 Increased intracranial pressure is a rise in the mmHg do CPP and cerebral perfusion decrease to a level

pressure inside the skull that can result from or cause brain that results in loss of consciousness. Any further elevations
injury. is the pressure in the skull that results from the will lead to brain infarction and brain death.
volume of three essential components: cerebrospinal fluid  In infants and small children, the effects of ICP differ
(CSF), intracranial blood volume and central nervous system because their cranial sutures have not closed. In infants, the
tissue. The normal intracranial pressure is between 5-15 fontanels, or soft spots on the head where the skull bones
mmHg. This is slightly lower than the mean systemic arterial have not yet fused, bulge when ICP gets too high.
pressure but considerably higher than venous pressure. 
Complications
 Death
 Permanent neurological problems
 Reversible neurological problems
 Seizures
 Stroke

Medical Mangement
 The treatment for IH depends on the etiology. In
addition to management of the underlying causes, major
considerations in acute treatment of increased ICP relates to
the management of stroke and cerebral trauma.
 A very common treatment for long-term, especially
idiopathic, cranial hypertension is medication with a special
 The intact cranium is essentially inexpandable
diuretic, especially one prescribed by a neurologist.
containing about 1400 grams of central nervous system
(CNS) or brain tissue, 75 ml of blood and about 75 ml of  In patients who have high ICP due to an acute injury it is
cerebrospinal fluid (CSF). These three components of the particularly important to ensure adequate airway, breathing,
cranial vault maintain a state of equilibrium. Their pressure and oxygenation. Inadequate blood oxygen levels (hypoxia)
and volume determine the condition of balance. or excessively high carbon dioxide levels (hypercapnia)
cause cerebral blood vessels to dilate, increasing the flow of
 According to Monro-Kellie hypothesis, any increase in blood to the brain and causing the ICP to [Link]
one of these elements must be balanced or compensated by
oxygenation also forces brain cells to produce energy using
a proportional constriction either or both of the other two
anaerobic metabolism, which produces lactic acid and lowers
components such as decreasing the volume of cerebral
pH, also dilating blood vessels and exacerbating the
blood flow, shifting CSF flow (into the spinal canal) or
[Link], blood vessels constrict when carbon
increasing CSF absorption. Absence of these compensatory
dioxide levels are below normal, so hyperventilating a
changes results to increased intracranial pressure. Once ICP
patient with a ventilator or bag valve mask can temporarily
reaches around 25 mmHg marked elevation in intracranial
reduce ICP. Hyperventilation was formerly a part of the
pressure will be [Link] intracranial pressure is a
standard treatment of traumatic brain injuries, but the
rise in the pressure inside the skull that can result from or
induced constriction of blood vessels limits blood flow to the
cause brain injury.
brain at a time when the brain may already be ischemic—
 AKA: ICP; Intracranial pressure – increased; Intracranial hence it is no longer widely used. Furthermore, the brain
hypertension; Acute increased intracranial pressure; Sudden adjusts to the new level of carbon dioxide after 48 to 72
increased intracranial pressure hours of hyperventilation, which could cause the vessels to
Causes rapidly dilate if carbon-dioxide levels were returned to
normal too [Link] is still used if ICP is
 Aneurysm rupture and subarachnoid hemorrhage resistant to other methods of control, or there are signs of
 Brain tumor brain herniation because the damage herniation can cause is
 Encephalitis so severe that it may be worthwhile to constrict blood
 Head injury vessels even if doing so reduces blood flow. ICP can also be
lowered by raising the head of the bed, improving venous
 Hydrocephalus (increased fluid around the brain)
drainage. A side effect of this is that it could lower pressure
 Hypertensive brain hemorrhage of blood to the head, resulting in a reduced and possibly
 Intraventricular hemorrhage inadequate blood supply to the brain. Venous drainage may
 Meningitis also be impeded by external factors such as hard collars to
 Subdural hematoma immobilize the neck in trauma patients, and this may also
increase the ICP. Sandbags may be used to further limit neck
 Status epilepticus movement.
 Stroke  In the hospital, the blood pressure can be artificially
 increased in order to increase CPP, increase perfusion,
Signs and symptoms oxygenate tissues, remove wastes and thereby lessen
swelling.[Since hypertension is the body’s way of forcing
 In general, symptoms and signs that suggest a rise in blood into the brain, medical professionals do not normally
ICP including headache, vomiting without nausea, ocular interfere with it when it is found in a patient with a head
palsies, altered level of consciousness, back pain and injury. When it is necessary to decrease cerebral blood flow,
papilledema. If papilledema is protracted, it may lead to MAP can be lowered using common antihypertensive agents
visual disturbances, optic atrophy, and eventually blindness. such as calcium channel [Link] there is an intact blood–
 In addition to the above, if mass effect is present with brain barrier, osmotherapy may be carried out by
resulting displacement of brain tissue, additional signs may administering IV mannitol to create a hypertonic solution
include pupillary dilatation, abducens palsies, and the within the blood to draw water out of the neurons. This helps
Cushing’s triad. Cushing’s triad involves an increased to reduce the fluid within the intracranial space, however
systolic blood pressure, a widened pulse pressure, prolonged administration may lead to increase in ICP.
bradycardia, and an abnormal respiratory [Link]  Struggling, restlessness, and seizures can increase
children, a low heart rate is especially suggestive of high metabolic demands and oxygen consumption, as well as
ICP. increasing blood [Link] and sedation
 Irregular respirations occur when injury to parts of the (particularly in the pre-hospital, ER, and intensive care
brain interfere with the respiratory drive. Cheyne–Stokes setting) are used to reduce agitation and metabolic needs of
respiration, in which breathing is rapid for a period and then the brain, but these medications may cause low blood
absent for a period, occurs because of injury to the cerebral pressure and other side [Link] if full sedation alone is
hemispheres or diencephalon. Hyperventilation can occur ineffective, patients may be paralyzed with drugs such as
when the brain stem or tegmentum is damaged. atracurium. Paralysis allows the cerebral veins to drain more
 As a rule, patients with normal blood pressure retain easily, but can mask signs of seizures, and the drugs can
have other harmful [Link] drugs are only
normal alertness with ICP of 25–40 mmHg (unless tissue
introduced if patients are fully sedated (this is essentially the
shifts at the same time). Only when ICP exceeds 40–50
same as a general anaesthetic)
  Intracranial pressure can be measured continuously with hypoglycemia or hyperglycemia, hyponatremia, anoxia);
intracranial transducers. A catheter can be surgically central nervous system infection; circulating disorders; drug
inserted into one of the brain’s lateral ventricles and can be toxicity; drug withdrawal states (alcohol, barbiturates); and
used to drain CSF (cerebrospinal fluid) in order to decrease congenital neurodegenerative disorders.
ICP’s. This type of drain is known as an EVD (extraventricular  Seizures are classified as partial or generalized by the
drain).In rare situations when only small amounts of CSF are origin of the seizure activity and associated clinical
to be drained to reduce ICP’s, drainage of CSF via lumbar manifestations.
puncture can be used as a treatment. There are many
clinical studies of non-invasive intracranial pressure
1. Simple partial seizures – manifest motor,
measurement methods currently being proposed, aimed to somatosensory, and psychomotor symptoms without
find reliable and accurate way to measure ICP non- impairment of consciousness.
invasively. Such method could improve diagnostics of  Complex partial seizures – manifest
traumatic brain injury and many other conditions associated impairment of consciousness with or without simple
with intracranial hypertension. partial symptoms.
 Craniotomies are holes drilled in the skull to remove  Generalized seizures – manifest a loss of
intracranial hematomas or relieve pressure from parts of the consciousness with convulsive or nonconvulsive
[Link] raised ICP’s may be caused by the presence of a behaviors and include tonic-clonic, myoclonic, atonic,
mass, removal of this via craniotomy will decrease raised and absence seizures.
ICP’s.  Simple partial seizures can progress to complex partial
 A drastic treatment for increased ICP is decompressive seizures, and complex partial seizures can secondarily
craniectomy, in which a part of the skull is removed and the become generalized.
dura mater is expanded to allow the brain to swell without  Seizures affect all ages. Most cases of epilepsy are
crushing it or causing [Link] section of bone identified in childhood, and several seizure types are
removed, known as a bone flap, can be stored in the particular to children.
patient’s abdomen and recited back to complete the skull Causes/ Risk Factors
once the acute cause of raised ICP’s has resolved.
Alternatively a synthetic material may be used to replace The origin of 50-70% of all cases of epilepsy is unknown. Epilepsy
the removed bone section. sometimes is the result of trauma at birth. Such causes include
insufficient oxygen to the brain; head injury; heavy bleeding or
 incompatibility between a woman’s blood and the blood of her
Nursing Intervention newborn baby; and infection immediately before, after, or at the
time of birth.
 Assess respiratory and neurological status
 Vital Sign’s Monitor and Documents (Plus,Blood Modifiable:
Pressure)
 Check Laboratory Test such as CPP  head trauma resulting from a car accident, gunshot
 Administration oxygen as order wound, or other injury.
 Give medication therapy as order  alcoholism
 Maintain Nutritional and food status  brain abscess or inflammation of membranes covering
the brain or spinal cord
 Maintain Diet plan give soft and healthy meal according  phenylketonuria (PKU, a disease that is present at birth,
to ditreation order
often is characterized by seizures, and can result in mental
 Sucction only as needed retardation) and other inherited disorders
 keep the patient in semi-Fowler’s positions  infectious diseases like measles, mumps, and diphtheria
 promot healthy and comfortable environmental  degenerative disease
 educate client’s about every kind of procedure  lead poisoning, mercury poisoning, carbon monoxide
 assist with turning,coughing,and deep breathing poisoning, or ingestion of some other poisonous substance
 Maintain the position and patency of the NG tube  suddenly discontinuing anti-seizure medication
 Enforce bed rest  hypoxic or metabolic encephalopathy (brain disease
 promote mouth care and skin care resulting from lack of oxygen or malfunctioning of other
 Maintain skin care change position every hourly to physical or chemical processes)
prevent bed sore  acute head injury
 Maintain seizure precautions  blood infection caused by inflammation of the brain or
 Provide emotional support client’s and his family the membranes that cover it
Non-Modifiable:
SEIZURES  Genetic factors
Assessment
 Also known as convulsions, epileptic seizures, and if
recurrent, epilepsy. 1. Generalized tonic-clonic (grand mal) seizure
 It is a sudden alterations in normal brain activity that  May be preceded by an aura such as a peculiar
cause distinct changes in behavior and body function. They
sensation or dizziness; then sudden onset of seizure
are thought to result from abnormal, recurrent, uncontrolled
with loss of consciousness.
electric discharges of neurons in the brain.
 Rigid muscle contraction in tonic phase which
clenched jaw and hands; eyes open with pupils dilated;
lasts 30 to 60 seconds.
 Rhythmic, jerky contraction and relaxation of
all muscles in clonic phase with incontinence and
frothing at the lips; may bite tongue or cheek, lasts
several minutes.
 Sleeping or dazed postictal state for up to
several hours.
2. Absence ( petit mal) seizure
 Loss of contact with environment for 5 to 30
seconds.
 Appears to be day dreaming or may roll eyes,
nod head, move hands, or smack lips.
 Resumes activity and is not aware of seizure.
 Pathophysiology of seizures is poorly understood but
seems to be related to metabolic and electrochemical 3. Myoclonic seizure (infantile spasm)
factors at the cellular level.  Seen in children or infants, caused by cerebral
 Predisposing factors include head or brain trauma, pathology, often with mental retardation.
tumors, cranial surgery, metabolic disorders (hypocalcemia,
  Infantile spasms usually disappear by age 4,  Antiepileptic drugs (AEDs) may be used singly or in
but child may develop other types of seizures. combination to increase effectiveness, treat mixed seizure
 Brief, sudden, forceful contractions of the types, and reduce adverse effects.
muscles of the trunk, neck, and extremities.  A wide variety of adverse reactions may occur, including
 Extensor type – infant extends head, spreads hepatic and renal dysfunction, vision disturbances,
arms out, bend body backward in “spread eagle” drowsiness, ataxia, anemia, leukopenia, thrombocytopenia,
position. psychotic symptoms, skin rash, stomach upset, and
 Mixed flexor and extensor types may occur in idiosyncratic reactions.
clusters or alternate. Surgical Interventions:
 May cause children to drop or throw  Surgical treatment of brain tumor or hematoma may
something. relieve seizures caused by these.
 Infant may cry out, grunt, grimace, laugh, or  Temporal lobectomy, extratemporal resection, corpus
appear fearful during an attack. callosotomy, or hemispherectomy may be necessary in
4. Partial (focal) motor seizure medically intractable seizure disorders.
 Rhythmic twitching of muscle group, usually 
hand or face. Nursing Interventions
 May spread to involve entire limb, other
extremities and face on that side, known as jacksonian  Monitor the entire seizure event, including prodromal
seizure. signs, seizure behavior, and postictal state.
 Monitor complete blood count, urinalysis, and liver
5. Partial (focal) somatosensory seizure function studies for toxicity caused by medications.
 Numbness and tingling in a part of the body.  Provide safe environment by padding side rails and
 May also be visual, taste, auditory, or olfactory removing clutter.
sensation.  Place the bed in low position.
6. Partial psychomotor (temporal lobe) seizure  Do not restrain the patient during seizure.
 May be aura of abdominal discomfort or bad  Do not put anything in the patient’s mouth during
odor or taste. seizure.
 Auditory or visual hallucinations, déjà vu  Maintain a patent airway until the patient is fully awake
feeling, or sense of fear or anxiety. after a seizure.
 Repetitive purposeless movements  Provide oxygen during the seizure if the patient become
(automatisms) may occur, such as picking at clothes, cyanotic.
smacking lips, chewing, and grimacing.  Place the patient on side during a seizure to prevent
 Lasts seconds to minutes. aspiration.
 Protect the patient’s head during the seizure.
7. Complex partial seizures – begin as partial seizures and
 Teach stress reduction techniques that will fit into the
progress to impairment of consciousness or impaired
patient’s lifestyle.
consciousness at onset.
 Tell the patient to avoid alcohol because it interferes
8. Febrile seizure with metabolism of AEDs and adds to sedation.
 Generalized tonic-clonic seizure with fever over  Encourage the patient to determine existence of
101.8 degrees Fahrenheit. triggering factors for seizures, such as skipped meals, lack of
 Occurs in children younger than age 5. sleep, and emotional stress.
 Treatment is to decrease temperature, treat  Remind the family the importance of following
source of fever, and control seizure. medication regimen and maintaining regular laboratory
 Long-term treatment to prevent recurrent testing, medical check ups, and visual examinations.
seizures with fever is controversial.  Encourage patient to follow a moderate lifestyle routine,
Diagnostic Evaluation including exercise, mental activity, and nutritious diet.

 EEG, with or without video monitoring, locates epileptic Discharge and Home Healthcare Guidelines
focus, spread, intensity, and duration, helps classify seizure
type.  Provide client teaching and discharge concerning:
 CT scanning or MRI identifies lesion that may cause of  Care during a seizure
seizure.  Need to continue drug therapy
 Single photon emission CT scanning (SPECT) or positron  Safety precautions/activity limitations
emission tomography (PET) identifies seizure foci.
 Need to wear Medic-Alert identification card
 Neuropsychological studies evaluate for behavioral
disturbances.  Potential behavioral changes and school problems
 Serum electrolytes, glucose, and toxicity screen  Availability of support groups/community agencies
determine the cause of first seizure.  How to assist the child in explaining disorder to peers
 Lumbar puncture and blood cultures may be necessary
if fever is present. CEREBROVASCULAR ACCIDENT
Primary Nursing Diagnosis
 A cerebrovascular accident (CVA), an ischemic stroke
 Risk for Trauma/Suffocation or “brain attack,” is a sudden loss of brain function resulting
Therapeutic Intervention from Cerebral Vascular Accident (Ischemic Stroke) a
disruption of the blood supply to a part of the brain.
 When a seizure occurs, the main goal is to protect the Description
person from injury. Try to prevent a fall. Lay the person on
the ground in a safe area. Clear the area of furniture or other  Stroke is the primary cerebrovascular disorder in the
sharp objects. United States.
 Cushion the person’s head.  Strokes are usually hemorrhagic (15%)
 Loosen tight clothing, especially around the person’s or ischemic/nonhemorrhagic (85%).
neck.  Ischemic strokes are categorized according to their
 Turn the person on his or her side. If vomiting occurs, cause: large artery thrombotic strokes (20%), small
this helps make sure that the vomit is not inhaled into the penetrating artery thrombotic strokes (25%), cardiogenic
lungs. embolic strokes (20%), cryptogenic strokes (30%), and other
 Look for a medical I.D. bracelet with seizure instructions. (5%).
 Stay with the person until he or she recovers, or until  Cryptogenic strokes have no known cause, and other
you have professional medical help. Meanwhile, monitor the strokes result from causes such as illicit drug use,
person’s vital signs (pulse, rate of breathing). coagulopathies, migraine, and spontaneous dissection of the
carotid or vertebral arteries.
Pharmacologic Interventions
  The result is an interruption in the blood supply to the  Disturbances in visualspatial relations (perceiving the
brain, causing temporary or permanent loss of movement, relation of two or more objects in spatial areas), frequently
thought, memory, speech, or sensation. seen in patients with right hemispheric damage
  Sensory losses: slight impairment of touch or more
Risk Factors severe with loss of proprioception; difficulty in interrupting
visual, tactile, and auditory stimuli
Nonmodifable Impaired Cognitive and Psychological Effects

 Advanced age (older than 55 years)  Frontal lobe damage: Learning capacity, memory, or
 Gender (Male) other higher cortical intellectual functions may be impaired.
 Race (African American) Such dysfunction may be reflected in a limited attention
Modifable span, difficulties in comprehension, forgetfulness, and lack
of motivation.
 Hypertension  Depression, other psychological problems: emotional
 Atrial fibrillation lability, hostility, frustration, resentment, and lack of
 Hyperlipidemia cooperation.
Assessment and Diagnostic Methods
 Obesity
 Smoking  History and complete physical and neurologic
 Diabetes examination
 Asymptomatic carotid stenosis and valvular heart  Noncontrast CT scan
disease (eg, endocarditis, prosthetic heart valves)  12lead ECG and carotid ultrasound
 Periodontal disease  CT angiography or MRI and angiography
Pathophysiology  Transcranial Doppler flow studies
 Transthoracic or transesophageal echocardiography
 Xenonenhanced CT scan
 Single photon emission CT (SPECT) scan
Prevention

 Help patients alter risk factors for stroke; encourage

patient to quit smoking, maintain a healthy weight, follow a
healthy diet (including modest alcohol consumption), and
exercise daily.
 Prepare and support patient through carotid
endarterectomy.
 Administer anticoagulant agents as prescribed (eg,
lowdose aspirin therapy).

Medical Management
 Recombinant tissue plasminogen activator (tPA),
unless contraindicated; monitor for bleeding
 Anticoagulation therapy
 Management of increased intracranial pressure
(ICP): osmotic diuretics, maintain PaCO2 at 30 to 35 mm Hg,
position to avoid hypoxia (elevate the head of bed to
promote venous drainage and to lower increased ICP)
 Possible hemicraniectomy for increased ICP from
brain edema in a very large stroke
 Intubation with an endotracheal tube to establish a
patent airway, if necessary
 Continuous hemodynamic monitoring (the goals for
blood pressure remain controversial for a patient who has
not received thrombolytic therapy; antihypertensive
treatment may be withheld unless the systolic blood
pressure exceeds mm Hg or the diastolic blood pressure
exceeds 120 mm Hg)
 Neurologic assessment to determine if the stroke is
evolving and if other acute complications are developing
Management of Complications
Clinical Manifestations
 Decreased cerebral blood flow: Pulmonary care,
General signs and symptoms include numbness or weakness maintenance of a patent airway, and administration of
of face, arm, or leg (especially on one side of body); confusion or supplemental oxygen as needed.
change in mental status; trouble speaking or  Monitor for UTIs, cardiac dysrhythmias, and
understanding speech; visual disturbances; loss of balance, complications of immobility.
dizziness, difficulty walking; or sudden severe headache.
Nursing Assessment
Motor Loss During Acute Phase (1 to 3 days)
 Hemiplegia, hemiparesis Weigh patient (used to determine medication dosages), and
 Flaccid paralysis and loss of or decrease in the deep maintain a neurologic flow sheet to reflect the following nursing
tendon reflexes (initial clinical feature) followed by (after 48 assessment parameters:
hours) reappearance of deep reflexes and abnormally
increased muscle tone (spasticity)  Change in level of consciousness or responsiveness,
Communication Loss ability to speak, and orientation
 Presence or absence of voluntary or
 Dysarthria (difficulty speaking) involuntary movements of the extremities: muscle tone,
 Dysphasia (impaired speech) or aphasia (loss of speech) body posture, and head position
 Apraxia (inability to perform a previously learned action)  Stiffness or flaccidity of the neck
Perceptual Disturbances and Sensory Loss  Eye opening, comparative size of pupils and pupillary
reactions to light, and ocular position
 Visualperceptual dysfunctions (homonymous
hemianopia [loss of half of the visual field])
  Color of face and extremities; temperature and moisture 
of skin Establishing an Exercise Program
 Quality and rates of pulse and respiration; ABGs,
body temperature, and arterial pressure  Provide full range of motion four or five times a day
 Volume of fluids ingested or administered and volume to maintain joint mobility, regain motor control,
prevent contractures in the paralyzed extremity, prevent
of urine excreted per 24 hours
further deterioration of the neuromuscular system, and
 Signs of bleeding enhance circulation. If tightness occurs in any area, perform
 Blood pressure maintained within normal limits rangeofmotion exercises more frequently.
Postacute Phase  Exercise is helpful in preventing venous stasis, which
Assess the following functions: may predispose the patient to thrombosis and
pulmonary embolus.
 Mental status (memory, attention span, perception,  Observe for signs of pulmonary embolus or excessive
orientation, affect, speech/language). cardiac workload during exercise period (eg, shortness
 Sensation and perception (usually the patient of breath, chest pain, cyanosis, and increasing pulse rate).
has decreased awareness of pain and temperature).  Supervise and support patient during exercises;
 Motor control (upper and lower extremity plan frequent short periods of exercise, not longer
movement); swallowing ability, nutritional and hydration periods; encourage patient to exercise unaffected side at
intervals throughout the day.
status, skin integrity, activity tolerance, and bowel and
bladder function.
 Continue focusing nursing assessment on impairment
of function in patient’s daily activities. Preparing for Ambulation

 Start an active rehabilitation program when
Diagnosis consciousness returns (and all evidence of bleeding is gone,
Nursing Diagnoses when indicated).
 Teach patient to maintain balance in a sitting
 Impaired physical mobility related to hemiparesis, loss position, then to balance while standing (use a tilt table if
of balance and coordination, spasticity, and brain injury needed).
 Acute pain related to hemiplegia and disuse  Begin walking as soon as standing balance is
 Deficient selfcare (bathing, hygiene, toileting, achieved (use parallel bars and have wheelchair available in
dressing, grooming, and feeding) related to stroke sequelae anticipation of possible dizziness).
 Disturbed sensory perception (kinesthetic, tactile,  Keep training periods for ambulation short and frequent.
or visual) related to altered sensory reception,
transmission, and/or integration BRAIN ABSCESS
 Impaired swallowing
 Impaired urinary elimination related to flaccid  A brain abscess is a collection of infectious material
bladder, detrusor instability, confusion, or difficulty in within the tissue of the brain.
communicating  Bacteria are the most common causative organisms. An
 Disturbed thought processes related to brain damage abscess can result from intra-cranial surgery, penetrating
 Impaired verbal communication related to brain damage head injury, or tongue piercing.
 Risk for impaired skin integrity related to hemiparesis  Organisms causing brain abscess may reach the brain
or hemiplegia, decreased mobility by hematologic spread from the lungs, gums, tongue, or
 Interrupted family processes related to catastrophic heart, or from a wound or intra-abdominal infection. It can
illness and caregiving burdens be a complication in patients whose immune systems have
been suppressed through therapy or disease.
 Sexual dysfunction related to neurologic deficits or fear
of failure

Collaborative Problems/Potential Complications
 Decreased cerebral blood flow due to increased ICP;
inadequate oxygen delivery to the brain; pneumonia.

Planning and Goals
The major goals for the patient (and family) may
include improved mobility, avoidance of shoulder pain,
achievement of selfcare, relief of sensory and perceptual
deprivation, prevention of aspiration, continence of bowel and
bladder, improved thought processes, achieving a form of
communication, maintaining skin integrity, restored family
functioning, improved sexual function, and absence of Prevention
complications. Goals are affected by knowledge of what the
patient was like before the stroke.  To prevent brain abscess, otitis media, mastoiditis,
rhinosinusitis, dental infections, and systemic infections
Nursing Interventions should be treated promptly.

Improving Mobility and Preventing Deformities


Clinical Manifestations
 Position to prevent contractures; use measures to
relieve pressure, assist in maintaining good body alignment,  Generally, symptoms result from alterations in
and prevent compressive neuropathies. intracranial dynamics (edema, brain shift), infection, or the
 Apply a splint at night to prevent flexion of location of the abscess.
affected extremity.  Headache, usually worse in morning, is the most
 Prevent adduction of the affected shoulder with a prevailing symptom.
pillow placed in the axilla.  Fever, vomiting, and focal neurologic deficits (weakness
 Elevate affected arm to prevent edema and fibrosis. and decreasing vision) occur as well.
 Position fingers so that they are barely flexed;  As the abscess expands, symptoms of increased
place hand in slight supination. If upper extremity spasticity intracranial pressure (ICP) such as decreasing level of
is noted, do not use a hand roll; dorsal wrist splint may consciousness and seizures are observed.
be used. 
 Change position every 2 hours; place patient in a Assessment and Diagnostic Methods
prone position for 15 to 30 minutes several times a day.
  Neuroimaging studies such as MRI or CT scanning to 12. Memory changes and confusion
identify the size and location of the abscess
 Aspiration of the abscess, guided by CT or MRI, to
culture and identify the infectious organism Primary Nursing Diagnosis
 Blood cultures, chest xray, electroencephalogram (EEG)
 Impaired physical mobility related to fatigue and
weakness.
Diagnostic Evaluation
Medical Management
 Cerebrospinal fluid (CSF) analysis reveals elevated
 The goal is to eliminate the abscess. protein level, increased white blood cells. Electrophoresis of
 Treatment modalities include antimicrobial therapy, CSF shows increased myelin basic protein and IgG bands.
surgical incision, or aspiration (CTguided stereotactic  Other Tests: No single test reliably diagnoses MS.
needle). Supporting tests include electroencephalography, evoked
 Medications used include corticosteroids to reduce the potential studies, computed tomography (CT) scan, and
inflammatory cerebral edema and antiseizure medications magnetic resonance imaging (MRI).
for prophylaxis against seizures (phenytoin, phenobarbital). Medical Management
 Abscess resolution is monitored with CT scans.
 Most medical treatment is designed to slow disease
 progression and address the symptoms of the disease, such
Nursing Management as urinary retention, spasticity, and motor and speech
deficits. Currently, however, physicians generally prescribe
 Nursing interventions support the medical treatment, as steroid therapy to reduce tissue edema during an acute
do patient teaching activities that address neurosurgical exacerbation.
procedures.  Consult with a physical therapist if the patient needs to
 Patients and families need to be advised of neurologic learn how to use assistive devices or needs to learn
deficits that may remain after treatment (hemiparesis, exercises to maintain muscle tone and joint mobility.
seizures, visual deficits, and cranial nerve palsies).  Muscle stretching for spastic muscles and selective
 The nurse assesses the family’s ability to express their strengthening exercises for weakness are prescribed.
distress at the patient’s condition, cope with the patient’s  A social service agency may be required to help the
illness and deficits, and obtain support. family deal with the often expensive and long-term financial
effect of the disease. Vocational redirection may also be
MULTIPLE SCLEROSIS required.
 For a patient who is experiencing depression, consider a
referral to a psychiatric clinical nurse specialist. Family
1. Multiple sclerosis is a chronic, progressive, non- counseling is often very helpful.
contagious, degenerative disease of the CNS characterized Pharmacologic Highlights
by demyelinization of the neurons.
2. Multiple sclerosis usually occurs between the ages of 20  Corticosteroids agents, such as Prednisone (Orasone);
methylprednisolone or (Solu-Medrol);
and 40 and consists of periods of remissions and
dexamethasone(Decadron) maybe used to help decrease
exacerbations.
symptoms and induce remissions through anti-inflammatory
3. The causes are unknown, but the disease is thought to effects.
be a result of an autoimmune response or viral infection.  Immunomodulatory agents, such as Interferon,
4. Precipitating factors include pregnancy, fatigue, stress,
cyclosporine, azathioprine, methotrexate maybe used to
help decrease symptoms and induce remissions; treatment
infection, and trauma. includes combination therapy using two or more of these
5. Electroencephalogram findings are abnormal agents.
 Other Drugs: Antianxiety agents, such as
6. A lumbar puncture indicates increased gamma globulin, chlordiazepoxide hydrochloride (Librium), may be prescribed
but the serum globulin level is normal. to manage mood swings; baclofen (Lioresal) or dantrolene
Causes (Dantrium) may be used to relieve muscle spasticity; and
patients with urinary symptoms may require behanechol
The cause of MS is unknown. Some evidence suggests that an
(Urecholine) or oxybutynin (Ditropan).
infective agent causes a predisposition to MS, although that agent
has not been identified. Some evidence supports immunologic, Nursing Interventions
environmental, or genetic factors as possible causes of the
disease. The risk of developing MS is 15 times higher when the 1. Provide bed rest during exacerbation.
disease is present in the patient’s immediate family. Conditions
such as pregnancy, infection, and trauma seem to precipitate the
2. Protect the client from injury by providing safety
onset of MS or cause relapses measures.
3. Place an eye patch on the eye for diplopia.
Assessment
4. Monitor for potential complications such as urinary tract
1. Fatigue and weakness infections, calculuses, decubitus ulcers, respiratory tract
infections, and contractures.
2. Ataxia and vertigo
5. Promote regular elimination by bladder and bowel
3. Tremors and spasticity of the lower extremities training.
4. Parasthesias 6. Encourage independence.

5. Blurred vision and diplopia 7. Assist the client to establish a regular exercise and rest
program.
6. Nystagmus
8. Instruct the client to balance moderate activity with rest
7. Dysphasia periods.
8. Decreased perception to pain, touch, and temperature 9. Assess the need for and provide assistive devices.
9. Bladder and bowel disturbances, including urgency, 10. Initiate physical and speech therapy.
frequency, retention, and incontinence
11. Instruct the client to avoid fatigue, stress, infection,
10. Abnormal reflexes, including hyperreflexia, absent overheating, and chilling.
reflexes, and a positive Babinski’s reflex
12. Instruct the client to increase fluid intake and eat a
11. Emotional changes such as apathy, euphoria, irritability, balanced diet, including low-fat, high-fiber foods and foods
and depression high in potassium.
 13. Instruct the client in safety measures related to sensory 3. Possible hypoventilation due to chest muscle weakness.
loss, such as regulating the temperature of bath water and
avoiding heating pads.
4. Difficulty with swallowing, chewing, speech, and gag,
indicating fifth (trigeminal) and ninth (glossopharyngeal)
14. Instruct the client in safety measures related to motor cranial nerve movement.
loss, such as avoiding the use of scatter rugs and using
assistive devices.
5. Reduce or absent deep tendon reflexes, position and
vibratory perception.
15. Instruct the client in the self-administration of prescribed 6. Autonomic dysfunction with orthostatic hypotension and
medications.
tachycardia.
16. Provide information about the National Multiple Sclerosis Diagnostic Evaluation
Society.
1. Lumbar puncture obtains cerebrospinal fluid samples,
which reveal low cell count and high protein levels.
Guillain-Barré Syndrome 2. Nerve conduction studies, which allow decreased
 Also known as polyradiculoneuritis. conduction velocity of peripheral nerves due to
demyelination.
 It is an acute inflammatory polyneuropathy of the
peripheral sensory and motor and nerve roots. 3. Abnormal laboratory studies may point to prior infection
 Affected nerves are demyelinated with possible axonal or illness.
degeneration. Primary Nursing Diagnosis
 It’s exact cause is unknown, Guillain-Barré Syndrome is
believed to be an autoimmune disorder that may be  Ineffective airway clearance related to
triggered by viral infection, Campylobacter diarrheal illness, weakness,problems in swallowing,and respiratory muscle
immunization, or other precipitating event. paralysis
 The syndrome is marked by acute onset of symmetric Therapeutic Intervention / Medical Management
progressive muscle weakness, most often beginning in the
legs and ascending to involve the trunk, upper extremities,
 GBS is considered a medical emergency; patient is
managed in an intensive care unit.
and facial muscles. Paralysis may develop.
 Complications may include respiratory failure, cardiac  Respiratory problems may require mechanical
ventilation
arrhythmias, and complications of immobility.
 Plasmapheresis (plasma exchange) or intravenous
immunoglobulin (IVIG) may be used to limit deterioration or
demyelination
 Continuous electrocardiogram (ECG) monitoring:
Observe and treat cardiac dysrhythmias and other labile
complications of autonomic dysfunction. Tachycardia and
hypertension are treated with short acting medication such
as alpha-adrenergic blocking agents. Hypotension is manage
by increasing the amount of intravenous fluid administered.
Pharmacologic Intervention
 Atrophine may be administered to avoid episodes of
bradycardia during endotracheal suctioning and physical
therapy. Anticoagulants and thigh-high elastic compression
stockings or sequential compression boots may be ordered
to prevent thrombosis and pulmonary emboli secondary to
immobility.
Nursing Intervention

1. Monitor respiratory status through vital capacity

measurements, rate and depth of respirations, and breath
sounds.
Pathophysiology 2. Monitor level of muscle weakness as it ascends toward
respiratory muscles. Watch for breathlessness while talking
GBS results from an autoimmune (cell-mediated and humoral) which is a sign of respiratory fatigue.
attack on peripheral nerve myelin proteins ( substances speeding
conduction of nerve impulses) . The Schwann cell( which produces 3. Monitor the patient for signs of impending respiratory
myelin in the peripheral nervous system) is paired in GBS, failure.
allowing for remyelination in the recovery phase of the disorder.
4. Monitor gag reflex and swallowing ability.
Causes 5. Position patient with the head of bed elevated to provide
Although the exact cause of GBS is unknown, two-thirds of for maximum chest excursion.
patients who develop it have had a viral or bacterial infection 1 to 6. Avoid giving opioids and sedatives that may depress
3 weeks before the development of symptoms. The most typical respirations.
site and cause of infections are a lung or intestinal infection
caused by Campylobacter jejuni(C. jejuni) or cytomegalovirus 7. Position patient correctly and provide range-of-motion
(CMV). Infections with Epstein-Barr virus and Mycoplasma exercises.
pneumoniae are also associated with GBS. Another 10% of
patients have had recent surgical procedures during the 4 weeks
8. Provide good body alignment, range-of-motion
before GBS developed. Other diseases that have been linked to exercises, and change of position to prevent complications
the development of GBS are lymphoma,human immunodeficiency such as contractures, pressure sores, and dependent edema.
virus (HIV) disease,gastroenteritis,Hodgkin’s disease, and lupus 9. Ensure adequate nutrition without the risk of aspiration.
erythematosus. In some cases,GBS develops after immunization
for influenza. 10. Encourage physical and occupational therapy exercises
to help the patient regain strength during rehabilitation
Assessment phase.
11. Provide assistive devices as needed (cane or wheelchair)
1. Acute onset (hours to weeks) of progressive, usually to maximize independence and activity.
ascending muscle weakness and fasciculation, possibly
leading to paralysis (maximal weakness is reached within 2 12. If verbal communication is possible, discuss the patient’s
weeks). fears and concerns.
2. Paresthesia and painful sensations.
 13. Provide choices in care to give the patient a sense of 8. Diminished breath sounds
control.
9. Respiratory paralysis and failure
14. Teach patient about breathing exercises or use of an Complications
incentive spirometer to reestablish normal breathing
patterns. Myasthenic Crisis

15. Instruct patient to wear good supportive and protective  This sudden onset of muscle weakness is usually the
shoes while out of bed to prevent injuries due to weakness result of undermedication or no cholinergic medication at all.
and paresthesia. Myasthenic crisis may result from progression of the disease,
emotional upset, systemic infections, medications, surgery,
16. Instruct patient to check feet routinely for injuries or trauma. The crisis is manifested by sudden onset of acute
because trauma may go unnoticed due to sensory changes. respiratory distress and inability to swallow or speak.
17. Urge the patient to maintain normal weight because Cholinergic Crisis
additional weight will further stress monitor function.  Caused by overmedication with cholinergic or
18. Encourage scheduled rest periods to avoid fatigue. anticholinesterase drugs, cholinergic crisis produces muscle
weakness and the respiratory depression of myasthenic
crisisas well as gastrointestinal symptoms (nausea,
MYASTHANIAS GRAVIS vomiting, diarrhea), sweating, increased salivation, and
bradycardia.
Primary Nursing Diagnosis
1. Myasthenia Gravis is a neuromuscular disease
characterized by considerable weakness and abnormal  Ineffective airway clearance related to difficulty in
fatigue of the voluntary muscles. swallowing and aspiration
Diagnostic Evaluation
 Injection of edrophonium (Tensilon) is used to confirm
the diagnosis (have atropine available for side effects).
Improvement in muscle strength represents a positive test
and usually confirms the diagnosis.
 MRI may demonstrate an enlarged thymus gland.
 Test includes serum analysis for acetylcholine receptor
and electromyography (EMG) to measure electrical potential
of muscle cells.

2. A defect in the transmission of nerve impulses at the

myoneural junction occurs.
3. Causes include insufficient secretion of acetylcholine,
excessive secretion of cholinesterase, and unresponsiveness
of the muscle fibers to acetylcholine.
Causes
MG, thought to be an autoimmune disorder, is caused by a loss of
acetylcholine (ACh) receptors in the postsynaptic neurons at the
neuromuscular junction. About 80% of all MG patients have
elevated titers for ACh receptor antibodies, which can prevent the Holding your arms above your shoulders until they drop is one exercise that may
ACh molecule from binding to these receptor sites or can cause be performed during the Tensilon test. In this test, the drug Tensilon is
damage to them. MG is often associated with thymic tumors. administered, and the response in the muscles are evaluated to help diagnose
myasthenia gravis or to help differentiate between myasthenia gravis and other
conditions.
Assessment Medical Management
1. Weakness and fatigue Management is directed at improving function through the
administration of anticholinesterase medications and by reducing
2. Difficulty chewing and removing circulating antibodies. Patients with MG are usually
3. Dysphagia
managed on an outpatient basis unless hospitalization is required
for managing symptoms or complications.

Pharmacologic Highlights
 Anticholinesterase drugs such as Pyridostigmine
bromide (Mestinon), neostigmine bromide (Prostigmine);
neostigmine methylsulfate can be given as a continuous
infusion if the patient cannot take oral medication.
Anticholinesterase drugs blocks the action of the enzyme
anticholinesterase, thereby producing symptomatic
improvement; atropine must be readily available to treat
cholinergic side effects and medications must be
4. Ptosis administered on time, or the patient may be too weak or
unable to swallow the drug.
5. Diplopia
 Prednisone is used to suppresses the autoimmune
6. Weak, hoarse voice activity of MG
 Nonsteroidal immunosuppressants such as Azathioprine
7. Difficulty breathing (Imuran), cyclophosphamide (Cytoxin) is used to suppress
 autoimmune activity when patients do not respond to
prednisone; can produce extreme immunosuppression and
toxic side effects
Nursing Interventions

1. Monitor respiratory status and ability to cough and deep

breathe adequately.
2. Monitor for respiratory failure.
3. Maintain suctioning and emergency equipment at the
bedside.
4. Monitor vital signs.
5. Monitor speech and swallowing abilities to prevent
aspiration.
6. Encourage the client to sit up when eating.
7. Assess muscle status. Characteristics/ Signs and Symptoms
8. Instruct the client to conserve strength. The disease course is divided into four stages, with progressive
9. Plan short activities that coincide with times of maximal
patterns of cognitive and functional impairments.
muscle strength. Pre-dementia
10. Monitor for myasthenic and cholinergic crises. Stage 1 is characterized by recent memory loss, increased
11. Administer anticholinesterase medications as irritability, impaired judgment, loss of interest in life, decline of
prescribed. problem-solving ability, and reduction in abstract thinking.
Remote memory and neurological exam remain unchanged from
12. Instruct the client to avoid stress, infection, fatigue, and baseline.
over-the counter medications.
Early
13. Instruct the client to wear a Medic-Alert bracelet.
Stage 2 lasts 2 to 4 years and reveals a decline in the patient’s
14. Inform the client about services from the Myasthenia ability to manage personal and business affairs, an inability to
Gravis Foundation. remember shapes of objects, continued repetition of a
meaningless word or phrase (perseveration), wandering or
circular speech patterns (circumlocution dysphasia), wandering at
ALZHEIMERS night, restlessness, depression, anxiety, and intensification of
cognitive and emotional changes of stage 1.

Moderate
Stage 3 is characterized by impaired ability to speak (aphasia),
inability to recognize familiar objects (agnosia), inability to use
objects properly (apraxia), inattention, distractibility, involuntary
emotional outbursts, urinary or fecal incontinence, lint-picking
motion, and chewing movements. Progression through stages 2
and 3 varies from 2 to 12 years.

Advanced
Stage 4, which lasts approximately 1 year, reveals a patient with
a masklike facial expression, no communication, apathy,
withdrawal, eventual immobility, assumed fetal position, no
appetite, and emaciation.
Description
Diagnostic Examination
 Alzheimer’s disease is an irreversible, progressive brain
disease that slowly destroys memory and thinking skills, and  Alzheimer’s disease is usually diagnosed clinically from
eventually even the ability to carry out the simplest tasks. In the patient history, collateral history from relatives, and
most people with Alzheimer’s, symptoms first appear after clinical observations, based on the presence of characteristic
age 60. neurological and neuropsychological features and the
 Alzheimer’s disease is the most common cause of absence of alternative conditions.
dementia among older people. Dementia is the loss of  Advanced medical imaging with computed tomography
cognitive functioning—thinking, remembering, and (CT) or magnetic resonance imaging (MRI), and with single
reasoning—to such an extent that it interferes with a photon emission computed tomography (SPECT) or positron
person’s daily life and activities. Estimates vary, but experts emission tomography (PET) can be used to help exclude
suggest that as many as 5.1 million Americans may have other cerebral pathology or subtypes of [Link],
Alzheimer’s. it may predict conversion from prodromal stages (mild
 Dementia involves progressive decline in two or more of cognitive impairment) to Alzheimer’s disease.
the following areas of cognition: memory, language,  Assessment of intellectual functioning including memory
calculation, visual-spatial perception, judgment, abstraction, testing can further characterize the state of the
and behavior. [Link] organisations have created diagnostic
Causes criteria to ease and standardize the diagnostic process for
practicing physicians. The diagnosis can be confirmed with
The cause of AD is unknown but knowledge about the hereditary very high accuracy post-mortem when brain material is
links is growing. Patients with Down syndrome eventually develop available and can be examined histologically.
DAT if they live long enough. There is a higher-than-normal Primary Nursing Diagnosis
concentration of aluminum in the brain of a person with DAT, but
the effect is unknown. A distinct protein, AZ 50, has been Self-care deficit related to impaired cognitive and motor function
identified at autopsy in the brains of DAT patients. This protein  Outcomes. Self-care: Activities of daily living—Bathing,
has been isolated from neurons that were not yet damaged, Hygiene, Eating, Toileting; Cognitive ability; Comfort level;
suggesting that its presence early in the degenerative process Role performance; Social interaction skills; Hope
might cause the neuronal damage. The life expectancy of a DAT  Interventions. Self-care assistance: Bathing and
patient is reduced 30% to 60%. Hygiene; Oral health management; Behavior management;
Body image enhancement; Emotional support; Mutual goal
setting; Exercise therapy; Discharge planning
 6. Encourage the patient to exercise as ordered to help
maintain mobility.
7. Encourage patient independence and allow ample time
for him to perform tasks.
8. Encourage sufficient fluid intake and adequate nutrition.
9. Take the patient to the bathroom at least every 2 hours
and make sure he knows the location of the bathroom.
10. Assist the patient with hygiene and dressing as
PET scan of the brain of a person with AD showing a loss of function in the necessary.

Other Nursing Diagnosis

temporal lobe
11. Frequently check the the patient’s vital signs.
Risk for Injury related to:
12. Monitor the patient’s fluid and food intake to detect
imbalances.
 Unable to recognize / identify hazards in the 13. Inspect the patient’s skin for evidence of trauma, such
environment. as bruises or skin breakdown.
 Disorientation, confusion, impaired decision making. 14. Encourage the family to allow the patient as much
 Weakness, the muscles are not coordinated, the independence as possible while ensuring safety to the
presence of seizure activity. patient and others.
Medical Management
There is no cure for Alzheimer’s disease; available treatments
offer relatively small symptomatic benefit but remain palliative in
nature.

The initial management of the patient begins with education of

the family and caregivers regarding the disease, the prognosis,
and changes in lifestyle that are necessary as the disease
progresses.
Basic collaborative principles include:

 Keep requests for the patient simple

 Avoid confrontation and requests that might lead to
frustration
 Remain calm and supportive if the patient becomes
upset
 Maintain a consistent environment
 Provide frequent cues and reminders to reorient the
patient
 Adjust expectations for the patient as he or she declines
in capacity
Pharmacologic Treatment
 Generally, therapy is focused on symptoms with an
attempt to maintain cognition.
 Donepezil (cholinesterase inhibitor; elevates
acetylcholine concentration in cerebral cortex by slowing
degradation of acetylcholine released by intact
neurons)which improves cognitive symptoms; improves
cognitive function in the early stages of the disease
only; drug effects diminish as the disease progresses
 Antidepressants (selective serotonin reuptake inhibitors;
increases activity of serotonin in the brain) which treats
depression, anxiety, and irritability
 Other Tests: Supporting tests include computed
tomography (CT) scan; magnetic resonance imaging (MRI);
positron emission tomography (PET). During the early stages
of dementia, CT and MRI may be normal, but in later stages,
an MRI may show a decrease in the size of the cerebral
cortex or of the area of the brain responsible for memory,
particularly the hippocampus. Genetic testing for the ApoE
gene is available and the presence of the gene is a risk
factor for AD. Genetic tests may be helpful in diagnosis, but
further studies are needed to confirm their reliability.
Nursing Intervention

1. Establish an effective communication system with the

patient and his family to help them adjust to the patient’s
altered cognitive abilities.
2. Provide emotional support to the patient and his family.
3. Administer ordered medications and note their effects. If
the patient has trouble swallowing, crush tablets and open
capsules and mix them with a semi soft food.
4. Protect the patient from injury by providing a safe,
structured environment.
5. Provide rest periods between activities because the
patient tires easily.