med surge 2 mod 3 study guide2

7/27/2019 Med Surge 2 Mod 3 Study Guide2

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Module III Review

I. GLASCOW COMA SCALE page 2240

Three areas assessed:

A) Eye opening

a. 4 - Spontaneous: Person spontaneously opens their eyes.

b. 3 - To voice: Person opens their eyes when spoken to.

c. 2 - To pain: Person opens eyes in response to pain.

d. 1- None: Person doesnt open their eyes.

B) Best verbal response

a. 5 - Oriented: Person. Place and time

b. 4 Confused: will not answer a question

c. 3 - Inappropriate words: using words or talking about something else; not in the same conversation

with you

d. 2 - Incomprehensible sounds: moaning, groaning, etc.

e. 1 - None:

C) Best motor response

a. 6 - Obeys command: moves arms or legs upon command; touch nose with finger

b. 5 - Localizes pain: moves to where the pain is located

c. 4 - Withdraws: withdraws from pain

d. 3 - Fexion: decorticate

e. 2 - Extension: Decerebrate (deepening brain injury compared to decorticate)

f. 1 - None:Total can be 3 15 and a score of 7 or less is considered coma.

Nursing assessment also includes

A) Evaluate the patients LOC

B) Vital signs

C) Compare previous assessments with your assessment

HESI HINT Use of the Glasgow Coma Scale eliminates ambiguous terms to describe neurologic status, such as

lethargic, stuporous, or obtunded.

NURSING ALERT!

If the patient begins to emerge from unconsciousness, every measure that is available and appropriate for calming and

quieting the patient should be used. Any form of restraint is likely to be countered with resistance, leading to self-injury or

to a dangerous increase in ICP. Therefore, physical restraints should be avoided if possible; a written prescription must beobtained if their use is essential for the patients well-being.

NURSING ALERT!

The body temperature of an unconscious patient is never taken by mouth. Rectal or tympanic (if not contraindicated)

temperature measurement is preferred to the less accurate axillary temperature.

II. DOLLS EYES PHENOMENON: Oculocephalic reflex (Dont attempt if suspect cervical spine injury)

A) Intact: eyes deviate to opposite direction in which the head is turned

B) Not intact (abnormal): eyes remain midline and move with the head indicating brain stem injury

Caloric Test: Eyes deviate to side being assessed as in checking temp in ear (Normal); (Abnormal) eyes dont deviate.

III. PATHOPHYSIOLOGY:

A) Increased ICP result of the amount of: brain tissue; intracranial blood, CSF

B) Monro-Kellie hypothesis: Increased volume of any one of those 3 contents above. The increase of one will

change the volume of the other two contents.

C) Causes of Increased ICP: increased intracranial blood volume, increased CSF volume, increased brain tissue

bulk (i.e. may have brain tumor, etc.- no room for expansion and will have herniation if not treated)

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D) Normal compensatory mechanism: within certain limits, the body can compensate, but it has a limited

window of opportunity (time). If no treatment is available, compensation runs out and the person can expire.

IV. SIGNS OF INCREASED ICP

A) Indications of increased ICP:

B) S/S: change in LOC (early sign), H/A, N/V change in vitals (Cushings triad late signs) increased systolicblood pressure, widening of the pulse pressure, bradypnea & bradycardia - compensatory mechanism has run

out

- Changes in level of responsiveness is the most important indicator of increased ICP

- Changes in vital signs:

a. Slowing of respirations or respiratory irregularities

b. Increase or decrease in pulse

c. Rising BP or widening pulse pressure

d. Temperature rise

- Vomiting (projectile)

- Pupillary changes reflecting pressure on optic or oculomotor nerves

a. Decrease or increase in size or unequal size of pupils

b. Lack of conjugate eye movement

c. Papilledema

HESI HINT Even subtle behavior changes such as restlessness, irritability or confusion, may indicate increased ICP

NURSING ALERT

The earliest sign of increasing ICP is a change in LOC. Slowing of speech and delay in response to verbal suggestions areother early indicators.

V. MANAGEMENT OF INCREASED ICP

A) Immediate management based on reducing the size of the brain by

1) decreased cerebral edema

2) lower CSF

3) decreased blood volumeB) Goals accomplished by:

1) Administering osmotic diuretics and steroids

2) Restricting fluids

3) Draining CSF

4) Controlling fever

5) Reducing metabolic demands6) Hyperventilation with mechanical ventilation

VI. MEDICAL MANAGEMENT:

A) Reduce volume ofbulk of brain, via surgical removal. (i.e. clot or tumor)

B) Osmotic diuretics: Mannitol, Glycerol and Urea; used to reduce edema; Mannitol removes fluid from normal

brain tissue, not the edematous tissue, making room for the edematous tissue to decrease the ICP. May use aloop diuretic (Lasix) with Mannitol.

Note: patient is critical and they will have a Foley. You will want to monitor their urine output.

Note: blood pressure drops, so they can severe hypotension, therefore, you really need to monitor the vital

signs.

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Drug Indications Adverse Reactions Nursing Implications

Mannitol

(Osmitrol)

Acts on renal tubules by

osmosis to prevent water

reabsorption.

In bloodstream, draws

fluid from the

extravascular spaces into

the plasma.

Disorientation,

confusion, and

headache

Nausea & vomiting

Convulsions and

anaphylactic reactions

Use for short-term therapy only

Never give to clients with cerebral

hemorrhage

IV infusion is usually adjusted to

urine output; filter and watch for

crystals

Never give to clients with no urineoutput (anuria); if output is


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Activities that increase ICP:

1. Change in bed position for caregiving and extreme hip flexion

2. Endotracheal suctioning

3. Compression of jugular veins (keep head straight and not to one side).

4. Coughing, vomiting, or straining of any type (no Valsalva: increased intrathoracic pressure increases ICP).

Collaborative Problems/ Potential Complication for ICP

1. Brain stem herniation

Results from an excessive increase in ICP in which the pressure builds in the cranial vault and the brain tissue

presses down on the brain stem

This increasing pressure on the brain stem results in cessation of blood flow to the brain, leading to

irreversible brain anoxia and brain death.

2. Diabetes insipidus

Result of decreased secretion of antidiuretic hormone (ADH).

The patient has excessive urine output, decreased urine osmolality, and serum hyperosmolarity.

Therapy consists of administration of fluids, electrolyte replacement, and vasopressin therapy.

3. SIADH

Result of increased secretion of ADH.

The patient becomes volume-overloaded, urine output diminishes, and serum sodium concentration becomes

dilute.

Treatment includes fluid restriction (


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HEADACHES

Headache is a symptom rather than disease state. May indicate organic disease (neurologic or other disease), a stress

response, vasodilation (migraine), skeletal muscle tension (tension headache or a combination of these).

Primary headaches no organic cause can be identified. Includes: migraine, tension-type, and cluster

Secondary headaches a symptom associated with an organic cause, such as brain tumor or an aneurysm

Various classifications

Muscle/Tension Headache

Migraine Headache

Cluster Headache

Temporomandibular Joint Pain: Unilateral facial pain either at the TMJ or it can be referred pain at any point on the face

and neck. Its causes are usually associated with malocclusion, joint disease (i.e. arthritis), or trauma. Bruxism (grinding of

the teeth) or clenching of the teeth make it worse.

Temporal Arteritis (Cranial arteritis): Inflammation of temporal arteries

S/S: fatigue, malaise, weight loss, fever,Very classic to this: heat, redness, tenderness and pain over the involved artery

Visual problems or blindness may occur from ischemia of involved structures.

Thrombosis of the central retinal artery.

Treatment: Corticosteroids (to prevent blindness) and (PRIMARILY) analgesics for comfort

MIGRAINE HEADACHES:pg 2198 KNOW DEFINITION!!!Symptom-complex characterized by periodic and recurrent attacks of severe headache. The cause is primarily a vascular

disturbance that occurs more commonly in women and has strong familial tendency.

Onset: primarily in youth (i.e. puberty or 20s); often occurs during a change in pace such as a weekend, holiday, surprise

of some kind, going to college, taking a new job, etc.

Migraine Personality: compulsive, perfectionist, sensitive to criticism, ambitious, and rigid

Pain is unilateral due to vasodilation of the superficial arteries (persists/throbbing)

Causative factor: basically combining the vasoconstriction initially to the vasodilation and what happens is that the blood

vessels stretch, putting pressure on the nerve ending, which causes pain.

(fatigue, hunger, bright lights)

Characterized by: aura (patient can usually sense that the headache is coming from tingling, dizziness, flash of light, etc.Note: during the aura phase, medication, such asImitrex, can be given to abort the headache

Duration: can last an hour or up to several days

Recovery phase: The patient may want to be left alone, lie down in a dark room, they dislike noise. As the headache

subsides the patient will go into a sleep that can last for a period of time due to exhaustion from the headache. Patient can

also have nausea and vomiting with the headache. Medication can be given during the aura phase, before the headache

begins in order to abort it.

Precipitating factors:

Certain foods containing tyramine, monosodium glucamate, milk products or nitrate may trigger headaches.

Tyramine is in foods that contain a vasoactive monoamine and have the potential for raising blood pressure.

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Environmental conditions: changes in weather, noise levels, or glare, etc.

(antihypertensive, antianginal drugs)

Some medications: such as oral contraceptives or nitroglycerin can accentuate the headache.

Mental and emotional excitement: surprises, sudden startle

Fatigue, hunger, smoking, alcohol

Treatment: trying to abort it through medication during the aura phase; get the meds on board before the patient gets a

full-blown headache. Look at predisposing factors and eliminate them. (Use warm or cool compresses)

Ergotamine preparations (po,sl,sq,IM,R,or inhalation): If given early, they can be effective in stopping the headache. The

key is that it must be taken with 30 minutes if not during the aura before headache gets full blown. Once the headache is a

full-blown migraine, these medications are of very limited benefit to these patients.

Ergotamine tartrate acts on smooth muscle, causing prolonged vasoconstriction of the cranial blood vessels.

Side effects: paresthesias of fingers and toes, muscle pain in extremities, nausea and vomiting, weakness in the

legs, and bradycardia.

Contraindications: (Look at if the headache is caused by vasodilation, what is the effect of the medication?

Vasoconstriction) - hyptertension, CAD, pregnancy, peripheral vascular disease. (impaired hepatic & renal function)

Cafergot a combination of ergotamine and caffeine can be utilized if given early

Sumatriptan (Imitrex) common drug used for treatment. Patient will have a prescription for this and will be taken

during the aura. May have tingling/numbness in extremities and this can be very frightening to them.

Management between attacks:

Prevention employs daily use of one or more agents that are thought to block the physiologic events leading to an

attack.

Most widely used and important drug for prevention of migraine:

Inderal: Propanolol 40mg tid-qid Do not stop abruptly and monitor pulse!

Beta-blocker inhibits the action of beta-receptors cells in the heart and brain that control the dilation of

blood vessels. (Heart rate, blood pressure)

Sansert: Methysergide maleate 2 mg bid or tid (not used often because of side effects)

Thought to inhibit or block (antagonist) the effects of serotonin, a substance possibly involved in mechanism of vascular

headaches.

Side effects: Blood dyscrasia (most serious), edema, weight gain, numbness, tingling.

Contraindications: (anything you wouldnt want vasoconstriction in) peripheral vascular disease, hypertension, renal

disease, hepatic disease

Nursing Implication: Must have a 1-2 month drug holiday every 6 months to prevent potential long-term complications

such as retroperitoneal fibrosis and pleuropulmonary and cardiac fibrosis.

(gradually take them off then, start them back on it) NOTES

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CLUSTER HEADACHES

A form of vascular headache; more common in men; NO AURA.

(Facial flushing)

Incidence: Unilateral pain of short duration which subsides abruptly. Very classic to being unilateral it is also localized

behind the eye watering of eye and nasal congestion. Can last 15 minutes up to 1 hour or 2; Patient will be up walkingthe floor rather than quiet in a dark room. More often at night rather than in the day and can wake the person up from a

sound sleep. (Person would rather pace than rest)

Treatment: some of the same medications, precipitating factors are the same as for Migraine Headaches**

Cluster headaches differ from migraine headaches in the following ways:

There is no vomiting and rarely nausea.

There is no significant family history

It affects many more men than women

There is no menstrual relationship

There are no neurological deficits except for ocular sympathetic paralysis

The average frequency of attacks is greater than that of migraine

Nocturnal attacks are more frequent than in migraines

There is no demonstrable decrease in serotonin at the onset of an attack as there is in the migraine.

MUSCLE CONTRACTION HEADACE (tension headache)

Causative factor: result of sustained contraction of the muscles of the neck and scalp, face, and upper back. (Such assitting in the same position for a period of time)

It is thought that when muscles are kept in a prolonged state of contraction, blood supply to the muscle becomes

diminished and metabolic wastes begin to accumulate.

Characteristics: Feels like a band-constricting around the top of the head; steady and constant feel of pressure; back of

neck up the base of the skull

Treatment: neck massage, discontinue whatever is causing it; analgesics/muscle relaxants. (Tylenol, ASA, Codeine,Darvon) (remove stimuli; warm heat)

CVA

Pathophysiology:

Cerebrovascular disease refers to any functional abnormality of the CNS caused by a pathologic condition of theindividual cerebral vessels or of the cerbrovascular system.

Includes any disorders of any of the vessels which furnish blood to the brain. As the brain tissue has insult, this area is

where you get your symptoms. Edema occurs with insult to the brain tissue.

Incidence: primarily with elderly; children with sickle cell; people with hypertension

Risk factors: 1) modifiable (diet, weight, smoking also includes disease process: hypertension, diabetes, heart disease

2) non-modifiable (age, gender, race)

MODIFIABLE RISK FACTORS FOR ISCHEMIC STROKE Hypertension (controlling hypertension, the major risk factor, is the key to preventing stroke)

Atrial fibrillation

Hyperlipidemia

Diabetes mellitus (associated with accelerated atherogenesis)

Smoking

Asymptomatic carotid stenosis

Obesity

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Excessive alcohol comsumption

Pathological causes of CVAs:

1) Cerebral thrombosis most common

2) Cerebral embolism 2nd most common

3) Cerebral ischemia

4) Cerebral hemorrhage

a. Epidural

b. Subdural

c. Intracerebrald. Subarachnoid

1. Cerebral thrombosis: clot that occludes a vessel; it usually doesnt develop abruptly; travels until it gets wedged; TIAs

in half the cases red flag. (Can occur at rest or on arising)

Major causes: atherosclerosis and the building up of the plaque

S/S: consciousness may or may not be lost the vessel may not be totally occluded, headache uncommon at

onset, possible dizziness, mental disturbance, convulsions/seizures, degree of involvement depends on rapidity of onset,

size of lesion and presence of collateral circulation. (Wont know improvement until edema subsides)

2. Cerebral Embolism: edema in area; embolism can be fat or blood; usually lodges in the middle cerebral artery branch

or carotid. (necrosis/edema of brain tissue)

Major causes: heart is closely associated, blood pooling in the heart can lead to clottingRisk factors: MI, atrial fibrillation, pulmonary infections

S/S: rapid in onset: * not related to activity (may want to ask patient or family member what they were doing

prior to this); usually do not have a TIA; headache before consciousness is lost; extent of damage depends on size of

damage and where it is located.

3. Cerebral Ischemia:page 2210 Insufficiency of blood supply to the brain (not total occlusion); due mainly to

atheromatous constriction of the arteries supplying the brain

Most common manifestation is TIA (may precede a stroke or due to atherosclerotic disease)**

Transient Ischemic Attacks: Transient or temporary episodes of neurological dysfunction commonly manifestedby a sudden loss of motor, sensory, or visual function, lasting a few seconds or minutes but no longer than 24 hours. Red

flag advanced stages of atherosclerotic heart disease. (warning of impending stroke)

(Percantine, ASA, hemorrhage)

4. Cerebral Hemorrhage: Stroke caused by cerebral hemorrhage is rapid in development, typically occurs during activity.

It can also be due to sudden rise in BP, rupture of cerebral aneurysm, or AVM (arterial venous malformation)

S/S result from either compression of cranial nerves or brain tissue puts pressure- displacing brain tissue

Severe headache, nuchal rigidity, tinnitus, dizziness, hemaphoresis, hemaplegia, visual disturbances (loss and

diplopia), seizure activity. (bleeding within head irritates meninges causing nuchal rigidity)

Events that may precede cerebral hemorrhage: severe occipital or nuchal headache (neck back of head and down neck);vertigo or syncope; parasthesia in extremities, nose bleeds, retinal hemorrhages

GREATEST RISK: 7th DAY!!

a. Epidural (extradual) hemorrhage: outside the dura mater; usually result of brain injury

and usually involves the middle menigeal artery (rupture); if patient is not treated within

hours of insult, there is very little chance of survival due to rapid progression of pressure on

the brain.

b. Subdural hemorrhage: Small vessels with venous tears; chronic primarily elderly due to

this area of brain taking longer time for hematoma to develop. (Elderly can take months

before showing symptoms)

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b. Receptive aphasia when patient can talk, but cant receive the information. Difficulty understanding

words. Must be spoken to in short increments at a time.**

c. Expressive aphasia cant express themselves

d. Behavioral style slow and cautious.

e. Dysarthria difficulty in speech secondary to paralysis of muscles responsible for producing speech.

Page 2213: Major goal of care in acute phase is directed toward life saving measures. Prevention of long term

complications and rehabilitation should begin immediately.

Assess movement relieve pressure

Prevent external rotation of hip

Prevent clawlike contracture deformity

Prevent footdrop

Bladder control

Assess sensations

Maintain skin integrity

Speech therapy to regain communication

BRAIN TUMOR LECTURE OUTLINE

INCIDENCE:

Brain tumors arise in all age groups and in both sexes, although they have a biphasic age distribution, peaking between theages of 5 and 8 years, and again between 55 to 60 years of age; males are at slightly higher risk than females.

Children are more likely to develop tumors of the cerebellum, whereas 90% of all tumors in adults are located above thetentorium. There is a higher incidence of whites than blacks..

Classification of intracranial tumors

1. TISSUE ORIGIN

a. Neural.neuroma

b. Connective..glioma

c. Meninges.meningio

d. Blood vessels..angioe. Glands.adenoma

2. LOCATION

a. supratentorial

b. infratentorial

3. RELATION TO BRAIN

a. Intrinsic

b. Extrinsic

Most common tumor to metastasize to the brain: cancer of the lung, followed by cancer of the breast

Metastases spread via the arterial system to form lesions in the cerebrum or cerebellumusually in the area supplied by

the terminal branches of the middle cerebral artery.

BRAIN TUMOR ASSESSMENT

The signs and symptoms vary greatly according to type and location of the tumor.features which are common to all

tumors: (change in LOC, nausea, inc systolic (widening pulse pressure) dec HR & Resp.)

1. S/S of increased ICP

2. focal disturbances (diplopia)

(EDEMA OF OPTIC NERVE, VISUAL ACUITY PROBLEMS, etc)

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Begin your assessment by taking a complete history.

- from patient

- from family members

Follow the history with a complete neuron examination.

- Primary tumors can arise in any tissue of the brain.

- Secondary tumors are a result of metastasis from other areas (most often from the lungs; followed by breast)

Classification of tumors according to the tissue where they originate: 2302

(most common is headache)***

1. Tumor arising from covering of the brain meninges.(meningioma)

- 15% of brain tumors

- Benign extrinsic

- Slow growing

- Presents between ages 30-60

- Females greater than males

- Presenting s/s vary according to the tumor location

- Prognosis: can pretty much remove the whole thing curable

2. Tumor involving cranial nerve (neuroma)Acoustic Neuroma page 2302 involves the cranial nerve VIII eventually will put pressure of the CN V trigeminal

- 5% of intracranial tumors

- Benign, intrinsic

Symptoms: vertigo, tinnitus, nerve deafness

Prognosis: if diagnosed early, can be completely removed; Can have facial paralysis.

Brain Tumor:

HESI HINT Benign tumors continue to grow and take up space in the confined area of the cranium, causing neural

and vascular compromise in the brain, increased intracranial pressure, and necrosis of brain tissue. Even benign tumorsmust be treated because they may have malignant effects.

3. Tumor arising form the glial(glioma)

- Always intrinsic develops within the brain itself

- Infiltrating

- Most common type of tumorcomprise between 40-50% of intracranial tumors- Usually malignant

- Female to male ratio is 2:1

Prognosis: poor cant be cured, will re-occur because of all of tentacles throughout tissue.

Two main types ofGliomas:

Astorcytomas graded 1 thru 4 in order of severity. * Not curable

- 40% of all gliomas * Penetrating

- Grades 1 and 2grow slowly * Cannot remove entire tumor - Grades 3 and 4 grow rapidly

- Grade 4 is most malignant; also called glioblastom multiform:

- Can occur at any age

- Adults usually in cerebrum

- Children usually in cerebellum

Medulloblastomas

- Highly malignant, rapid growing

- 10% of the gliomas- Frequently in children

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- Seeds through CSF

- Most commonly located in cerebellum

4. Tumor of blood vessels (hemangioma)

Hemangioblastoma.also called angioblastoma- tumor of immature blood vesselsforms a cyst, the tumor itself remaining as a little nodule in the cyst wall.

Incidence:

Symptoms: (usually form in cerebellum) vertigo; visual problems; as ICP increases, can have mystagnis, nuchal

rigidity, positive rhomberg

Prognosis: curable

5. Tumor of the ductless glands (adenoma)

Pituitary gland tumor tumor sitting on top of the pituitary gland

- Compromise between 7-10% of IC tumor

- Pituitary function may be increased if decreased by the presence of a tumor

- Increased function secondary to increased secretion of the growth hormone.

o Accelerates growth: hyperpituitarism

o Children: giantism

o Adults: acromegaly

o Cushings syndrome: moonface, buffalo hump, hypoglycemia, obese trunk

- Decreased function secondary to tumor presence in the anterior portion of the pituitary gland.

o Hypopituitarism

o Marked adiposity and loos of sexual function

o Loss of libido, sterility, impotence, amenorrhea

o Loss of visionpressure on optic nerve

- Surgery: transsphenoidal hypophysectomy (2181- incision made under lip in nasal cannul, maxillary

gingiva..)

Symptoms according to site/location

The site or location of any of the tumors can be identified by assessing the dysfunction of the brain

other sites cannotdue to silten areas of the brain

Frontal Lobe Tumor s/s: bifrontal headache, changes in mood, personality emotions, expressive aphasia,

hemophoresis, hemaplegia, seizures (also unexpected use of obscene language) [impaired judgement]

Temporal Lobe Tumor: problems with short-term memory, hemanoxia,psychomotor seizures, receptive aphasia

[auditory hallucinations]

Parietal Lobe Tumors: [sensory loss] parasthesia (hypo to hyper) sensitivity to touch

Occipital Lobe Tumor: homonymous hemaniopsia, flashes of light

Pineal tumor (tumor of the ductless glands)

- Produces symptoms by growth and can cause obstructive hydrocephalus due to pressure on the Aqueduct ofSylvius

- Rx: shunt or radiotherapy or total removal

Pituitary gland tumors

- Bifrontal headache.pain radiating between two temples

Tumors of the 3rd Ventricle

- Symptoms arise from increase ICP

Cerebellar tumor (Tendency to fall wherever lesion is in cerebellum)**

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- Symptoms: unsteady gain, dizziness, intentional tremor, negative finger-to-nose, positive Rhomberg,

niastagmus.

Brain tumor: diagnosis

History and Neuro exam

Progression of diagnostic studies:

1. Skull x-ray

- Can detect tumors containing calcium, i.e. menigioma or oligodendroglioma

- Displacement of pineal gland (calcified)

2. EEG

- Abnormal waves detected in region occupied by tumor

3. CT Scan

- Can determine tumor location, shape and size; can also track the tumors response to therapy

4. Angiography (cerebral arteriogram reveals any vessels displaced by tumor growth

Other tests:

- MRI can detect tumors

- Lumbar puncture often not done in establishing a diagnosis but will be done provided increased ICPdoesnt exist

- CSF analysis: protein usually increased; normal protein is 15-45 mg/mL; pressure increased and

normal pressure is usually 60-180 mL H2O- Brain scan an abnormal amount of radioactive material will be present in area of tumor

- Audiometry or vestibular function studies suspected cases of acoustic neuroma.

- Visual-field testing determines the limit of peripheral vision; pituitary adenomas, meningiomas,

creaniopharynigiomas, or gliomas (supratentorial tumors).frequently produce visual-field changes

Nursing care planning and implementation will be the same as for any patient with increased intracranial pressure

Traditional methods of treatment for brain tumor include surgery, radiation therapy, and to a lesser degree,

chemotherapy.

Radiation therapy may be prescribed for lesions inaccessible to excision, as adjunctive therapy when remnants of

the tumor can be removed surgically, and palliation in metastatic tumors.

The objective of radiation therapy is to destroy tumor cells without injury to normal onestumor cells are moreradiosensitive than non-tumor cells.

- Observe for signs of increasing ICP

- Probably be on steroids prior to and during treatment

- Alopecia- Skin reaction

- N/V

- Drowsiness- Itching

- Fatigue

- Adequate nutritional intake

- Thrombocytopenia

- Leucopenia

Chemotherapy

- Drugs with certain pharmacologic properties cross the blood-brain barrier to concentrate within the

brain tumors.

- Side effects: N/V, leucopenia, thrombocytopenia, erthyrocytopenia

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Radiation and chemotherapy require management of side effects and assessment for tolerance.

- Patients with N/V/D may require

o Fluid replacement

o Antiemetics

o Antidiarrheal meds

o Monitoring of CBC to note hemopoietic depression may requires: whole blood, packed cells,

platelets If dangerously low white countmay require reverse isolation

Avoid crowds and people with infections

Planned periods of rest

Diet high in protein, iron, vitamin C

Monitor for easy bruising: gums that bleed, petechiae, hematuria, tarry stools

Use soft toothbrush, electric razor

Brain Tumor: prognosis

An untreated brain tumor inevitably leads to death, either from progressively increasing ICP or from

primary brain damage

Brain tissue doesnt regenerate

The earlier the tumor is recognized and surgery performed, the better are the changes for recovery.

The prognosis depends on the type of tumor, size, and its location.

INTRACRANIAL SURGERY LECTURE OUTLINE

Assessment and intervention pre-op

- Psychological assessment and intervention

- Apprehensive

- Reinforce and repeat the information

- Different expected responses: depression and withdrawl; crying, denial, anger, acceptance- Psychological support to patient and family frightening experience

- Treatments and procedures explained

- Family questions

- What to expect post-opo Oxygen

o Suctioning

o IVs

o Arterial lines

o Frequent neuron checks and vital signs

o Cranial dressings and drainslater scrub cap, wig or turban

o Foley

o Transfusions

o Periorbital edema and ecchymosis

o Leg exercises

o

Deep breathing

Baseline neurological assessment and intervention

- Knowledgeable of the patients symptoms preoperativelyto determine if patients condition worsens,improves or stays the same.

- Other pre-operative anticipatory measures

o Pre-op steroids to decrease brain edema

o Foley

o Prophylactic Dilantin

o TED hose

HESI HINT Craniotomy preoperative medications:

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Corticosteroids to reduce swelling

Agents and osmotic diuretics to reduce secretions (atropine, Robinul)

Agents to reduce seizures (phenytoin)

Prophylactic antibiotics

APPROACHES anytime brain is manipulated watch for increased ICP (allows expansion of inoperable tumor)

- Craniectomy portion of skull is removed to accommodate cerebral edema (do not put patient on operative side)- Cranioplasty repair or a cranial defect

o Indications: cosmetic effect as well as protection to brain

o Precautions:

- Observe dressing for bleeding and CSF leakage

- Observe dressing for increasing tightness, indicating edema

- Do not allow patient to lie on portion of the head where the skull has been removed

- Take precautions not to accidentally hit the head

- Do not remove dressing without an order strict aseptic technique

- Craniotomy surgical opening of the skull to gain access to intracranial structures

o Supratentorium above the tentorium into the supratentorial compartment

o Infratentorium below the tentorium into the infratentorial (posterior fossa) compartment

Postoperative nursing management- Monitor for sings of increased ICP 2184- Establish and maintain adequate airway and ventilation

- Maintain body alignment after suprotentorial

o HOB elevated 15 to 30 degrees according to doctors orders

o Position client on side or back to facilitate drainage**

o If tumor is large, and removed, patient must not be placed on the affected side because of displacement of

brain tissue due to gravity.

o Neutral head position, can have pillow, but no neck flexion, head is flat, not on their back**

o Assess surgical dressing for: [Large pillow behind head/shoulders]

CSF leakage DEXTROSE STICK**

Excessive bleeding [Reinforce any dressings] -Meningitis**

Do not change dressings until ordered - Infection**

Ventricular drainage

Purpose: to drain excess CSF and to prevent increased ICP monitor the drainage for

CSF and/or blood

Monitor elimination

Provide for patient comfort

o Headache may persist for 24 to 48 hoursattributing to stretching or irritation of the

nerves of the scalp that occurs during surgery

Activities to avoid: coughing, sneezing, straining, vomiting (can give antiemetic), suction

IC surgery complications:

Meningitis: due to irritation of the meninges due t infection in the subarachnoid space or due to prolonged use of

intracranial monitoring devices 2nd/3rd day post surgery

S/S: headache + Kernigs

Chills + Brudzinski

Fever

Irritability Delirium

Nuchal rigidity Convulsions

Soreness of skin and muscles

Increased cells in CSF

P/I: Strict aseptic technique

Antibiotics

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Seizures give prophylactic meds

- greater risk of seizures with supratentorial surgery

- P/I: Padded side railsSide rails

Dilantin prophylactically

- Status epilepricus occurrence of prolonged seizures without recovery of consciousness

Stress Ulcers hyperacidity of gastric secretions can cause gastritis with ulceration and frank hemorrhage

Diabetes insipidus surgery in the area of the hypothalamus and pituitary gland causes edema and interferes

with the production of antidiuretic hormone, resulting in excessive urinary output.

o S/S: excessive urination (5-10mL); dilute urine (specific gravity of 1.001 to 1.006); excessive thirst

o P/I: fluid replacement and vasopressin

IC surgery

Transsphenoidal hypophysectomy approach

Indication: pituitary tumor

Procedure:- incision is made in the maxillary gingival

- tumor cavity is packed with muscle or fat taken from the thigh, or lower abdomen.

- nasal cavities packed with Vaseline gauze with bacitracin ointment..2-3 days

- upper gums sutured

- moustache dressing under nose to hold the packing in place

P/I:

- patient in high Fowlers position to promote venous drainage and prevent bleeding

- replacement hormones and steroids

- no nasopharyngeal suctioning

Diabetes Insipidus caused by edema of the pituitary stalk from surgical manipulation resulting in failure of the

posterior pituitary to secrete ADH temporary. Diapid Nasal Spray after packing removed and tissues healed (7 days for sutures in upper gum to absorb, and at

least one month is required for healing of nasal mucosa).

Patient teaching:

- Not to bend over, to prevent placing undue pressure on the graft site that could dislodge the graft

- Mouth breathing until nasal packing removed

- No nose blowing, sneezing or coughing- No tooth brush

Postoperative complications:

Hypothyroidism

Hypoglycemia

CSF lead [Dextrose stick positive at risk for meningitis]**

SEIZURES 2190

DEFINITION

A seizure disorder is a sudden alteration in normal brain activity that causes distinctive changes in behavior and body

function. (Hesi: Uncontrolled electrical discharges of neurons in the brain.)

Seizures are frequently symptoms of an underlying illness.

They may accompany a variety of disorders, or they may occur spontaneously without any apparent cause.

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Seizures resulting from systemic and metabolic disturbances are not considered epilepsy if the seizures cease when the

underlying problem is corrected.

CLINICAL MANIFESTATIONS

The preferred method of classifying seizures is the International Classification System proposed in 1970 and revised in

1981.

It is based on the clinical and EEG manifestations of seizures.

Seizures are divided into TWO major classes:

1. generalized

2. Partial

1) GENERALIZED SEIZURES: entire brain affected at onset; no warning or aura; loss of consciousness from

seconds to minutes can occur in tonic clonic motions; cyanosis, excess salivations, tongue and cheek biting,

incontinence, no memory or activity

a. The most common generalized seizure is the gran mal seizure (tonic clonic)

Characterized by: tonic loss of consciousness

1. generalized stiffeningof entire body

2. clonic jerking spasm followed by relaxation

(Post muscle soreness, very tired, may sleep for hours)**Some persons may not feel normal for several hours or days after a seizure. The client has no memory of the seizure

activity.

b. Absence orpetit mal seizures usually occurs only in children and rarely continues beyond adolescence.

It may cease altogether as the child matures, or it may evolve into another type of seizure.

Characterized by: brief staring spells that last only for a few seconds; can have up to 100 episodes a day and may

also experience twitching of facial muscles. (problem progressing in school)

2) PARTIAL SEIZURES: Begin in a specific region of the cortex, as indicated by the eEG and by the clinical

manifestations.

May be confined to one side of the brain and remain partial or focal in nature, or may spread to involve

the entire brain, culminating in generalized tonic-clonic seizure.S/S:Automatism lip smacking, picking at clothes, walking away from conversation.

Partial seizures further divided into those with:

a. simple motor (Jacksonian)

b. those with complex symptoms (psychomotor) involves temporal lobeSimple partial seizures: only a finger or hand may shake or mouth may jerk uncontrollably. Person may talke

untintelligibly, may be dizzy, and may experience unusual or unpleasant sights, sounds, odors, or tastes, but

without loss of consciousness.

Status Epilepticus state which seizures recur in rapid excession 2197Complex partial seizures: person either remain motionless or moves automatically but inappropriately for time

and place, or may experience excessive emotions of fear, anger, elation, or irritability. Person doesnt remember

the episode when it is over. May have lip-smacking; Automatism: inappropriate behavior such as picking anclothing, fumbling with objects, or walks away while being talked to

Valium, Ativan, Cerebryx Halt seizures immediately; Dilantin, Phenobarbital - Maintenance

Other complications are severe injury and even death to trauma suffered during a seizure. Death can result from

head injury incurred in a fall, drowning in a bathtub, or from severe burns.

HESI HINT Do notuse tongue blade, padded or not, duringa seizure. It can cause traumatic damage to the

oral cavity.

PSYCHOSOCIAL:

Attitudes have improved in recent years, but still carries social stigma.

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It used to be associated with supernatural powers, possession by the devil and insanity.

Today the stigma probably exists because of the characteristics of seizures are in direct conflict with modern

societal values of self-control, conformity, and independence.

DIAGNOSTIC STUDIES

Aimed at determining type of seizures, their frequency and severity and the factors that precipitate them.

MANAGEMENT: *page 2192*

SEE NURSING MANAGEMENT DURING A SEIZURE IN BRUNNER

Observe and record sequence of symptoms

Nature of seizure usually indicates type of treatment used.

Nursing care During Seizure

a. Provide privacy and protect the patient from curious onlookers. (The patient who has an aura may

have time to seek a safe, private place)

b. Ease the patient to the floor, if possiblec. Protect the head with a pad to prevent injury (from striking a hard surface).

d. Loosen constrictive clothing.

e. Push aside any furniture that may injure the patient during the seizure.f. If the patient is in bed, remove pillows (to open airway)** and raise side rails.

g. If an aura precedes the seizure, insert an oral airway to reduce the possibility of the patients biting

the tongue or cheek.

h. Do not attempt to pry open jaws that are clenched in a spasm or to insert anything. Broken teeth and

injury to the lips and tongue may result from such action.

i. No attempt should be made to restrain the patients during the seizure, because muscular contractions

are strong and restraint can produce injury.

j. If possible, place the patient on one side wit head flexed forward, which allows the tongue to fall

forward and facilitates drainage of saliva and mucus. If suction is available, use it if necessary to clearsecretions

Nursing care after seizure:

a. Keep the patient on one side to prevent aspiration. Make sure the airway is patent.

b. Make sure the airway is patent. [stay with patient, allow to sleep]

c. There is usually a period of confusion after a grand mal seizure.d. A short apneic period may occur during or immediately after a generalized seizure.

e. The patient, on awakening, should be reoriented to the environment.

f. If the patient becomes agitated after a seizure (postictal), use calm persuasion and gentle restraint.

Things to have ready in the hospital room for seizure patient:

Oxygen and suction apparatus available

Privacy provided as soon as possible

Side rails up and padded

Oxygen tubing

Patient in side-lying position (immediately postseizure)

Bed in lowest position

Pillow under head

Loose clothing for client

Chronic management:

g. medication must be taken regularly and continuously

h. Teach family members

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i. Medical-alert items

PHARMACOLOGICAL MANAGEMENT: 2194

The primary goal of antiepileptic drug therapy is to obtain maximum seizure control with a minimum of toxic side

effects.

The principle of drug management is to: control rather than cure seizures

Serum levels of the drug: decreased levels can cause seizures to start occurring again; manifestation of drug

toxicity are variable, and any organ system may be involved. Monitor therapeutic drug levels.

Monitor therapeutic drug levels regularly every 6 months**

Side effects of antiseizure medications may be divided into three groups:

1. idiosyncratic or allergic disorders, which manifest primarily as skin reactions

2. acute toxicity, which may occur when the medication is initially prescribed

3. chronic toxicity, which occurs late in the course of therapy

If seizure control is not achieved with a single drug, a second drug is used.

Primary drugs for generalized tonic-clonic and partial seizures:

a. phenytoin (Dilantin)

b. carbazepine (Tegretol)

c. Phenobarbital

d. Primidone (Mysoline)e. Divalproex sodium (Depakote)

Primary drugs for absence, akinetic, and myoclonic seizures:

a. ethosuximide (Zaronitn)

b. divalproex sodium (Depakote)

c. clozaepam (Klonopin)

NURSING ALERT

Nurses must take care when administering lamotrigine (Lamictal), an antizeizure medication. The drug packaging was

recently changed in an attempt to reduce medication errors, because this medication has been confused with Lamisil,

Trandate, Epivir, Ludiomil, and Lomotil. Patients with epilepsy are at risk for status epilepticus from having theirmedication regimen interrupted.

HESI HINT Medication noncompliance is the most common cause of increased seizure activity.

Drugs Indications Adverse Reactions Nursing Implications Phenobarbital

(Luminal)

Tonic-clonic and partial

seizures

Is the longest acting of

common barbiturates

Usually combined withother drugs

Drowsiness

Nystagmus

Ataxia

Paradoxic excitement

Therapeutic levels, 15 40

mcg/mL

Avoid rapid IV infusion

Monitor BP during IV infusion

Phenytoin

(Dilantin)

Tonic-clonic and parital

seizures

Gingival hyperplasia

Dermatitis

Ataxia

Nausea, anorexia

Bone marrow depression

Nystagmus

(causes drowsiness,

discolors urine (brownish)

EXPECTED!)

Therapeutic levels 10 to 20

mcg/mL

Monitor any drug interactions

Ensure meticulous oral hygiene

Monitor CBC

Report to MD if any rash develop

For IV administration, flush IV

before and after with normal

saline only

Do not administer with milk

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Fosphenytoin

sodium (Cerebyx)

Generalized convulsive

status epilepticus

Prevention and treatment

of seizures during

neurosurgery

Short-term parenteral

replacement for phenytoin

oral (Dilantin)

Rapid IV infusion can cause

hypotension

Severe: ataxia, CNS

toxicity, confusion, gingival

hyperplasia, irritability,

lupus erythematosus,

nervousness, nystagmus,

paradoxic excitement,

Stevens-Johnson syndrome,toxic epidural necrosis

Use for short-term parenteral use

only

Should always be prescribed and

dispensed in phenytoin sodium

equivalents

Prior to IV infusion, dilute in

D5W or NS to administer solution

of 1.5 to 25mg PE/mL

Infuse at IV rate of no more than150 mg PE/minute

Valproic acid

(Depakene)

Absence seizures

Myoclonic seizures

Hepatotoxicity, especially in

children less 2 years old

Prolonged bleeding times

GI disturbances

Monitor liver function

Potentiates Phenobarbital and

Dilantin, altering blood level

Therapeutic levels: 50 to 100

mEq/mL

Carbamazepine

(Tegretol)

Tonic-clonic mixed

seizures

Drowsiness

Ataxia

Hepatitis

Agranulocytosis

Monitor liver function while on

therapy

Therapeutic level: 6 to 12

mcg/mL

Lamotrigine

(Lamictal)

Partial seizures

Tonic-clonic seizures Absence seizures

Dizziness

Headache Nausea

Rash

Withhold drug if rash develops

Do not discontinue abruptly

Clonazepam

(Klonopin)

Absence seizures

Myoclonic seizures

Drowsiness

Hyperactivity

Agitation

Increased salivation

Therapeutic levels of 20 to 80

mcg/mL

Do not abruptly discontinue drug

Monitor liver function, CBC, and

renal function periodically.

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