Medsurg Finals Theory

MED SURG FINALE b.
Hypoxic encephalopathies: severe congestive heart

failure, chronic obstructive pulmonary disease, severe
anemia,
The human brain requires a constant supply of prolonged hypertension
oxygen and glucose for normal function. Interruption c. Toxicity: heavy metals, carbon monoxide, drugs
of this supply will cause loss of consciousness within (opiates, barbiturates and alcohol)
a few seconds and may also cause even permanent d. Extremes of body temperature: heat stroke,
brain damage hypothermia
e. Seizures
Introduction
• Altered level of consciousness is not a disorder Pathophysiology
itself, rather it is a result of multiple pathophysiological • The underlying causes of neurologic dysfunction are
phenomena. disruption in the cells of the nervous system,
neurotransmitters, or brain anatomy due to the
• The cause may different etiologic factor
1. neurogenic( HI,BT,CVA etc.)
2. toxicological ( alcohol, poison & drug overdose} 1. Cellular brain edema or disrupting the chemical
3. metabolic ( hepatic, renal failure) transmission at the receptor site, resulting in faulty
impulse transmission and impeding communication
Altered Level of Consciousness within the brain or from the brain to other body parts
• Consciousness is a state of wakefulness and 2. Brain trauma, brain edema, tumor pressure,
awareness of self and the environment. increased or decrease blood or cerebrospinal fluid
• Altered level of consciousness is defined as a result in disruption in the anatomic structure of the
condition of being less responsive to and aware of brain and faulty impulse transmission and impeding
environmental stimuli. communication within the brain or from the brain to
• LOC is gauged on a continuum with a normal state another body part
of alertness and full cognition
(consciousness) on one end and coma on the other Clinical Manifestations
end. • As the patient’s state of alertness and
consciousness decreases, there will be
• Alert or conscious- attends to the changes in:
environment, responds appropriately to a. pupillary response
commands and questions with minimal b. eye opening response,
stimulation c. verbal response
• Confused-disoriented to surroundings, may have d. motor response.
impaired judgment, may need cues to respond to •Can be assessed using Glasgow Coma scoring
commands
• Lethargic-drowsy, needs gentle verbal or touch
stimulation to initiate a response
• Obtunded- responds slowly to external
stimulation, needs repeated stimulation to
maintain attention and response to the
environment
• Stupors- responds only minimally with
vigorous stimulation may only moan as a verbal
response
• Comatose- no observable response to any
external stimuli
Etiology of Unconsciousness
1. Structural
a. Trauma: concussion, contusion, traumatic
intracerebral hemorrhage, cerebral edema,
subdural and epidural hematoma
b. Vascular disease; infarction, intracerebral
hemorrhage, subarachnoid hemorrhage
c. Infection: meningitis, encephalitis, brain abscess
d. Neoplasms: primary brain tumor, metastatic tumors
2. Metabolic
• Initial changes may be reflected by subtle behavioral
a. Systemic metabolic derangement: hypoglycemia,
changes such as:
diabetic
ketoacidosis, hyperglycemic nonketotic hyperosmolar restlessness or increased anxiety
state, uremia, hepatic encephalopathy, hyponatremia, there will be a decrease in wakefulness
myxedema decrease attention to the environment
confusion, disorientation,
1
JOHN 3:30 HE MUST INCREASE, BUT I MUST DECREASE
agitation present.
• Assess alertness by the patient’s ability to open the
poor memory
eyes spontaneously or to a stimulus.
decrease ability to carry out activities of daily • Periorbital edema or trauma, which may prevent the
living patient from opening the eyes.
decreased mobility • Motor response includes spontaneous,
incontinence purposeful movement, movement only in
response to noxious stimuli, or abnormal
hallucination and delusions
posturing (decorticate or Decerebrate).
• Respiratory status and pattern of respiration.
Diagnostic Studies
• Eye signs, and reflexes.
• Complete blood count to rule out severe anemia
• Corneal reflex.
evidenced by low RBC, and decreased PCV.
• Facial symmetry.
infection,
• swallowing reflex.
evidenced by elevated WBCs and differentials count .
• Deep tendon reflex.
➢ Blood Glucose to rule out Hypo/Hyper
glycemia
➢ Electrolytes: Urea, Creatinine to rule
outelectrolyte imbalances as well as uremic
encephalopathy.
➢ Calcium level
➢ Partial thromboplastin and prothrombin time
➢ Procedures used to identify the cause of
unconsciousness include
➢ Scanning
➢ Computed tomography
➢ Magnetic resonance imaging
➢ Positron emission tomography
➢ Electroencephalography
Nursing Diagnosis
Ineffective airway clearance related to
Potential Complications of Patient with
Altered LOC altered level of consciousness.
• 1.Respiratory failure Risk of injury related to a decreased level
• 2.Pneumonia of consciousness.
• 3.Pressure ulcers Deficient fluid volume related to inability to
• 4.Aspiration. take in fluids.
Impaired oral mucous membranes related
Medical Management
to mouth breathing, absence of pharyngeal
• Obtain and maintain a patent airway
reflex, and altered fluid intake.
a. Intubation or a tracheostomy may be
performed. Risk for impaired skin integrity related to
b. Mechanical ventilator is used to maintain immobility.
adequate oxygenation. Impaired tissue integrity of cornea related
c. The circulatory status (blood pressure, heart rate) to diminished or absence of corneal reflex.
is monitored to ensure adequate perfusion to the body Ineffective thermoregulation related to
and brain. damage to the hypothalamic center
• An intravenous catheter is inserted to provide
Impaired urinary elimination (incontinence
access for fluids
or retention) related to impairment in
• Intravenous medications.
neurologic sensing and control.
• Nutritional support, using either a feeding tube or a
gastrostomy tube Bowel incontinence related to impairment
• Determine and treat the underlying causes of altered in neurologic sensing and control.
LOC Disturbed sensory perception related to
.• Pharmacological management of complications neurologic impairment.
and strategies to prevent complications. Interrupted family processes related to a
health crisis.
NURSING PROCESS
THE PATIENT WITH AN ALTERED LEVEL Nursing Interventions
OF CONSCIOUSNESS
• Maintaining the airway
Assessment 1. Remove accumulated secretion to eliminate the
• Level of responsiveness or consciousness danger of aspiration.
• Verbal response. 2. Elevating the head of the bed to 30 degrees helps
• Patient’s orientation to time, person, and place, the prevent aspiration.
patient is asked to identify the day, date, or season of 3. Position the patient in a lateral or semi-prone
the year and to identify where he or she is or to position to promote drainage of secretions.
identify the clinicians, family members, or visitors
2
4. Suction orally to remove secretions from the 5. Maintain correct body position, passive exercise of
posterior pharynx and upper trachea. the extremities to prevent contractures.
5. Hyper oxygenate and hyperventilate the patient 6. Use of splints or foam boots aid in the prevention of
before and after suctioning to prevent hypoxia foot drop and eliminate the pressure of bedding on
6. Chest physiotherapy and postural drainage to the
promote pulmonary hygiene. toes.
7. Auscultate the chest at least every 8 hours to 7. Trochanter rolls supporting the hip joints keep the
detect adventitious breath sounds or absence of legs in proper alignment
breath sounds. 8. The arms should be in abduction, the fingers lightly
8. Maintaining the patency of the endotracheal tube or flexed, and the hands in slight supination. The heels
tracheostomy for the intubated patient. of the feet should be assessed for pressure areas.
9. Providing frequent oral care. 9. Specialty beds, such as fluidized or low-air-loss
10. Monitoring arterial blood gas measurements. beds, may be used to decrease pressure on bony
prominences
Protecting the Patient
1. Padded side rails and raised at all times. Preserving Corneal Integrity
2. Prevent injury from invasive lines and equipment 1. Eyes may be cleansed with cotton balls moistened
(eg, restraints, tight dressings, environmental irritants, with sterile normal saline to remove debris and
damp bedding or dressings, tubes and drains). discharge.
3. Protecting the patient’s dignity during altered 2. If artificial tears are prescribed, and may be
LOC is providing privacy and speaking to the patient instilled every 2 hours.
during nursing care activities to preserve the patient’s 3. Observe for periocular edema (swelling around the
humanity. eyes) often occurs after cranial surgery. Cold
4. No negative speaking about the patient’s compresses may be prescribed, and care must be
condition or prognosis in the patient’s presence. exerted to avoid contact with the cornea.
4. Eye patches should be used cautiously because of
Maintaining Fluid Balance and Managing the potential for corneal abrasion from the cornea
Nutritional Needs coming in contact with the patch.
1. Assess hydration status by examining tissue turgor
and mucous membranes. Maintaining Body Temperature
2. Monitor intake and output, • Unconscious patients often develop very high
3. Analyze laboratory data. temperatures. Such temperature elevations must be
4. Fluid needs are met initially by giving the required controlled.
fluids intravenously. • Persistent hyperthermia with no identified
a. intravenous solutions for patients with intracranial clinical source of infection indicates brain stem
conditions must be administered slowly. damage and a poor prognosis.
b. Restrict fluid administration to minimize the 1. Adjustment of the environment depending
possibility of producing cerebral edema. on the patient’s condition to promote a normal body
c. Enteral feeding to the patient with inadequate fluid temperature.
and calories intake by mouth. 2. If body temperature is elevated, a minimum amount
of bedding, perhaps only a small drape is used.
Providing Mouth Care 3. The room may be cooled to 18.3°C• If the patient is
1. Mouth is inspected for dryness, inflammation, and elderly and does not have an elevated temperature, a
crusting. warmer environment is needed because of damage to
2. Oral care because there is a risk of parotitis. The the heat-regulating center in the brain
mouth is cleansed and rinsed carefully to remove 4. Frequent temperature monitoring is indicated to
secretions and crusts and to keep the mucous prevent an excessive decrease in temperature and
membranes moist. shivering.
3. Apply a thin coating of petrolatum on the lips to 5. Administering repeated doses of acetaminophen
prevent drying, cracking, and encrustations. as prescribed
4. If the patient has an endotracheal tube, the tube 6. Provide a cool sponge bath and allowing an electric
should be moved to the opposite side of the mouth fan to blow over the patient to increase surface
daily to prevent ulceration of the mouth and lips. cooling
7. Using a hypothermia blanket
Maintaining Skin and Joint Integrity
1. Regularly schedule of turning to avoid pressure, Preventing Urinary Retention
which can cause breakdown and necrosis of the skin. 1. Indwelling urinary catheter attached to a closed
2. Turning also provides kinesthetic (sensation of drainage system is inserted. A catheter may be
movement), proprioceptive (awareness of position), inserted during the acute phase of illness to monitor
and vestibular (equilibrium) stimulation. urinary output.
3. After turning, the patient is carefully repositioned to 2. Observe the patient for fever and cloudy urine.
prevent ischemic necrosis over pressure areas. 3. The bladder is palpated at intervals to determine
4. Dragging the patient up in bed must be avoided whether urinary retention is present
because this creates a shearing force and friction on 4. If indicated an external catheter (condom catheter)
the skin surface. for the male patient and absorbent pads for the
female patient can be used
3
for the unconscious patient who can urinate MONROE KELLIE DOCTRINE
spontaneously although involuntarily. • Pathologic states that an increase in the volume of
5. As soon as consciousness is regained, a one component necessitates a decrease in the
bladder-training program is initiated. volume of another to maintain normal Intra- Cranial
6. Frequently skin monitoring for irritation and skin Pressure. Brain, CSF.
breakdown.
Cerebral blood volume
Promoting Bowel Function • CSF can be displaced through the foramen magnum
1. Assess the abdomen for distention by listening for into the spinal theca. The spinal dural sheath can
bowel sounds and measuring the girth of the accept a quantity of CSF as it does not fit the canal
abdomen with a tape measure. closely, being surrounded by a layer of loose areolar
2. Monitors the number and consistency of bowel tissue & plexus of epidural veins.
movements • In states of increased ICP there is an increase in the
3. Performs a rectal examination for signs of fecal passage of blood through venous emissaries.
impaction. Intracranial pressure is a result of at least 2 factors
4. Stool softeners may be prescribed
• A glycerin suppository may be indicated to facilitate 1. The volume of the brain is constant has limited
bowel emptying. space to expand
• The patient may require an enema every 2. Compensation is accomplished by shifting or
Providing Sensory Stimulation diminishing CSF or decreasing the blood volume.
1. Encourages family members to touch and Any obstruction to venous outflow will entail an
talks to the patient. increase in the volume of intracranial blood and
2. The nurse should communicate and touch the ICP. As the ICP increases, the cerebral venous
patient when rendering care and spending enough pressure increases in parallel so as to remain 2
time with him or her. to 5 mm higher or else the venous system would
3. Avoid making any negative comments about the collapse.
patient’s status or prognosis in the patient’s presence. • Causes of increased intracranial pressure can be
4. Minimize the stimulation to the patient by limiting classified by the mechanism in which ICP is
background noises, having only one person speak to increased:
the patient at a time. • mass effect such as brain tumors, infarction with
5. Giving the patient a longer period of time to edema, contusions, subdural or epidural hematoma,
respond, and allowing for frequent rest or quiet times. or abscess all tend to deform the adjacent brain.
6. Orients the patient to time and place at least once • generalized brain swelling can occur in
every 8 hours. ischemic-anoxia states, acute liver failure,
7. Family members can read to the patient from a hypertensive encephalopathy, pseudotumor cerebri,
favorite book and may open radio and television hypercarbia, and Reye hepato cerebral syndrome.
programs that the patient previously enjoyed as a These conditions tend to decrease the cerebral
means perfusion pressure but with minimal tissue shifts.
of enriching the environment and providing familiar • increase in venous pressure can be due to venous
input. sinus thrombosis, heart failure, or obstruction of
superior mediastinal or jugular veins.
• obstruction to CSF flow and/or absorption can
Meeting Families’ Needs occur in hydrocephalus (blockage in ventricles or
1. Reinforce and clarify information about the patient’s subarachnoid space at base of brain, e.g., by
condition. Arnold-Chiari malformation), extensive meningeal
2. Permit the family to be involved in care. disease (e.g., infectious, carcinomatous,
3. Listen and encourage ventilation of feelings and granulomatous, or hemorrhagic), or obstruction in
concerns while supporting them in their cerebral convexities and superior sagittal sinus
decision-making process about post-hospitalization (decreased absorption
management and placement.
—------------------------------------------------------------ ETIOLOGY
Infections
INCREASED INTRACRANIAL PRESSURE
Tumors
The skull is a rigid structure. Stroke

It contains Aneurysm
1. Brain tissue 1,400g Epilepsy
2. Blood 75ml
Seizures
3. Cerebrospinal fluid (CSF) 75ml
The volume and pressure of these 3 are usually in a Hydrocephalus
state of Hypertensive brain injury
equilibrium and produces ICP Hypoxemia
❑ Any increase in these contents and/or the
Meningitis
addition of any mass will lead to an increase in the
pressure (the Monroe-Kellie doctrine).
Elevation in ICP can be graded as follows:
4
• MRI
Normal ICP 0 - 15mm Hg
Mild Elevation 16 - 20 mm Hg
Moderate elevation 21 - 30 mm Hg
Severe elevation 31 - 40 mm Hg
Very severe elevation 41 mm Hg and above
SIGNS AND SYMPTOMS

• Early Signs
• decreased level of consciousness
• confusion
• Restlessness
• lethargy, Medical Management
• difficulty with memory and thinking • Pharmacologic management
• pupillary dysfunction 1. Corticosteroids- Dexamethasone
• changes in vision 2. Osmotic diuretic- Mannitol
• deterioration of motor function 3. Analgesics
• Headache, 4. Anti-epileptic drugs- Diazepam,
• personality changes Clonazepam
• decreasing Glasgow Coma Score 5. Barbiturate therapy- It will offset ICP
lowering the effect on cerebral perfusion
LATER SIGNS: pressure.
● Continued decrease in level of • Pharmacologic Methods

consciousness (stuporous, comatose) Osmotic Diuretics: Mannitol
● Dilated pupils, no reaction to light MOA: reduces the water content of the brain
● hemiplegia that progresses due to the establishment of an osmotic
● Vomiting gradient between the brain and
● Bradycardia the intravascular compartment.
● Hyperthermia Mannitol is a large molecule and will not
● Papilledema cross the BBB.
• Decreased LOC with difficulty to arouse and Contraindications:

further decrease in the Glasgow Coma Score. Patients with anuria related to renal disease,
• Pupils will become unilaterally enlarged pulmonary edema, severe dehydration, or
progressing to fixed and dilated. Eventually active intracranial bleeding used with Lasix
becoming bilaterally fixed and dilated with
noted papilledema. Loop Diuretics: Furosemide, Ethacrynic
• Decorticate or decerebrate posturing to Acid
flaccidity will occur. • MOA: inhibit sodium and chloride
• Speech may be absent with only moaning. reabsorption in the loop of Henle resulting in
• Respiration will be irregular advancing to contraction of the blood volume which may
Neurogenic hyperventilation and respiratory mobilize cerebral edema
arrest. • . usually administered with mannitol to
• Loss of corneal and gag reflexes. increase the therapeutic effect
• Abnormal reflexes such as positive Babinski
reflex. • Corticosteroids
• Vital signs will present the Cushing triad only proven to be effective in reducing
○ hypertension, cerebral edema associated with brain
○ bradycardia, tumors; role in traumatic cerebral edema is
○ widening pulse pressure uncertain
Goals of Therapy: MOA: exact mechanism unknown; may

1. Maintain cerebral perfusion pressure. decrease CSF production
2. Prevent focal or global cerebral ischemia and stabilize brain cell membranes
and focal brain compression
• Non-pharmacologic:
Diagnostic Evaluation Elevating head of bed to improve
• Medical history and physical exam venous drainage.
including a neurological exam to test senses, Oxygenation and ventilation to
balance and mental status keep Pao2 >100, PaCo2 30-35
• Lumbar puncture reduces ICP by avoiding coughing.
• CT Scan
5
Surgical management • Decrease environmental stimuli which
Decompressive Craniotomy can increase ICP.
1. Dim all lights
Dietary management 2. Speak softly
• A low salt low-fat diet 3. Touch gently and only when needed
• Avoid red meat and processed meats like 4. Space all nursing interventions
pork, bacon, and beef. 5. Limit noxious stimuli such as suctioning to
• Foods that are rich in vitamin A may have only as needed
an adverse impact on
intracranial hypertension • Meeting Oxygenation needs
1. Attach a pulse oximeter to monitor
Assessment Oxygen saturation
1. Change in LOC - drowsiness, lethargy 2. Insert an oral airway if client is comatose.
2. Early behavioral changes: restlessness, 3. Administer oxygen.
irritability, confusion, and apathy
3. Falling score on the GCS • - For mechanically ventilated clients,
a. Change in orientation: disorientation to ensure that the ventilator delivers the
time, place, or person prescribed tidal volume at the ordered
b. Difficulty or inability to follow commands rate.
c. Difficulty or inability in verbalization or in
responsiveness to auditory stimuli • Prevention of Infection
d. Change in response to painful stimuli (eg, 1. Keep wounds clean and dry.
purposeful to inappropriate or absent 2. Use aseptic technique when handling any
responses) part of the intracranial monitoring device or
e. Posturing (abnormal flexion or extension) changing a dressing applied after surgery.
3. Administer antibiotic therapy, if prescribed.
4. Changes in vital signs caused by 4. Tilt or turn client from side to side every 2
pressure on brain stem. hours. - Avoid friction by using a lift sheet.
5. Use a pressure-relieving mattress or
NURSING DIAGNOSIS mechanical bed for clients whose position
1. Ineffective cerebral tissue perfusion cannot be readily changed.
related to increased ICP as 6. Keep skin clean and dry.
evidenced by decreased LOC,
sluggish pupil response, Maintain fluid balance
papilledema, and posture 1. Measure I & O.
2. Risk for ineffective breathing pattern 2. Overhydration will lead to cerebral edema.
and ineffective airway clearance 3. Monitor electrolytes as these patients are
related to diminished LOC and prone to hypernatremia, hypoglycemia, and
herniation of the brain stem hypokalemia
secondary to increased ICP • Avoid activities that can increase ICP such
3. Risk for infection related to impaired as suctioning or gagging.
skin and tissue integrity secondary • Treat hyperthermia as it increases the
to surgery, invasive diagnostic or metabolic needs of the brain
monitoring procedures, or original • Sponge bath
head injury • Light linen or drapes only to reduce heat
4. Risk for impaired skin integrity
related to low capillary blood flow SEIZURES DISORDER
secondary to pressure and inactivity • Seizure disorders include disturbance of
brain’s electrical activity periodically,
resulting in some degree of temporary brain
NURSING INTERVENTION dysfunction.
• Maintain Perfusion • Our normal brain function requires an
1. Keep head of the bed slightly elevated orderly, organized , coordinated discharge of
and the head in the midline (straight). electrical impulses. Electrical impulses
2. Avoid extreme hip flexion. enable the brain to communicate with spinal
3. Avoid range-of-motion (ROM) exercises cord, nerves, and muscles as well as within
until ICP approaches normal itself.
4. Administer reduced fluid volumes at an
even rate for 24 hours. Definition
5. Give diuretics as prescribed; note client's • An abnormal electrical discharge in the
response to therapy. brain that interrupt normal function.
6. Hyperventilate the mechanically ventilated • Seizures are episodes of abnormal motor,
client sensory, autonomic, or psychic activity (or a
7. Keep suctioning brief, without exceeding combination of these) resulting from sudden
10-15 seconds per pass of the catheter. excessive discharge from cerebral neurons.
• Seizures are sudden abnormal electrical
6
discharges from the brain that result in
changes in sensation, behavior, movements,
perception, or consciousness.
• Epilepsy is a chronic disorder of recurrent
seizures.
• An isolated, single seizure cannot be
considered epilepsy
An epileptic syndrome consists of recurrent

episodes of one or more of the following
manifestations:
– Loss of consciousness.
– Convulsive movements or other motor
activity. • Seizure activity increases cerebral oxygen
– Sensory phenomena . consumption and the need for ATP.
– Behavioral abnormalities. • Supplies of oxygen and glucose are rapidly
consumed.
• Epilepsy occurs when permanent changes • To meet these demands, cerebral blood
in the brain cause it to be too excitable or flow increases during a seizure.
irritable. • If the seizure is ongoing (as in status
• As a result, the brain sends out abnormal epilepticus), severe hypoxia and lactic
signals. This leads to repeated unpredictable acidosis
seizures. occur and may result in brain tissue
Epilepsy may be due to a medical condition destruction.
or injury that affects the brain or the cause
may be unknown. Clinical Manifestation
1. Impaired consciousness
INCIDENCE 2. Disturbed muscle tone or movement.
• The incidence rates are high in during the 3. Disturbance of behavior Mood Swing
first year of life, decline through childhood 4. Sensation or perception disturbance
and adolescence, plateau in middle age, and 5. Uncontrollable jerking movements of the
rise sharply again among the elderly. arms and legs.
• The population with the highest prevalence 6. Psychic symptoms—out-of-body feelings
of new-onset epilepsy is those over the age or not feeling “in the moment”
of 60. 7. Memory lapses.
Common Causes of Epilepsy DIAGNOSTIC EVALUATION

Stroke or TIA. – Dementia (like • History
Alzheimer’s • Physical examination
disease). • Blood test
Traumatic brain injury. • LP
• CT and MRI
Infections include brain abscess,
• EEG
meningitis,
• Single-photon emission computerized
encephalitis, and HIV/AIDS. tomography (SPECT).
Brain problems that are present at • Single-photon emission computerized
birth tomography (SPECT).
(congenital birth defects). • A SPECT test uses a small amount of low-
Brain injury that occurs during or dose radioactive material that's injected into
near birth. a vein to create a detailed, 3-D map of the
blood flow activity in brain that happens
Metabolism disorders present at
during a seizure.
birth
(phenylketonuria).
Classification of Seizures
Brain tumor. • Seizures Partial seizure
Abnormal blood vessels in the a. Simple Partial seizure
brain. b. Complex Partial seizure
Other illness that damages or • Generalize seizure
a. Absence seizure
destroys brain tissue.
b. Generalized tonic-clonic seizure
c. Myoclonic seizure
d. Tonic seizure
e. Clonic seizure
f. Atonic seizure
ABSENCE SEIZURE- Tulala
7
• Simple absence seizure is a vacant stare, STAGES OF SEIZURES
which may be mistaken for a lapse in
attention that lasts about 10 seconds, though Aura Phase
it may last as long as 20 seconds, without • This phase happens right before a seizure
any confusion, headache or drowsiness starts,
afterward. over 5 to 20 minutes, and usually last 60
• (Decrease minutes.
• Neurotransmitter) • an aura may be:
• Vision problems
GENERALIZED TONIC-CLONIC SEIZURE • Dizziness
• Generalized tonic-clonic • Numbness or “pins and needles”
seizure, Electric discharges involve the • Headache
entire brain. The person • Nausea
loses consciousness right • Feelings of intense fear
from the beginning of the
Ictal Phase
seizure. A tonic-clonic
• This is a stage of seizure. There is intense
seizure usually lasts one
electrical changes happen in brain.
to three minutes, but may
• Some common signs of this stage are:
last up to five minutes.
• Loss of awareness (black out)
• Feeling confused
MYOCLONIC SEIZURES
• Seeing flashing lights
• Muscle jerks can have causes that aren't
• Trouble speaking
due to underlying disease.
• Loss of muscle control
Examples include infrequent muscle
• Repeated movements (lip, arms)
twitches, low magnesium levels or
muscle fatigue. Postictal Phase
• During this final phase, brain tries to get
TONIC SEIZURE nerve cells to stop misfiring body begins to
• Tonic seizures are characterized by facial relax. The physical after effects of the
and truncal muscle spasms, flexion or seizure also set in.
extension of the upper and lower extremities, • The postictal phase can last for seconds,
and impaired consciousness minutes, hours, and sometimes even days.
• Most commonly experience:
-Drowsiness
-Confusion
COMPLICATIONS
• Fracture of bone.
• Impair intelligence.
• Unable to get job, driver’s license, life
insurance.
CLONIC SEIZURES
• Socially stigma
• Muscles have spasms, which often
• Reduced quality of life.
make face, neck, and arm muscles jerk
• ‘’sudden unexpected death in epilepsy’’.
rhythmically.
Medical Management
• They may last 3-5 minutes.
• Goals of management of clients with
seizures and epilepsy are
ATONIC SEIZURE
1. To prevent injury during seizures,
• Muscles have spasms, which often make
2. To eliminate factors that precipitate
face, neck, and arm muscles jerk
seizures, and
rhythmically. They may last 3-5 minutes.
3. To control/abort seizures
• During the seizures the major goals are:

1. To maintain the airway.
2. To prevent injury to client.
3. To observe the seizure activity.
4. To administer appropriate anticonvulsant
drugs.
• In a hospital setting, suction equipment
should be readily available.
• The person experiencing a seizure usually
requires protection from the environment.
• Objects should be moved out of the way
so that the client does not strike his/her head
or extremities.
8
impaired, oxygen and glucose cannot be delivered to
PHARMACOLOGY the brain.
• Anticonvulsant- Carbamazepine 500 mg
• Valproic acid. Blood flow can be compromised by a variety of
• Antiseizures : Phenytoin 50 mg IV mechanisms; neurological deficit of cerebrovascular
• Surgical management cause that persists beyond 24 hours or is interrupted
• Vagus Nerve Stimulation: A device by death within 24 hours
implanted underneath the skin of the chest
stimulates the vagus nerve in neck, sending AKA stroke or brain attack
signals to brain that inhibit seizures. With
vagus nerve stimulation, client may still Is a sudden disruption in normal cerebral circulation
need to take medication, but may be able to due to a lack of blood flow
lower the
• Responsive neurostimulation May result from:
• During responsive neuro stimulation, a - Occlusion
device implanted on the surface of the brain - Hemorrhage in the brain
or within brain tissue can detect seizure
activity and deliver electrical stimulation to Mechanisms that Compromise the Blood Flow to
the detected area to stop the seizure. the Brain
Nursing Care ● Blockage of an artery

1. Any tight clothing is loosened. ● Arteriosclerosis- hardening of the arteries
2. Put a pillow or folded blanket under the leading to the brain
affected person’s head, but not flex the neck ● Atherosclerosis- arteries becomes narrow
sharply or close the airway. because of plaque or cholesterol embolism
3. Turning the client to his/her side displaces to the brain from the heart
the tongue and usually opens the airway ● Rupture of an artery (hemorrhage)
once the tonic phase has ceased. Cerebral hemorrhage (Bleeding within the
• Do not attempt to open the airway with your brain substance)
fingers. ● The most common reason to have bleeding
• A jaw thrust maneuver (head tilt - chin lift) within the brain is uncontrolled high blood
will open the airway without the potential to pressure
harm the client or the caregiver. ● Other situations include aneurysms that
4. Eliminate the factors that precipitate leak or rupture or arteriovenous
seizure, if possible. malformations(AVM) in which there is an
5. Eating a balanced diet, restricting abnormal collection of blood vessels that are
excessive caffeine and alcohol intake fragile and can bleed.
6. Provide adequate sleep
7. Avoiding seizure triggers ( means
initiations ) CLASSIFICATION OF STROKE
(ex.- flashing lights), and minimizing
emotional 1. ISCHEMIC STROKE
stress may be helpful in preventing seizures. - In an ischemic stroke, blood supply to part of the
8. Note and Observer descriptions of a brain is decreased, leading to dysfunction and
seizure and time necrosis of the brain tissue in that area.
9. Instruct the family & unlicensed assistive
personnel to make - There are four reasons why this might happen:
the following observations: Thrombosis (obstruction of a blood vessel by a blood
• How long did the seizure last? clot forming locally)
• Where in the body did the seizures begin
and how did they progress? TYPES OF ISCHEMIC STROKE
• Did the client’s eyes or head deviate?
• Were the respirations labored or frothy? 1. Thrombotic Stroke
• Was the client incontinent? - a thrombus (blood clot) usually forms around the
• Did the client lose consciousness? atherosclerotic plaques.
• What were the types of movements and - since blockage of the artery is gradual, onset of
what body parts symptomatic thrombotic strokes is slower
moved? - a thrombus itself (even if non-occluding) can lead to
an embolic stroke. If the thrombus breaks off.
- thrombotic stroke can be divided into two types
CEREBROVASCULAR ACCIDENT(CVA) depending on the type of vessels the thrombus is
formed on:
Other terms: “stroke’, “brain attack”, “acute ● Large vessel disease
ischemic cerebrovascular syndrome” occurs when ● Small vessel disease
blood supply to part of the brain is disrupted, causing
brain cells to die. When blood flow to the brain is
9
- Embolism (due to an embolus from elsewhere in the - A distinct is made between intra-axial hemorrhage
body) (blood inside the brain) and extra-axial hemorrhage
(blood inside the skull but outside the brain)
- Systemic hypoperfusion (general decrease in blood
supply, e.g., in shock) venous thrombosis - Intra- axial hemorrhage is due to intraparenchymal
- Stroke without an obvious explanation is termed hemorrhage or intraventricular hemorrhage (blood in
cryptogenic shock (of unknown origin) the ventricular system)
- The main types of extra-axial hemorrhage: Epidural
- Sickle cell anemia, which can cause blood cells to hematoma (bleeding between the dura mater and the
clump up and block blood vessels, can also lead to skull) Subdural hematoma (in the subdural space)
stroke. Stroke is the second leading killer of people Subarachnoid hemorrhage (between the arachnoid
under 20 who suffer from sickle-cell anemia mater and pia mater). Most of the hemorrhagic stroke
syndromes have specific symptoms (e.g., headache,
2. Embolic stroke previous head injury)
- Refers to the blockage of an artery by an
embolus, a traveling particle or debris in the arterial - Intracerebral hemorrhage (ICH) is bleeding directly
bloodstream originating from elsewhere. into the brain tissue, forming a gradually enlarging
hematoma (pooling of blood)
- An embolus is most frequently a thrombus, but it
can also be a number of other substances including - It generally occurs in small arteries or arterioles and
fat (e.g. from bone marrow in a broken bone), air, is commonly due to hypertension, trauma, bleeding
cancer cells or clumps of bacteria disorders, illicit drug use (e.g., amphetamines or
cocaine) and vascular malformations.
- The source of the embolus must be identified.
Because the embolic blockage is sudden in onset, - The hematoma enlarges until pressure from
symptoms usually are maximal at start. surrounding tissue limits its growth, or until it
decompresses by emptying into the ventricular
- Also, symptoms may be transient as the embolus system.
is partially resorbed and moves to a different location
or dissipates altogether. - CSF or the pial surface. A third of intracerebral
bleed is into the brain’s ventricles. ICH has a mortality
- Emboli most commonly arise from the heart rate of 44 percent after 30 days, higher than
(especially in atrial fibrillation) but may originate from ischemic stroke or even the very deadly subarachnoid
elsewhere in the arterial tree. hemorrhage
- In paradoxical embolism, a deep vein thrombosis DIAGNOSTICS

embolism through an atrial or ventricular septal defect - Lumbar tap may be bloody, if hemorrhagic type
in the heart into the brain - CT scan shows edema, lesions, structural details
with high accuracy
3. Systemic hypoperfusion is the reduction of blood - MRI delineates size and location only
flow to all parts of the body Angiography shows arterial vessel shadow and can
identify narrowing, blockage or rupture
It is most commonly due to cardiac pump failure from - EEG can assess localized damage
cardiac arrest or arrhythmias, or from reduced cardiac
output as a result of myocardial infarction, pulmonary SURGICAL MANAGEMENT
embolism, pericardial effusion, or bleeding - Craniectomy- surgical procedure wherein a portion
of the cranium is removed to relieve pressure on the
Hypoxemia (low blood oxygen content) may brain structures by providing space for expansion
precipitate the hypoperfusion
- Craniotomy - surgical procedure wherein the
4. Venous thrombosis Cerebral venous sinus cranial vault is opened to visualize and relieve
thrombosis leads to stroke due to locally increased pressure on the brain
venous pressure, which exceeds the pressure
generated by the arteries. MEDICAL MANAGEMENT
● Osmotic diuretics (Mannitol)
Infarcts are more likely to undergo hemorrhagic ● Corticosteroids (Dexamethasone)
transformation (leaking of blood into the damaged ● Anticonvulsants (Tegretol, Dilantin)
area) than other types of ischemic stroke ● Muscle relaxants (Valium)
● Analgesics (Morphine sulfate)
● Anti-coagulants (Coumadin)
2. HEMORRHAGIC STROKE ● Anti-hypertensive (Nicardipine)
- Intracranial hemorrhage is the accumulation of ● Neuroprotective (Nootropil)
blood anywhere within the skull vault
10
SIGNS AND SYMPTOMS OF STROKE 2. HEMORRHAGIC- when blood vessels
- Are related to the anatomical location of the BURST leaking blood into brain tissue or
damage; nature and severity of the space.
symptoms can therefore vary widely.
ETIOLOGY
Ischemic Strokes usually only affect regional areas 1. HTN
of the brain perfused by the blocked artery. 2. Hypercholesterolemia
3. Atherosclerosis
Hemorrhagic Strokes can affect local areas, but 4. Atrial Fibrillation
often can also cause more glocal symptoms due to 5. Obesity
bleeding and increased intracranial pressure. On the 6. Smoking, alcohol
basis of the history and neurological 7. DM; Sickle Cell; TIA
- If the area of the brain affected contains one of the PATHOPHYSIOLOGY

three prominent Central Nervous System pathways—
the spinothalamic tract, corticospinal tract, and dorsal 1. Normally the brain receives blood flow at 60
column(medial lemniscus), symptoms may include: to 70 ml/100g of brain tissue.
● Hemiplegia (paralysis that affects only one a. When the rate slowed to 25ml, loss
side of your body) of function begins due to lack of
● Muscle weakness of the face aerobic metabolism.
● Numbness b. If blood flow will not be restored,
● Reduction in sensory or vibratory sensation soon cell death begins within a few
minutes of deprivation of O2, occur
A stroke affecting the brainstem therefore damaged permanently.
can produce symptoms relating to deficits in 2. Location of tissue damage and the
these cranial nerves. availability of collateral circulation will help
determine the patient's prognosis.
3. Weakness/paralysis on 1 side of body.
Altered smell, taste, hearing, vision
4. Inability to maintain balance
(total/partial)
5. Blurred vision, diplopia
Ptosis (drooping eyelids) & weakness of 6. Slurred speech
ocular muscles 7. Fatigue
decreased reflexes; gag; swallow; pupil
reactive to light COLLAB MANAGEMENT
Dec. sensation and weakness muscle in the 1. Respiratory Support
face. 2. Mech Vent
3. IV fluids.
Balance prob; Nystagmus (uncontrolled
4. Bed rest
movement of eyes)
5. Fowler pos
Altered breathing & HR weakness in 6. ROM exercise
sternocleidomastoid muscle with an inability 7. Diet
to turn head to one side weakness in the 8. Surgery
tongue (inability to protrude &/or move from
side to side) DIAGNOSTIC EVALUATION
If cerebral cortex is involved, the CNS 1. CSF analysis-blood (hemorrhagic)
pathways can be affected. 2. CT scan or MRI
Apraxia- altered voluntary movements visual 3. Cerebral Angiogram- site of rupture.
4. EEG
field defect.
5. CBC
Memory deficit- (temporal lobe)
6. PT, PTT- Partial thromboplastin Time.
If cerebellum is involved, the pt may have *Important
the ff:
Trouble walking PHARMACOLOGY
🥺
Altered movement coordination > vertigo & 1. Anticoagulant- heparin, warfarin,
syaparin - to prevent blood clotting
disequilibrium
2. Antiplatelet- prevent platelet from clumping
LOC, headache, & vomiting, usually occurs together and blocking blood vessel
more often in hemorrhagic stroke than in 3. Calcium Antagonist
thrombosis because of the IICP from the 4. tPA (Tissue Plasminogen Activator)- should
leaking blood compressing on the brain be given within 60 minutes in ED to break up
clots. * Important
2 MAIN TYPE
1. ISCHEMIC- damage to the brain due to the NR INTERVENTION
CLOGGED artery. 1. Promote oxygenation
2. Monitor pulse oximeter and ABG levels
3. CBR
11
4. DIET
a. Low Sodium MEDICAL MANAGEMENT
b. Low cholesterol ● Anticoagulant Therapy- prevent future
c. Low fat attacks and massive cerebral infarction.
5. Assess gag reflex. ● Platelet Inhibiting Meds-
6. IVF ● Endarterectomy- removal of atherosclerotic
7. Monitor I&O plaque.
8. Seizure precaution
9. Verbalization of feelings. NR MGT
1. Monitor Neurologic status
Board Exam Q: 2. Monitor BP; Sodium Nitroprusside uses to
produce BP.
URINARY INCONTINENCE- Avoid catheters as it 3. Assess difficulty in swallowing; hoarseness
causes infection, and use condom cath instead for of voice; cranial nerve dysfunction.
males. 4. Have emergency airway ready.
*USE GCS
TRANSIENT ISCHEMIC ATTACK
COMPLICATION IN ENDARTERECTOMY
- TIA is a temporary episode of neurologic
dysfunction manifested by a sudden loss of 1. Stroke
motor sensory or visual function. 2. Cranial nerve Injury
3. Infection/hematoma of wound
- Last for seconds to minutes but not last 4. Carotid artery disruption.
longer than 24 hours. ___________________________________________
HEAD INJURY AND SPINAL CORD INJURY
- It can precede to stroke; It may serve as
WARNING of impending stroke. Traumatic Brain Injury (TBI) is the leading cause of
death and disability in children and adults from ages 1
to 44.
RISK FACTORS
It is the most common cause of death in young adults
1. HTN (age 15-24 years) Males are about twice as likely as
2. Type 1 DM females to experience a TBI.
3. Cardiac disease
4. Hx of smoking • Incidence - 450 cases /100 000/ year. About 4
5. Hx of stroke million people experience head injury annually.
6. Hx of alcoholism
Around 500 000 children with head injury attend
hospital every year and head injury admissions
CLINICAL MANIFESTATION account for nearly 10% of all pediatric hospital
admissions.
1. Sx and Sy depend upon the
location of vessel affected. Road traffic accidents (RTAs) are the most common
cause of TBI followed by falls and assaults.
★ Ophthalmic- middle cerebral and anterior
cerebral arteries; lateral signs such as Definition
• Traumatic brain injury (TBI) is a non-degenerative,
1. Amaurosis Fugax- sudden painless loss of non- congenital insult to the brain from an external
vision in one eye, due to retinal artery mechanical force, possibly leading to permanent or
ischemia.= kulang Oxygen sa retinal artery temporary impairment of cognitive, physical, and
2. Contralateral Aphasia- speaking problem psychosocial functions, with an associated diminished
or altered state of consciousness.
★ Posterior, Cerebral & Cerebellar arteries
1. Vertigo Types of Brain Injuries
2. Diplopia- naduduling
3. Numbness/ Paresthesia 1. Primary- one that is a result of a direct trauma to
4. Ataxia- no balance the brain, an insult to the brain caused by an external
physical force which may produce a diminished or
DIAGNOSTIC altered state of consciousness and result in the
disturbance of behavioral 'or emotional functioning
● Bruit heard on Carotid Artery/ (-) pulsation
on CA 2. Secondary - occur as a result of an injury to the
● Carotid Phonoangiography- a direct brain due to hypoxia, cerebral edema, hypertension,
visualization. increased ICP, or hypercapnia. This occur hours to
● Oculoplethysmography- measures days after the initial body's response to initial injury.
pulsation in blood flow in ophthalmic artery.
12
Secondary brain injury include a lack of oxygen, Epidural hematomas - These are usually caused by
hypotension or inflammatory process that result in fracture of the temporal bone and rupture of the
swelling of brain tissue call and release of chemicals middle meningeal artery.
that damage healthy brain tissue.
Subdural hematomas – The hematomas are usually
Two Types Traumatic Head Injury caused by rupture of the bridging veins in the
subdural space. loss
A traumatic brain injury can be closed or open brain
injury: Subarachnoid hematomas - These result from
damage to blood vessels in the posterior fossa stalk.
• Closed Brain Injury -without the skull being broken
or penetrated and the brain has not been exposed. Extracranial hematoma- scalp lacerations, nasal
Example: when the rapid movement of the head injuries, injuries to the face and neck can lead to
backward and forward (acceleration-deceleration significant blood loss.
movement) causes the brain to move inside the skull
and slam against its hard inner bone. 3. Concussion - A concussion is a brain injury that
occurs when the brain bounces against the hard walls
• Open Brain Injury - open or penetrating head injury. of your skull. Concussion-temporary disruption of
A TBI can be focal or diffuse, meaning damage may synaptic activity, brief loss of consciousness The loss
be isolated to one specific area of the brain in focal of function associated with concussions is temporary,
injuries or wide spread in the case of diffuse injuries. repeated concussions can eventually lead to
permanent damage.
Brain injury type:
- Fractures 4. Contusion bruising of brain tissue with slight
• Depressed bleeding of the small cerebral vessels into
• Comminuted surrounding tissue at site of impact or opposite to the
• Linear site as a result of rebound reaction.
- Hemorrhages 5. Edema- Any brain injury can lead to edema, or

• Epidural swelling. Injuries cause swelling of the surrounding
• Subdural tissues, but it’s more serious when it occurs in your
• Intracerebral brain. The skull can’t stretch to accommodate the
swelling, which leads to a buildup of pressure in your
Etiology brain. This can cause your brain to press against your
● Falls skull.
● Vehicle-related collisions.
● Violence. 6. Skull Fracture- The skull doesn’t have bone
a. gunshot wounds, marrow. This makes the skull very strong and difficult
b child abuse like Shaken baby syndrome to break. A broken skull is unable to absorb the
● sports injuries. impact, making it more likely that there will also be
а. Soccer damage to the brain.
b. boxing,
c. football, or extreme sports. Pathophysiology
• Head injury may be divided into primary injury and
Major Types of Head Injuries secondary injury.
1. Hematoma - A hematoma is a collection, or
clotting, of blood outside the blood vessels. It can be • Primary injury is induced by mechanical force and
very serious if a hematoma occurs in the brain. The occurs at the moment of injury.
clotting can cause pressure to build up inside the
skull, which can cause, loss consciousness. • Secondary injury is not mechanically induced. It
may be delayed from the moment of impact, and it
2. Hemorrhage - A hemorrhage is uncontrolled may superimpose injury on a brain already affected by
bleeding. There can be bleeding in the space around a mechanical injury.
the brain, which is a subarachnoid hemorrhage, or
bleeding within the brain tissue, which is an • The injured blood vessel and disrupted neurons
intracerebral hemorrhage. Subarachnoid bleeds and cell bodies, may bleed, bleeding damage the
often cause headaches and vomiting. brain tissue, increasing the ICP
The severity of intracerebral hemorrhages depends • Secondary process of auto destructive factors will
on how much bleeding there is, but over time any cause additional injury like cellular anoxia, depletion
amount of blood can cause pressure to build. of energy stores, cell membrane lipid metabolites,
intracellular calcium overload, release of free radicals
Hematomas are categorized as follows: and inflammatory process.
13
• So, when energy supply is low because of poor 5. Leaking CSF from the ears and nose
blood flow and poor oxygenation mechanism to 6. Nausea & vomiting
maintain normal intracellular calcium level fails. 7. Respiratory distress
8. Dizziness, poor motor control, fatigue,
• As a result of inadequate perfusion, cellular ion inability to maintain balance and ringing in
pumps may fail, causing a cascade involving the ear.
intracellular calcium and sodium. Resultant calcium 9. Hemiparesis, hemiplegia
and sodium overload may contribute to cellular 10. Seizures
destruction. 11. Impaired speech, aphasia, dysarthria
11. Sexual dysfunction
Excessive release of excitatory amino acids, such as 12. Cognitive symptoms like confusion
glutamate and aspartate, exacerbates failure of the inability to concentrate
ion pumps. As the cascade continues, cells die, 13. Impaired memory
causing free radical formation, proteolysis, and lipid 14. Difficulty in reading and writing
peroxidation. These factors can ultimately cause 15. Difficulty in planning, sequencing,
neuronal death. impaired judgment
16. Behavioral symptoms like agitation,
• Brain glucose utilization and blood flow is also mood swings
altered and this leads to further injury to the area of 17. Anxiety and restlessness
injury. 18. Delusions, paranoia
• Inflammatory process and cellular edema leads to POSTURE

increased ICP
Decorticate Posture
• Increase ICP result in compensatory mechanism
that raises the BP in an attempt to increase cerebral
• The arms are rigidly flexed at the elbows and
pressure and lead to further injury.
wrists.
• The legs also may be flexed with toes rigidly
• As pressure increases, downward pressure is
pointed.
placed on brain stem and thus damage the CN3
• Indicates a lesion in the brain.
causing changes in pupil and later may dilate pupils.
• In some instances the posture may be produced
by applying a painful stimulus to a comatose
• There is also pressure in respiratory center that
patient.
leads to changes in respiratory rate and rhythm and
may lead to respiratory arrest. Other cranial structure
are affected leading to inability to maintain
temperature regulation and fluid balance.
Decerebrate Posture
Signs and symptoms

• The arms are rigidly straight and internally
• Mild traumatic brain injury :
rotated
- Loss of consciousness for a few seconds to
• The legs are extended with the toes rigidly
a few minutes
pointed.
- Memory or concentration problem
• It is usually observed in patients afflicted by
- Headache
compression of the brainstem at a low level.
- Dizziness or loss of balance
- Nausea or vomiting
- Difficulty sleeping
Diagnostic Evaluation
• Moderate to severe traumatic brain injuries: ● X-ray
- Loss of consciousness from several minutes ● Cervical Spine X-rays. Focus from 1 – 7 to
to hours see that they have no injury.
- Slurred speech ● PET
- Inability to awaken from sleep ● Transcranial Doppler studies.
- Weakness or numbness in fingers and toes Looking for vasospasm
- Loss of coordination ● CT scan: standard modality
- Persistent headache or headache that ● Glasgow coma Scale (GCS).
worsens ● MRI
● Bleeding from the ear or nose in cases of
Assessment Findings suspected CSF leak -"halo" or "ring" sign ,
1. Physical signs when dabbed on a tissue paper
wound, contusion, ecchymosis (Raccoon eye) ● CSF leak - analyzing the glucose level and
2. Impaired consciousness, brief or prolonged loss of by measuring using a dextro strips
consciousness, lethargy, coma
3. Visual disturbance, blurring photosensitivity,
pupillary changes, reaction to light.
4. Headache and neck pain
14
Preventive Measures Health Promotion ● The GCS score decreases by 2 or more
points between the time of injury and
Prevent car and motorcycle accidents hospital evaluation
1. Wear safety helmets use of safety seat belts ● The patient presents with fixed and dilated
2. Preventative measures include safer roads, pupils
barriers to prevent falls, and gun control ● The intracranial pressure (ICP) exceeds 20
legislation. mm Hg
3. Bicycle and motorcycle helmets, seatbelts, Exception :
airbags, and soft surfaces on playgrounds ● In Subdural hematoma with GCS=15-
are effective. hematoma >10mm ,or >5mm midline shift
4. 25-30% of head injuries in infants are the ---- requires
result of an abuse - healthcare professionals ● Surgical decompression : when a cerebral
need to be trained in safeguarding and to aneurysm is identified on angiography,
raise concerns without delay. clipping and coiling is done to prevent
re-bleed
First Aid
If severe head trauma occurs 4. Pharmacotherapy
1. Keep the person still. Until medical help Phenytoin- prevent traumatic seizure
arrives, keep the injured person lying down Anti-anxiety- to calm the client since alertness and
and quiet, with the head and shoulders restlessness increases ICP
slightly elevated. Anticoagulant to help prevent blood clot formation
2. Don't move the person unless necessary, Beta blocker
and avoid moving the person's neck. If the Anticonvulsant like carbamazepine, Depakote
person is wearing a helmet, don't remove it.
3. Stop any bleeding. Apply firm pressure to the 5. Hemodynamic/fluid management
wound with sterile gauze or a clean cloth. ● Monitoring required for a critically
Don't apply direct pressure to the wound if head-injured patient should include
you suspect a skull fracture.4 continuous arterial blood pressure
4. Watch for changes in breathing and monitoring , core body temperature,
alertness. If the person shows no signs of respiration rate and pattern and continuous
circulation — no breathing, coughing or ECG.
movement — begin CPR. ● These patients may develop arrhythmias due
to induced hypothermia and/or electrolyte
imbalances.
Emergency Management ● ICP monitoring should be employed in
1) Supportive Measures: head-injured patients who are ventilated and
● Endotracheal intubation for patients with paralyzed where neurological deterioration
decreased level of consciousness and poor cannot be readily observed clinically.
airway ● ECG monitoring and regular electrolyte
● Cautiously lower blood pressure to a MAP observation is essential.
less than 130 mm Hg, but avoid excessive ● Blood glucose control Hyperglycemia is
hypotension. known to exacerbate cerebral lactic acidosis
● Rapidly stabilize vital signs, and and consequently aggravates cerebral
simultaneously acquire emergent CT scan. ischemia in head injury. Therefore glucose
● Maintain euvolemia, using normotonic rather solutions should be avoided, and initially
than hypotonic fluids, to maintain brain hourly blood sugar monitoring/insulin
perfusion without exacerbating brain edema infusion implemented to keep blood glucose
● Avoid hyperthermia. below 11mmol/L.
● Facilitate transfer to the operating room or
ICU Positioning
● Elevation of the head from 15 to 30 degrees
2) Decrease cerebral edema: this will decrease in ICP
● Modest passive hyperventilation to reduce ● Nutritional support
PaCO2 ● Severe head injury is associated with a
● Mannitol 0.5-1.0 gm/kg slow iv push hypermetabolic state with, the metabolic rate
● Furosemide 5-20 mg iv increasing, It is therefore important to begin
● Elevate head 15-30 degrees, avoid any neck feeding as early as possible, preferably
vein compression or turning head to one side enteral.
Sedate if necessary with morphine ● The feeding tube should always be passed
(struggling, coughing etc will elevate via the nosogastric route in head-injured,
intracranial pressure) unless a basal skull fracture has been
definitively ruled out.
3) Surgical Evacuation of hematoma:
● No surgical intervention if collection <10ml Complications
Indication of surgical decompression: ● Amnesia is common, and may be retrograde
and/or anterograde.
15
● Increased intracranial pressure, cerebral ● Compression stocking/boots to prevent
edema. DVT.
● Cerebral herniation. ___________________________________________
● Meningitis: following skull fracture, may
occur weeks to years later. SPINAL CORD INJURY
● CSF leak (test fluid for glucose or drop on An injury to the spinal cord, vertebral column,
filter paper to see double halo) supporting soft tissue, or intervertebral disc caused by
● Bleeding from the ear - possible fracture of trauma
petrous temporal bone, may involve VII/VIII
th nerves. Risk factor:
● Bleeding from the nose - possible fracture Younger age, male, alcohol and drug user
of cribriform plate, may originate from ear,
leak may require surgery, don't blow nose Major cause of death
or insert nasogastric tube. Pneumonia, pulmonary embolism, sepsis
Nursing Diagnosis Definition

● Acute Confusion related to altered cerebral • Spinal cord injury (SCI) is damage to the spinal cord
blood flow. that results in a loss of function such as mobility or
● Risk for Ineffective cerebral tissue perfusion feeling.
● Disturbed sensory perception related to • A spinal cord injury (SCI) is damage to the spinal
injury. cord that causes temporary or permanent changes in
● Fatigue related to cerebral edema its function.
● Deficient fluid volume related to decreased • Symptoms may include loss of muscle function,
LOC sensation, or autonomic function in the parts of the
● Risk for injury body served by the spinal cord below the level of the
● Risk for Imbalance temperature injury.
● Risk for impaired skin integrity
● Impaired memory Impaired social interaction Usually results from a traumatic force to the vertebral
column. Typically has lifelong consequences,
Nursing Management classified by:
1. Maintaining airway ● Type
2.Monitoring Neurological Function ● Level
3.Monitoring FE ● Degree
4.Promoting Adequate nutrition ● Mechanism
5.Preventing injury ● Force of Injury
6.Maintaining Body temperature
7.Maintaining Skin Integrity Etiology
● Cervical and lumbar areas more frequent
Nursing Interventions because these segment are more mobile
● Assess status ● Trauma like automobile accident, gunshot
– neurologic –changes in GCS, pupil responses. wound, diving accident- inflict severe
– Respiratory-Pulse oximetry, prepare for intubation damage to the spinal cord.
and Mechanical ventilator ● Tumor, degenerative disease and infections
also impair the functions of spinal cord and
● Observe for signs of increasing ICP its branches.
● Monitor
– VS- slowing of heart rate, Increase BP, temperature Types of Injury
– I/O – increase urinary output - Concussion
– hemodynamic variables – specific gravity - Contusion
- Laceration
● Monitor CPP (cerebral perfusion pressure) - Transaction
CPP is the difference between the ICP and the mean - Hemorrhage
arterial pressure.
Normal CPP is 70-95 mmHg Classification according to Anatomical Location
Keep the environment calm and quiet, limiting visitor. 1. Cervical
Keep the head of the bed at 15- 30 degrees 2. Thoracic
Do not stress and hyperextend the neck. 3. Lumbar or sacral
● Provide suctioning Level of injury are classified as:

● Maintain seizure precautions Cervical- may result in quadriplegia
● Administer medications as to decrease ICP Thoracic and Lumbar- may result in paraplegia
and pain.
● Allow a rest period between nursing care ● Upper motor neuron (UMN)
● Skin care, turned every 2 hours, use pillows – Modulated by cerebrum, cerebellum, basal
as support to all extremities. ganglia, reticular neurons
16
– Injury = paralysis, hypertonicity, • Hemodynamic will be unstable and result to
hyperreflexia decrease in BP and hypoxia of the cord.
• The inflammatory process injure the myelin covering
● Lower motor neuron (LMN) the axon so the chemical and electrolytes changes
– Originated in CNS interrupt the nerve impulse transmission
– Injury = flaccidity, hyporeflexia,
fasciculations Clinical Manifestations
Incidence Cervical region damage

• SCI is highest among persons age 16-30, in whom 1. Paralysis and loss sensory perception in
53.1 percent of injuries. both arms and both legs (Quadriplegia)
2. Severe injury to the cord above the fifth CV
• Males represent 81.2 percent of all reported SCIs fatal- because phrenic nerve that innervate
and 89.8 percent of all sports-related SCIs. the diaphragm originates in 3rd, 4th and 5th
cervical segment - respiratory problem
• Both genders are affected. Three leading causes of 3. Interruption of the thoracic cord through L1
SCI: and L12 cause paraplegia
1. auto accidents, If injury not severe may result in temporary
2. falls and paralysis and subside when swelling
3. gunshots decreases
• Sports and recreation-related SCI injuries primarily Assessment Findings

affect people under age 29 ● Complete or incomplete loss of the following
function below the level of injury:
Causes - Voluntary motor movement
• Road Traffic accidents. - Pain
• Bullet or stab wound - Problems on light touch,
• Traumatic injury temperature, pressure and
• Electric shock proprioception
• Extreme twisting of the middle of the body - Reflex activity
• Landing on the head during a sports injury - Autonomic activity
• Fall from a great height - Bowel and bladder dysfunction
Pathophysiology
• Fracture, dislocation or subluxation (partial
dislocation) of the vertebral column result in spinal
cord injury
• Cord injury is caused by compression, pulling,

twisting or tearing of the cord.
• 1. Penetrating trauma from gunshot wound or knife

injury causes severe compression or contusion of
spinal cord
2. Extreme flexion or hyperextension of the neck,

falling on buttocks, causes flexion of lower thoracic
and lumbar spine.
3. Tumor growth compress or destroy spinal tissue.

Any injury to spinal cord may cause nerve
transmission to the brain or from the brain not to
occur below the level of the damage causing paralysis
Microscopic bleeding in the gray matter affect after
the injury.
• Irritation of the cells causes edema to develop and

- Respiratory distress
spread to one or two cord segment.
Complete Spinal Cord Injuries
• Edema peaks in 2-3 days and subsides in 7 days
• Tetraplegia(Quadriplegia)- Spinal cord injury above
after the injury.
the first thoracic vertebra, or within the cervical
sections of C1-C8. The result is some degree of
• This edema causes temporary loss of sensation and
paralysis in all four limbs—the legs and arms.
function.
• Paraplegia- Spinal cord injuries below the first

thoracic spinal levels (T1-L5).
17
Paraplegics are able to fully use their arms and • CAUDA EQUINA SYNDROME
hands, but the degree to which their legs are disabled Known as Horse tail Syndrome.
depends on the injury. • Cause: Injury or lesion at the lumbosacral nerve root
below the conus medularris.
• Complete paraplegia: It is described as permanent • Characteristics:
loss of motor and nerve function at T1 level or below, 􏰀 Areflexia loss of reflexes(Lower Extremities). Leg
resulting in loss of sensation and movement in the weakness
legs, bowel, bladder, and sexual region. 􏰀 Bladder/bowel dysfunction
• CENTRAL CORD SYNDROME SIGNS AND SYMPTOMS

• Cause: Injury or edema of the central cord, usually
of the cervical area and cervical lesions CERVICAL (NECK) INJURIES
• Characteristics: Motor deficits (in the upper ✔ Breathing difficulties
extremities sensory loss varies in the upper ✔ Loss of normal bowel and bladder control
extremities). ✔ Numbness
✔ Sensory changes
• ANTERIOR CORD SYNDROME ✔ Spasticity (increased muscle tone)
• Cause: acute disk herniation associated with
fracture-dislocation of vertebra and also occur injury THORACIC (CHEST LEVEL) INJURIES
to anterior spinal Artery and lesion. ✔ Loss of normal bowel and bladder control
• Characteristics: Loss of pain, temperature, and ✔ Numbness
motor function is noted below the level of the lesion or ✔ Sensory changes
injury; light touch, position, and vibration sensation ✔ Spasticity (increased muscle tone)
remain intact. ✔ Weakness, paralysis
• POSTERIOR CORD SYNDROME LUMBAR SACRAL (LOWER BACK)INJURIES

• Cause: an infarct in the posterior spinal artery and is ✔ Loss of normal bowel and bladder control (patient
caused by lesions on the posterior portion of the may have constipation, leakage, and bladder spasms)
spinal cord. ✔ Numbness Pain
Characteristics: loss of proprioceptive sensation, ✔ Sensory changes Weakness and paralysis
fine touch, pressure, and vibration below the lesion;
deep tendon areflexia. Diagnostic Test
• Complete blood count (e.g. Hb, RBC, WBC)
• BROWN- SEQUARD SYNDROME • Arterial blood gas level
Known as Lateral Cord Syndrome. • PaO2:85-95 mm of Hg
• Cause: The lesion is caused by a transverse hemi • PaCO2:35-45 mm of Hg
section of the cord, as a result of a knife or missile • X- RAYS:
injury, fracture dislocation of a unilateral articular • COMPUTERIZED TOMOGRAPHY (CT)SCANS
process. • MAGNETIC RESONANCE IMAGING (MRI)
• Characteristics: Ipsilateral paralysis or paresis is • MYELOGRAPHY:
noted, together with ipsilateral loss of touch, pressure,
and vibration and contralateral loss of pain and Collaborative Management
temperature. ● Respiratory management
● Immobilization and rest
● Traction (crutchfield and Gardner- wells tong
● Urinary management indwelling catheter
● Special bed
Management
Airway
– C1-4 injuries require definitive airway
– Injuries below C4 may also require airway due to
• Work of breathing
• Weak thoracic musculature
Breathing
– Adequacy of respirations
• SpO2
• Tidal volume
• Effort
• Pattern
• CONUS MEDULARRIS SYNDROME
Known as Lateral Cord Syndrome. Circulation
• Cause: blow to the back- such as Gunshot and – Neurogenic shock
spinal tumor. • Injuries above T6
• Characteristics: Bowel and bladder dysfunction, • Hypotension
Flaccid lower extremities. Sexual dysfunction.
18
• Bradycardia –treat symptomatic only • Gardner-Wells tongs
• Warm and dry –Surgical
• Poikilothermic – keep warm
– Fluid resuscitation Stabilization
– Identify and control any source of bleeding – Cervical collar – convert to padded collar as soon
– Supplement with vasopressors as possible
– CTO or TLSO for low cervical, thoracic, lumbar
injuries
NEUROGENIC SHOCK
⬇️
Injury to T6 and above
Loss of sympathetic innervation ➡️

Increase in
⬇️ ⬇️
venous capacity
.
↘️↘️ ⬇️
Bradycardia Decrease in venous return
↙️
Hypotension
⬇️
Decreased cardiac output
Decreased tissue perfusion

ROTATIONAL BED THERAPY
Urine output – Maintain alignment and traction
– Urinary retention – Prevent respiratory complications of immobility
• Atonic bladder
– Foley SURGICAL
• Initially avoid intermittent catheterization – Determined by
• High urine output from resuscitation fluids • Degree of deficit, location of injury,
instability, cord impingement
Pain • Anterior vs. posterior decompression/ both
– Frequent physical and verbal contact
– Explain all procedures to patient – Emergent
– Patient-family contact as soon as possible • Reserved for neurologic deterioration when
– Appropriate short-acting pain medication and evidence of cord compression is present
sedatives
Prevention of Complication
• Surgery to stabilize the injured spine • Respiratory
– Complications of immobility
• Medications: • Atelectasis, Pneumonia
– Analgesic • Pulmonary embolism
• acetaminophen (Tylenol)
• codeine • Cardiovascular
– Anticoagulant: heparin – Neurogenic shock
– Anxiolytic: lorazepam (Ativan) – Orthostatic hypotension
– Glucocorticoid: methylprednisolone (Solu-Medrol) – Poikilothermia
– Laxative – Venous thromboembolism
• Other Pharmacologic agents Complication

– Lazaroids (21-aminosteroids) Gastrointestinal
– Opiate antagonists (Naloxone) – Ileus
– EAA receptor antagonists – Gastric/ intestinal ulcers
– Calcium channel block – Pancreas dysfunction
– Nutritional deficiencies
Communication – Constipation/ impaction
– Blink board – Cholecystitis
– Adapted call bell system
– Speech and occupational therapy Urinary
– Setting limits/boundaries for behavior • Areflexive bladder
– Hypothermia • Urinary tract infection
• Recommends 33oC intravascular cooling • Renal calculi
• Rapid application, Monitor closely • Skin breakdown
temperature
Musculoskeletal
Reduction • Spasticity
– Cervical traction • Contractures
• Halo
19
Psychological complication Nursing Diagnosis
• Pain/Depression ● Impaired physical mobility related to loss of
motor function
Male sexuality ● Fluid volume deficit related to decrease LOC
– Erection – parasympathetic ● Risk for injury related to loss of motor
– Ejaculation – sympathetic function
– Fertility – decreased sperm motility and quality ● Urinary retention related to level of injury
● Risk for Impaired skin integrity related to
Female trauma
– Lack innervation to pelvic floor ● Knowledge deficit regarding the treatment
– Pregnancy should be closely monitored to prevent modalities and current situation.
complications ● Anxiety related to outcome of diseases as
evidenced by poor concentration on work,
Complication isolation from others
Autonomic Dysreflexia Objectives of Care

– An uncontrolled, massive sympathetic reflex 1. To save the victims life.
response to noxious stimuli, below the level of the 2. To prevent further injury to the cord by proper
lesion handling of patient.
3. To repair as much of the damage to the cord.
An exaggerated and uninhibited sympathetic 4. To establish a routine of care that will improve and
response to a noxious stimulus that occurs in clients maintain state of health and prevent complication
with a spinal cord injury about T7
Nursing Interventions
– Precipitating factors • Assess VS and neurologic status.
• Full bladder • Immobilize, reduce, and align the injured area of the
• Distended bowel spinal column.
• Skin irritation, ingrown toenail – Crutchfield, Vinke, or Gardener-Wells
• UTI tongs with cervical traction
• Uterine spasms, penile stimulation – Halo external fixation device; a body jacket
• Tight clothing, wrinkled sheets – Minerva jacket
Signs and Symptoms of Autonomic Dysreflexia .Minerva cast Minerva jacket:

– Signs and symptoms: (Rarely used)
• Hypertension It is applied to trunk and head, with spaces cut out for
• Pounding headache face and ears. It extends fromsternum and distal rib
• Flushing border anteriorly & across the distal rib border
• Diaphoresis posteriorly
• Blurred vision
• Bradycardia. Cervical traction:
•Treatment consists of removing the noxious stimulus – Assess and clean the pin sites as prescribed
– Make sure the weights are free-hanging
• This response is potentially dangerous, because it
can produce vasoconstriction of the arterioles with an • Halo external fixation device
immediate elevation of blood pressure. The sudden – Assess and clean the pin sites as prescribed –
hypertension can cause seizure, retinal hemorrhage Keep a torque screwdriver readily available
or stroke.
• Less serious effect includes: • Provide bed rest on a firm surface
1. severe headache • Maintain a patent airway and administer
2. changes in PR, oxygen
3. Sweating and flushing above the level of spinal • Assess the client for signs and symptoms of
cord lesion Autonomic Dysreflexia
4. pallor and “goose bump • Most stimulation that can cause Autonomic
Dysreflexia are related to bladder, bowel and skin of
Autonomic Dysreflexia Management patient
• Observe for bradycardia and hypertension • Example: Change of catheter
• Sit patient upright to produce orthostatic • Insertion of rectal suppositories, enema
hypotension(Fowler’s position) • Bladder distention
• Monitor BP every 5 minutes • Sudden change in position
• Monitor neurologic status (GCS)
• Eliminate the offending stimulus TRIGEMINAL NEURALGIA
– Empty bladder, bowel; identify skin lesion
• Administer anti-hypertensives if the above fails • FACIAL NERVE the nerve which is most commonly
• Education –family and patient associated with facial nerve pain is trigeminal nerve.
• The facial pain cause by this nerve is called
• trigeminal neuralgia (Tic Douloureux).
20
• It is a chronic neuropathic condition affecting any 􏰀 Chewing and swallowing
part of the face, head, neck, shoulders and is 􏰀 Touching and washing face
considered one of the most painful conditions. 􏰀 Light breeze or wind on face
• It can affect any of the three branches.
• Is a painful disorder of one or more branches of the DIAGNOSTIC EVALUATION
fifth cranial (trigeminal) nerve that produces • Skull X-rays
paroxysmal attacks including facial pain. • Tomography
• CT scan rule out sinus or tooth infections, and
INCIDENCE tumors
• Incidence: • MRI
– above 40 or middle aged – more common in women
– affected right side MEDICAL MANAGEMENT
• Can subside spontaneously Pharmacology
• With remissions lasting from several months to • Anti seizure drug- Carbamazepine(tegretol)
years • Baclofen.
• Oxycarbazepine with lamotrigine or phenytoin may
ETIOLOGY also be use.
INTRACRANIAL CAUSES • During refractory period, gabapentin is most
1. compression-internal carotid artery pulsations commonly used.
2. Multiple sclerosis
3. Intracranial tumors- at the cerebellopontine angle SURGERY
4. Intracranial vascular abnormalities-basilar artery • Those patients who do not respond to medications
aneurysm, superior cerebellar artery abnormality and are physically fit can go for invasive procedures.
• Peripheral Injections Longer-acting anesthetic
EXTRACRANIAL CAUSES agents Agents like bupivacaine without adrenaline but
Vascular factors with or without corticosteroids are injected to the
Dental etiology peripheral nerve end.
Post traumatic neuralgia Infections
Viral etiology Peripheral Neurectomy
• Mostly performed on the infraorbital nerve, inferior
PATHOPHYSIOLOGY alveolar nerve, mental nerve and rarely lingual nerve.
• Affect the CN V , three branches of this nerve are • Nerve blocks to relieve pain(Glycerol rhizotomy)
the ophthalmic, mandibular and maxillary. The Cryotherapy -direct application of cryoprobe
ophthalmic nerve is not involved or rarely involved (temperature -60◦) intraorally to the affected nerve • In
• Pressure by an artery next to trigeminal nerve this, the nerve is not sectioned but destroyed.
causes neuralgia.
• Pain may also be due to increased afferent firing in NURSING DIAGNOSES
the nerve or failure of inhibitory mechanism • Acute pain
• Trigeminal neuralgia is associated with • Powerlessness
neurovascular compression in the trigeminal root • Anxiety
entry zone, which can lead to demyelination and a
dysregulation of voltage-gated sodium channel NURSING INTERVENTION
expression in the membrane. • Observe and record the characteristics of each
• These alterations may be responsible for pain attack.
attacks in trigeminal neuralgia patients. • Provide adequate nutrition:
– small frequent meals at room temperature, soft food
CLINICAL MANIFESTATION • Place food in the unaffected side of his mouth when
• Pain occur several times a day or a week, followed chewing.
by pain- free or refractory period. The pain worsens • Health teachings on good oral hygiene.
with time and mostly affects only one side of the face. • Reinforce natural avoidance of stimulation
• If both sides of the face are involved then it is called • Provide instruction about preventive strategies, like
bilateral trigeminal neuralgia. use of room temperature water when washing face.
• The cheek, jaw, teeth, gums, and lips are most ___________________________________________
commonly affected. BELL’S PALSY
• may have anxiety because they are uncertain when
the pain will return Is a condition in which the muscles on one side of the
face become weak or paralyzed.
TRIGGER FACTORS
􏰀 Light touch to a sensitive area of the face (trigger Affects only one side of the face at a time, causing it
zone) to droop or become stiff on that side.
􏰀 Exposure to hot or cold temperature
􏰀 Eating, smiling, or talking Caused by some kind of trauma to the seventh
􏰀 Drinking hot or cold beverages cranial nerve, called the “facial nerve”
􏰀 Hair brushing and cleaning of teeth
􏰀 Tilting head and shaving Stress and tiredness
􏰀 Cold and hot weather
21
DEFINITION MEDICAL MANAGEMENT
Is a form of facial paralysis resulting from a SURGERY:
dysfunction of the cranial nerve VII (the facial nerve) Decompression surgery was used to
that results in the inability to control facial muscles on relieve the pressure on the facial nerve by opening
the affected side the bony passage where the nerve passes through.
Facial nerve injury and permanent hearing loss are
RISK FACTORS possible risks associated with this surgery.
• Bell's palsy occurs more often in people who:
1. Are pregnant, especially during the third trimester, • . Electrotherapy after the 14th day of prednisone
or who are in the first week after giving birth therapy (stimulation of nerve)
2. Have an upper respiratory infection, such as the flu – help prevent facial muscle atrophy
or a cold • Moist heat
3. Diabetes Mellitus • Eye patch
4. Exposure to cold risk factor • Medication:
– Corticosteroid: prednisone (Deltasone)
CAUSES – Acyclovir if associated with Herpes
• Blockage of the seventh cranial nerve (Facial) – Use of eye drops – keep eye lubricated
– Infection
– Hemorrhage NURSING DIAGNOSES
– Tumor • Acute pain
– Meningitis • Disturbed sensory perception
– Local trauma • Disturbed body image
– Herpes simplex • Alteration in Nutritional Status
– Herpes zoster
– Influenza NURSING INTERVENTIONS
– Stress • Massage the client’s face
– Exposure to cold risk factor – gentle upward motion
– 2-3x/day for 5 to 10 minutes
PATHOPHYSIOLOGY • Arrange for privacy at mealtimes
• Bell’s Palsy result from a lower neuron dysfunction • Oral care (as the residue is common)
causing a unilateral facial nerve (CN Vll) paresis or • Psychological support.
paralysis on one side of the face – Give reassurance that recovery is likely
within 1 to 8 weeks
DIAGNOSTIC EVALUATION ___________________________________________
Electromyography (EMG) PERIPHERAL NEUROPATHY
Test can confirm the presence of nerve damage and • Refers to nerves outside the brain and spinal cord.
determine its severity. EMG measures the electrical • Broken down into:
activity of a muscle in response to stimulation and the Sensory
nature and speed of the conduction of electrical Motor
impulses along a nerve. Autonomic
▪ Parasympathetic
Imaging scans. Magnetic resonance imaging ▪ Sympathetic
(MRI) or computerized tomography
(CT) may be needed on occasion to rule out other • Is caused by damage to peripheral nerve/
possible sources of pressure on the facial nerve, such • Peripheral neuropathy, a result of nerve damage,
as a tumor or skull fracture. often causes pins and pain in your hands and feet.
• Patients experience the anxiety of peripheral
CLINICAL MANIFESTATION neuropathy as burning, while they may explain the
• Inability to close eye completely on the affected side loss of feeling to the feeling of wearing a thin sack
occurring within hours or day • Peripheral Neuropathy can affect:
• Pain around the jaw or ear • Sensory pathways
• Unilateral facial weakness • Motor pathways
• Eye rolls upward and tears excessively when the • Autonomic pathways
client attempts to close it
• Ringing in the ears Neuropathies might be acute or chronic
• Taste distortion on the affected anterior portion of 1. Mononeuropathy – affecting a single nerve
the tongue 2. Polyneuropathy – a diffuse, symmetrical disease
• Facial droop and difficulty making facial usually starting peripherally.
expressions, like smiling 3. Mononeuritis multiplex – affects several or
• Drooling multiple nerves.
• Increased sensitivity to sound on the affected side 4. Radiculopathy – a disease affecting nerve roots
• Headache
• Changes in the amount of tears and saliva produce Mononeuropathies
• Affects one nerve
• Direct injury to a nerve, ischemia, or inflammation.
22
• Most likely the cause is a physical compression, May also cause pain :
localized trauma, or infection • e.g. carpal tunnel, deep, aching pain worse at night frequently in the
cubital tunnel lower back, hip, or leg
• "pins-and-needles" sensation of one's
• Peripheral nerve compression and entrapment • In diabetes typically encountered as acute,
• Carpal tunnel syndrome is a common mono unilateral, severe thigh pain followed by anterior
neuropathy – Median nerve entrapment muscle weakness and loss of knee reflex.
• Clinical presentation
- Pain, tingling, and paresthesia on the palmar MECHANISMS OF PERIPHERAL NERVE
aspect of hand and fingers DEGENERATION
- Weakness of thenar muscles and wasting of 1. Demyelination – e.g. Guillain-Barre Syndrome
abductor pollicis brevis 2. Axonal degeneration - e.g. toxic neuropathies
- Nocturnal Pain may extend to arm and 3. Wallerian degeneration
shoulder 4. Compression – e.g. carpal tunnel syndrome
- Tinel’s and Phalen’s tests are positive. 5. Infarction – e.g. diabetes
6. Infiltration – e.g. leprosy and granulomas
POLYNEUROPATHY
● Affects many nerve cells in various parts of CAUSES OF PERIPHERAL NEUROPATHY
the body - often unknown
● Symmetrical - two main causes are:
● Progresses slowly ● Diabetic Neuropathy
● Caused by processes affecting the whole ● Nutritional, including alcohol (B1 deficiency)
bod
Other causes:
SENSORY POLYNEUROPATHY MANIFESTATION - Infection – HIV, leprosy, diptheria, tetanus, botulism
- Paresthesia - Heavy metal poisoning e.g. Lead and mercury
- Numbness - Malignancy
- Burning pain - Metabolic – hypothyroidism, liver failure, renal
- Loss of vibration sense and position sense failure
- Difficulty using small objects e.g. needles - Post Infective polyneuritis – Guillain-Barre
- Subacute with ataxia due to loss of sense of Syndrome
posture - Sarcoidosis
- Feet are usually affected first - Drugs – isoniazid, vincrinstine, phenytoin, gold,
excess vitamin B6
AUTONOMIC POLYNEUROPATHY
MANIFESTATION DIABETIC NEUROPATHY
Clinical Presentation: ● Directly related to the duration and degree of
● Postural hypotension abnormal metabolic control – occurring
● Urinary retention relatively early in disease
● Erectile dysfunction ● Due to metabolic disturbance and
● Diarrhoea/constipation accumulation of fructose and sorbitol in
● Diminished sweating Schwann cells degradation
● Impaired pupillary response ● Types of Diabetic neuropathy
● Cardiac arrhythmias Symmetrical mainly sensory neuropathy
Might occur in: Acute painful neuropathy
● Diabetes Mononeuropathy
● Amyloidosis Mononeuritis multiplex
● Guillain-Barre syndrome Diabetic amyotrophy
MOTOR NEUROPATHY MANIFESTATION ALCOHOLIC NEUROPATHY

Clinical presentation: • Chronic alcohol abuse leads to polyneuropathy Calf
● Progressive weakness or clumsines pain is common
● Difficulty walking (falling or stumbling • Deficiency in thiamine due to alcoholism also
● Respiratory difficulties (falling vital capacity) causes neuropathy
● Wasting • Can lead to Wernicke-Korsakoff syndrome
● Foot or wrist drop
● Reflexes absent or reduced Common presentation
▪ Eye signs
MONONEURITIS MULTIPLEX ▪ Ataxia
• Simultaneous or sequential involvement of individual ▪ Cognitive change
noncontiguous nerves, either partially or completely, ▪ Delirium tremens
evolving over days to years asymmetric ▪ Hypothermia and hypotension
• Typically presenting with acute or subacute loss of GUILLAIN-BARRE SYNDROME MANIFESTATION

sensory and motor function of individual nerves • Acute polyneuropathy – acute inflammatory or post
infective neuropathy
23
• Usually demyelinating but can be axonal cells in an area of the brain known as the substantia
Monophasic – following Campylobacter jejuni nigra.
• Infection induces antibody responses against
peripheral nerves • These cells normally produce dopamine, a chemical
- Paralysis 1-3 weeks following infection (neurotransmission) that transmits signals between
- Weakness of distal limb muscles and/or areas in the brain that when working normally
distal numbness coordinates smooth and balanced muscle movement .
- Symptoms progress proximally
- Loss of tendon reflexes • Parkinson’s disease cause these nerve cells to die
- Facial muscle weakness and, as a result, body movement is affected.
- Autonomic features – uncommon
- Might need ventilatory support EPIDEMIOLOGY
- SC heparin is required to reduce risk of ● Parkinson disease occurs worldwide and is
thrombosis present in all races.
- Spontaneous recovery begins after several ● Males are more affected than females.
weeks ● Prevention of Parkinson disease increase
with increasing age of 1% of person from
DIAGNOSTIC EVALUATION age 60.
• Urine – glucose, protein ● YOPD starts between 21 -40 years of age
• Hematology – FBC, ESR, vitamin B12, folate affecting 5 to 10% of Parkinson disease
• Biochemistry – fasting glucose, RFT, LFT, TSH patients.
• Neurophysiology testing ● China is the country world's the largest
• Nerve conduction studies prevalence of Parkinson's disease.
• Needle electromyography
• Nerve biopsy DEFINITION
Parkinson's disease is characterized by tremors at
MEDICAL MANAGEMENT rest, rigidity and slowness or difficulty in initiating and
● Need to find cause then treat the cause of executing movement (Akinesis or Bradykinesis).
neuropathy.
● If pain can give antiepileptic, antidepressant This combination of clinical features is collectively
drugs or tramadol, Codeine, Aspirin known as Parkinsonism.
● Corticosteroid injection for inflammation
● Foot care – good shoes Parkinsonism is a syndrome with numerous cause of
● Weight reduction which Parkinson disease is the most common.
● Walking aids for those with severe leg
weakness ANATOMY
● Occupational therapy • The substantia nigra is a nucleus in the mid brain
● Physiotherapy which is part of the Basal Ganglia.
NURSING INTERVENTION • The substantia nigra is made up of two automatically

• Nursing care depend upon the type and cause of and functionally distinct portion :
neuropathy Substantia nigra pars compacta –more darkened
• Teach patient: Substantia Nigra pars reticulata –less darken.
• Daily inspection of foot
• Wear white socks so you can see blood Most of the dopamine neuron of the brain originate
more easily in the midbrain and are found in either the substantia
• Don’t cut your own toe nails Nigra.
• Wear sensible shoes
• Exercise. Regular exercise, such as The Dopamine neurons in the substantia Nigra
walking three times a week, can reduce neuropathy express a high level of pigment called Neuromelanin
pain, improve muscle strength and help control blood which accounts for thin dark colour .
sugar levels. Gentle routines such as yoga and tai chi
might also help The substantia Nigra par compacta contain more
• Quit smoking. dopamine neurons while pars Reticulate contains
• Eat healthy meals. Good nutrition is more GABA neurons .
especially important to ensure that you get essential
vitamins and minerals. Include fruits, vegetables, CLINICAL SIGNIFICANCE
whole grains and lean protein in your diet. • Parkinson disease is associated with the death of
• Avoid excessive alcohol. dopamine Neuron in the substantia Nigra pars
compacta which is due to neuro-degeneration .
PARKINSON’S DISEASE • when a significant number of this neuron have died,

the individual will likely to start to experienced
• Parkinson disease is a slowly progressive , chronic movement –related problems like:
neurological disease that effects a small area of nerve • tremors,
• rigidity,
24
• slowness of movement and Degeneration of dopaminergic activity particularly in
• postural instability the nigro-striatal pathway
• These are the hall mark symptoms of ↓
Parkinson disease. Depletion of dopamine store
↓
ETIOLOGY/RISK FACTORS Imbalance between excitatory (Acetylcholine) and
Advancing age : Above 60 years mostly seen while inhibiting (dopamine) neurotransmitter in the corpus
young onset Parkinson disease is called a patients striation
develop Parkinson disease between 21-40 years. ↓
Impairment of extrapyramidal tract controlling
Sex: male are more likely to get than female. complex body movement
↓
Family History: Having one or more close relatives Tremors Rigidity. Akinesia. Postural instability
with the disease increase the rise of getting.
SIGNS AND SYMPTOMS
Low Estrogen Level: most menopausal women who Four cardinal sign:
don’t use hormone replacement therapy are more risk - Resting tremor
of getting the disease. - Rigidity
- Akinesia
Agricultural work: exposure to environmental toxin - Postural instability Cog-wheeling
such as pesticide ,herbicides ,inhabits dopamine
production and promote free radical damage. these AKINESIA: Bradykinesia Hypokinesia Hypophonia
involved in farming and are exposed to such toxins Micrographia
have a greater risk of getting the disease.
DYSAUTONOMIA: it includes sweats,facial flushing.
Low level of vitamins: researchers de was found Dyspnea, urinary frequency, urgency. GI
that people with low level of vitamin B develop severe dysfunction-constipation. Dysphagia, Orthostatic
Parkinson symptoms. hypotension and sexual dysfunction Cognitive and
psychiatric disturbance: Anxiety, Apathy, mental,
Head Trauma: Trauma to the head ,neck and upper irritability, impaired executive function, depression
cervical spine increase the chance of getting psychosis (delusions ) dementia
Parkinson’s.
● Parkinsonian gait
Genetic Mutation: people who have both young ● Slowed movement
onset Parkinson’s disease and a strong family history ● Reduced armswing
of the disease are more likely carry genes linked to ● Rigidity Freezing
Parkinson’s disease which includes; ● Mask like face
• Alpha Synuclein: Autosomal dominant. ● Asymmetric resting tremor
• LRRK2(leucine rich repeat kinesis2): Autosomal. ● Postural instability Shuffling steps
• PINK1/PARKIN/DJ-1: Autosomal recessive
• GBA(Glucocerebrocidase): Autosomal recessive POSTURAL DISTURBANCE:
• Alpha synuclein and LRRK2 gene mutation is • Stooped or fixed positive
linked with Young onset Parkinson Disease. • Disequilibrium or postural instability
• Retropulsion –backward motion
Other causes: • Propulsion – forward motion
Secondary Parkinson’s: which are caused by other • Sleep disturbance: Frequent awakening
disorders such as Neoplasm, multiple cerebral • Daytimes sleepiness’
infarction and infection of the brain. • Sensory impairment: pain, restlessness and
Drug induces Parkinsonism: which are irreversible. Akathisia.
causative drugs include : Neuroleptics – haloperidol
,risperidone, olanzapine. Antiemetic- • Bradykinesia- condition exhibiting slow movement
metachlopramine, prochlorperazine. and speech that produces poor body balance and a
Parkinson’s disease caused by Degenerative characteristic gait.
disease in which symptoms of Parkinson’s disease • Tremor-a rhythmic, purposeless, fine trembling or
are combines with neurologic deficit yet patients fail to quick movement resulting from the involuntary
response to Anti-Parkinson drugs therapy . These alternating contracting and relaxation of opposing
disorders include group of muscle
- Multiple system atrophy (MSA). • Rigidity- muscle stiffness that affect the skeletal
- Alzheimer’s Disease -often accompanied muscle.
with mild signs of Parkinsonism. • Lead-pipe rigidity- stiffness and inflexibility that
remain uniform through out the range of passive
PATHOPHYSIOLOGY movement
Destruction of Dopaminergic neuronal cells in the • Cogwheel rigidity is an abnormal movement when
substantia nigra in the basal Ganglia Neuronal cells the limb is passively stretched.
loss and depigmentation • Akinesia loss of movement
↓
25
COMMON SECONDARY MANIFESTATION receptors . They mimic or copy the function of
1. Fine motor deficit Dopamine in the brain. Dopamine agonists can be
2. Monotonic voice taken alone or in combination with
3. Generalized muscle weakness Levodopa/carbidopa. Most commonly drugs used are
4. Drooling, constipation Ergot derivatives : Bromocriptine or
5. Orthostatic hypotension pergolite.
6. Urinary dysfunction Non-ergot Derivatives: Ropinirole
,pramipexole.
STAGES OF PARKINSON’s DISEASE
Parkinson’s disease is typically classified by the 3. MONOAMINE OXIDIZED INHIBITORS: It blocks
worsening of clinical manifestation. The modified an enzymes that caused premature of levodopa and
Hoehn and Yohr scale is one method use to rate the are used primarily to treat motors fluctuation
severity of Parkinson’s disease. associated with levodopa treatment .most commonly
drugs used are Seligiline, Rosagiline.
• STAGE 0: No evidence of Parkinson’s disease.
• Stage 1: Unilateral involvement . • AMANTADINE : it is the most commonly used
• Stage 1.5: Unilateral and Axial involvement . medication for early onset Parkinson’s disease to tract
• Stage 2: Bilateral involvement, balance in contact . tremor .It reduce dyskinesia’s that occur with
• Stage 2.5: Bilateral involvement, recovery on pull Levodopa.
test .
• Stage 3: Mild to moderate impairment with postural COMT INHIBITORS(Catechol-o-methyl-transferase):
instability . such is Tolcapone and entacapone response the
• Stage 4: Severe impairment but still able to stand or newest class of Parkinson’s drugs .
walk un assisted.
• Stages 5: Confinement to a wheel chair or bed . • It does not have direct effect on Parkinson’s disease
symptoms, it prolong the effect of levodopa by
DIAGNOSTIC EVALUATION: blocking its metabolism.
Criteria for making diagnosis of Parkinson’s disease
include the following • ANTI-CHOLINERGIC: it is helpful in controlling
tremors and rigidity.
1. Through patients’ history and performed • It decrease the activity of acetylcholine, a
complete neurological examination. neurotransmitter that regulates movement ,most
2. CT scan or MRI of head to rule out secondary commonly used are:
cause. • Benzotropine mesylate
3. PET-scan to evaluate levodopa uptake and • Trihexyphenidyl
conversion to Dopamine in the corpus Striatum .
4. Present of two or more cardinal features (resting • HCL ANTI-DEPRESSANT :
tremors, rigidity, Akinesia, postural instability). • Amitriptyline is typically prescribe because of its
5.Final diagnosis usually made by the pressure of Anticholinergic and Antidepressant effect.
heavy bodies in the brain during Autopsy. • Serotonins reuptake inhibitors; Fluoxetine
Hydrochloride and Bupropion hydrochloride, they are
MEDICAL MANAGEMENT effective for treating depression in patients with
• There are no complete cure for Parkinson’s disease. Parkinson’s disease.
• Treatment is directed at controlling symptoms and • Physical therapy
maintaining functional independence. • Speech therapy
• There are no medical or surgical approaches that
prevent disease progression. SURGICAL MANAGEMENT:
• Care is individualized for each patients based on THALATOMY:
preventing symptoms and social occupational and • It involves destruction of part of the Thalamus,
social needs. generally the ventral’s intermediates (VIM) to relieve
• Pharmacologic management is the main stay of tremor.
treatment.
• The VIM nucleus is considered the best target for
ANTI-PARKINSONISM MEDICATION: tremor suppression with excellent short and long term
1. LEVEDOPA (L-Dopa): it is the most effective tremor suppression in 80-90% of patients with
agents and the mainstay of treatment, for controlling Parkinson’s diseases.
the symptoms particularly Bradykinesia and rigidity.
• When rigidity and Akinesia are prominent other
SINEMET: it is made up of Levodopa and carbidopa targets ,deep brain stimulation of both Globus pallidus
.Levodopa enters the brain and is converted to interna (Gpi) and subthalami nucleus (STN)are
Dopamine while carbidopa increase its effectiveness preferred.
and prevents the side effects of levodopa such as
nausea, and vomiting. 10 Early Signs of Parkinson's Disease
● Tremor
2. DOPAMINE RECEPTOR AGONISTS: this are the ● Trouble Moving or Walking
drugs that activate or stimulate the dopamine ● Loss of smell
26
● Trouble sleeping ● Promote independence along with safety
● Small handwriting measures.
● Soft or Low Voice ● Avoid rushing the client with activities.
● Constipation ● Assist with ambulation and provide assistive
● MaskedFace devices.
● Stooped or Hunched Over ● Instruct client to rock back and forth to
● Dizziness or fainting initiate movement.
● Instruct the client to wear low-heeled shoes.
DEEP BRAIN STIMULATION: ● Encourage the client to lift feet when walking
• Deep brain stimulation is a neurological procedure and avoid prolonged sitting.
which Parkinson’s diseases symptoms. ● Provide a firm mattress, and position the
client prone, without a pillow, to facilitate
• More recently in 2016 DBS surgery was approved proper posture.
for the earlier stages of Parkinson’s for those with at ● Instruct in proper posture by teaching the
least four years disease duration with motors client to hold the hands behind the back to
complication that are not controlled with medications. keep the spine and neck erect.
● Promote physical therapy and rehabilitation.
• Deep brain stimulation involves the implantation of ● Administer anticholinergic medications as
permanents thin electrodes into selected deep parts prescribed to treat tremors and rigidity and to
of the brain . inhibit the action of acetylcholine.
● Administer antiparkinsonian medications to
• The targets area of the brain depends on the increase the level of dopamine in the CNS.
presenting symptoms, the most common targets area ● Instruct the client to avoid foods high in
are thalamus, subthalamic nucleus(STN)and Globus vitamin B6 because they block the effects of
pallidus in terna(Gpi). antiparkinsonian medications.
NURSING DIAGNOSIS: DISCHARGE INSTRUCTION

1. Impaired physical mobility related to Bradykinesia, ● To assist in maintaining balance, concentrate
rigidity and tremors on taking larger steps with feet apart,
2. Imbalance nutrition less than body requirement keeping back straight and swinging the
related to motor difficulties with feeding, chewing, and arms;
swallowing ● To overcome akinesia, tape the “frozen” leg
3. Impaired verbal communication related to to initiate movement;
decreased speech volume ● To reduce tremors, hold objects (coins, keys,
4. Constipation related to diminished motor function or purse) in the hand;
and inactivity ● To obtain partial control of tremors when
5. Ineffective coping related to physical limitation and seated, grasp chair arms;
loss of independence. ● To reduce rigidity before exercise, take a
warm bath;
NURSING INTERVENTION ● To initiate movement, rock back and forth;
Nursing Assessment: ● To prevent spine flexion, periodically lie
● Obtain a history of symptoms and their effect prone and avoid using a neck pillow; and
on functioning, mobility, feeding, ● Teach the patient to eliminate loose
communication, and self-care difficulties. carpeting, install grab bars, and elevate the
● Assess cranial nerves, cerebellar function toilet seat. Use of chair lifts can also be
(co-ordination) and motor function. beneficial
● Observe gait and performance of activities
● Assess speech for clarity and space
● Assess for sign of depression
● Assess family supports and access to social
service.
● Diet
• Low protein at day, high protein at night
(Levodopa is slowed down by high protein
food and Vitamin B6) soft diet with small,
frequent feedings.
● Assess the client’s gag reflex.
● Institute safety measures to prevent injury.
● Provide ample time for communicating.
● Administer medications, as ordered.
● Provide ample time for the client to perform
ADL.
● Allow verbalization of feelings.
● Assess ability to swallow and chew
● Increase fluid intake to 2000 mL/day.
● Monitor for constipation.
27

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MED SURG FINALE b.

Hypoxic encephalopathies: severe congestive heart

The skull is a rigid structure. Stroke

Very severe elevation 41 mm Hg and above

SIGNS AND SYMPTOMS

● Continued decrease in level of • Pharmacologic Methods

• Decreased LOC with difficulty to arouse and Contraindications:

Goals of Therapy: MOA: exact mechanism unknown; may

An epileptic syndrome consists of recurrent

Common Causes of Epilepsy DIAGNOSTIC EVALUATION

• During the seizures the major goals are:

Nursing Care ● Blockage of an artery

- In paradoxical embolism, a deep vein thrombosis DIAGNOSTICS

- If the area of the brain affected contains one of the PATHOPHYSIOLOGY

- Hemorrhages 5. Edema- Any brain injury can lead to edema, or

• Inflammatory process and cellular edema leads to POSTURE

Signs and symptoms

Nursing Diagnosis Definition

● Provide suctioning Level of injury are classified as:

Incidence Cervical region damage

• Sports and recreation-related SCI injuries primarily Assessment Findings

• Cord injury is caused by compression, pulling,

• 1. Penetrating trauma from gunshot wound or knife

2. Extreme flexion or hyperextension of the neck,

3. Tumor growth compress or destroy spinal tissue.

• Irritation of the cells causes edema to develop and

• Paraplegia- Spinal cord injuries below the first

• CENTRAL CORD SYNDROME SIGNS AND SYMPTOMS

• POSTERIOR CORD SYNDROME LUMBAR SACRAL (LOWER BACK)INJURIES

Loss of sympathetic innervation ➡️

Decreased tissue perfusion

• Other Pharmacologic agents Complication

Autonomic Dysreflexia Objectives of Care

Signs and Symptoms of Autonomic Dysreflexia .Minerva cast Minerva jacket:

MOTOR NEUROPATHY MANIFESTATION ALCOHOLIC NEUROPATHY

• Typically presenting with acute or subacute loss of GUILLAIN-BARRE SYNDROME MANIFESTATION

NURSING INTERVENTION • The substantia nigra is made up of two automatically

PARKINSON’S DISEASE • when a significant number of this neuron have died,

NURSING DIAGNOSIS: DISCHARGE INSTRUCTION

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