CNS depression. For those patients
receiving anesthetics that are quick acting and whose effects are reversed quickly, dosages of analgesics
may not need to be altered.
For intravenous anesthesia, all resuscitative equipmentas well as a drug antidoteare usually readily
available in case of cardiorespiratory distress or arrest. Neurologic indicators (e.g., reflexes, response to
commands, level of consciousness), electrocardiogram, pulse oximetry readings, and vital signs are some
of the parameters that need to be monitored frequently. Additional nursing interventions with anesthesia
include the following: status of breath sounds should be assessed by auscultation (hypoventilation may be
a complication of general anesthesia) and neurologic changes and status (no matter how small) and any
change in sensations, such as noted with nerve blocks (local anesthesia), should be documented and
reported. If changes occur in body parts distal to the site of local anesthesia or in locations where
restraints were placed, the body part should be assessed for temperature, color, and presence or absence
of pulses and the findings should be documented and reported to the physician. Improper positioning
during surgery may lead to the injury of arteries and nerves and should be reported immediately.

Patients undergoing moderate sedation as the method of anesthesia should receive education about the
technique. As noted earlier, recovery from this type of anesthesia is more rapid and the safety profile
better than with general anesthesia, which has inherent cardiorespiratory risks.
With regard to the use of topical or local anesthetics (e.g., lidocaine with or without epinephrine), solutions
that are not clear and appear cloudy or discolored should not be used. Some anesthesiologists mix the
solution with sodium bicarbonate to minimize local pain during infiltration, but this also causes a more
rapid onset of action and a longer duration of sensory analgesia. If an anesthetic ointment or cream is
used, the nurse should thoroughly cleanse and dry the area to be anesthetized before application of the
drug.
If a topical or local anesthetic is being used in the nose or throat, the nurse must remember that it may
cause paralysis and/or numbness of the structures of the upper respiratory tract, which can lead to
aspiration. Exact amounts of the drug should be used, and it should be administered only at the
prescribed times. Local anesthetics are not to be swallowed unless the physician has so instructed. Should
this occur, the nurse must closely observe the patient, check his or her gag reflex, and expect to withhold
food or drink until the patient's sensation and/or gag reflex has returned.
A patient who receives an NMBA should be monitored closely during and after anesthesia or initiation of
mechanical ventilation. Vital signs and other parameters should be constantly monitored, with
measurement of blood pressure, pulse, respirations (rate, depth, pattern, quality), SpO2, and hand grasp
strength (for neuromotor assessment). Intake and output are also monitored. Recovery from NMBAs is
manifested by a decrease in paralysis of the face, diaphragm, legs, arms, and remainder of the body. The
health care provider must reassure the patient of his or her condition as the patient begins to recover,
because the patient may become frightened if communication is difficult during the recovery process.
Once anesthesia and procedures are completed and the patient is to be discharged or transferred, some
general areas of patient teaching must be completed. One major focus is sharing information regarding
health care resources available to the patient at home, should assistance be necessary. Home health care
is often required and ordered by the physician, and if it is not ordered, there may be a need for additional
resources for assistance at home. Education about home health care resources and assistance-in-living
programs should be guided by the findings of an at-home nursing assessment and the needs identified.
Assistance with activities of daily living and/or assistance with health carerelated procedures or
interventions may be required. Some examples of health care procedures for which help might be needed
are wound care, dressing changes, surgical site care, drawing of samples for laboratory studies,
intravenous infusions, and administration of various medications through the intravenous, intramuscular,
or subcutaneous route. Pain management may also need to be addressed (Chapter 10) with thorough
teaching for the patient and those involved in care at home. Simple instructions provided using ageappropriate teaching strategies are always important (Chapter 6). Sharing of information about
community resources is also important, especially for those who may need transportation, assistance with
meals and housekeeping during the patient's recovery, and possibly rehabilitation at home. Some of these
community resources may be agencies that are supported by city or state social service programs, Meals
on Wheels, senior citizen support groups, and church-sponsored support resources. Many of these
resources are free or have income-based fees. Teaching tips important for patients receiving general or
local anesthesia are given in the Patient Teaching Tips.
Malignant hyperthermia (MH), first identified in the 1960s, is a serious and potentially fatal complication of
general anesthesia. Even though MH occurs most commonly during induction or surgical procedure, it can
occur or recur in the PACU or on the nursing unit 24 to 72 hours after surgery. MH reportedly occurs in 1
in 50,000 adults and 1 in 15,000 children.[32] More common in males and adolescents, the incidence of MH
decreases after age 50.[33] Other syndromes associated with an increased incidence of MH include central
core disease and Duchenne's muscular dystrophy.[28] With prompt recognition and treatment, the mortality
rate is less than 10%.[8]
MH is a genetic autosomal-dominant defect resulting in altered muscle metabolism. It is triggered by
certain anesthetic agents (Box 14-3
Box 14-3

Anesthetic Agents Triggering Malignant Hyperthermia

Inhalation Agents
Halothane
Enflurane
Isoflurane
Desflurane
Sevoflurane
Neuromuscular Blocking Agent
Succinylcholine
Nondepolarizing Muscle Relaxant
d-Tubocurarine chloride

A genetic defect in the muscle cell membrane permits anesthetic agents to trigger a sudden increase of
calcium ions within the muscle cells. The rapid increase of calcium starts a series of biochemical reactions
that elevate the metabolic rate, causing hyperthermia (with temperatures rising to 109.4 F [43 C]),
muscle rigidity, respiratory and metabolic acidosis, hypercapnia, and cell breakdown. Muscle rigidity occurs
in approximately 75% of patients with MH.[14] Diagnostic findings include hypercalcemia, metabolic and
respiratory acidosis, hyperkalemia, hypermagnesemia, hypercapnea, and elevated serum creatine
phosphokinase (CPK).
Masseter muscle spasms or fasciculations after administration of succinylcholine during induction should
alert the anesthesiologist to the potential for an MH episode. The earliest and most consistent clinical sign
of MH is unexplained ventricular dysrhythmia, specifically tachycardia or premature ventricular
contractions, associated with an increase in end tidal carbon dioxide. Additional clinical symptoms include
tachypnea, cyanosis, other dysrhythmias, skin mottling, unstable blood pressure, elevated levels of CPK,
and elevated levels of myoglobin. As a result of desaturation, blood at the surgical field may appear dark.
The patient's temperature may rise 1.8 to 3.6 F (1 to 2 C) every 5 minutes and may exceed 109.4 F
(43 C). Because it occurs in the late stages, an elevated temperature is not a reliable indicator of MH.
The patient's urine may appear dark due to rhabdomyolysis (breakdown of striated muscle with excretion
of myoglobin in urine). Other late clinical manifestations of MH include hyperkalemia, acute renal failure,
left-sided heart failure, disseminated intravascular coagulation, pulmonary embolus, and neurologic
deficits.
Treatment of the patient experiencing MH includes immediately ceasing the inhalation agent or muscle
relaxant, hyperventilating with 100% oxygen, cooling with ice packs or cooling blankets, lavaging body
cavities with iced saline, restoring acid-base balance, treating hyperkalemia, and providing rapid
intravenous infusion of dantrolene. Cooling measures should be discontinued when the patient's
temperature reaches 100.4 F (38 C).
Dantrolene is the only known treatment able to stop an MH crisis. Dantrolene relaxes skeletal muscle and
retards the biochemical actions that cause muscle contractions. Dosage recommendations by the
Malignant Hyperthermia Association of the United States (MHAUS) include an initial bolus of 2 to 3 mg/kg
with subsequent dosing of up to10 mg/kg.[22] Dantrolene should be continued for at least 24 hours after
initial treatment.
All perioperative personnel should be aware of the protocol for patients who develop MH. Many institutions
have an MH kit or cart containing necessary supplies for treatment. More information is available from
MHAUS at www.mhaus.org. The MH hotline number for physician consultation in emergencies is 800-MHHYPER.
Identification of patients at risk is the primary method for prevention of MH. The preoperative history
should include an assessment of the patient's previous experience with surgery, a history of heatstroke in
the patient or family, or known muscular abnormalities. The CPK level may also be elevated, but this is not
specific to MH, since elevations may also occur as a result of alcoholism or muscle disease. The key
assessment finding is familial history of unexplained death under general anesthesia. For persons with
suspected MH, diagnosis is confirmed by preoperative muscle biopsy. Prophylactic administration of

dantrolene for MH-susceptible patients is no longer recommended.[22] Anesthetic agents known to trigger
MH should not be administered to persons who are at significant risk for developing MH. Family members
of individuals with known MH should undergo diagnostic testing as a prophylactic measure.
ACS-cardiac enzymes
Depending on the cause of the reduced cardiac output, clients may present with differing clinical
manifestations.[59] Dysrhythmias are self-evident on cardiac monitoring. The most prominent
manifestations associated with a decrease in cardiac output include chest pain, skin pallor, diaphoresis,
hypotension, nausea, and agitation or a decrease in level of consciousness.[70] External chest wall injury
may be evident with cardiac contusions. Cardiac tamponade produces the additional findings of distended
jugular neck veins and muffled heart sounds. Fever may be present with cardiac infections.
Diagnostic tests include cardiac monitoring, electrocardiography (ECG), chest radiography,
ultrasonography, laboratory studies, noninvasive stress testing, two-dimensional echocardiography,
myocardial perfusion imaging, CT scans, and invasive coronary angiography. Levels of the cardiac
enzymes creatine kinase (CK) and the CK-MB fraction and of the cardiac markers myoglobin and troponin
T (cTnT) and troponin I (cTnI) are especially important in diagnosing the occurrences of a myocardial
infarction.
Blood Tests
Biomarkers provide definitive information about the presence and severity of myocardial damage and are
drawn immediately in patients experiencing unrelenting chest pain. Biomarkers are especially valuable in
evaluating patients who are seen for possible thrombolytic therapy. The most specific biomarker for MI is
serum troponin, which is composed of troponin C, troponin I, and troponin T. Any elevation of serum
troponin indicates myocardial cell damage. Cardiac troponin I that is already elevated on admission is
associated with an increase in both complications and mortality (Table 29-4).

Table 29-4

Cardiac Enzyme

Elevation (hr)

Peak Elevation (hr)

Duration (hr)

Creatine kinase MB

39

1218

13

Troponin T

35

1024

1014

Troponin I

36

1024

Myoglobin

46

12

However, elevated troponin levels may also reflect minor myocardial injury from causes other than ACS.
Injured myocardial cells release another biomarker, the enzyme creatine kinase (CK), during AMI. CK
elevation confirms the presence of myocardial damage. Brain tissue and skeletal muscle also release CK
with injury, but the isoenzyme CK-MB is specific to the myocardium. Myoglobin, an oxygen-binding protein
found in cardiac and skeletal muscle, is another early biomarker for MI.
Blood chemistry tests and a complete blood count (CBC) are performed to determine concurrent disease
states and help with differential diagnosis. C-reactive protein, another measure of inflammation, is also
considered a marker for an increased risk of cardiovascular disease. The AHA and CDC have established
risk guidelines for C-reactive protein as follows: concentrations of less than 1.0 mg/L are considered low
risk, 1.0 to 3.0 mg/L are average risk, and higher than 3.0 mg/L are high risk. People in the high-risk
group have about a twofold increase in relative risk for cardiovascular disease compared with those in the
low-risk group.

Cardiac Enzymes
Enzymes are drawn to evaluate myocardial damage and to identify myocardial infarction (MI).
Lactate dehydrogenase (LDH): isoenzyme LDH-1 specific for cardiac damage. Normal is 14% to 26%
of total LDH. Increases 24 to 48 hours after MI; peaks in 48 to 72 hours; returns to normal 5 to 10 days.
Creatinine kinase (CK): CK isoenzyme MB (CK-MB2) is specific for myocardial injury. It increases within
3 to 6 hours after an MI, peaks in 12 to 24 hours, and returns to normal in 12 to 48 hours. Levels are
calculated according to a ratio.
Cardiac troponin T and cardiac troponin I: normal level is <0.2 ng/ml (for T) and < 0.03 bg/dl (for I).
Levels are elevated within 4 to 6 hours after an MI and peak within 10 to 24 hours.

Nursing Implications

1. Enzymes must be drawn on admission and obtained in a serial manner thereafter.

There is a characteristic pattern to the increases and decreases of enzyme levels in a client with an
MI.

2. The larger the infarction, the larger the enzyme response.

3. The increased levels of troponin and CPK are the most significant and are diagnostic of
myocardial damage. Evaluate serial levels of the enzymes.
4. Intramuscular injections, medications, other disease entities, and tissue
injury
will affect enzyme changes; however, isoenzymes help discriminate
myocardial tissue
damage from other tissue injury.
NURSING PRIORITY:

For a client with an increase in CK-MB2and an increase in cardiac troponin levels, it is important to assess the clien
MI. Serum levels may be checked every 6 to 8 hours during the acute phase of an MI.

Clinical Manifestations
The first symptom of acute myocardial infarction is usually sudden, severe chest pain. The pain is similar
to angina pectoris but more severe and persistent and is not relieved by nitrates. It may be described as
heavy and crushing, such as a truck sitting on my chest. Radiation to the neck, jaw, back, shoulder, or
left arm is common. Some individuals, especially those who are elderly or have diabetes, experience no
pain, thereby having a silent infarction. Infarction often stimulates a sensation of unrelenting
indigestion. Nausea and vomiting may occur because of reflex stimulation of vomiting centers by pain
fibers. Vasovagal reflexes from the area of the infarcted myocardium also may affect the gastrointestinal
tract. Catecholamine release results in sympathetic stimulation, producing diaphoresis and peripheral
vasoconstriction that cause the skin to become cool and clammy. Fever may develop in the first 24 hours
and persist for 1 week because of inflammatory activity within the myocardium.
Various cardiovascular changes are found on physical examination:

1. Blood pressure initially decreases.

2. The sympathetic nervous system is reflexively activated to compensate, resulting in a
temporary increase in heart rate and blood pressure.
3. Abnormal extra heart sounds reflect left ventricular dysfunction.
4. Pericardial friction rub (roughened membranes rubbing against each other) and cardiac
murmurs may result from inflammation.

Laboratory data reveal leukocytosis and elevated sedimentation rate, both of which indicate inflammation.
The individual's blood sugar is usually elevated, and the glucose tolerance level may remain abnormal for
several weeks. Hypoxemia develops, particularly in individuals not given supplemental oxygen.

A transient rise in plasma enzyme levels can confirm the occurrence of myocardial infarction and indicate
its severity. The enzymes released by myocardial cells include creatine kinase (CK), lactic dehydrogenase
(LDH), and to a lesser extent, aspartate aminotransferase (AST). These enzymes exist in several different
active molecular forms called isoenzymes, which are present in different amounts within particular tissues.
If serologic tests show abnormally high levels of isoenzymes associated with cardiac tissue (CK-MB, LDH1), acute myocardial infarction has probably occurred. Of the three isoenzymes, CK-MB is most specific for
myocardial infarction, although its level also may increase in individuals with other conditions. Assays
based on monoclonal antibodies against troponin I and troponin T are more sensitive and specific markers
for myocardial injury than CPK/MB and are usually measured along with the other three cardiac
isoenzymes.[78,79] Elevation of troponin I, CK-MB, LDH-1, and AST will be noted at characteristic times. The
higher the serum concentration of CK-MB and troponin I, the more extensive the tissue damage that has
occurred. Blood is drawn for enzyme determinations as soon as possible after the onset of symptoms and
for serial enzyme levels every 4 hours for three additional measurements. If these consecutive
measurements reveal no significant enzyme elevation, then myocardial infarction is ruled out.
Myocardial infarction can occur in various regions of the heart wall and may be described as anterior,
inferior, posterior, lateral, subendocardial, endocardial, subepicardial, epicardial, intramural, or transmural,
depending on the anatomic location and extent of tissue damage from infarction. Twelve-lead
electrocardiograms (ECGs) help to localize the affected area through identification of Q waves and changes
in ST segments and T waves (Figure 23-23). The infarcted myocardium is surrounded by a zone of hypoxic
injury, which may progress to necrosis or return to normal. Infarcted tissue is electrically silent and does
not contribute to the ECG. Transmural infarcts are large enough to create inscription of a Q wave on the
ECG (Q wave infarction). Small infarcts are usually subendocardial and do not create a Q wave (nonQ
wave infarction). Adjacent to the zone of hypoxic injury is a zone of reversible ischemia. Ischemic and
injured myocardial tissue causes ST and T wave changes. As the myocardium heals, the ST segment and T
waves gradually return to normal, but abnormal Q waves generally persist.

Figure 23-23 Electrocardiographic alterations associated with the three zones of myocardial
infarction.
Radionucleotide imaging with thallium-201 and single proton emission computed tomography (SPECT) can
provide a diagnostic picture in individuals with acute or healed myocardial infarction. Technetium-99m
pyrophosphate also is taken up by areas of myocardial infarction, which appear as hot spots.
Unfortunately, the area of infarction must be large enough to visualize the hot spot, and the scan may
remain positive for many months after infarction.
Although the incidence of sudden cardiac death is decreasing, about 350,000 to 400,000 people in the
United States alone present with sudden cardiac death annually.[6] Sudden cardiac death is a multifactorial
problem. Risk factors for sudden death are related to three factors: ischemia, left ventricular dysfunction,
and electrical instability. These factors interact with each other (Figure 23-24).

Figure 23-24 Three interacting factors related to sudden cardiac death. The three factors are
ischemia, left ventricular dysfunction, and electrical instability. (*See key terms list for
references to further discussion.)
Complications.
The number and severity of postinfarction complications depend on the location and extent of necrosis,
the individual's physiologic condition before the infarction, and the availability of swift therapeutic
intervention. Table 23-5 lists the most common complications.
TABLE 23-5
Type

Characteristics

Dysrhythmias

Disturbances of cardiac rhythm that affect 90% of cardiac infarction pati

Caused by ischemia, hypoxia, autonomic nervous system imbalances, la
conduction pathways or conduction abnormalities, drug toxicity, or hemodynam

Left ventricular failure

(congestive heart failure)

Characterized by pulmonary congestion, reduced myocardial contractility

Cardiogenic shock can develop

Inflammation of the
pericardium (pericarditis)

Includes pericardial friction rubs

Often noted 2 to 3 days later and associated with anterior chest pain tha

Dressler postinfarction
syndrome

Essentially a delayed form of pericarditis that occurs 1 wk to several mo

Thought to be immunologic response to necrotic myocardium and marke

Organic brain syndrome

Occurs if blood flow to brain is impaired secondary to MI

Transient ischemic attacks or cerebrovascular accident may occur if thro

Rupture of heart structures

Caused by necrosis of tissue in or around papillary muscles

Affects papillary muscles of chordae tendineae cordis
Predisposing factors include thinning of wall, poor collateral flow, shearin
marked necrosis at terminal end of blood supply and aging of myocardium with

Rupture of wall of infracted

ventricle

Can be caused by aneurysm formation when pressure becomes too grea

Left ventricular aneurysm is late (month to years) complication of MI

Infarctions around septal

structures

Occur in those structures that separate heart chambers and lead to sept
Associated with audible, harsh cardiac murmurs, increased left ventricul

Systemic
thromboembolism

Commonly found in postmortem examinations of individuals who died of

May disseminate from debris and clots that collect inside dilated aneurys
Especially common are pulmonary emboli and deep venous thrombi of le


Sudden death

Reduced incidence associated with early mobilization and prophylactic an

Dysrhythmias frequently causative, particularly ventricular fibrillation

Knowledge of CPR has increased survival
Risk of death increased by age more than 65 yr, previous angina pectori
at time of admission, diabetes mellitus, dysrhythmias or conduction defects, an

Data Base
A.

Etiology and pathophysiology

1. Atherosclerosis: deposition of fatty plaques and fibrous tissue along inner wall of
coronary arteries leads to inflammation, narrowing, and possible obstruction; also affects
peripheral and cerebral vessels

2. Angina pectoris: episodic pain experienced when oxygen supplied by the blood cannot
meet the metabolic demands of the muscle. In addition to atherosclerosis, this temporary ischemia
may be precipitated by coronary artery spasms, strenuous exercise, hyperthyroidism, exposure to
cold and emotional stress; classified as unstable preinfarction, chronic stable, nocturnally resting
(Prinzmetal)

3. Myocardial infarction (MI): acute necrosis of the heart muscle caused by interruption of
oxygen supply to the area (ischemia), resulting in altered function and reduced cardiac output

4. Risk factors
0
a. Family history
1
b. Increasing age
2
c. Gender: males and females especially after menopause (estrogen seems to
provide some degree of protection)
3
d. Race: risk appears higher in African-Americans
4
e. Cigarette smoking (contributes to vasoconstriction, platelet activation, arterial
smooth muscle cell proliferation, and reduced oxygen availability)
5
f.
Hypertension
6
g. Hyperlipidemia: increased total cholesterol; increased low-density lipoprotein
cholesterol (LDL); increased ratio of total cholesterol or LDL to HDL; decreased high-density
lipoprotein cholesterol (HDL); HDL seems to protect against CAD; increased triglycerides
7
h. Obesity (particularly abdominal obesity)
8
i.
Sedentary lifestyle (contributes to obesity and reduced HDL)
9
j.
Diabetes
10
k. Stress (an innate competitive, aggressive type A personality seems less
important than amount of stress and client's psychologic response)
l.
Metabolic syndrome: a cluster of signs including
hyperlipidemia, low HDL, abdominal obesity, increased BP, and
impaired glucose utilization

B.

0
1
0
1
2
3

Clinical findings
1. Subjective: retrosternal chest pain; pain may radiate to arms, jaw, neck, shoulder, or
back; pain described as pressure, crushing, or viselike; pain of angina is associated with
activity and generally subsides with rest; palpitations; apprehension, feeling of dread; dyspnea;
nausea; asymptomatic with silent ischemia
2. Objective
a. ECG changes may reveal ischemia (inverted T wave, elevated ST segment) or
evidence of MI (presence of Q wave); a Holter monitor may be used to detect changes
associated with ADL
b. Elevated serum enzymes and isoenzymes with MI
(1) Cardiac troponin T (cTnT) levels increase within 3 to 6 hours and remain
elevated for 14 to 21 days; very accurate for assessing cardiac disease
(2) Cardiac troponin I (cTnI) levels rise 7 to 14 hours after an MI and remain
elevated for 5 to 7 days; highly specific for myocardial damage
(3) Creatinine kinase (CK); elevated 3 to 6 hours after infarction, peaking at
24 hours, and returning to normal within 72
(4) CK-MB: elevated 4 to 6 hours after pain, peaking within 24 hours, and

returning to normal within 72 hours; specific for myocardial damage

(5) Myoglobin: elevated in 1 to 3 hours; returning to normal within 12 hours

4
2
3

c. C-reactive protein (CRP): elevation suggests inflammation of the vascular

endothelium and coronary artery calcification
d. Doppler flow studies
e. Cardiac nuclear scanning (thallium, MUGA) or echocardiographic studies can
help determine extent of vessels involved
f.
Sympathetic nervous system responses: pallor, rapid pulse, diaphoresis,
vomiting
g. Signs associated with MI: dysrhythmia and elevated
temperature, sedimentation rate, and WBCs

4
5
6

C.

0
1
2
3
4
5

Therapeutic interventions
1. Prevention of MI
a. Supervised exercise program to avoid ischemia but promote collateral circulation
and increase HDL; weight control; smoking cessation; dietary restriction of sodium,
cholesterol, and total and saturated fat; management of hypertension and diabetes
b. Pharmacologic management: nitrates, beta-blocking agents, calcium channelblocking agents, antilipidemics, antiplatelet agents (ASA)
c. Supplemental oxygen during anginal attack as needed
d. Percutaneous transluminal coronary angioplasty (PTCA)
e. Coronary artery bypass graft (CABG) if medical regimen not successful
f.
Intracoronary stent placement
g. Transmyocardial revascularization: involves creating laser
channels in the myocardium to promote vascular growth or
angiogenesis
2.

0
1
2
3
4

0
1
2
3

0
1
2
3

0
1
2
3
4

Management of acute MI
a. Improvement of perfusion
(1) Administer ASA immediately, often on way to hospital
(2) Begin beta blocker and IV nitroglycerin
(3) Thrombolytic therapy within 6 hours of MI; anticoagulants
(4) Antidysrhythmics to maintain cardiac function
(5) Intraaortic balloon pump that inflates during diastole and deflates during systole
to decrease cardiac workload by decreasing afterload for cardiogenic shock
b.

Promotion of comfort and rest

(1) Administer analgesics such as intravenous morphine sulfate
(2) Oxygen administration to alter tissue hypoxia
(3) Maintain bed or chair rest to decrease oxygen tissue demands
(4) Diet therapy may be 2-gram sodium diet or clear liquids, depending on presence
of nausea
c.

Monitoring client
(1) Pulse oximetry
(2) Cardiac monitoring
(3) Vital signs
(4) Swan-Ganz catheter

d.

Assessment for complications of MI

(1) Cardiogenic shock
(2) Pulmonary edema caused by acute heart failure
(3) Thromboembolism
(4) Extension of MI
(5) Pericardial effusion and cardiac tamponade

Nursing Care of Clients with Ischemic Heart Disease


0
1
2
3
4
5
6
7
8

0
1
2
3

0
1
2
3
4
0
1
2
3

A.

Assessment
1. History of chest, arm, shoulder, neck, jaw pain
2. Precipitating factors (e.g., exercise, cold)
3. Risk factors (nonmodifiable and modifiable)
4. Vital signs
5. Intake and output (fluid volume overload is dangerous if cardiac output is
compromised)
6. Adventitious breath sounds and dependent edema with impending failure
7. Restlessness, dyspnea
8. Skin: diaphoresis; pallor; cyanosis
9. If MI is suspected, continuous ECG monitoring to detect: changes in rate,
rhythm, and conduction of heartbeat; life-threatening dysrhythmias (ventricular fibrillation
and ventricular standstill); dysrhythmias such as premature ventricular complexes close to a
T wave, ventricular tachycardia, and atrial fibrillation
B.

C.

Planning/Implementation
1. Teach signs and management of cardiac ischemia (rest; nitrates; emergency
care if ineffective)
2. Encourage prophylactic administration of nitrates
3. Reinforce need to avoid exertion (e.g., shoveling snow) and exposure to cold
4. Support involvement in smoking cessation programs
5. Encourage the following dietary program
a. Low cholesterol, low fat (especially saturated)
b. Replace vegetable oils high in PUFA with those high in MUFA, such as
olive oil and avocado oil
c. Eat fish high in omega-3 fatty acids several times per week (salmon,
tuna)
d. Follow DASH diet; increase intake of high-fiber foods such as fruits,
vegetables, cereal grains, and legumes; soluble fiber is particularly effective in
reducing blood lipids (oat bran, legumes); low-fat dairy

5
6
7
8
0

6.
7.
8.

Educate client about medications

Provide emotional support regarding alteration in lifestyle
Care of client after acute MI
a. Document dysrhythmia and respond per protocol: medication,
defibrillation, or CPR
b. Reduce cardiac demand; administer oxygen, analgesics, vasodilators,
and other medications as ordered
c. Recognize risk for sensory overload: orient to unit and equipment; allow
time to express feelings; encourage short visits by significant others
d. Use measures to prevent sequelae to diminished activity:
thrombophlebitis, pneumonia, constipation

1
2
3
9

0
1
2
3

Analysis/Nursing Diagnoses
1. Activity intolerance related to dyspnea
2. Decreased cardiac output related to myocardial ischemia
3. Ineffective sexuality pattern related to chest pain
4. Anxiety related to anticipated lifestyle changes

D.

Myxedema coma

Evaluation/Outcomes
1. Remains free of chest pain
2. Verbalizes a reduced level of anxiety
3. Adheres to prescribed regimen (dietary, pharmacologic, and exercise)
4. Maintains oxygen saturation at 95% on room air

Any client with hypothyroidism who has any other health problem or who is newly diagnosed is at risk for
myxedema coma. Factors leading to myxedema coma are listed in Table 67-3. Problems that often occur
with this condition include the following:

Coma
Respiratory failure
Hypotension
Hyponatremia
Hypothermia
Hypoglycemia

Untreated myxedema coma leads to shock, organ damage, and death. Assess the client with
hypothyroidism every shift for changes that indicate increasing severity, especially changes in mental
status.
Treatment is instituted quickly according to the client's manifestations and without waiting for laboratory
confirmation. Best practices for emergency care of the client with myxedema coma are listed in Chart 677.

CHART 67-7
BEST PRACTICE for
Emergency Care of the Client During Myxedema Coma

Maintain a patent airway.

Replace fluids with IV normal or hypertonic saline.
Give levothyroxine sodium IV as prescribed.
Give glucose IV as prescribed.
Give corticosteroids as prescribed.
Check the client's temperature hourly.
Monitor blood pressure hourly.
Cover the client with warm blankets.
Monitor for changes in mental status.
Turn every 2 hours.
Institute aspiration precautions.

CONSIDERATIONS FOR OLDER ADULTS

Metabolic rate and production of thyroid hormone both decrease with advancing age (Chart 67-8),
particularly among people older than 80 years of age. Until recently, however, data regarding normal
levels of T3 and T4 were established only for adults between the ages of 20 and 30 years. By such criteria,
older people with T3 and T4 levels 15% to 20% below normal levels (established for a younger
population) were considered to have hypothyroidism and therapy with thyroid hormone was initiated. In
fact many of these clients were not truly hypothyroid, and therapy caused pseudohyperthyroidism,
stressing many tissues and organs. Daily thyroid hormone therapy decreases the activity of the anterior
pituitary gland and the thyroid gland, creating actual hypothyroidism. Health care providers need to
assess more than just laboratory data to determine hypothyroidism in the older adult.

CHART 67-8
Nursing Focus on the older adult
Thyroid Problems

Teach the client the following facts about changes in the thyroid gland related to aging:

The thyroid gland decreases in size with increasing age.

Thyroid hormone secretion decreases with age, but the hormone level remains stable because ce
hormone also decreases with age.

The basal metabolic rate decreases with age, usually as a result of decreased activity. This decre
composition from predominantly muscular to predominantly fatty.

Older clients require lower doses of replacement thyroid hormone. Too large a dose may adverse
muscle.

Clinical Manifestations
The manifestations of hypothyroidism depend on whether it is mild, severe (myxedema), or complicated
(myxedema coma).
Mild Hypothyroidism
Clients with mild hypothyroidism (the most common form) may be asymptomatic or may experience
vague manifestations so ordinary as to escape detection. For example, clients may experience sensitivity
to cold, lethargy, dry skin or hair, forgetfulness, depression, and some weight gain. Constipation and fecal
impaction related to slowed peristaltic action and lack of normal physical activity may be reported.
As the degree of hypothyroidism worsens, the thyroid may enlarge (goiter) in an attempt to produce
enough T4. Typically, clients seek medical advice when the goiter grows large enough to distort the
appearance of the neck. They may also experience respiratory distress and dysphagia if the goiter is very
large.
Diagnostic tests for hypothyroidism confirm the clinical picture of hypometabolism and depressed thyroid
activity. The serum TSH level is elevated in primary hypothyroidism. Radioactive iodide uptake is
decreased in hypothyroidism.
Myxedema
Myxedema may develop in clients with undiagnosed or undertreated hypothyroidism who experience
stress. Stressors include infection, drugs (phenothiazines, barbiturates, opioids, anesthetics), respiratory
failure, heart failure, cerebral vascular accident, trauma, prolonged exposure to cold, metabolic
disturbances, surgery, and seizures.
Myxedema is characterized by a dry, waxy type of swelling with abnormal deposits of mucin in the skin
and other tissues. The edema is of the nonpitting type and is common in the pretibial and facial areas.
Myxedema is most commonly diagnosed in hypothyroid women in their 60s. Untreated myxedema has
been associated with severe atherosclerosis and has been attributed to the increase in serum cholesterol
concentrations, particularity low-density lipoproteins. TH replacement improves these changes.
Clients with myxedema may also have hypercholesterolemia, hyperlipidemia, and proteinemia as a result
of T4 changes in the synthesis, mobilization, and degradation of serum lipids. Elevated lipid levels may
contribute to the later development of cardiac problems. Dilutional hyponatremia may develop as a result
of the marked impairment of water excretion because of decreased delivery of sodium and volume to the
distal renal tubules associated with decreased renal blood flow. Elevated creatine phosphokinase,

aspartate aminotransferase, and lactate dehydrogenase may also develop secondary to altered
metabolism.
Myxedema Coma
Hypothyroidism generally affects all body systems, with the extent of the symptoms closely related to the
degree of TH deficiency. The onset is usually insidious over months or years. The lowered levels of TH
result in decreased energy metabolism and heat production. The individual develops a low basal metabolic
rate, cold intolerance, lethargy, tiredness, and slightly lowered basal body temperature. Many organ
systems are affected (Table 21-2).
The major complication of hypothyroidism is myxedema coma, an extremely rare condition with a
mortality rate approaching 100%. Myxedema coma is characterized by a drastic decrease in metabolic
rate, hypoventilation leading to respiratory acidosis, hypothermia, and hypotension. Complicating
conditions include hyponatremia, hypercalcemia, secondary adrenal insufficiency, hypoglycemia, and water
intoxication. Myxedema coma may be brought on by stressas from surgery or infectionor by
noncompliance with thyroid treatment.

System

Clinical Manifestations

Neurologic

Confusion, syncope, slowed speech and thinking, memory loss; lethargy, headaches,
hearing loss, night blindness; slow, clumsy movements; cerebellar atazia; slow alphawave
activity and loss of amplitude in EEG; reduced cAMP response to epinephrine, glucagons,
and PTH stimulation; decreased appetite

Endocrine

Increased TSH production in primary hypothyroidism; enlarged pituitary thyrotropes,

increase in serum prolactin levels with galactorrhea; decreased rate of cortisol turnover but
with normal serum cortisol levels

Reproductive

Decreased androgen secretion in men, increased estriol formation in women; low total
hormone values but with increased amounts of unbound hormone; anovulation, decreased
libido, and a high incidence of spontaneous abortion in women; erectile dysfunction,
decreased libido, and oligospermia in men

Hematologic

Decrease in red cell mass leading to normocytic, normochromic anemia; macrocytic anemia
associated with vitamin B12 deficiency and inadequate folate or iron absorption in the
gastrointestinal tract

Cardiovascular

Reduction in stroke volume and heart rate causing lowered cardiac output; increased
peripheral vascular resistance to maintain systolic blood pressure; normal response to
exercise but with alterations in circulatory system at rest (prolonged circulation time and
decreased blood flow to tissues); cool skin and cold tolerance; enlarged heart; decreased
intensity of heart sounds and variety of ECG changes (sinus bradycardia, prolonged PR
interval, depressed P waves, flattened or inverted T waves, and lowamplitude QRS
complexes); cardiac tamponade (although rare) (See Chapter 30)

Pulmonary

Dyspnea; myxedematous changes in respiratory muscles leading to hypoventilation and

carbon dioxide retention, which contribute to myxedema coma

Renal

Reduced renal blood flow and glomerular filtration rate leading to decreased renal excretion
of water; increase in total body water and dilutional hyponatremia; reduced production of
erythropoietin

Gastrointestinal

Constipation, weight gain, and fluid retention; decreased absorption of most nutrients;
decreased protein metabolism leading to retarded skeletal and soft-tissue growth and
slightly positive nitrogen balance; edema; decreased glucose absorption and delayed
glucose uptake; elevated serum lipid values

Musculoskeletal

Muscle aching and stiffness; slow movement and slow tendon jerk reflexes; decreased bone
formation and resorption, increased bone density; aching and stiffness in joints

Integumentary

Dry, flaky skin; dry, brittle head and body hair; reduced growth of nails and hair, slow
wound healing
Myxedema
Cool skin

The decrease in TH leads to increases in TSH production and may cause goiter.
The characteristic sign of severe or long-standing hypothyroidism is myxedema, which is histologically
similar to the pretibial myxedema deposits that often occur with Graves disease. Myxedema is a result of
an alteration in the composition of the dermis and other tissues. The connective fibers are separated by an
increased amount of protein and mucopolysaccharides.
This protein-mucopolysaccharide complex binds water, producing nonpitting, boggy edema, especially
around the eyes, hands, and feet and in the supraclavicular fossae.
Myxedema is also responsible for thickening of the tongue and the laryngeal and pharyngeal mucous
membranes. This results in thick, slurred speech and hoarseness, both common in hypothyroidism.
Myxedema coma, a medical emergency, is a diminished level of consciousness associated with severe
hypothyroidism.[63] Signs and symptoms include hypothermia without shivering, hypoventilation,
hypotension, hypoglycemia, and lactic acidosis. Older individuals with severe vascular disease and with
moderate or untreated hypothyroidism are particularly at risk for developing myxedema coma. It also may
occur after overuse of narcotics or sedatives or after an acute illness in hypothyroid individuals.
Hypothyroidism
Hypothyroidism, a decrease in thyroid hormone secretion, can have either a primary cause (thyroid
gland disorder) or a secondary cause (lack of TSH secretion). Primary hypothyroidism occurs more
frequently. Decreased T4 and elevated TSH levels indicate primary hypothyroidism, the causes of which are
acute or chronic inflammation of the thyroid gland, radioiodine therapy, excess intake of anti-thyroid
drugs, and surgery. Myxedema is severe hypothyroidism in the adult; symptoms include lethargy, apathy,
memory impairment, emotional changes, slow speech, deep coarse voice, edema of the eyelids and face,
thick dry skin, cold intolerance, slow pulse, constipation, weight gain, and abnormal menses. In children,
hypothyroidism can have a congenital (cretinism) or prepubertal (juvenile hypothyroidism) onset. Drugs
containing T4 and T3, alone or in combination, are used to treat hypothyroidism.
Drug Therapy: Hypothyroidism
Levothyroxine sodium (Levothroid, Synthroid) is the drug of choice for replacement therapy for the
treatment of hypothyroidism. It increases the levels of T3 and T4. Levothyroxine is also used to treat
simple goiter and chronic lymphocytic (Hashimoto's) thyroiditis.
Liothyronine (Cytomel) is a synthetic T3 that has a short half-life and duration of action; it is not
recommended for maintenance therapy. Liothyronine is better absorbed from the GI tract than
levothyroxine, and because of its rapid onset of action and short half-life, it is frequently used as the initial
therapy for treating myxedema.
Liotrix (Euthroid, Thyrolar) is a mixture of levothyroxine sodium and liothyronine sodium in a 4:1 ratio.
There is no significant advantage to the use of liotrix for treating hypothyroidism over levothyroxine
sodium used alone because levothyroxine converts T4 to T3 in the peripheral tissues.
The drug thyroid is seldom used. Some clients with hypothyroidism may benefit from this agent.
Alterations of Thyroid Function

1. Thyrotoxicosis is a general condition in which thyroid hormone (TH) levels are elevated
and produce an exaggerated physiologic response in tissues. The condition can be caused by a

the

variety of specific diseases, each of which has its own pathophysiology and course of treatment.
2. In general, hyperthyroidism has a range of endocrine, reproductive, gastrointestinal,
integumentary, and ocular manifestations. These are caused by increased circulating levels of TH
and by stimulation of the sympathetic division of the autonomic nervous system.
3. Graves disease, the most common form of hyperthyroidism, is caused by an
autoimmune mechanism that overrides normal mechanisms for control of TH secretion.
4. Manifestations of Graves disease can include symptoms of hyperthyroidism, diffuse
thyroid enlargement, disorders of the skin, and enlargement of extraoccular muscles.
5. The cutaneous manifestation of Graves disease is pretibial myxedema, a condition
characterized by subcutaneous swelling of the legs and, occasionally, the hands.
6. Ocular manifestations of Graves disease are caused by hyperactivity of the sympathetic
division of the autonomic nervous system and by immune-induced infiltration of extraoccular
muscles.
7. Toxic nodular goiter and toxic multinodular goiter occur when hyperplastic regions of
the thyroid become autonomous.
8. Toxic nodular goiters are follicular-cell adenomas that produce symptoms similar to
those of Graves disease.
9. Toxic multinodular goiters result from multiple functioning adenomas.
10. Thyrotoxic crisis is a severe form of hyperthyroidism that often is associated with
physiologic stress. Without treatment, death occurs quickly.
11. Hypothyroidism is caused by deficient production of TH by the thyroid gland. The
condition may be primary or secondary.
12. Primary hypothyroidism transiently occurs in either subacute or painless thyroiditis and
spontaneous resolution of hypothyroidism is nearly universal. Chronic lymphocytic thyroiditis, an
autoimmune disease, is associated with permanent hypothyroidism.
13. Subacute thyroiditis, a form of hypothyroidism, is a self-limited nonbacterial
inflammation of the thyroid gland. The inflammatory process damages follicular cells, causing
leakage of triiodothyronine (T3) and thyroxine (T4). Hyperthyroidism then is followed by transient
hypothyroidism, which is corrected by cellular repair and a return to normal levels in the thyroid.
14. Autoimmune thyroiditis is associated with infiltration or fibrosis of the thyroid,
circulating thyroid antibodies, and gradual loss of thyroid function. Autoimmune thyroiditis occurs in
those individuals with a genetic susceptibility to an autoimmune mechanism that causes thyroid
damage and eventual hypothyroidism.
15. Hypothyroidism also can be caused by hypothalamicpituitary dysfunction in which TRH
and TSH are not produced in sufficient amounts.
16. Thyroid carcinoma is a relatively rare cancer. The most consistent causal risk factor
associated with thyroid carcinoma is exposure to ionizing radiation, especially in childhood.
17. Hypothyroidism affects all body systems. Symptoms depend on the degree of TH
deficiency. Common manifestations include decreased energy metabolism and heat production.
18. Myxedema is the characteristic sign of hypothyroidism. Myxedema is caused by
alterations in connective tissue with water-binding proteins. The excess water leads to edema and
thickened mucous membranes.
19. Myxedema coma is a severe form of hypothyroidism, which may be life threatening
without emergency medical treatment.
20. Congenital hypothyroidism occurs with thyroid agenesis and results in hypothyroidism,
growth failure, and mental retardation from absence of thyroxine.
21. Thyroid carcinoma is probably caused by exposure to ionizing radiation
with
development of nodules and normal thyroxine levels.

Treatments
The patient with myxedema coma is frequently in both respiratory and cardiac failure and requires close
monitoring in an intensive care unit. Manifestations are those of severe hypothyroidism with an emphasis
on (1) hypothermia; (2) respiratory dysfunction related to respiratory muscle weakness (myopathy), sleep
apnea, and decreased ventilatory drive in response to hypoxia and hypercapnia; (3) reduced cardiac
output caused by bradycardia and decreased stroke volume (or overt congestive cardiac failure in patients
with underlying cardiac disease); (4) slowed drug metabolism and clearance resulting in potential drug
toxicity (e.g., digoxin toxicity); and (5) concurrent adrenal insufficiency, which may require stress doses of
glucocorticoids.

Therapy for the patient with myxedema coma includes supportive care (cardiovascular, respiratory, and
fluid balance support) and administration of thyroid hormone. Intubation and mechanical ventilation may
be necessary for patients in respiratory failure. The hypothermic patient needs to be gradually rewarmed
and additional heat loss prevented; however, rapid rewarming can cause vascular collapse. Treatment
protocols vary; options for thyroid hormone therapy include T4 and T3. Some patients with myxedema
coma may also have adrenal insufficiency; intravenous hydrocortisone in stress doses should be
maintained until the serum cortisol value is greater than 20 mcg/dl or the cosyntropin test is within
normal limits without exogenous glucocorticoids.
Nursing interventions include care of the comatose patient; surveillance of respiratory, cardiovascular, and
fluid status; care of the patient with respiratory insufficiency; preventive care for problems of immobility;
and assistance with the medical regimen.
Blood sugar-verify symptoms
Self-Monitoring of Blood Glucose
Self-monitoring of blood glucose (SMBG) can be used for monitoring blood glucose (BG) levels or
determining carbohydrate tolerance or insulin-to-carbohydrate ratio (the amount of insulin required to
cover carbohydrate intake). Recommended times to test BG levels include before meals to help determine
insulin doses with type 1 diabetes or 1 to 2 hours postprandially to determine carbohydrate tolerance with
type 2 diabetes. This is referred to as pattern management because patterns may be noted that give an
indication of when hyperglycemia or hypoglycemia may be predicted based on SMBG and food and activity
records. Self-monitoring consists of taking a drop of blood and placing it on a strip that is inserted into a
BG meter. Several types of meters are available, as are automatic lancet devices.
Typically, a meal can be expected to raise the blood sugar by 50 points. With a fasting blood sugar level of
100 mg/dL, an ideal meal should keep the blood sugar level at about 150 mg/dL approximately 1 to 2
hours after the meal. If the BG level goes higher than this, it indicates either excess carbohydrates in the
meal, per individual needs, or a need for increased medication.
The advantage of SMBG is the knowledge and flexibility it affords in diabetes management. Less
guesswork is involved, and SMBG allows the person with diabetes greater objectivity in decision making to
prevent both hyperglycemia and hypoglycemia.
Alternatives to fingersticks for BG monitoring do exist. Increasingly, persons with diabetes are using the
forearm to measure glucose levels. A continuous glucose sensor has been developed that works by having
a biosensor inserted just below the surface of the skin. Eventually this system will be designed to talk
with an insulin pump, thus serving as an artificial pancreas. Other devices and means to monitor glucose
levels are in the development stage.
Short-Term Control
HBGM is a critical component of the treatment regimen for patients with either type 1 or type 2 DM.
Glucose levels are vital signs to persons with diabetes. HBGM is the only accurate method of monitoring
glucose control on a daily basis and allows the person with diabetes to make any necessary changes in the
diabetes regimen. Results should be recorded in a logbook. Minimally, nonpregnant individuals with type 1
DM should perform HBGM before meals and at bedtime. Patients using an insulin pump perform HBGM up
to 12 or more times per day. The frequency of HBGM in type 2 DM patients is determined by the
treatment regimen and varies from once to several times per day. Postprandial HBGM is critical even in the
diabetic patient with a normal HbA1c. Approximately 50% of persons with diabetes who have a normal
HbA1c have a 2-hour postprandial glucose level in excess of 200 mg/dl. The higher the HbA 1c, the more
likely it is that a patient will have an elevated postprandial glucose level. Unfortunately, according to
Healthy People 2010, only 42% of persons with diabetes 18 years of age or older perform HBGM at least
once daily.[101,108] A recent study demonstrated that the provision of free glucose monitoring supplies by a
health maintenance organization to enrollees with DM improved the frequency of HBGM, medication
compliance, and glycemic control
HBGM uses capillary whole blood obtained by a fingerstick and correlates well with laboratory values when

accurate techniques are used. Plasma glucose values are approximately 10% higher than whole blood
values (see Guidelines for Safe Practice box). The majority of available glucose meters use a no blot
techniquethe user does not blot or wipe the blood off the test strip. The user inserts a test strip into the
meter and applies a drop of capillary blood to the strip, which is impregnated with either glucose oxidase
or another chemical. A chemical reaction occurs, and the meter displays the result. Test time varies among
manufacturers, ranging from 5 to 45 seconds. All marketed glucose meters must be approved by the FDA
and yield accurate results when proper technique is used. Meters must be calibrated to each test strip lot
according to manufacturers' specifications. The most common source of errors in HBGM results is user
technique, followed by problems with the test strips. Because a chemical is embedded in the test strip,
any factors that can affect the chemical (light, heat, cold, humidity) will alter the result. Use of control
solution is the only way to test the accuracy of the strips. Control solution, produced by the meter's
manufacturer, is glucose solution in a known concentration that yields a standard result. Unfortunately,
control solution is often not readily available in pharmacies and is an additional cost to the individual, the
insurance company, or both.
Alternate site testing (the use of anatomic sites other than the fingertips) is FDA approved for certain
blood glucose meters. Blood glucose results from alternate site testing do not correlate with fingerstick
blood glucose results when blood glucose levels are rapidly changing, such as postprandially and when the
patient is hypoglycemic. Therefore patients should always monitor blood glucose via a fingerstick
postprandially or if they suspect hypoglycemia. Alternate site testing can be accurately used in the fasting
and premeal states.[30,54,57] Many patients have difficulty obtaining an adequately sized sample from
alternate sites, most commonly the forearm. Additionally, because a larger aperture in the lancing device
is needed to obtain an alternate site sample, and pressure is placed on the anatomic site, areas of skin
puncture and erythema can develop, which can be cosmetically displeasing.
A continuous glucose monitoring system, the Medtronic CGMS System Gold, measures interstitial glucose
every 5 minutes for 72 hours. The system consists of a sensor that is inserted subcutaneously in the
abdomen and a reading device that is worn at the waist. Fingerstick blood glucose levels are used to
calibrate the device before use and then at least four times daily to provide reference points for
comparison. To obtain the most valuable data analysis, the patient should also enter into the system meal
times, exercise, etc. The system does not provide a real-time display of blood glucose levels; data are
downloaded to a computer and then retrospectively analyzed. The CGMS System Gold is currently not
available for purchase and daily use by individuals with diabetes. Another system, the GlucoWatch G2
Biographer, monitors interstitial blood glucose levels. The watchlike device uses alkaline batteries to create
a low electrical current that wicks interstitial fluid into sensors on the underside of the device. Skipped
readings are common because of glitches such as the device being bumped, excessive perspiration, or
rapid temperature changes. The displayed readings are approximately 17 minutes behind capillary
readings because of the delay in compartmentalization of glucose. Mild to moderate skin irritation occurs
as a result of the wicking process. The GlucoWatch G2 Biographer is FDA approved for trend detection in
glucose levels, not to replace HBGM. Fingerstick blood glucose readings must be done every 12 hours to
calibrate a new sensor, and should be done anytime medication is taken or hypoglycemia is suspected,
since the GlucoWatch is not FDA approved for adjusting doses. The GlucoWatch G2 biographer retails for
approximately $875, with the disposable autosensors costing about $150 for 16 autosensors.
Signs, Symptoms, and Management of Hypoglycemia
Individuals with hypoglycemia may begin to perspire; they may experience hunger and nervousness; their
skin may become pale, cold, and clammy; and they may experience mental confusion, physical tremors,
weakness, headache, rapid heartbeat, numbness in the tongue, and double or blurred vision.
Hypoglycemia also alters mood states. Irritability is well known to occur with the combination of stress
and hypoglycemia.
When symptoms of hypoglycemia are noted, the blood sugar level should be checked to verify
hypoglycemia. However, not all individuals with diabetes experience these symptoms, especially children,
elderly persons, and persons who have frequent episodes of hypoglycemia. The last situation can be
resolved by meticulous prevention of hypoglycemia for at least 2 weeks. The health professional or close
family member should suspect hypoglycemia, and treat it accordingly, when a child with diabetes becomes
unusually quiet or fretful or when the older adult with diabetes becomes weak or faint. A physician should
be consulted if the cause is not readily apparent or if hypoglycemia occurs frequently.

The treatment for a person who can swallow is to give 15 g of a rapid-acting carbohydrate source, such as
4 oz of orange juice, 4 teaspoons of sugar mixed in water, or three or four glucose tablets. Liquid sources
of sugar will correct hypoglycemia the most quickly. The carbohydrate has to get through the stomach
before it can significantly affect blood sugar levels. The blood sugar should be rechecked in 15 minutes,
and the procedure repeated until the blood sugar returns to normal. This is referred to as the 15:15 rule.
For severe hypoglycemia, the amount of carbohydrate may be increased to 30 g because every 15 g of
carbohydrate raises the BG level by only 50 points (mg/dL). Squeezing cake icing or honey inside the
cheek is appropriate only if the person is alert enough to swallow.
A person may or may not need a follow-up snack to maintain glucose levels in the normal range after
hypoglycemia has been corrected with the 15:15 rule. With experience in using SMBG, a person may
better gauge the necessity of having a snack. As a general guideline, if the next meal will be several hours
later, such as in the middle of the night, it may be beneficial to have a more substantial snack (e.g., half a
sandwich). A bedtime snack containing carbohydrates for a person using insulin is advised if the BG level
is less than 100 mg/dL.
If the person becomes unconscious, glucagon can be injected or an intravenous solution of glucose may be
administered in the hospital or ambulance setting. Long-term treatment includes diet, activity, insulin
modification (the lists on page 265 show factors that raise or lower blood sugar levels), or education to
help prevent future episodes. Hypoglycemia can result in a severe headache, sometimes referred to as a
diabetic headache.
Hypoglycemia
Hypoglycemia (blood glucose < 50 mg/dl) occurs when insulin levels exceed insulin needs. A major cause
of insulin excess is overdose. Imbalance between insulin levels and insulin needs can also result from
reduced intake of food, vomiting and diarrhea (which reduce absorption of nutrients), excessive
consumption of alcohol (which promotes hypoglycemia), unaccustomed exercise (which promotes glucose
uptake and utilization), and parturition (which reduces insulin requirements).
Diabetic patients and their families should be familiar with the signs and symptoms of hypoglycemia.
Some symptoms result from activation of the sympathetic nervous system, whereas others arise from the
central nervous system (CNS). When glucose levels fall rapidly, activation of the sympathetic nervous
system occurs, resulting in tachycardia, palpitations, sweating, and nervousness. However, if glucose
declines gradually, symptoms may be limited to those of CNS origin. Mild CNS symptoms include
headache, confusion, drowsiness, and fatigue. If hypoglycemia is severe, convulsions, coma, and death
may follow.
Rapid treatment of hypoglycemia is mandatory; if hypoglycemia is allowed to persist, irreversible brain
damage or even death may result. In conscious patients, glucose levels can be restored with a fast-acting
oral sugar (e.g., glucose tablets, orange juice, sugar cubes, honey, corn syrup, nondiet soda). However, if
the swallowing reflex or the gag reflex is suppressed, nothing should be administered by mouth. In cases
of severe hypoglycemia, IV glucose is the preferred therapy. Parenteral glucagon is an alternative method
of treatment. (The pharmacology of glucagon is discussed at the end of the chapter.)
In anticipation of hypoglycemic episodes, diabetic patients should always have an oral carbohydrate
available (e.g., Life Savers, candy, glucose tablets, sugar cubes). Many physicians recommend that
patients keep glucagon on hand as well. Patients should carry some sort of identification (e.g., Medic Alert
bracelet) to inform emergency personnel of their condition.
In some patients, hypoglycemia occurs without producing the symptoms noted above. As a result, the
patient remains unaware of hypoglycemia until blood sugar has become dangerously low. Hypoglycemia
unawareness is a particular problem among patients practicing tight glucose control. The risk of dangerous
hypoglycemia can be minimized by frequently monitoring blood glucose.
Severe hypoglycemia and diabetic ketoacidosis (see below) can both produce coma. Of the two causes,
hypoglycemia is the more common. Since treatment of these two conditions is very different
(hypoglycemia involves withholding insulin, whereas ketoacidosis requires giving insulin), it is essential
that coma from these causes be differentiated. The most definitive diagnosis is made by measuring

plasma or urinary glucose levels: in hypoglycemic coma, glucose levels are very low; in ketoacidosis,
glucose levels are very high.
Other Complications
Lipodystrophies.
Altered deposition of subcutaneous fat (lipodystrophy) can occur at sites of insulin injection. Two types of
change may be seen: (1) lipoatrophy (loss of subcutaneous fat), and (2) lipohypertrophy (accumulation of
subcutaneous fat).
Lipoatrophy produces a depression in the skin at the site of insulin injection. The cause of atrophy appears
to be immunologic. Accordingly, fat atrophy is most likely with use of insulin preparations that have a high
concentration of antigenic contaminants. Because the insulin preparations in use today are much purer
than those used in the past, lipoatrophy is now rare. When lipoatrophy occurs, subcutaneous fat can often
be restored by injecting a highly purified insulin preparation (e.g., human insulin) directly into the site of
fat loss. Some improvement can be seen in 4 weeks, but full recovery can take 3 to 6 months.
Lipohypertrophy occurs at sites of frequent insulin injection. Fat accumulates because insulin stimulates
fat synthesis. When use of the site is discontinued, excess fat is eventually lost. Lipohypertrophy can be
minimized through systematic rotation of injection sites.
Allergic Reactions.
Insulin injection can produce local and systemic allergic responses. Fortunately, allergic reactions are rare.
With local reactions, the injection site becomes red and hardened. These reactions are usually delayed,
taking several hours to develop. Local reactions occur in response to a contaminant in the insulin
preparationnot to the insulin itself. Because insulins in use today are highly purified, local reactions are
uncommon.
Systemic reactions take place rapidly, and are characterized by the widespread appearance of red and
intensely itchy welts. Breathing difficulty may develop. Systemic reactions occur in response to insulin
itself, not to a contaminant. Beef insulin, which differs from human insulin by three amino acids, is the
most frequent cause of systemic allergy. Generalized reactions are least likely with pork and human
insulins. If severe allergy develops in a patient who nonetheless must continue insulin use, a
desensitization procedure can be performed. This process entails giving small initial doses of purified pork
or human insulin, followed by a series of progressively larger doses.
WHAT IS THE ROLE OF HYPERINSULINEMIA IN THE INSULIN RESISTANCE SYNDROME?
A person with a genetic predisposition to insulin resistance tends to have an altered insulin response. With
insulin resistance there is often a delayed production of meal-related insulin. This can result in a transient
state of hyperglycemia (high levels of blood glucose). When the body does respond to the
hyperglycemia, it is often with excess insulin production over a prolonged period. Persons with insulin
resistance have been noted to produce up to 10 times the amount of insulin to control blood glucose levels
as compared with other insulin-sensitive individuals. This hyperinsulinemia can result in symptoms of
hypoglycemia (low levels of blood glucose) if meals are delayed.
The symptoms of reactive hypoglycemia are common among persons with insulin resistance, but medically
the condition is rarely diagnosed. The blood glucose criteria for diagnosis of reactive hypoglycemia are
more stringent than for persons with diabetes on medication. Physicians generally will not make the
diagnosis unless blood glucose levels are below 50 mg/dL. Symptoms of hypoglycemia, however, may
occur years before the onset of diabetes and are likely because of hyperinsulinemia and excess release of
counterregulatory hormones.
Counterregulatory hormones correct hypoglycemia by causing the liver to release its stored sugar, called
glycogen. The symptoms that occur because of these hormones, however, can be unpleasant. Altered
glucagon (a counterregulatory hormone that is the first one produced in response to low levels of blood
glucose) secretion has been noted in reactive hypoglycemia. Glucagon in excess leads to feelings of
nausea. Glucagon release is inhibited with hyperinsulinemia. It may be for this reason that persons with
insulin resistance experience the symptoms of hypoglycemia as the body needs to release other
counterregulatory hormones such as adrenalin (epinephrine). Adrenalin causes an increased heart rate

and physical tremors, which is an unpleasant and potentially frightening experience if the person has not
associated it with the need to eat a carbohydrate source.
The symptoms of hypoglycemia do affect the quality of life. However, most persons with hypoglycemia
symptoms are not in an immediate health emergency. Severe hypoglycemia requiring medical assistance
is usually limited to persons taking insulin or insulin-stimulating medications such as the sulfonylurea
medications.
Hyperinsulinemia is found with central obesity. It is still, however, a bit of a chicken-and-egg question.
Which came first? Hyperinsulinemia and central obesity are known to worsen insulin resistance. However,
it may be that the genetic predisposition to insulin resistance is what first sets up excess production of
insulin in relation to carbohydrate intake. Some health care professionals suggest that hyperinsulinemia
encourages the gain of abdominal weight in the first place. This is the basis of the low-carbohydrate diets.
Within a group of obese children, 40% were found to have hyperinsulinemia, and over 10% had impaired
glucose tolerance as based on an OGTT. About one third of obese children had dyslipidemia (disordered
fats in the blood; generally referring to elevated triglycerides and low levels of HDL-C) and hypertension.
The metabolic syndrome was found in 30% of children under 12 years of age (Viner et al., 2005).
With regard to dyslipidemia, it has been clearly shown that the enzyme lipoprotein lipase (an enzyme
that helps the breakdown of triglycerides) is altered in the presence of hyperinsulinemia. This results in
reduced breakdown of triglycerides, leading to high serum triglyceride levels. Thus elevated triglyceride
levels in the blood are generally associated with hyperinsulinemia, especially if the person also has central
obesity. This occurs even in childhood, with triglyceride levels correlating with insulin levels in children
(Reinehr et al., 2005). Reduction in hyperinsulinemia generally improves dyslipidemia. One study showed
that an intake of 250 mg EPA/DHA omega-3 fats for only 6 weeks significantly decreased both fasting and
postprandial triglyceride levels (Brady et al., 2004).
Hypertension is now a well-recognized aspect of insulin resistance and the metabolic syndrome. There are
still unanswered questions regarding the specific mechanism related to hypertension and the underlying
cause of insulin resistance. The role of hyperinsulinemia is being suggested as the link, as a result of
altered vasodilation. Therefore advice to follow a low-glycemic index diet may contribute to management
of hypertension (Kopp, 2005). A person with central obesity and hypertension likely has insulin resistance.
Hyperinsulinemia is now believed to be related to early heart disease, because of the incidence of heart
disease occurring before the diagnosis of diabetes. It is well known that diabetes is associated with
increased risk of atherosclerosis.
Type 2 diabetes is described as a relative insufficiency of insulin production. Hyperinsulinemia is usually
present with type 2 diabetes; there just is not enough insulin for the demand or to overcome severe
insulin resistance at the cellular level. However, hyperinsulinemia can worsen insulin resistance, making it
more difficult for the body to regulate blood glucose levels.
Certain cancers are found with the metabolic syndrome. Middle-aged men with the metabolic syndrome
were found to be more likely to develop prostate cancer (Laukkanen et al., 2004). Excess weight in
women is found with hyperinsulinemia, low HDL-C, increased levels of estrogen, and breast cancer
(Furberg et al., 2005).