Background

Medulloblastoma (seen in the image below) is the most common

malignant brain tumor in children, accounting for 10-20% of primary
CNS neoplasms and approximately 40% of all posterior fossa tumors.
Inline figure

MRI showing a medulloblastoma of the cerebellum.

/Inline figure
It is a highly invasive embryonal neuroepithelial tumor that arises in
the cerebellum and has a tendency to disseminate throughout the CNS
early in its course.
Morphologically similar tumors arising in the pineal region are termed
pineoblastomas, and those arising in other CNS locations are called
primitive neuroectodermal tumors (PNETs).
With aggressive surgery, craniospinal radiotherapy and chemotherapy,
more than 50% of children with medulloblastoma can be expected to
be free of disease 5 years later. Using current treatments, 80-90% of
those without disseminated disease can be cured; however, treatment
for this disease often results in significant endocrinological and
intellectual sequelae.
Pathophysiology
Medulloblastoma is a cerebellar tumor arising predominantly from the
cerebellar vermis. The histogenesis of medulloblastoma remains
controversial.
One view suggests that the cell of origin derives from the external
granular layer of the cerebellum. This is supported by the finding that
the proliferation of precursor neurons in this layer is controlled by sonic
hedgehog (shh), whose receptor PTCH is mutated in a subset of
sporadic medulloblastomas. Furthermore, suppression of shh was
recently shown to eliminate medulloblastoma that spontaneously
develops in the PTCH +/- heterozygote mouse.[1]
Another hypothesis proposes that medulloblastomas have more than
one cell of origin. This is based on studies showing differential

immunoreactivity to a neuronal calcium-binding protein that is not

expressed in the external granular layer and to a beta-tubulin isotype
that is expressed in the neuronal cells of the ventricular matrix and
external granular layer. Numerous molecular alterations that appear to
modulate the biological behavior of medulloblastoma or its response to
therapy have been reported. For example, studies suggest that
medulloblastoma expression of neurotrophin (NT3) and its cognate
receptor, Trk C, may modulate the behavior of these tumors by
inducing apoptosis, thereby retarding tumor progression and resulting
in a more favorable prognosis.[2]
Other studies have shown that overexpression of the oncogenes
ERBB2 and MYCC are associated with worse outcome, and that MYCC
can induce the potentially more aggressive large cell anaplastic variant
of medulloblastoma. Finally, amplification of the oncogene OTX2 has
been most recently described in association with medulloblastoma.
As the tumor grows, obstruction of cerebrospinal fluid (CSF) passage
through the fourth ventricle generally occurs, resulting in
hydrocephaly. The tumor may spread contiguously, to the cerebellar
peduncle and/or the floor of the fourth ventricle; anteriorly, to the
brainstem; inferiorly, to the cervical spine; or superiorly, above the
tentorium. It also may spread via the CSF intracranially or to the
leptomeninges and spinal cord. Of all the pediatric CNS neoplasms,
medulloblastoma has the greatest propensity for extraneural spread,
especially to bone and bone marrow; however, the rate of such events
is less than 4%.
Epidemiology
Frequency
United States
Approximately 250 new patients are diagnosed annually.
International
Exact figures are unknown. In general, brain tumors occur at a rate of
2.5-4 per 100,000 at-risk children per year. Of these, approximately
18% are medulloblastoma.
Mortality/Morbidity
Risk group stratification is continuing to evolve but is currently based
on 3 principal features, including age, extent of postoperative residual
disease, and the metastasis stage (M stage) derived from the Chang
classification staging system. The M stage classification is as follows:
M0 - No gross subarachnoid or hematogenous metastasis
M1 - Microscopic tumor cells found in CSF
M2 - Gross nodular seeding in cerebellum, cerebral subarachnoid
space, or in the third or fourth ventricles
M3 - Gross nodular seeding in spinal subarachnoid space
M4 - Extraneuraxial metastasis.
The specific risk groups based on this classification scheme are defined
below.

 Average-risk disease: This risk group is defined as patients older

than 3 years who are at stage M0 with less than 1.5 cm2 of
residual tumor postoperatively. The 5-year survival rate for this
group is currently more than 80%
Poor-risk disease: This risk group is defined as patients older than
3 years who are at stage M1-M4 and/or with more than 1.5 cm2
of residual tumor postoperatively. The 5-year survival rate for this
group is currently 30-60%.
Infants: This group is defined as patients younger than 3 years.
This group has the worst prognosis, regardless of M stage and
extent of postoperative residual disease. The 5-year survival rate
is approximately 30%; however, patients with metastatic disease
do considerably worse. Those infants with desmoplastic tumors
are more likely to survive.
Various biologic parameters have been related to outcome. In
retrospective studies, children with tumors that have increased
expression of TRKC and WNT are more likely to survive, whereas those
with increased amplification of MYCC oncogene or increased ERBB2
expression have a poorer prognosis. Real-time biologic tumor analysis
will likely supplement, if not supplants, clinical parameters used for
stratification in the future. In addition, histologic features of severe
anaplasia have been associated with poorer survival.
Despite successful treatment, a significant number of patients have
neurocognitive and endocrinologic deficits. Although most long-term
survivors have normal intelligence, many subsequently develop
learning difficulties that require individualized educational programs.
Biochemical growth deficiency is observed in 70-80% of patients, and
some degree of growth impairment is present in well over half of
patients after treatment. Thyroid and gonadotropin hormonal
deficiency may also occur. Craniospinal radiation, a mainstay of
treatment, has been implicated as a major cause of these deficits.
Race
No racial predisposition is noted. The latest data from the Surveillance,
Epidemiology, and End Results (SEER) program showed that patients
aged 0-14 years in the United States have an incidence rate per million
population of 5.7 in whites and 5 in blacks.[3]
Sex
US incidence per 1 million population for patients aged 0-14 years is
6.1 for boys and 4.5 for girls.
Age
Peak age of incidence is 3-5 years. Approximately 80% of patients are
diagnosed in the first 15 years of life.
History

Although 70-90% of patients with medulloblastomas present with a

history of headaches, emesis, and lethargy, these symptoms are
generally intermittent and subtle. Duration of symptoms for 3 months
or more before diagnosis is common.
Increased intracranial pressure (ICP)
Early symptoms are secondary to increased ICP. The classic triad
consists of morning headaches, vomiting, and lethargy. Headache
consists of head pain present upon arising that is relieved by vomiting
and gradually lessens during the day. Cushing triad (ie, hypertension,
bradycardia, and hypoventilation), an uncommon finding in children
with increased intracranial pressure, usually indicates impending
herniation.
Initial signs of increased ICP are usually subacute, nonspecific, and
nonlocalizing.
School-aged children may complain of vague intermittent headaches
and fatigue. They may demonstrate declining academic performance
and personality changes.
Infants may present with irritability, anorexia, and developmental
delay.
Cerebellar dysfunction
With increasing tumor size and invasion into the surrounding brain
tissue, more characteristic symptoms appear.
One symptom is progressively worsening ataxia involving the lower
extremities, often with relative sparing of the trunk and upper
extremities.
Brain stem deficits
Tumor infiltration of the brain stem or increased ICP may result in
diplopia and multiple other cranial nerve findings, such as facial
weakness, tinnitus, hearing loss, head tilt, and stiff neck.
Metastatic disease
Uncommonly, patients may present with back pain or leg weakness
secondary to spinal metastasis.
Physical
The earliest signs are nonlocalized and caused by increased ICP. Later
signs are generally due to tumor invasion of the surrounding tissue.
Increased ICP
Funduscopic evaluation reveals papilledema or optic pallor in infants.
Palsy of cranial nerve VI resulting in the inability to abduct one or both
eyes is common.
Infants may have the "setting sun" sign. This is demonstrated by
impaired upgaze and seemingly forced downward deviation of the
eyes.
Measurement of head circumference in infants with open cranial
sutures also may reveal macrocephaly.
Cerebellar findings

Localized deficits in truncal steadiness, upper extremity coordination,

and gait are common.
Brain stem findings
Invasion into the brain stem may cause loss of conjugate gaze (gaze
palsy) or the inability to adduct one eye on attempted lateral gaze.
This is observed most commonly in combination with deficits of cranial
nerves V, VII, and IX.
Invasion into the cerebellopontine angle results in facial weakness and
hearing loss, often with associated unilateral cerebellar deficits.
Causes
Environmental
Epidemiological studies investigating parental occupational exposures,
environmental exposures and maternal nutritional intake have not
proven a direct link between such factors and the development of
childhood brain tumors.
Familial and heritable disease
Medulloblastoma is associated with recessively inherited Turcot and
ataxia-telangiectasia syndromes.
As many as 5% of patients with autosomal dominant nevoid basal cell
carcinoma (Gorlin) syndrome develop medulloblastoma. These tumors
demonstrate loss of heterozygosity at band 9q22-q23, the region
containing the PTCH tumor suppressor gene associated with Gorlin
syndrome.
Genetic associations
The most frequent cytogenetic abnormality in sporadic
medulloblastoma is an isochromosome 17q [i(17q)]. Of tumors
analyzed, 40-50% have a deletion of the short arm of chromosome 17,
implicating the presence of a tumor suppressor gene that maps to 17p,
which is distinct from the p53 gene. Alternatively, a gene on 17q may
be related to transformation because of increased copy number.

DifferentialDiagnoses

Astrocytoma
Ependymoma
Meningitis, Aseptic
Meningitis, Bacterial
Laboratory Studies
The routine pretreatment laboratory evaluation for medulloblastoma
includes CBC count, electrolytes, liver, and renal function tests.
Baseline thyroid function studies and viral titers are also
recommended.

maging Studies
CT scanning
A CT scan of the head with and without contrast has more than 95%
sensitivity for the detection of brain tumors.
On CT scans, prominent hydrocephalus and a solid, homogeneous,
isodense to hyperdense, contrast-enhancing, midline cerebellar mass
are characteristic of (although not diagnostic of) medulloblastoma.
MRI
Head and spinal MRI with and without gadolinium should be performed
in all patients with CT or clinical findings consistent with
medulloblastoma.
Other midline posterior fossa tumors, such as cerebellar astrocytoma
and ependymoma, may have a similar appearance on CT.
MRI can be useful in such instances by better demonstrating the
anatomic origin and extent of tumor (see the image below).
Inline figure

MRI showing a medulloblastoma of the cerebellum.

/Inline figure
Preoperative and postoperative MRI is required for detection and
measurement of residual disease following surgical resection.
Postoperative MRI evaluation should be performed within 72 hours of
surgery to delineate residual tumor from the postsurgical inflammatory
changes that are visualized on MRI at this time.
Spinal MRI is the most sensitive method available for detection of
spinal cord metastasis.
Bone scan
Because medulloblastoma can metastasize outside the CNS, especially
to bone, a bone scan with plain film correlation may be useful in
symptomatic patients.
Other Tests

A baseline hearing test (audiography or brainstem auditory-evoked

response [BAER]) is recommended because of the potential toxicity
from radiation and chemotherapy.
Some investigational treatment protocols may require additional tests,
such as echocardiography, pulmonary function tests, or other more
specific tests, for the purposes of monitoring treatment-related toxicity.
Procedures
Lumbar puncture
CSF cytologic examination is useful for the detection of microscopic
leptomeningeal tumor dissemination. However, neither clinical
symptoms nor negative CSF cytologic findings can be relied on to
indicate the presence of nodular spinal cord disease. As many as 50%
of patients with positive spine MRI studies are asymptomatic and have
negative cytologic results.
Funduscopic examination (or CT or MRI) must be performed before
lumbar puncture (LP) to rule out the presence of hydrocephaly.
In known cases of medulloblastoma, LP generally is deferred until 2
weeks postoperation to avoid the presence of tumor cells that have
disseminated as a result of surgery.
Bone marrow aspirate and biopsy
Medulloblastoma rarely metastasizes to bone marrow.
These tests should be reserved for patients who demonstrate abnormal
peripheral blood findings that have no clear etiology.
Histologic Findings
Medulloblastomas are undifferentiated embryonal neuroepithelial
tumors of the cerebellum. They are highly cellular, soft, and friable
tumors composed of cells with deeply basophilic nuclei of variable size
and shape, little discernible cytoplasm, and often abundant mitoses
(see the image below).
Inline figure

This section displays a typical medulloblastoma, composed of

undifferentiated cells with deeply basophilic nuclei of variable size and
shape and little discernible cytoplasm.
/Inline figure
These characteristics give the microscopic appearance of a small,
round, blue cell tumor. Morphologically identical tumors arising in the

pineal region are termed pineoblastomas, and those arising in other

CNS locations are called primitive neuroectodermal tumors (PNETs).
Homer-Wright rosettes (ringlike accumulations of tumor cell nuclei
around a neuropil-containing or fibrillary core) and pseudorosettes are
variably present (see the image below).
Inline figure
Section displaying Homer-Wright rosettes and pseudorosettes of a
medulloblastoma.
/Inline figure
These tumors express neuronal and neuroendocrine markers, including
synaptophysin and neurofilament proteins.
Various degrees of glial or neuroblastic differentiation are noted,
suggesting that the primitive cell of origin possesses the capacity for
bipotential differentiation. A histologic variant with abundant stromal
component, desmoplastic medulloblastoma, occurs dominantly in the
lateral cerebellar areas of adolescents and adults. Another more
recently described variant is characterized by marked features of
anaplasia that is associated with MYCC oncogene amplification.
Medical Care
Standard therapy for medulloblastoma consists of aggressive surgery
followed by radiation to the entire craniospinal axis with boost to both
the primary tumor site and focal CNS metastatic sites. Recently,
adjuvant chemotherapy has also been shown to be beneficial.[4]
Radiation Therapy
Average-risk disease
Reducing the amount of craniospinal radiation in an attempt to
decrease morbidity without jeopardizing survival appears to be
successful in this group. In a report by the International Society of
Pediatric Oncology, children with average-risk medulloblastoma
randomly received either the standard 36 Gy or a reduced dose of 24
Gy to the neuraxis.[5] It was found that no statistical difference in
progression-free survival rates was demonstrated between the groups
as long as the initiation of radiotherapy was not delayed by the
administration of chemotherapy before radiation.
The dose for average-risk medulloblastoma patients enrolled on
Children's Oncology Group (COG) last completed trial was 23.4 Gy to
the craniospinal axis followed by 32.4 Gy boost directly to the primary
tumor site.[6] In both the poor-risk and average-risk groups, the total
radiation dose to sites of known disease is 55.8 Gy. An ongoing study is
investigating further reduction of the craniospinal dose to 18 Gy in a
subset of children with average-risk disease.
Verma et al conducted a retrospective study comparing results
obtained with prone positioning for craniospinal irradiation with results
obtained with supine positioning in the treatment of medulloblastoma.
[7]
The study cohort consisted of 46 children, 23 of whom were

irradiated in the prone positioning, and 23 in the supine position. The

median ages for each group was 8.1 years and 7.2 years, respectively.
Data were collected with regard to age; sex; risk group; need for
general anesthesia; radiation therapy dose and fractionation;
acceptance or rejection of weekly port films during treatment; and
outcomes, including neuraxis recurrence and possible complications,
such as myelitis. High-risk disease was seen in 26% of patients
receiving irradiation in the prone position and in 35% of those receiving
irradiation in the supine position. There was no difference in use of
general anesthesia between the 2 groups. The rejection rate of cranial
port films was significantly higher for patients treatedintheprone
position (35%) than for patients in patients in the supine position (8%).
The rate for 5-year progression-free survival was 62% for patients in
the prone position and 76% for supine patients. The rate for overall
survival was 67% for patients in the prone position and 84% for supine
patients. There were no isolated junctional failures or occurrences of
radiation myelitis in either group. The investigators concluded that
irradiation positioning had no bearing on survival outcomes but that
prone positioning was associated with a higher rate of rejection of
cranial port films.[7]
Min et al conducted a study of the relationship between the skin dose
of proton irradiation and permanent alopecia in pediatric patients with
medellublastoma.[8] The study cohort comprised 12 children (aged 4-15
years) with medulloblastoma. Permanent alopecia was assessed and
graded after completion of therapy. Skin threshold doses of permanent
alopecia were calculated on the basis of skin dose from the
craniospinal irradiation plan, using the concept of generalized
equivalent uniform dose. The investigators took into account the
intensity of chemotherapy that was employed. Monte Carlo simulations
were used to assess uncertainties associated with beam range
prediction and the presence of secondary particles. The investigators
found that increasing the dose of the irradiation field or the dose given
by the boost field to the posterior fossa increased total skin dose
delivered in that region. It was found that permanent alopecia
correlated with irradiation dose with a threshold of about 21 Gy
(relativebiological effectiveness) with high-dose chemotherapy and 30
Gy with conventional chemotherapy. The investigators concluded that
the risk for permanent alopecia could be predicted on the basis of the
information in the treatment plan.[8]
Poor-risk disease
The current recommendation is 36 Gy to the craniospinal axis, followed
by a boost of 19.8 Gy to the primary tumor site and an additional 19.8
Gy to focal metastatic sites. The amount of boost that can be given is
limited by the presence of the optic nerves within the radiation field or
if more than two thirds of the supratentorial compartment volume is
within the radiation field.

Spinal disease that is visible after 30.6 Gy of the prescribed 36 Gy to

the craniospinal axis receives an additional boost up to a total of 45 Gy
if the tumor is located above the termination of the spinal cord and as
much as 50.4 Gy if the tumor is located below the termination of the
cord.
Infants
Radiotherapy for patients younger than 3 years, the poorest risk group,
remains controversial. Because the effects of radiotherapy on
intellectual development are most severe in this age group, attempts
have been made to delay or omit radiation by using chemotherapy.
However, in the most recent COG study, infants receiving
chemotherapy alone had a 29% 3-year progression-free survival rate
for those without dissemination and only 11% for those with
metastasis. The Pediatric Oncology Group (POG) reported that, in
infants with medulloblastoma treated initially with chemotherapy
followed by delayed radiation, the 2-year progression-free survival rate
was 34%.[9]
Trials are currently underway to avoid or delay radiotherapy in this
population by using cycles of high-dose chemotherapy followed by
autologous stem cell rescue. Initial reports have indicated a good
response rate to chemotherapy, and, although overall survival (3040%) is comparable to prior studies, most patients who survived in the
latest trials did not receive radiotherapy. Infants with desmoplastic
tumor treated with chemotherapy fare better than those with classic
tumors because 70% or more can be successfully treated without
radiotherapy.
Chemotherapy
Average-risk disease
The most encouraging results with adjuvant chemotherapy have been
reported in children with nondisseminated medulloblastoma receiving
8 cycles of lomustine (CCNU), vincristine, and cisplatin chemotherapy
for approximately 1 year following conventional dose radiotherapy and
concomitant vincristine.
Latest trials indicate that children aged 3-10 years who received this
regimen with reduced-dose craniospinal radiation have a superior
survival rate compared to those who received standard radiation alone.
The current 3-year progression-free survival rate for those receiving
adjuvant chemotherapy is approximately 80%.
Poor-risk disease
Chemotherapeutic agents that have been found to be most effective
for this disease are cisplatin, carboplatin, cyclophosphamide, and
vincristine.
To improve survival rates in this group, current trials are investigating
the use of high-dose chemotherapy (most commonly using
carboplatinum and thiotepa-containing regimens) and autologous stem

cell rescue after a course of conventional craniospinal radiotherapy

and chemotherapy.
Studies using chemotherapy (carboplatin and vincristine) concurrent
with radiotherapy are also underway.
Retinoic acid as a maturation agent following radiation is under
investigation in a randomized trial.
Infants
In children younger than 3 years, evidence suggests that some do
respond, at least partially, to chemotherapy. In patients with minimal
residual postoperative disease, this response may be long-lasting.
Ongoing trials are investigating high-dose chemotherapy (carboplatin
and thiotepa) and stem cell rescue, following induction with
chemotherapeutic agents similar to those used in the treatment for
older children with poor-risk disease. Whether radiotherapy can be
safely delayed or omitted altogether in certain subgroups has not yet
been determined.
Methotrexate, both intrathecally and intravenously, is being added to
more conventional chemotherapy in some studies; primarily for infants
with partially resected and/or disseminated tumors.
Relapsed disease
Current studies investigating the use of biologic agents that specifically
target the most common molecular alterations described in this
disease, such as tyrosine kinase inhibitors that block the function of
EBB2, are ongoing.
Surgical Care
Suboccipital craniotomy
Because the tumor is often friable, gentle suction is used.
Microdissection is used to remove adherent portions.
Modern neurosurgical techniques permit complete or near-complete
resection with little or no significant increase in morbidity and mortality
rates compared with more conservative surgery.
Because surgical estimates of the extent of resection may not be
reliable, postoperative MRI evaluation for residual disease is required
within several days of the procedure.
As many as 40% of patients have some degree of new neurologic
dysfunction postoperatively. One ill-defined syndrome is posterior fossa
syndrome, characterized by mutism, cerebellar dysfunction,
supranuclear cranial nerve palsy, and hemiparesis that occurs 12-48
hours after surgery. As many as 50% of patients have residual deficits.
Ventriculoperitoneal shunt
Approximately 50% of patients require placement of a
ventriculoperitoneal shunt at the time of operation (or shortly
thereafter) because of unresolving obstructive hydrocephaly. Third

ventriculostomy is increasingly used to avoid the placement of a

permanent ventricular shunt.
Diet
No specific dietary restrictions or requirements are indicated.
Patients who develop severe anorexia or weight loss as a result of
therapy may need supplemental nutrition to maintain daily
requirements. Most patients can tolerate enteral supplementation, but
some may need parenteral support.
Activity
Most patients have no restrictions on activity other than limitations
from neurologic deficits caused by the tumor and treatment.
Patients with ventriculoperitoneal shunts may be restricted from
performing high-impact sports (eg, diving).
School performance needs to be carefully monitored, as most children,
especially those younger than 7 years at diagnosis, require added
support at school.
Medication Summary
Chemotherapeutic agents are continually evolving. Historically, the
most active drugs have been DNA alkylators. These agents cause DNA
damage and disrupt DNA replication. The agents with the longest
clinical history in the treatment of medulloblastoma are vincristine,
lomustine (CCNU), and cisplatin.
Class Summary
These agents disrupt DNA replication, which inhibits tumor growth and
promotes tumor cell death.
View full drug information
Vincristine (Oncovin)
Plant-derived vinca alkaloid used during radiotherapy and in
combination with other chemotherapeutic agents. Acts as a mitotic
inhibitor by binding tubulin.
View full drug information
Lomustine (CeeNU)
DNA alkylator used in combination with other chemotherapeutic
agents. Causes interstrand and intrastrand DNA-DNA crosslinks
resulting in damage to the DNA template and inhibition of DNA
replication.
View full drug information
Cisplatin (Platinol)

A heavy metal coordination complex that exerts its cytotoxic effect by

platination of DNA. A mechanism analogous to alkylation, leading to
interstrand and intrastrand DNA crosslinks and inhibition of DNA
replication. Used in combination with other chemotherapeutic agents.

Patient Education
Patients and family members should be instructed about the care of
the central venous catheter.
Patients should be instructed about protection against infection and
what to do should infection be suspected during therapy.
For excellent patient education resources, visit eMedicineHealth's
Cancer Center. Also, see eMedicineHealth's patient education article
Brain Cancer.
Complications
Complications include the following:
Obstructive hydrocephaly
Neurologic impairment
1 Holland et al conducted a study to identify factors associated
with academic difficulties in survivors of pediatric
medulloblastoma.[10] The study focused on school competence
and fluent academic performance. Thirty-six patients (aged 718 years) were recruited for the study. Participants completed
a neuropsychological screening battery that included selected
Woodcock-Johnson III Tests of Achievement subtests. Parents
completed the Child Behavior Checklist. Basic academic skill
development was found to be broadly average, in contrast to
fluent academic performance, which was significantly worse
than average. The investigators concluded that school
competence may have utility in estimating levels of
educational success in survivors of pediatric medulloblastoma
and that academic difficulties in these patients may be better
assessed through measures of deficits in fluent academic
performance rather than academic skills.[10]

Pain secondary to metastasis

Chemotherapy-induced effects
1 Anemia
2 Thrombocytopenia and increased risk for bleeding
3 Neutropenia and increased risk for life-threatening bacterial,
viral, and fungal opportunistic infections
4 Nephrotoxicity, ototoxicity, hepatotoxicity, and neurotoxicity

 Radiation-induced effects
1 Neurocognitive and endocrinologic dysfunction
2 Mineralizing microangiopathy with ischemia or infarct
3 Secondary CNS and thyroid malignancies

http://reference.medscape.com/article/987886-followup#a2649
nursing care plan
Brain Tumor
A brain tumor, or tumour, is an intracranial solid neoplasm, a tumor
(defined as an abnormal growth of cells) within the brain or the central
spinal canal.
A brain tumor begins when normal cells in the brain change and grow
uncontrollably, forming a mass. A tumor can be benign (noncancerous)
or malignant (cancerous). In general, primary CNS tumors do not
spread outside of the CNS. Malignant brain tumors are further
classified using a grade: low, intermediate, or high.
Brain tumors can occur at any age. The exact cause of brain tumors is
not clear.
There most common type of primary brain tumors among adults are
astrocytoma, meningioma, and oligodendroglioma.
The most common type of primary brain tumors in children are
medulloblastoma, grade I or II astrocytoma, ependymoma, and brain
stem glioma.
The most common symptoms of brain tumors include headaches;
numbness or tingling in the arms or legs; seizures, memory problems;
mood and personality changes; balance and walking problems; nausea
and vomiting; changes in speech, vision, or hearing.
Assessment for Brain Tumor (Intracranial Tumor)
Focal neurological disorders. In the frontal lobe, occurred
personality disorders, affective disorders, the motor system
dysfunction, seizures, aphasia. Precentral gyrus can be found on
Jacksonian seizures. In the occipital lobe, visual disturbances,
and headache. Temporal lobe can occur auditory hallucinations,
visual or gustatory and psychomotor seizures, aphasia. In the
parietal lobe can be found the inability to distinguish left right,
sensory deficit (contralateral).
Increased ICT: lethargy, decreased HR, decreased level of
consciousness, papilledema, projectile vomiting, seizures,
changes in breathing patterns, changes in vital signs.
Mental. Personality changes, depression, decreased memory and
ability to make decisions.
Pituitary dysfunction. Cushings syndrome, acromegaly,
giantisme, hypopituitarism.

 Pain. Persistent headache.

Seizure activity.
Fluid status. Nausea and vomiting, decreased urine output, dry
mucous membranes, decreased skin turgor, decreased serum
sodium, BUN, Hb, Hct, hypotension, tachycardia, weight
decreased.
Psychosocial. Anger, fear, mourning and hostility.
Nursing Diagnosis for Brain Tumor (Intracranial Tumor)
1. Disturbed Body Image related to hair loss, and changes in the
structure and function of the body.
2. Impaired Skin Integrity related to the effects of chemotherapy
and radiation therapy.
3. Acute Pain related to severe headaches and side effects of
treatment.
4. Risk for Fluid Volume Deficit related to the side effects of
chemotherapy and radiation therapy.
Nursing Interventions for Brain Tumor (Intracranial Tumor)
1. Disturbed Body Image related to hair loss, and changes in the
structure and function of the body.
Goal:
Patients express a positive self-image
Expected outcomes:
Patients received a change in body image.
Interventions:
1. Assess the patients reaction to body changes.
2. Observation of patient social interaction.
3. Maintain a therapeutic relationship with the patient.
4. Instruct the patient to open communication with health care or other
important person.
5. Help patients find effective coping about body image.
Rational:
1. Determine the patients reaction to changes in body image.
2. Social withdrawal may occur due to rejection.
3. Facilitate a therapeutic relationship.
4. Expression of fears openly to reduce anxiety.
5. Help patients find coping strategies that can reduce anxiety and
fear.
2. Impaired Skin Integrity related to the effects of chemotherapy and
radiation therapy.
Goal:
Patients skin integrity is maintained
Expected outcomes:
Intact skin,

There is no redness or damage.

Interventions:
1. Assess skin integrity every 4 hours.
2. Keep skin clean and dry, use soap and water to bathe the patient.
3. Repositioning the patient every 2 hours.
4. Advise for fluid intake and adequate nutrition.
Rational:
1. Red, dry, and injuries can occur in the area of radiation,
chemotherapy can cause rash, hyperpigmentation and hair loss.
2. Prevent skin damage.
3. Improve circulation and prevent pressure sores.
4. Dehydration and malnutrition may increase the risk of developing
pressure sores.
3. Acute Pain related to severe headaches and side effects of
treatment.
Goal:
The patient does not feel pain
Expected outcomes:
Reported no discomfort,
Not grimace, cry,
Vital signs within normal limits,
Participate in activities appropriately.
Interventions:
1. Assess the location, and duration of headache and pain in the
incision every 2 hours.
2. Set giving analgesics / narcotics.
3. Give comfort to the patient.
Rational:
1. Sudden changes or severe pain may indicate increased ICT and
should be reported to the doctor.
2. Giving narcotic, sedative effect.
3. Eliminating discomfort and anxiety.
4. Risk for Fluid Volume Deficit related to the side effects of
chemotherapy and radiation therapy.
4. Risk for Fluid Volume Deficit related to the side effects of
chemotherapy and radiation therapy.
Goal:
Adequate fluid balance can be maintained
Expected outcomes:
Intake and output balance,
Skin turgor and moist mucous membranes,
Serum electrolytes, Hb, Hct, and vital signs within normal limits
Interventions:

1. Skin turgor, mucous membranes, thirst, blood pressure, HR, monitor

serum electrolytes, albumin and CBC.
2. Monitor intake and output.
3. Encourage adequate intake. Set intravenous fluids, appropriate
orders.
4. Set antiemtek administration, appropriate orders.
rational:
1. Determine dehydration status.
2. Vomiting may occur in patients with chemotherapy and radiation
therapy.
3. Help maintain adequate hydration.
4. Reduce nausea and vomiting.