Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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CARE OF THE ELDERLY PATIENT

447

failure in this population, intravenous fluid administration

must be individualized and approached cautiously.

As stated earlier, aging is associated with a change in body

composition with increase in fat content and a concurrent

decrease in muscle mass and total body water. Decrease in

muscle mass and a reduction in physical activity result in a

fall in total energy expenditure with increasing age. Energy

requirements may decrease by about a third between the ages

of 30 and 80 years. However, during periods of stress such as

trauma, surgery, or infection, daily energy requirements may

be more than doubled. In addition to the total energy intake,

attention should be paid to macronutrient and micronutri-

ent requirements.

The elderly are particularly vulnerable to malnutrition.

The reported incidence of malnutrition in elderly hospital-

ized patients varies from 17% to 65%. As the duration of

hospital stay increases, the likelihood of malnutrition rises.

In the elderly, a functional nutritional assessment should

include evaluation of sight, taste, smell, dentition, degree of

cognitive impairment, presence of depression, swallowing

abnormalities, respiratory dysfunction, hand-to-mouth coor-

dination, level of assistance required at meals, and perhaps

drug-appetite and drug-nutrient interactions.

Whenever possible, feeding should be started as soon as

possible in hospitalized or postoperative elderly patients. The

enteral route is greatly preferred, but parenteral nutritional

support can be used, if needed. Increased mortality occurs in

underweight people, but mortality is not clearly increased in

overweight elderly patients.

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Special Considerations

The current disease-oriented model of acute medical care

promotes a sequential approach to diagnosis and treatment

that generally ignores the practice of restorative care until

after the patient is discharged from the hospital. In the frail

elderly, this approach may lead to a decline in functional

abilities despite effective treatment of acute medical illnesses.

The high rate of delirium and psychological decompensa-

tion in the acutely hospitalized elderly may lead to excessive

bed rest with accompanying loss of mobility, muscle atrophy,

contractures, pressure sores, greater tendency to fall, throm-

boembolism, incontinence, anorexia, constipation, and lack

of motivation. This has been called the “cascade of illness and

functional decline.”

Since the physiologic characteristics of the aging popula-

tion include both a decreased functional reserve and large

individual variation, medical management should be indi-

vidualized with the focus on maintenance of functional sta-

tus, protection from the hazards of immobility, and low risk

of complications from treatment.

Delirium

Approximately one-third to one-half of elderly patients will

have a delirious episode during the course of hospitalization

for medical or surgical care. It can be as high as 70% in ICUs.

Delirium is often unrecognized and is associated with pro-

longed hospitalization, greater need for nursing home place-

ment, and increased mortality. The presence of altered level

of consciousness, easy distractibility, rambling conversation,

illogical flow of ideas, unpredictable switching from subject

to subject, perceptual disturbances, and psychomotor agita-

tion or retardation should clue the clinician to the diagnosis

of delirium. Risk factors are listed in Table 19–3. Prior cog-

nitive impairment is the most frequent independent risk

factor for delirium. Other factors that predispose to the

development of delirium include unfamiliar surroundings,

social isolation, structural brain disease, concurrent chronic

illness, sleep deprivation, and alcohol or drug abuse. Delirium

could be the presenting symptom of a variety of illnesses

(Table 19–4). Early diagnosis is important because most

patients can recover if the underlying cause is recognized and

treated. The use of sedatives, psychotropic drugs, or physical

restraints to treat delirium could worsen the existing situa-

tion, placing the patient at higher risk for aspiration pneu-

monia, pressure ulcers, and other immobility-related

complications (cascade effect).

Prior cognitive impairment

Fracture on admission

Age over 80 years

Infection

Male sex

Impaired activities of daily living (ADLs)

Sensory impairment (blindness, deafness)

Polypharmacy (psychoactives, anticholinergics etc.)

Dehydration

Immobility

Bladder catheters

Table 19–3. Risk factors for delirium.

Decreased cardiac output Fecal impaction

Congestive heart failure Hypothermia and hyperthermia

Acute myocardial infarction Metabolic disorders

Acute blood loss Electrolyte abnormalities

Dehydration Acid-based disturbances

Infections Hypoxia

Fractures Hypercapnia

Stroke Hypoglycemia and hyperglycemia

Poorly controlled pain Azotemia

Drugs Transfer to unfamiliar surroundings

Urinary retention

Table 19–4. Common causes of delirium.

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CHAPTER 19

448

The DSM-IV criteria for diagnosis of delirium include

the following: (1) disturbances of consciousness (ie, reduced

clarity of awareness of the environment) in conjunction with

reduced ability to focus, sustain, or shift attention, (2) a

change in cognition (such as memory deficit, disorientation,

or language disturbance) or the development of a perceptual

disturbance that is not better accounted for by a preexisting,

established, or evolving dementia, (3) development of the

disturbance during a brief period (usually hours to days) and

a tendency for fluctuation during the course of the day, and

(4) evidence from the history, physical examination, or labo-

ratory findings that the disturbance is caused by a general

medical condition. The Confusion Assessment Method is a

validated tool to assess delirium. With appropriate training,

it can achieve more than 95% sensitivity and specificity in

the diagnosis of delirium, even in groups with a high preva-

lence of dementia. In contrast with dementia, delirium gen-

erally has an abrupt onset, disturbance of consciousness,

fluctuations during the course of the day, and frequently, an

identifiable and potentially reversible cause.

The decreased attention span seen in delirium can be

assessed by several bedside tests. A simple test is the A test, in

which the interviewer vocalizes letters at a rate of one per

second, and the patient indicates by a sign every time the let-

ter A is mentioned. In the one-tap, two-taps test, the patient is

instructed to tap twice each time the interviewer taps once

and vice versa. More complex tests include spelling the word

world backward or subtracting 7 from 100 each time until 72

is reached (ie, 100, 93, 86, 79, 72). These tests are often abnor-

mal in patients with delirium.

Delirium is indicative of diffuse brain dysfunction and

has been associated with four classes of diseases: (1) primary

cerebral diseases, such as CNS infections, brain tumors, and

stroke, (2) systemic illnesses that secondarily affect brain

function, including cardiac disease, pulmonary failure,

hepatic dysfunction, uremia, deficiency states, anemia,

endocrine disturbances, systemic infections, and inflamma-

tory diseases, (3) intoxication with exogenous substances (eg,

alcohol, illicit drugs, prescribed medications, and industrial

toxins), and (4) withdrawal from dependency-producing

agents (eg, alcohol, barbiturates, and benzodiazepines).

The approach to patients with delirium includes a

focused history and physical examination, review of medica-

tions, and basic laboratory studies such as complete blood

count, serum electrolytes, serum urea nitrogen, glucose, and

urinalysis. Further specialized tests can be done in individual

patients. These include chest radiography, electrocardiogra-

phy, pulse oximetry, selected drug levels, selected cultures,

vitamin B

level, thyroid function tests, brain imaging, lum-

bar puncture, and electroencephalography.

Treatment of delirium should include identification and

treatment of the underlying cause and review of the medica-

tion regimen. Neuroleptics, opioids, or any medication with

high anticholinergic or sedative side effects should be discon-

tinued or reduced in dosage whenever possible. When avail-

able, constant observation is preferable to restraints. A

well-lighted and predictable environment, use of eyeglasses

and hearing aids, frequent reorientation by family and care-

givers, simple explanations of any procedure or confusing

stimuli, encouragement to stay awake during the daytime, and

nursing routines that permit uninterrupted nighttime sleep

are all valuable in the management of delirium. Finally, it may

be necessary to treat agitated behavior with medication.

Generally, the lowest effective doses of one of the atypical

antipsychotics (eg, risperidone or olanzapine) should be used

because of the low incidence of extrapyramidal side effects.

Complete resolution of symptoms can take days to months.

Communicating with the Elderly Patient

Many elderly patients have hearing and vision problems that

interfere with communication and cause difficulty in orien-

tation and adaptation to a new environment. Being able to

see and hear properly becomes critical when one must cope

with new experiences such as ventilatory support devices and

other invasive interventions.

Communication problems generate great anxiety in the

patient and frustration in the caregiver. There is a risk of mis-

labeling the patient as “confused” and disregarding the patient’s

role as a participant in health care decisions. The elderly patient

who reacts to an unfamiliar situation by becoming “agitated” is

at risk for the use of physical restraints or psychotropic medica-

tions. This causes worsening of the clinical status and may lead

to the cascade effect described earlier. The importance of efforts

to maximize communication with the elderly individual thus is

emphasized, especially in the ICU setting.

Adequate vision makes communication easier, especially

for those who have impaired hearing or comprehension. Eye

contact helps the caregiver to assess the extent to which the

older person hears and understands what is being said. If the

patient wears glasses, they should be clean and within reach

of the patient. The head of the bed should be elevated so that

the patient can see the speaker’s lips and eyes. A glare-free

light source coming from behind the patient helps the

patient to see the face and lips of the speaker. If the patient

has a hearing impairment, background noise should be

reduced by turning the television or radio off, by closing the

door, and by asking others in the area to be quiet. The

speaker should lean forward so that the lips can be seen, but

shouting should be avoided. Most elderly people suffer from

a selective high-frequency hearing loss with decreased ability

to identify high-frequency tones and pitches in the conso-

nants s, f, t, hard g, and j. Increasing the volume of sound is

of little help, and shouting may be misinterpreted as hostility

or anger. The manner of speaking should be natural and not

distorted by exaggerated lip movements. When it is necessary

to repeat a comment or question, it is better to rephrase than

to say the same thing in a louder voice. If the patient has a

hearing aid, it should be properly in place and in good work-

ing condition. Older people are often not aware of their hear-

ing inadequacies, and their perceptions of what they have

heard may not be accurate. Therefore, an attempt should be

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CARE OF THE ELDERLY PATIENT

449

made to determine whether the patient has properly inter-

preted what has been communicated.

Health care personnel and family members should not

whisper or speak together in low tones near a hearing-

impaired older adult. A few words may be heard that will

result in misinterpretation, increasing the possibility of

unwarranted fears, paranoid behavior, or hostility. Glasses

and hearing aids should be worn consistently during the day.

If the patient is able to talk, dentures should be in place to

facilitate clear speech.

Immobility

Elderly patients are particularly vulnerable to the untoward

effects of immobility. Contractures, pressure ulcers, and

deconditioning can develop rapidly. Some of the other con-

sequences of immobility include muscle atrophy, deep

venous thrombosis, increased calcium mobilization from

bone, atelectasis, hypostatic pneumonia, constipation, func-

tional fecal and urinary incontinence, and loss of motivation.

Pressure ulcers are a common and frequent complication

of immobility. Any disease process leading to immobility

(eg, severe congestive heart failure, respiratory failure, delir-

ium, fractures, complicated postoperative course, or spinal

cord injury) places the elderly patient at high risk for devel-

opment of a pressure ulcer. Sites commonly involved are the

sacrum, ischial tuberosities, hip, heel, elbow, knee, ankle, and

occiput. More than 50% of pressure ulcers occur in persons

over age 70. Their prevalence among patients expected to be

confined to a bed or a chair for at least 1 week is as high as

28%. Pressure ulcers generally occur within the first 2 weeks

of hospitalization. Moreover, the development of pressure

sores has prognostic implications; the mortality rate among

those who develop pressure ulcers during the first 2 weeks has

been as high as 73%. Sepsis is the most serious complication

of pressure ulcers. Among bacteremic patients with a pres-

sure ulcer as the probable source of infection, the in-hospital

mortality rate can be as high as 60%.

Frequent repositioning (whether supine or in the sitting

position) has been the primary method of preventing pres-

sure ulcers. The evidence of structural changes in experimen-

tal animal models has led to the recommendation for

repositioning every 2 hours. Repositioning should be per-

formed so that a person at risk is positioned without pressure

on vulnerable bony prominences. This is accomplished in

practice by positioning patients horizontally with the

back resting partially over pillows that maintain the body at

a 30-degree angle to the support surface. Additional pillows

between the legs and supporting the arms will aid in main-

taining optimal positioning. A person with limited ability to

change position who must sit in a chair or have the head of

the bed elevated should not remain in this position for more

than 2 hours at a time. To diminish the shearing forces over

the sacral area, the head of the bed should not be elevated

more than 30 degrees. Particulate matter (eg, food crumbs)

should be removed from the bed. Sheets should be loose, and

tucking of the sheet at the foot of the bed should be avoided

so that movement is not restricted and the feet can assume

their natural position. Heels and elbows should be protected

by raising them with pillows to avoid direct pressure over

bony prominences. Patients should be lifted, not dragged.

The skin should be patted dry, not rubbed. Moisture control

depends on timely skin care. The evaluation and manage-

ment of urinary and fecal incontinence are of crucial impor-

tance in these patients.

In high-risk patients, pressure-relieving devices such as

constant low-pressure supports, alternating-pressure sup-

ports, or pressure-relieving cushions may be needed.

Attention also should be directed toward proper nutrition,

hydration, and pain control.

Educational programs aimed at physicians, nurses, and

other caregivers; family members; and the patients them-

selves have beneficial results. One study found that when

physicians ordered preventive measures for high-risk

patients, the incidence of pressure ulcers was half that for

patients for whom such orders were not written.

Bed rest also results in immobility and loss of weight-

bearing forces on joints. These effects cause changes in peri-

articular and articular structures that result in joint

contractures and changes similar to those of osteoarthritis.

Changes in periarticular tissues occur within days. Muscles

that bridge the immobilized joint shorten. These changes

produce decreased range of motion that can be permanent,

depending on the length of immobilization.

Bed rest is accompanied by progressive cardiovascular

deconditioning with exaggeration of the hemodynamic

changes normally seen with standing, as manifested by

orthostatic intolerance and decreased exercise tolerance.

Although orthostatic hypotension is not always documented,

signs and symptoms of orthostatic intolerance such as tachy-

cardia, nausea, diaphoresis, and syncope are common after

prolonged bed rest. A decrease in coordination, as measured

by pattern tracing and a marked increase in body sway in a

standing position, has been documented after several weeks

of bed rest.

The rate of decrease in muscular strength may be as high

as 5% per day and varies with the degree of immobility. Leg

muscles tend to lose strength about twice as fast as arm mus-

cles. For some elderly patients who normally use 100% of

their quadriceps muscle strength just to stand up, a loss of 5%

per day results in significant loss of function in a short time.

Given the numerous complications resulting from immo-

bility, early mobilization of the elderly patient in the ICU set-

ting should be a high priority. The rate of loss of muscle

strength will slow when active contraction of muscles is

encouraged, particularly if resistance is added. Simple

devices such as elastic fabrics (Theraband) make exercise

against resistance available for patients in beds or chairs.

Active movement in bed and full range-of-motion exercises

should be encouraged in alert patients. For other patients,

passive full range of motion should be done on every nurs-

ing shift.

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450

Intermittent sitting—and standing when possible—will

reduce the frequency of orthostatic hypotension. The sitting

position also improves oxygenation and diminishes cardiac

work because cardiac output and stroke volume decrease in the

sitting position. Finally, rehabilitation service consultation may

be useful in the management of elderly patients in the ICU.

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451

0020

Critical Care of the

Oncology Patient

∗

Darrell W. Harrington, MD

Darryl Y. Sue, MD

Several complications of cancer may require critical care for

palliative management. These include (1) acute CNS disor-

ders (eg, spinal cord compression and increased intracranial

pressure), (2) severe metabolic disorders (eg, hypercalcemia,

hypocalcemia, tumor lysis syndrome, hyponatremia, hyper-

glycemia, hypoglycemia, and hypokalemia with ectopic

adrenocorticotropic hormone [ACTH] production),

(3) orthopedic disorders (eg, pathologic fracture), (4) uro-

logic disorders (eg, hematuria, hemorrhagic cystitis, and

acute obstructive uropathy), (5) general surgical disorders

(eg, GI bleeding, bowel perforation, bowel obstruction,

extrahepatic biliary obstruction, and intraabdominal abscess

formation), (6) malignant effusions (eg, pericardial effusion

with cardiac tamponade and pleural effusion with lung

compression), (7) complications of chemo- and radiother-

apy, and rarely, (8) superior vena cava syndrome. CNS disor-

ders, metabolic disorders, and superior vena cava syndrome

are addressed in this chapter.

CENTRAL NERVOUS SYSTEM DISORDERS



Spinal Cord Compression

ESSENTIALS OF DIAGNOSIS

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Axial (back) pain that may radiate to arms or legs or

bandlike discomfort around the chest.



History of malignancy (may be initial presentation of

cancer).



Neurologic deficits (ie, motor, sensory, or autonomic).



Abnormal images of spine: MRI (preferred), plain x-rays,

CT scan, CT or planar myelography.

General Considerations

Spinal cord compression from epidural metastases is a

potentially devastating complication in cancer patients. It

occurs in about 5% of cancer deaths and therefore will

develop in about 25,000 of the annual 500,000 cancer deaths.

The most common primary tumors that cause spinal cord

compression are cancers of the lung, breast, and prostate;

lymphomas; and multiple myeloma. Cord compression also

can be seen in patients with leukemia (chloroma) and a wide

range of other solid tumors. It may present as the first and

only manifestation of cancer, but it is postulated that pro-

longed survival from initial diagnosis of cancer will increase

the incidence of spinal cord compression.

Epidural spinal cord compression develops via two mecha-

nisms: (1) by metastatic spread to the vertebral bodies, from

where the tumor expands and erodes into the epidural space,

and (2) by cancerous involvement of the paravertebral region

with extension into the epidural space through the interverte-

bral foramina. Bone scans and spine x-rays may be normal in

the latter cases but usually are abnormal in the former. Vertebral

body metastases account for epidural spinal cord compression

in approximately 85% of patients with solid tumors and 25% of

patients with lymphomas. In the 70% of cancer patients with

metastases at death, metastases to the spine are found in 40%.

Epidural metastases extend from the paravertebral region in the

remainder. In addition to spinal cord compression, sudden irre-

versible spinal dysfunction may occur from vascular compro-

mise, resulting in spinal cord infarction.

The thoracic spine occupies 47% of the total length of the

spine but is the affected area in approximately 70% of

patients, the lumbar spine occupies 30% and is affected in

20%, and the cervical region occupies 22% and is affected in

10% of patients. Spinal cord involvement may occur at mul-

tiple levels in 10–38% of patients. The greater chance of tho-

racic spine involvement may be related to the presence of

physiologic kyphosis and the narrower spinal canal in this

region. Metastases never traverse the intervertebral disks and

rarely traverse the dura.

∗

Darrell W. Harrington, MD, and Hassan J. Tabbarah, MD, were the

authors of this chapter in the second edition.

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CHAPTER 20

452

Clinical Features

A. Symptoms and Signs—The clinical presentation of

epidural spinal cord compression is well known and depends

on the level of spinal involvement. Axial pain is the most

common presenting symptom (prodromal phase), occurring

in 95% of adults and 80% of children with epidural spinal

cord compression. Therefore, spinal cord compression

should be considered in any patient with cancer and axial

pain. The local pain corresponds to the site of the lesions and

is described as dull and aching. Tenderness over the affected

spinal element is usually readily elicited. Approximately 15%

of patients will develop paraplegia despite a long duration of

painful symptoms (compressive phase), because spinal cord

compression was not anticipated. Pain may persist for several

weeks or months before symptoms of radiculopathy are

manifested. Cervical or lumbar disease usually but not

always presents as unilateral radiculopathy, whereas thoracic

disease produces bilateral symptoms resulting in a bandlike

distribution of pain. Radicular pain may be accompanied by

sensory or motor loss, as determined by the involved nerve

root, and may be easily confused with disk herniation. Pain is

usually worse at night and is aggravated by movement,

coughing, or the Valsalva maneuver. Because midthoracic

back pain is less likely to be due to benign causes, any patient

localizing pain and tenderness to this area regardless of a his-

tory of malignancy should be evaluated carefully.

Neurologic deficits seen in spinal cord compression usu-

ally begin with motor impairment. These are seen more com-

monly in the distal part of the body or the lower extremities

owing to the greater frequency of thoracic and lumbar spine

involvement. Anterior spinal cord compression is more com-

mon than posterior involvement. Accordingly, patients usu-

ally have more motor than sensory disability, at least in the

early stages. Sensory impairment follows, parallels the devel-

opment of motor deficit, and is present in half of patients at

the time of diagnosis of spinal cord compression. Autonomic

dysfunction occurs later and is present in half of cases.

The neurologic deficit is caused either by mechanical

compression by the tumor on the spinal cord or cauda

equina or by destruction of a vertebral body sufficient to

make it collapse and compress the spinal cord. Once spinal

cord compression occurs, progression may be very rapid.

Therefore, the presence of myelopathy is a neurologic emer-

gency. Disease presentation and progression depend on the

level of spinal involvement. For example, high cervical cord

lesions (C3–5) may be life-threatening because both quadri-

plegia and respiratory muscle impairment are common fea-

tures. Involvement of the thoracic cord typically is

characterized by identification of a sensory level on the

trunk. In addition, lower extremity weakness and autonomic

dysfunction may accompany thoracic cord compression. The

specific site of lumbosacral spinal cord compression is less

easily determined by physical examination. Patients may

present with radiculopathy and loss of associated reflexes or

with isolated autonomic dysfunction as seen in the conus

syndrome. It is important that each patient have a complete

neurologic examination, paying close attention to subtle

asymmetries in muscle strength and reflexes. It is important

to note that patellar and ankle reflexes provide information

only about L4 and S1 nerve roots, respectively. Therefore,

normal reflexes of the lower extremity should not be used to

exclude the presence of significant myelopathy.

B. Laboratory Findings—A histologic diagnosis of malig-

nancy is rarely necessary in a patient with a known preexist-

ing malignancy. However, it is prudent to specifically identify

malignancy causing spinal cord compression in an individual

without an underlying history of cancer. This is so because

localized infection causing spinal cord compression may

mimic malignancy. In the presence of complete blockage of

the spinal canal and to avoid worsening of neurologic status,

only a few drops of cerebrospinal fluid (CSF) should be

removed and sent for cytologic examination and protein

determination. Additional studies are sent to exclude infec-

tion. Lumbar puncture otherwise should be reserved for

patients suspected of concomitant leptomeningeal dissemi-

nation of tumor. CSF may have elevated protein, normal or

low glucose, and a lymphocytic pleocytosis.

C. Imaging Studies—MRI is the diagnostic study of choice

to evaluate spinal cord compression, but plain x-rays of the

involved area and planar or CT myelography are potentially

useful or necessary (especially if MRI is unavailable or cannot

be performed). It is critical that imaging should be acquired

as early as possible and should not be delayed more than a few

hours in patients with neurologic symptoms and signs.

The most important attribute of MRI is its ability to eval-

uate directly the full length of the cord, thus making it possi-

ble for multiple levels of compression to be identified and to

determine whether these lesions are related or unrelated to

bony erosion or bone destruction by tumor. At least 35% of

patients who present with focal symptoms have evidence of

subclinical epidural compression at other sites along the

spine. MRI also can determine the number of segments and

vertebrae involved, the location of a compressive mass, if

present (anterior, posterior, or encircling), and perhaps the

percentage loss of bone mass. Imaging of the entire spine is

usually not done because of the length of time needed (as

much as 3 hours), but not taking the time may miss lesions

that cause later neurologic compromise. MRI is comparable

to myelography and CT scanning with contrast material in

detecting leptomeningeal metastasis. However, MRI may be

inadequate in patients who may have had previous spinal

surgery because metal-induced artifacts may be seen or the

patient’s movements cannot be controlled.

Vertebral metastases can be seen on unenhanced T

weighted images as foci of low signal intensity (dark) that

contrast with the adjacent high signal intensity (bright) of

normal adult bone marrow. The administration of gadolin-

ium results in normalization of the tumor, making its appear-

ance similar to that of the marrow. Vertebral metastases rarely

cross the disk space, as often seen in infection. However, it

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CRITICAL CARE OF THE ONCOLOGY PATIENT

453

sometimes may be difficult to distinguish between malig-

nancy and infection with MRI. Diffuse bone marrow

involvement may make interpretation by MRI difficult. This

is also true in younger patients with relatively little fatty mar-

row. MRI is superior to CT scanning with and without

intrathecal contrast material (CT myelogram).

Plain x-rays may be helpful in localizing the anatomic

origin of compression symptoms. Hematologic malignancies

less often are manifested by abnormal plain spine x-rays than

solid tumors. The most common findings include loss of

pedicles, destruction of the vertebral body, and vertebral

body collapse. Plain x-rays will, however, be unsuccessful in

identifying up to 20% of vertebral body lesions and also will

fail to demonstrate paravertebral masses that spare vertebral

body destruction but encroach on the epidural space via the

intervertebral foramina. The overall diagnostic sensitivity of

plain spine films is about 83%.

CT scans can assess the extent of a paravertebral mass,

detect small areas of bone destruction, quantify the extent

and characterize the direction of spinal cord impingement,

and assess response to treatment. CT scans cannot investigate

multiple levels of involvement without extensive scanning

and may miss the area of maximal impingement if CT scan

“cuts” are too widely spaced.

CT myelography remains an important diagnostic

method for epidural spinal cord compression, especially

when MRI is unavailable. Water-soluble contrast media are

preferred. Once a complete block of the spinal canal is

demonstrated by a lumbar myelogram, a C1–2 or suboccipi-

tal myelogram should be done to define the upper level of

block. Myelography may disclose silent epidural metastasis.

Lumbar myelography may cause further deterioration of neu-

rologic findings in approximately 14% of patients even with

the removal of only a small amount of CSF. Myelography has

been associated with complications such as headaches, seizures,

allergic reactions, and deterioration of neurologic status.

The role of radionuclide bone scans is unclear in the set-

ting of suspected epidural spinal cord compression. Bone

scans are less accurate than plain spine x-rays in predicting

epidural involvement. Moreover, bone scans often will suggest

multiple areas of abnormality without identifying the level

associated with pain or neurologic deficit. Bone scans may

not reflect the extent of vertebral involvement. These studies

are reserved for patients with skeletal pain, negative plain x-

rays, and a low suspicion for spinal cord compression.

Differential Diagnosis

The differential diagnosis of spinal cord compression includes

intervertebral disk herniation, vascular disease (eg, hemor-

rhage or infarction), infectious processes such as epidural

abscess, benign neoplasms (eg, meningioma, neurilemoma,

and chordoma), neurologic disorders (eg, multiple sclerosis

and amyotrophic lateral sclerosis), transverse myelitis, lep-

tomeningeal carcinomatosis, and paraneoplastic syndromes

(eg, necrotizing myelopathy and carcinomatous neuropathy).

Treatment

Early recognition, diagnosis, and treatment of epidural

spinal cord compression are of utmost importance. Either

the presence of neurologic symptoms or radiographic evi-

dence of epidural compression is sufficient to justify begin-

ning treatment. Cord compression diagnosed after the onset

of myelopathy has the most profound impact on the patient’s

quality of life. The drastic difference is between 2 and 6

months of ambulatory survival versus 2–6 months of bed or

wheelchair confinement with a urinary catheter, potential

urosepsis, pneumonia, and decubiti—and dependence on

professional care or family members. In one study, 70% of

patients with malignant spinal cord compression had pro-

gression of symptoms from initial symptoms and onset of

treatment. Reasons for delay included lack of recognition by

the patient but also delays in diagnostic evaluation.

Although median survival after treatment for spinal cord

compression is short, two factors appear to predict a good

prognosis for recovery of function: a normal pretreatment

neurologic examination and urgent appropriate treatment.

Other prognostic factors include the rate and onset of pro-

gression of neurologic dysfunction, histologic features of the

primary tumor (eg, myeloma, lymphoma, breast, and

prostate have a better prognosis), the presence of vertebral

collapse, and the location of the compressing lesion (anterior

or posterior). In general, if patients are ambulatory before

the start of treatment, two-thirds will remain ambulatory

after treatment. If patients are paraparetic before treatment,

one-third will be ambulatory after treatment, but if patients

are paraplegic (especially if unresponsive to dexamethasone

therapy), only a few—if any—will become ambulatory after

treatment. The most commonly used treatment regimen

consists of high-dose corticosteroid therapy plus external-

beam radiation. Surgery is used selectively either as initial

treatment or when specifically indicated.

A. Corticosteroids—To reduce edema of the cord adjacent

to the tumor, corticosteroids are used frequently in the treat-

ment of spinal cord compression. These should be started as

soon as the diagnosis is suspected. Delaying therapy while

awaiting formal studies is unnecessary and may lead to fur-

ther progression of the neurologic deficit. These drugs clearly

improve the initial rate of neurologic recovery and often lead

to stabilization of the neurologic deficit. Randomized trials

support the benefit of corticosteroids in those treated subse-

quently with radiotherapy. The optimal dose of corticos-

teroids is not known, but almost all recommendations

support “high doses” in the range of 16–100 mg dexametha-

sone. Some studies have shown both a higher likelihood of

benefit from the highest dosages and more complications of

therapy. One recommendation is to vary the dose with the

degree of neurologic impairment. With pain or radiculopa-

thy alone, dexamethasone, 16 mg intravenously, followed by

4–6 mg intravenously or orally every 6 hours, is adequate.

Patients with rapidly progressive symptoms or significant



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454

myelopathy should be treated with dexamethasone, 100 mg

intravenously, followed by 24 mg intravenously every 6 hours.

Therapy should be continued until benefit is demon-

strated from definitive therapy (ie, radiation or surgery)

or neurologic deficits are considered irreversible. Tapering of

corticosteroids is accomplished by reducing the dose by

about one-third every 3–4 days over a period of 2–3 weeks.

Corticosteroids should be reinstituted if neurologic deficits

recur. Patients failing to improve after a 7-day trial at 100

mg/day should be rapidly tapered to the lowest dose that will

maintain stable neurologic function. Such steroid regimens

do not appear to be toxic, although vaginal burning may

occur with rapid intravenous administration of dexametha-

sone. Conversely, corticosteroids may result in serious and

fatal complications when used in high doses for more than 40

days or when given to patients with serum albumin concen-

tration of less than 2.5 g/dL.

B. Radiation Therapy—Radiation therapy alone produces

neurologic improvement in 30–50% of patients with epidural

spinal cord compression. Pain relief is obtained in the major-

ity of patients with radiation therapy. Radiation-sensitive

tumors such as hematologic malignancies and seminomas

have the best outcome, breast and prostate cancer have mod-

erately good outcomes, and lung and renal cancer, sarcomas,

and melanoma are radioresistant and have the worst out-

comes. Radiation therapy and surgical therapy appear to be of

equal effectiveness in the treatment of radiosensitive tumors.

The usual dose of radiation is 3000–4000 cGy over a period of

3–4 weeks. There are few differences reported between vari-

ous radiotherapy protocols (ie, dose, number of fractions, and

total duration). Complications of radiation therapy include

radiation myelopathy and impaired wound healing in

patients who undergo subsequent surgery.

C. Surgery—The surgical approach selected—laminectomy,

anterior surgical decompression, or posterolateral surgical

decompression—depends on several variables, including the

specific element of vertebral involvement, cord level, and sta-

bility of the spine. The concept that surgery is not indicated

in the treatment of spinal cord compression is based on ret-

rospective analysis of several surgical series that compared

decompressive laminectomy followed by radiation therapy

with radiation therapy alone. No difference in neurologic

outcome was reported initially. Better understanding of the

pathogenesis of cord compression combined with advances

in operative technique and materials have resulted in

improved outcomes after surgical decompression. For exam-

ple, in 54 patients with cord compression in whom laminec-

tomy or vertebral body resection was performed, all 54

improved, and 23 of 25 patients surviving for 2 years

remained ambulatory. The 30-day mortality rate in this

series was 6%, and the morbidity rate was 15%.

Surgery is a major procedure associated with a significant

rate of complications. Therefore, surgery should be used only

in patients who have less extensive disease and longer life

expectancy. In the absence of medical contraindication,

surgery may be considered (1) when the diagnosis is not

known or is in doubt, (2) when there is spinal instability or

bone deformity, (3) when there is failure to respond to radi-

ation therapy, (4) when there is a history of previous radia-

tion therapy up to cord tolerance, (5) when there is high

cervical spinal cord compression (because of the danger of

respiratory failure), (6) in the presence of a radioresistant

tumor, especially when the onset of signs is rapid and com-

plete block is present, (7) when atlantoaxial compression is

present, (8) when a solitary spinal cord metastasis is present,

and (9) as a form of primary treatment before radiation ther-

apy. When possible, it is recommended that adjuvant

chemotherapy be delayed for 3–6 weeks after surgical ther-

apy to minimize wound complications.

Table 20–1 offers an approach to the patient with known

or suspected malignancy that presents with back pain and

possible spinal cord compression.

Conway R, Graham J, Kidd J, Levack P. Scottish Cord Compression

Group: What happens to people after malignant cord compres-

sion? Survival, function, quality of life, emotional well-being

and place of care 1 month after diagnosis. Clin Oncol (R Coll

Radiol) 2007;19:56–62. [PMID: 17305255]

Graham PH et al: A pilot randomised comparison of dexam-

ethasone 96 mg vs 16 mg per day for malignant spinal-cord

compression treated by radiotherapy: TROG 01.05 Superdex

study. Clin Oncol (R Coll Radiol) 2006;18:70–6. [PMID:

16477923]

Husband DJ, Grant KA, Romaniuk CS: MRI in the diagnosis and

treatment of suspected malignant spinal cord compression. Br J

Radiol 2001;74:15–23. [PMID: 11227772]

Loblaw DA et al: Systematic review of the diagnosis and manage-

ment of malignant extradural spinal cord compression: The

Cancer Care Ontario Practice Guidelines Initiative’s Neuro-

Oncology Disease Site Group. J Clin Oncol 2005;23:2028–37.

[PMID: 15774794]

Patchell RA et al: Direct decompressive surgical resection in the

treatment of spinal cord compression caused by metastatic can-

cer: A randomised trial. Lancet 2005;366:643–8. [PMID:

16112300]

Prasad D, Schiff D: Malignant spinal-cord compression. Lancet

Oncol 2005;6:15–24. [PMID: 15629272]



Increased Intracranial Pressure Due

to Malignancy

ESSENTIALS OF DIAGNOSIS



Mental deterioration, lethargy, somnolence, or confusion.



Changes in heart rate and blood pressure.



Pupillary changes.



Neurologic deficits, focal or nonfocal.



Abnormal brain CT or MRI diagnostic or suspicious of

intracranial tumor or metastases.



CRITICAL CARE OF THE ONCOLOGY PATIENT

455

General Considerations

Increased intracranial pressure (ICP) can cause neurologic

damage either directly or indirectly by way of herniation of

the cerebellar tonsil or uncus or by secondary vascular com-

promise. It is essential that prompt management be insti-

tuted in order to prevent loss of cerebral function or death.

The closed cranium means that any increase in volume of

any intracranial component must result in increased pres-

sure. A tumor increases ICP by adding its bulk or localized

edema to the normal components of brain tissue, CSF, and

vessels within the cranium.

Increased ICP can result from primary or metastatic

tumors. At least one-fourth of patients dying from malig-

nancy will have brain metastases discovered at autopsy.

Hematogenous spread is the most common route of dissem-

ination. Thus most lesions (approximately 80%) are supra-

tentorial. The most common cancers found include lung,

renal, breast, and melanoma. Brain metastases from chorio-

carcinoma, melanoma, and breast cancer more often

undergo hemorrhagic transformation. The metastatic

tumors may be single or multiple and should be distin-

guished from diffuse infiltrative processes that also may

cause increased ICP. Leukemic meningitis and diffuse

leukemic infiltration also can cause increased ICP but with-

out the focal neurologic or radiographic findings usually

seen in primary or metastatic brain tumors. In diffuse

processes, ICP increases without evidence of other concomi-

tant findings (eg, localizing findings from a mass lesion).

Brain edema results from leakage of plasma into the

parenchyma through dysfunctional capillaries (ie, vasogenic

edema). Studies on the formation, speed, and resolution of

brain edema have concluded that increased capillary perme-

ability occurs within the brain tumor itself and not in the

surrounding brain tissue. This increased capillary permeabil-

ity varies depending on the histology of the tumor and its

size. Brain edema occurs preferentially in the cerebral white

matter. Vascular endothelial growth factors may contribute

to dysfunction of tight junctions. It is not clear how brain

edema results in neurologic dysfunction, but it is thought to

be related to ischemia from a mass effect or from metabolic

abnormalities in the surrounding extravascular fluid.

Untreated, metastatic brain tumors ultimately lead to

progressive neurologic dysfunction and death. The median

survival in this setting is 4–6 weeks.

Clinical Features

A. Symptoms and Signs—Headache, nausea, vomiting,

mental deterioration, lethargy, somnolence, and confusion

are key findings in patients with increased ICP. Flexor or

extensor posturing may occur. In addition, decrease in

Other Clinical Findings Diagnostic Studies Treatment

Normal neurologic examination

Normal plain spine x-rays

MRI for high-risk tumors or in the presence

of other metastatic disease. If MRI is not

available, then CT, CT with myelography, or

myelography.

Observe closely for low-risk primary tumors.

Treatment depends on MRI or CT findings.

Normal neurologic examination

Abnormal plain spine films

None.

MRI, or CT with myelography.

Radiation therapy to symptomatic vertebral metastases

without further imaging. Advantages: No delay in treat-

ment, no further expense. Disadvantages: May miss

other sites of disease that may become symptomatic

later and compromise further radiotherapy because of

overlapping radiation therapy ports. Disadvantages

reduced if x-ray of entire spine is obtained, radiation

port includes two segments above and below lesions, or

bone scan is performed to document that disease is lim-

ited to one area of the spine.

Treatment depends on MRI or CT findings.

Abnormal neurologic examination

Abnormal or normal plain spine x-rays

MRI of symptomatic area to identify adjacent

levels of involvement.

If MRI is unavailable, consider CT with

myelography.

Treatment (radiation therapy) depends on MRI or CT

findings. Consider selective surgery.

Table 20–1. Management of patients with back pain and suspected malignancy.

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456

heart rate, increase in blood pressure, and abnormal respira-

tory pattern (Cushing’s triad) often can be present but are

late findings. Cerebellar masses may, however, have a

reversed clinical picture. Dilation of one or both pupils sug-

gests rapid and significant increases in ICP. Focal neurologic

deficits and abnormal reflexes may be found. Early diagnosis

is usually based on the timely observation of subtle alter-

ations in the mental status or state of consciousness of the

patient.

B. Laboratory Findings—Lumbar puncture for diagnosis is

to be discouraged because removal of fluid from the

intrathecal sac may result in an acute drop in infratentorial

pressure, thereby precipitating or worsening herniation.

C. Imaging Studies—Head CT scan and MRI are the most

useful diagnostic tests. The size and location of a tumor mass

or masses, the amount of peritumoral edema, shifts in

intracranial structures, and ventricular size can be deter-

mined easily. No test is completely accurate in predicting risk

of herniation. MRI is more sensitive than CT scan for find-

ing tumor, especially when evaluating lesions of the posterior

fossa. However, CT scan may better detect bony involvement

of the skull. Both non-contrast- and contrast-enhanced CT

scans are recommended because the combination not only

may detect hemorrhagic lesions (non-contrast-enhanced)

but also may allow detection of small lesions (contrast-

enhanced).

Differential Diagnosis

The differential diagnosis of increased ICP includes metabolic

encephalopathy (eg, hypo- and hypernatremia, hypercal-

cemia, uremia, hypoxemia, hypoglycemia, and thyroid dys-

function), CNS infection, cerebrovascular disease (especially

intracranial hemorrhage), drug-induced encephalopathy (eg,

sedatives and analgesics), and nutritional deficiencies.

Treatment

A. Medical Treatment—If signs of cerebral herniation are

evident, emergent reduction of ICP is warranted. Emergent

maneuvers include elective intubation and hyperventilation

to maintain Pa

between 25 and 30 mm Hg, followed by

administration of mannitol, 1–1.5 g/kg intravenously every

6 hours. Some recommend following serum osmolality as a

guide to dosing mannitol. Use of mannitol should be avoided

when definitive therapy (surgery or radiation) is delayed. In

any case, hypotonic fluids may be harmful and should not be

given. Early corticosteroid (eg, dexamethasone) administra-

tion and fluid restriction appear to be the best means of

achieving a decrease in ICP and brain edema. The specific

mechanism of action of corticosteroids on brain edema is

not known. These agents may either decrease edema produc-

tion or increase edema resorption. Corticosteroids appear to

decrease tumor capillary permeability and alter the exchange

of sodium and water across the endothelial cells and decrease

CSF production at the choroid plexus. Corticosteroid

administration may result in symptomatic improvement

within 4–5 hours, but more commonly such improvement

occurs gradually over several days, with 70% of patients

showing late significant clinical improvement. Dexamethasone

is administered at a dosage of 16 mg/day in four divided

doses, and the dosage may be increased to 100 mg/day. Some

patients must remain on corticosteroids for long periods and

whenever they undergo definitive treatment such as sur-

gery or radiation. Patients are subject to the risks and side

effects of high-dose corticosteroids if administered for long

enough time.

Preemptive antiseizure medications are frequently

administered, but their value is controversial. Because

patients with malignancy have a high risk for venous throm-

boembolism, deep venous thrombosis prophylaxis is recom-

mended despite the theoretical risk of hemorrhage from

primary or metastatic brain tumor.

B. Surgical and Radiation Treatment—Surgery and radi-

ation therapy are important methods of treatment of pri-

mary and metastatic brain tumors either as initial or as

adjunctive therapy. Candidates for surgical resection should

be patients with solitary lesions and limited systemic disease.

Radiation therapy usually involves the whole brain and

requires an average of 3000 cGy. Most recently, radiosurgery

has evolved as a new technique to deliver a single large dose

of radiation to a specific target. Local control rates appear to

be equal to those achieved with surgery. Radiosurgery is

especially useful in patients with multiple or poorly accessi-

ble lesions.

Aoyama H et al: Stereotactic radiosurgery plus whole-brain radia-

tion therapy vs stereotactic radiosurgery alone for treatment of

brain metastases: A randomized, controlled trial. JAMA

2006;295:2483–91. [PMID: 16757720]

Chang JE, Robins HI, Mehta MP: Therapeutic advances in the

treatment of brain metastases. Clin Adv Hematol Oncol

2007;5:54–64. [PMID: 17339829]

Kaal EC, Niel CG, Vecht CJ: Therapeutic management of brain

metastasis. Lancet Neurol 2005;4:289–98. [PMID: 15847842]

Khuntia D et al: Whole-brain radiotherapy in the management of

brain metastasis. J Clin Oncol 2006;24:1295–304. [PMID:

16525185]

Klos KJ, O’Neill BP: Brain metastases. Neurologist 2004;10:31–46.

[PMID: 14720313]

Langer CJ, Mehta MP: Current management of brain metastases,

with a focus on systemic options. J Clin Oncol 2005;23:6207–19.

[PMID: 16135488]

Mehta MP, Khuntia D: Current strategies in whole-brain radiation

therapy for brain metastases. Neurosurgery 2005;57:S33–44;

discusssion S1–4. [PMID: 16237287]

Peacock KH, Lesser GJ: Current therapeutic approaches in patients

with brain metastases. Curr Treat Options Oncol 2006;7:

479–89. [PMID: 17032560]

Tsao MN et al: Whole brain radiotherapy for the treatment of mul-

tiple brain metastases. Cochrane Database Syst Rev

2006;3:CD003869. [PMID: 16856022]