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  • In any case suspected of meningitis based on the clinical signs, a lumbar puncture is essential. Sometimes parents are afraid of the procedure and fear it is harmful to the child. It should be emphasized to them that treatment is highly dependent on CSF results. A lumbar puncture may be postponed or withheld in the following situations: presence of significant cardiac or respiratory distress and shock, sign of increased intracranial pressure, infection in the area that the spinal needle will traverse to obtain CSF, and hematologic problems such as thrombocytopenia and coagulation defects.
  • The following are the CSF findings that will make you confirm the diagnosis of meningitis: the CSF pressure may be elevated, there is leukocytosis with predominance of PMNs, the glucose is low, the CSF blood to glucose ratio is <0.40, and the protein is elevated. The stained smears of CSF may be (+) for bacteria. Culture of CSF should be done whenever it is available, but a negative culture does not rule out meningitis.

 neurological  disorders neurological disorders Presentation Transcript

  • DISTURBANCE IN PERCEPTION & COORDINATION
  • CRANIOCEREBRAL TRAUMA (HEAD INJURIES)
    • Defined as any injury to the scalp, skull/cranium, or brain.
    • Motor vehicle accidents are most common cause
    • Other causes:
      • Gunshot
      • Hacking
      • Falls
      • accidents
    • 3 mechanisms that contribute to head trauma:
    • Acceleration
      • Occurs when head is struck by a moving object and set in motion
    • Deceleration
      • Occurs when moving head strikes a solid, immobile object.
    • Deformation
      • Injuries in which the force results in deformation and disruption of the integrity of the impacted body part (skull fracture)
    CRANIOCEREBRAL TRAUMA (HEAD INJURIES)
    • By description of injury
      • Blunt trauma
        • Results from acceleration-deceleration injuries
      • Penetrating injuries
        • Injuries made by foreign bodies (knives, bullets) or those made by bone fragments from skull fracture
      • High velocity objects
        • As in bullets produce shock waves in the skull and brain. The shock waves may significantly damage brain structures beyond those in the object’s path.
      • Coup injury
        • Occurs immediately at the point of impact. The same blow may cause injury on the opposite side of the brain
    CRANIOCEREBRAL TRAUMA (HEAD INJURIES)
    • According to Structures Damaged
    • Primary head injury
      • Refers to impact damage, the severity of which is estimated by initial s/sx.
      • Includes injuries to the scalp, skull, or brain or all of these.
    CRANIOCEREBRAL TRAUMA (HEAD INJURIES)
    • a. Scalp Injuries – include lacerations, hematomas and contusions or abrasions
    • Immediate interventions:
    • Do not attempt to remove foreign or any penetrating objects from the wound
    • Cover head wounds and apply pressure to bleeding scalp.
    • b. Skull Injuries – often caused by a force sufficient to cause both fracture and brain injury
    • 3 Types of Skull Fractures:
      • Linear skull fracture
        • appears as thin lines on X-rays and do not require treatment.
      • Depressed skull fracture
        • may be palpated and seen on x-ray. It results when the bone is forced below the line of normal contour from impact with moving object, which may caused brain abrasion or laceration.
      • Basilar skull fracture
        • occurs in bones over the base of the frontal and temporal lobes.
  • c. Traumatic brain injury
    • 1. CONCUSSION
    • Involves jarring of head without tissue injury
    • Temporary loss of neurologic function lasting fore a few minutes to hours
    • Is a head trauma producing brief loss of consciousness (5 min) followed by confusion and/or memory loss (amnesia), may also experience dizziness and nausea and vomiting.
  •  
  • Traumatic brain injury
    • 2. CONTUSION
    • Involves structural damage
    • Is a damage to the brain substance itself, causing multiple areas of petecheal and punctuate hemorrhage and bruised areas.
    • The patient becomes unconscious for hours
        • TYPES OF CEREBRAL CONTUSION:
          • Temporal Lobe Contusion
            • Person is agitated, confused but remains alert
          • Frontal Lobe Contusion
            • Hemiparesis inn an alert head-injured client
          • Frontal-Temporal Contusion
            • Aphasic head-injured person
          • Brain Stem Contusion
            • Renders a person immediately unresponsive or partially comatose
  •  
  • Traumatic brain injury
    • 3. Diffuse Axonal injury
    • Involves widespread damage to the neurons
    • Patient has decerebrate and decorticate posture
  • Traumatic brain injury
    • 4. Intracranial hemorrhage
    • Epidural Hematoma- blood collects in the epidural space between skull and dura mater. Usually due to laceration of the middle meningeal artery
    • Symptoms develop rapidly
  •  
  • Traumatic brain injury
    • 4. Intracranial hemorrhage
    • Subdural hematoma- a collection of blood between the dura and the arachnoid mater caused by trauma. This is usually due to tear of dural sinuses or dural venous vessels
    • Symptoms usually develop slowly
  •  
  • Traumatic brain injury
    • 4. Intracranial hemorrhage
    • Intracerebral Hemorrhage and hematoma- bleeding into the substance of the brain resulting from trauma, hypertensive rupture of aneurysm, coagulopahties, vascular abnormalities
    • Symptoms develop insidiously, beginning with severe headache and neurologic deficits
  •  
  • Traumatic brain injury
    • MANIFESTATIONS
    • 1. Altered LOC
    • 2. CSF otorrhea
    • 3. CSF rhinorrhea
    • 4. Racoon eyes and battle sign
      • HALO SIGN- blood stain surrounded by a yellowish stain
      • Periorbital ecchymosis (bruise around the eye)
  • Traumatic brain injury
    • NURSING MANAGEMENT
    • 1. Monitor for declining LOC- use of Glasgow
    • 2. Maintain patent airway
    • Elevate bed, suction prn, monitor ABG
  • Traumatic brain injury
    • NURSING MANAGEMENT
    • 3. Monitor F and E balance
    • Daily weights
    • IVF therapy
    • Monitor possible development of DI and SIADH
  • Traumatic brain injury
    • 4. Provide adequate nutrition
    • 5. Prevent injury
    • Use padded side rails
    • Minimize environmental stimuli
    • Assess bladder
    • Consider the use of intermittent catheter
  • Traumatic brain injury
    • 6. Maintain skin integrity
    • Prolonged immobility will likely cause skin breakdown
    • Turn patient every 2 hours
    • Provide skin care every 4 hours
    • Avoid friction and shear forces
  • Traumatic brain injury
    • 7. Monitor potential complications
    • Increased ICP
    • Post-traumatic seizures
    • Impaired ventilation
  • Increased Intracranial Pressure
  • Increased Intracranial pressure
    • Intracranial pressure more than 15 mmHg
    • Brunner= Normal intracranial pressure 10-20 mmHg
    • Black = Normal ICP 5-15 mmHg
    • Causes:
    • Head injury
    • Stroke
    • Inflammatory lesions
    • Brain tumor
    • Surgical complications
  • Increased Intracranial pressure
    • Pathophysiology
    • The cranium only contains the brain substance, the CSF and the blood/blood vessels
    • MONRO-KELLIE hypothesis- an increase in any one of the components causes a change in the volume of the other
    • Any increase or alteration in these structures will cause increased ICP
  • Increased Intracranial pressure
    • Pathophysiology
    • Compensatory mechanisms:
    • 1. Increased CSF absorption
    • 2. Blood shunting
    • 3. Decreased CSF production
  • Increased Intracranial pressure
    • Pathophysiology
    • Decompensatory mechanisms:
    • 1. Decreased cerebral perfusion
    • 2. Decreased PO2 leading to brain hypoxia
    • 3. Cerebral edema
    • 4. Brain herniation
  • Decreased cerebral blood flow
    • Vasomotor reflexes are stimulated initially  slow bounding pulses
    • Increased concentration of carbon dioxide will cause VASODILATION  increased flow  increased ICP
  • Cerebral Edema
    • Abnormal accumulation of fluid in the intracellular space, extracellular space or both.
  • Herniation
    • Results from an excessive increase in ICP when the pressure builds up and the brain tissue presses down on the brain stem
  • Cerebral response to increased ICP
    • Steady perfusion up to 40 mmHg
    • Cushing’s response
      • Vasomotor center triggers rise in BP to increase ICP
      • Sympathetic response is increased BP but the heart rate is SLOW
      • Respiration becomes SLOW
  • Increased Intracranial pressure
    • CLINICAL MANIFESTATIONS
    • Early manifestations :
    • Changes in the LOC- usually the earliest
    • Pupillary changes- fixed, slowed response
    • Headache
    • vomiting
  • Increased Intracranial pressure
    • CLINICAL MANIFESTATIONS
    • late manifestations :
    • Cushing reflex- systolic hypertension , bradycardia and wide pulse pressure
    • bradypnea
    • Hyperthermia
    • Abnormal posturing
  • Increased Intracranial pressure
    • Nursing interventions:
    • Maintain patent airway
    • 1. Elevate the head of the bed 15-30 degrees- to promote venous drainage
    • 2. assists in administering 100% oxygen or controlled hyperventilation- to reduce the CO2 blood levels  constricts blood vessels  reduces edema
  • Increased Intracranial pressure
    • Nursing interventions
    • 3. Administer prescribed medications- usually
      • Mannitol- to produce negative fluid balance
      • corticosteroid- to reduce edema
      • anticonvulsants-p to prevent seizures
  • Increased Intracranial pressure
    • Nursing interventions
    • 4. Reduce environmental stimuli
    • 5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning
  • Increased Intracranial pressure
    • Nursing interventions
    • 6. Keep head on a neutral position. ACOID- extreme flexion, valsalva
    • 7. monitor for secondary complications
      • Diabetes insipidus- output of >200 mL/hr
      • SIADH
  • Assessment of IIP
    • Subjective
      • Diplopia
      • Personality change
      • Thought processes change
      • Headache
      • Nausea
  • Assessment of IIP
    • Objective
      • Decreasing LOC
      • Hyperthermia
      • Weakness
      • Vomiting
      • Seizures
      • Papilledema
      • Posturing
      • Wide pulse pressure
      • Bradycardia
      • Altered respirations
      • Pupils fixed & dilated
  • Assessment of IIP
    • Diagnostic tests:
      • CT scan, MRI
      • Close observation
      • Craig’s screw
  • Medical Management of IIP
    • Craniotomy
    • Craniectomy
    • Tumor removal
    • Drainage of ventricles
    • Drainage of hematoma
    • Intubation
  • Medical Management of IIP
    • Medications
      • Osmotic diuretics - Mannitol
      • Corticosteroids - Decadron
      • Anticonvulsants - Dilantin
    • Internal monitoring
  • Nursing Care of the Patient With IIP
    • Elevate HOB
    • Neck in neutral position
    • Avoid flexion hips, waist and neck
    • Avoid isometric activity or Valsalva
    • Restrict fluids
    • Foley
    • Suctioning
    • O2
    • Hypothermia blanket
  • Altered LOC
  • ALTERED LEVEL OF CONSCIOUSNESS
    • Consciousness
      • Is a state of being with 2 important aspects: the wakefulness and awareness of self, environment (including place) and time.
    • Wakefulness
      • ability to maintain an awake state or to be easily aroused from sleep.
    • Awareness of self
      • the client can identify himself or herself.
    • Awareness of place
      • client can identify his or her present location and reason for being there.
    • Awareness of time
      • client knows the date, month and year and can identify common current facts, such as season.
    • Unconsciousness
      • Can be brief, lasting for a few seconds to minutes, or sustained, lasting for an hour or longer.
      • To produce unconsciousness:
        • Disrupt the ascending reticular activating system, which extends the length of the brain stem and up into the thalamus
        • Significantly disrupt the function of both cerebra; hemisphere
        • Metabolically depress overall brain function, like drug overdose
    ALTERED LEVEL OF CONSCIOUSNESS
    • Coma
      • State of sustained unconsciousness in which the patient:
        • does not respond to verbal stimuli
        • may have varying responses to painful stimuli
        • does not move voluntarily
        • may have altered respiratory patterns
        • may have altered pupillary responses to light
        • does not blink.
      • The longer the coma lasts, the more likely it is irreversible.
    ALTERED LEVEL OF CONSCIOUSNESS
    • Etiology and Risk Factors
      • Structural lesions in the brain
        • Place pressure on the brain stem or the structures within the posterior cranial fossa (cerebellum, midbrain, pons and medulla) affecting the RAS
        • Head trauma, ischemic or hemorrhagic stroke, brain tumor, vehicular accidents, gunshot wounds and falls
        • Ischemic stroke = occur with interruption on blood supply to the brain. It can directly affect involved the structure in consciousness or cause swelling of the brain leading to coma
        • Hemorrhagic stroke = occur as a consequence of hypertension or from rupture of a vascular anomaly.
        • Hemorrhage = cause coma by placing pressure on the brain.
        • Tumor = can metastasize and can increase the pressure on the brain leading to coma
    ALTERED LEVEL OF CONSCIOUSNESS
      • Etiology and Risk Factors
      • Metabolic disorders and diffuse lesions
        • Impair wakefulness and awareness by reducing the supply of oxygen and glucose, by allowing waste products to accumulate in the brain, or by altering other cerebral metabolic processes.
        • Metabolic means any problem that alters brain metabolism.
        • Hypoxia = most common cause of metabolic coma
        • Blood loss, high altitudes or carbon monoxide poisoning deprive the brain of oxygen
    ALTERED LEVEL OF CONSCIOUSNESS
      • Coma may be induced to treat neurologic disorders
        • giving propofol to produce coma to rest the brain and hopefully prevent further brain injury
        • therapeutic coma may be induced with extreme brain swelling secondary to brain injury, stroke or metabolic stroke.
    ALTERED LEVEL OF CONSCIOUSNESS
      • Pathophysiology
        • Consciousness is controlled by RAS and its integrated components.
        • RAS begins in the medulla, located in the midbrain, which connects to hypothalamus and thalamus, this in turn connect with the limbic system via hypothalamus. Feedback systems also connect at the brain stem level.
        • Reticular formation produces wakefulness
        • RAS produces awareness of self and the environment.
        • Diffuse cortical connections allow maximum integrations of all conscious-related activities.
    ALTERED LEVEL OF CONSCIOUSNESS
      • Pathophysiology
        • Disorders affecting any part of the RAS produces coma.
        • To produce coma, a disorder must affect both cerebral hemispheres or the brain stem itself.
        • Disorders affect these areas in 1 of 3 ways:
          • Direct compression or destruction of structures responsible for consciousness.
            • Tumor, hemorrhage in brain stem, swelling in the cerebral hemispheres
          • Decrease in availability of oxygen or glucose = both needed for cerebral metabolism.
            • Ischemia, hypoxia
          • Toxic effects of substance on structures of the RAS
            • Toxic wastes from liver, kidney, bacterial invasions from meningitis and metabolites from drugs.
        • The anatomic location and severity of the problem determine the depth of coma.
    ALTERED LEVEL OF CONSCIOUSNESS
      • Clinical manifestations
        • Supratentorial lesions
          • (located above the dura roofing the cerebellum)
            • Headache
            • Localized sensorimotor deficits
            • Seizures
            • Manifestation depends on the specific area of the brain affected
    ALTERED LEVEL OF CONSCIOUSNESS
      • Clinical manifestations
        • Infratentorial area
          • (located beneath the dura roofing the cerebellum)
          • Cause sudden loss of consciousness
          • Unusual respiratory patterns
          • Brain stem houses the rhythmic breathing, its function is loss as consciousness decreases, the lower brain stem begins to regulates breathing by responding to changes primarily in the carbon dioxide levels and acid-base and oxygen levels = result to irregular breathing pattern and depth.
          • Compression on the cranial nerves leads to cranial nerve deficits.
    ALTERED LEVEL OF CONSCIOUSNESS
      • Clinical manifestations
          • Metabolic coma
            • Confusion and stupor = 1st sign
            • Motor manifestation is symmetrical
            • Tremors
            • Asterixis (flapping tremors of the hands
            • Myoclonus (single, sudden jerking movement)
            • Seizures
    ALTERED LEVEL OF CONSCIOUSNESS
      • Diagnostic Test
        • CT scan – tumors and bleeding
        • MRI
        • Lumbar puncture – after CT scan/ MRI is done, when there is no expanding intracranial mass – to prevent risk of herniation caused by sudden changes in CSF pressure.
          • CSF cloudy = infection
          • CSF bloody = bleeding in ventricles/subarachnoid space
        • EEG = can be used to determine if comatose due to continuous seizures. Results are commonly abnormal to patient with coma
    ALTERED LEVEL OF CONSCIOUSNESS
      • Diagnostic Test
        • Reflexes
          • (+) Oculocephalic response (OCR) = doll’s eye reflex
            • Done in unconscious patient
            • Absence of reflex means brain stem function is preserved
            • Should not be done for known cervical spine injury
    ALTERED LEVEL OF CONSCIOUSNESS
      • Medical Management
        • Goal = to preserve brain function and to prevent additional brain injury
        • Focus is to maintaining supply of oxygen and glucose to the brain.
        • ABC must be maintained.
        • Intubation may be needed if respiratory pattern is ineffective
        • Ventilation and supplemental oxygen
        • Monitoring BP and maintaining systolic pressure between 100 and 160 mmHg, lower/higher cause alteration in cerebral perfusion pressure
    ALTERED LEVEL OF CONSCIOUSNESS
  • RUN DOWN on Altered LOC
  • Altered level of consciousness
    • Etiologic Factors
    • Head injury
    • Stroke
    • Drug overdose
    • Alcoholic intoxication
    • Diabetic ketoacidosis
    • Hepatic failure
  • Altered LOC – Etiology (Mnemonics)
    • Vowel
    • A lcohol
    • E pilepsy
    • I nsulin
    • O piates
    • U rates (renal failure)
    • TIPPS
    • T rauma
    • I nfection
    • P sych
    • P oisons
    • S hock
  • Altered level of consciousness
    • Patient is not oriented
    • Patient does not follow command
    • Patient needs persistent stimuli to be awake
    • COMA= clinical state of unconsciousness where patient is NOT aware of self and environment
  • Altered level of consciousness
    • Assessment
    • Orientation to time, place and person
    • Motor function
      • Decerebrate
      • Decorticate
    • Sensory function
  • Altered level of consciousness
    • ASSESSMENT
    • Behavioral changes initially
    • Pupils are slowly reactive
    • Then , patient becomes unresponsive and pupils become fixed dilated
    • Glasgow Coma Scale is utilized
  • Altered level of consciousness
    • Nursing Intervention
    • 1. Maintain patent airway
    • Elevate the head of the bed to 30 degrees
    • Suctioning
    • 2. Protect the patient
    • Pad side rails
    • Prevent injury from equipments, restraints and etc.
  • Altered level of consciousness
    • Nursing Intervention
    • 3. Maintain fluid and nutritional balance
    • Input and output monitoring
    • IVF therapy
    • Feeding through NGT
    • 4. Provide mouth care
    • Cleansing and rinsing of mouth
    • Petrolatum on the lips
  • Altered level of consciousness
    • Nursing Intervention
    • 5. Maintain skin integrity
    • Regular turning every 2 hours
    • 30 degrees bed elevation
    • Maintain correct body alignment by using trochanter rolls, foot board
    • 6. Preserve corneal integrity
    • Use of artificial tears every 2 hours
  • Altered level of consciousness
    • Nursing Intervention
    • 7. Achieve thermoregulation
    • Minimum amount of beddings
    • Rectal or tympanic temperature
    • Administer acetaminophen as prescribed
    • 8. Prevent urinary retention
    • Use of intermittent catheterization
  • Altered level of consciousness
    • Nursing Intervention
    • 9. Promote bowel function
    • High fiber diet
    • Stool softeners and suppository
    • 10. Provide sensory stimulation
    • Touch and communication
    • Frequent reorientation
  • HEADACHE
  • Headache
    • Is a clinical manifestation rather than a disease
    • Head pain is caused by stimulation of pain sensitive structures in the head
    • Affects more than 45 million individuals annually
    • Classified as:
      • Primary headache- no organic cause
      • Secondary headache- with organic cause
  • Headache
    • Cephalalgia
    • Types:
      • Migraine headache
        • periodic attacks of headache due to vascular disturbance
      • Tension headache
        • the most common type- due to muscle tension
    • Types:
      • Tension type
        • Most common type
        • Characterized by a steady pressure in the head
        • Generally bilateral
        • Referred to as muscle contraction, psychogenic or rheumatic headache
        • no aura (the perception of a strange light, an unpleasant smell or confusing thoughts or experiences )
        • May occur daily
    Headache
    • Types:
      • Tension type
        • Manifestations:
          • Photophobia
          • Phonophobia
          • Pressure or tightness bilaterally
          • Worse with activity
    Headache
    • Type:
      • Migraine
        • Characterized by unlilateral or bilateral throbbing pain
        • Maybe be preceded by prodrome and aura (sensation of light/warmth)
        • Aura may last for 30 minutes
        • Etiology unknown b maybe neurological, vascular or chemical
        • May be triggered by chocolate, alcohol, bright lights, menstruation or stress
        • May last for hour to days
        • Generally occurs after awakening and improves with sleep
    Headache
    • Type:
      • Migraine with aura
        • Manifestations:
          • Unilateral numbness, tingling, or burning sensations in the lips, hands, or face
          • Dizziness
          • Confusion
          • Weakness
          • Scintillating scotomata (perceived flashing light in 1 quadrant or visual field)
    Headache
    • Type:
      • Migraine without aura
        • Manifestations:
          • Unilateral, severe, pulsating head pain that is worse with activity
          • Nausea and vomiting
          • Photophobia
          • Phonophobia
    Headache
  • headache
    • Migraine
    • Prodrome stage
    • Aura phase
    • Headache
    • Recovery phase
    • Type:
      • Cluster
      • Episodic headaches peaking in 10 minutes anf lasting 90 minutes occurring for weeks or months followed by remission
      • Generally occurs unilaterally around or behind one eye and is severe
      • More frequent in men between the ages of 20-50 y.o.
      • Characterized by an abrupt onset without a prodrome
    Headache
  • Neurological Problems
    • Headache
      • Vascular – migraine, cluster, hypertensive
      • Tension – stress
      • Traction-inflammatory – infection, occlusion vessels
    • Diagnostic testw
      • Complete history and physical
      • CT scan or MRI if there is neurological abnormality on assessment
    Headache
  • headache
    • Nursing Interventions
    • 1. Avoid precipitating factors
    • 2. modify lifestyle
    • 3. relieve pain by pharmacologic measures
      • Beta-blockers
      • Serotonin antagonists- “triptan"
    • Nursing Interventions
      • Biofeedback
      • Relaxation therapy
      • Stress management
      • Provide the client medication instructions
      • Encourage the client to keep a diary of the characteristics of the headaches
      • Instruct to avoid trigger-producing foods (caffeine, alcohol, cheese, chocolate, onions, ice cream, salt, vinegar-containing products and nicotine)
  • Seizures
  • SEIZURES
    • Episodes of abnormal motor, sensory, autonomic activity resulting from sudden excessive discharge from cerebral neurons
    • A part or all of the brain may be involved
  • SEIZURES
    • PATHOPHYSIOLOGY
    • An electrical disturbance in the nerve cells in one brain section  EMITS ELECTRICAL IMPULSES excessively
  • SEIZURES
    • ETIOLOGIC FACTORS
    • Idiopathic
    • Fever
    • Head injury
    • CNS infection
    • Metabolic and toxic conditions
  • Seizures
    • Generalized:
      • Tonic-clonic – grand mal
      • Absence - Petit mal
      • Myoclonic
      • Atonic or akinetic
    • Localized: (Focal)
      • Partial (Jacksonian)
      • Psychomotor
  • Seizures
    • Causes:
      • Hypoglycemia
      • Infection
      • Electrolyte imbalance
      • Trauma
      • IIP
      • Toxins
  • Seizure Medications
    • Dilantin (Phenytoin)
    • Phenobarbital
    • Mysoline
    • Tridione
    • Valium (Diazepam)
    • Depakene
    • Clonopin
    • Mesantoin
    • Neurontin
    • Lamictal
    • Felbatol
    • Cerebyx
  • SEIZURES
    • Nursing Interventions
    • During seizure
    • 1. remove harmful objects from the patient’s surrounding
    • 2. ease the client to the floor
    • 3. protect the head with pillows
    • 4. Observe and note for the duration, parts of body affected, behaviors before and after the seizure
  • SEIZURES
    • Nursing Interventions
    • During seizure
    • 5. loosen constrictive clothing
    • 6. DO NOT restrain, or attempt to place tongue blade or insert oral airway
  • SEIZURES
    • Nursing Interventions
    • POST seizure
    • 1. place patient to the side to drain secretions and prevent aspiration
    • 2. help re-orient the patient if confused
    • 3. provide care if patient became incontinent during the seizure attack
    • 4. stress importance of medication regimen
  • Seizure Medications
    • Nursing:
      • Medications
      • Continue meds
      • Medic alert ID
      • Avoid alcohol, avoid driving, get adequate rest
      • If on Dilantin, instruct on oral hygiene
  • Seizures: Nursing Care
    • Protect
      • Lower to the floor; pad side rails; pillow under head; don’t restrain
      • No bite block or padded tongue blade
      • Allow for post-ictal rest
    • Prevent aspiration (airway)
      • Turn side; loosen clothing around neck
    • Document everything
  • EPILEPSY
    • A group of syndromes characterized by recurring seizures
    • CAUSES
    • 1. idiopathic 6. brain tumors
    • 2. Birth trauma 7. head Injury
    • 3. perinatal infection 8. metabolic disorders
    • 4. infectious disease 9. CVA
    • 5. ingestion of toxins
  •  
  • EPILEPSY
    • Recurring seizures may be classified as GENERALIZED or PARTIAL SEIZURES
    • Generalized Seizures- cause a generalized electrical abnormality within the brain
    • Partial seizures- these seizures arise from a localized part of the brain and cause specific symptoms
  • GENERALIZED SEIZURES
    • 1. General Tonic-Clonic seizure- ( Grand mal ) characterized by loss of consciousness and alternating movements of the extremities
    • 2. Absence Seizure ( Petit mal )- common in children, begins with a brief change in the LOC, indicated by blinking, rolling of eyes and blank stares
  • GENERALIZED SEIZURES
    • 3. Myoclonic seizure- characterized by brief, involuntary muscular jerks of body extremities
    • 4. Akinetic seizure- general loss of postural tone and a temporary loss of consciousness- a drop attack
  •  
  • PARTIAL SEIZURES
    • 1. Simple partial seizure- typically limited to one cerebral hemisphere
    • 2. Complex partial seizure- begins with an aura, then with impaired consciousness, with purposeless behaviors like lip-smacking, chewing movements
  • Epilepsy
    • DIAGNOSTIC TESTS
    • 1. EEG
    • 2. CT
    • 3. MRI
    • 4. LP
    • 5. Angiography
  • Epilepsy
    • Medical treatment
    • 1. Anticonvulsants- most commonly phenytoin, phenobarbital and carbamazepine
    • Ethosuximide and valproic acid for absence seizure
    • 2. surgery
  • Epilepsy
    • Nursing Intervention
    • 1. Care of patients during seizure
    • 2. care of patients after seizures
    • 3. patient teaching
  • SEIZURE: STATUS EPILEPTICUS
  • What is Epilepsy?
    • Epilepsy is a seizure disorder resulting from sudden bursts of electrical energy in the brain. These electrical discharges produce seizures which vary from one person to another in frequency and form. Sometimes the electrical signal only reaches part of the brain where a part of the body, like an arm or a leg may move on its own. If the signal goes through all of the brain, the person may shake all over, fall and lose consciousness.
    • It is not a disease, psychological disorder or contagious .
    • Please view the Video ‘ All about Epilepsy’
    • http://www.epilepsyontario.org/allaboutep.wmv
  • Epilepsy and GABA
    • A seizure occurs when the message delivery system becomes unbalanced.
    • Under normal circumstances, the neurotransmitter GABA (gamma-amino
    • butryic acid) triggers signals.
    • When there is not enough GABA, a person has a seizure because the
    • receiving neurons is flooded with signals.
    • SEIZURE
    • sudden, excessive, disorderly electrical discharges of the neurons.
    • EFFECTS OF SEIZURE: alteration in the following
    • mental status
    • LOC
    • sensory and special senses
    • motor funtion
    • CLASSIFICATION OF SEIZURES
    • A. Primary Generalized Seizure
    • B. Partial Seizure
    • GENERALIZED SEIZURES:
    • GRAND MAL (Tonic-Clonic)
    • most common type of seizure
    • The phases are as follows:
    • The phases are as follows:
  •  
    • PETIT MAL (Absence Seizure or Little Sickness)
    • not preceeded by AURA
    • little or no tonic-clonic
    • characteristic: blank facial expression, automatism like lip-chewing, cheek smacking
    • regain of consciousness as rapid as it was for 10-20secs
    • usually occurs during childhood and adolescence
    • JACKSONIAN / FOCAL SEIZURE
    • common for patients with organic brain lesion like frontal lobe tumor
    • aura is present(numbness, tingling, crawling feeling)
    • charac by tonic-clonic movements of group muscle e.g. hands, foot, or face then it proceeds to grand mal seizure
    • FEBRILE SEIZURE
    • this is common for children 6 mos to <5yo, when temp. is rising
    • PSYCHOMOTOR SEIZURE
    • aura is present (hallucinations or illusion)
    • charac by mental clouding (being out of touch with the envt)
    • appears intoxicated
    • the client may commit violent or antisocial acts, e.g. Going naked public, running
  • PARTIAL SEIZURE 2 TYPES OF PARTIAL SEIZURES: A. Simple Partial Seizure B. Complex Partial Seizure
    • Simple Partial Seizure
    • Awareness Preserved
    • Memory Preserved
    • Consciousness Preserved
    • Complex Partial Seizure
    • Awareness Preserved
    • Memory Preserved
    • Consciousness Preserved
    • CAUSES OF SEIZURES IN CHILDREN
    • Birth Traumas
    • Infections – Meningitis
    • Congenital Abnormalities
    • High Fever
    • CAUSES OF SEIZURES IN MIDDLE YEARS
    • Head Injuries
    • Infections
    • Alcohol
    • Stimulant Drugs
    • Medications its Side Effects
    • CAUSES OF SEIZURES IN THE ELDERLY
    • Brain Tumors
    • Strokes
    • CHEMICAL IMBALANCES CAUSE SEIZURE
    • Alcohol
    • Cocaine
    • Other Drugs
    • Low blood sugar, low oxygen, low blood sodium, low calcium, kidney and renal failure
  • Nursing Management During a Seizure
    • The nursing goal is to prevent injury to the patient. This includes not only physical support but psychological support as well.
    • Provide privacy
    • Ease the patient on the floor, if possible
    • Protect the head with a pad to prevent injury
    • Loosen constrictive clothing
    • If aura precedes the seizure, place a padded tongue blade between the teeth
    • Do not attempt to pry open jaws that are clenched in a spasm to insert anything
    • No attempt should be made to restrain the patient during the seizure
    • Place the patient on one side with head flexed forward
    • The patient should be reoriented to the environments and happening upon awakening
  • Nursing Assessment during a Seizure
    • Observe and to record the sequence of symptoms.
    • Description of the circumstances before the attack.
    • The first thing a patient does in an attack.
    • The type of movements in the part of the body involved.
    • The size of both pupils.
    • Whether or not there is automatisms
    • Duration of each phase of the attack
    • Unconsciousness, ability to speak, consciousness
  • Epilepsy
    • Disorders of brain function characterized by recurring seizures.
    • Disturbance in consciousness, movement, behavior, mood, sensation, perception. It is not a disease but a symptom.
    • Electrical disturbance in one section of nerve cells causing uncontrolled electrical discharges.
  • How is Epilepsy Diagnosed?
    • History
    • Physical Exam
    • Electroencephalogram
    • MRI (Neuro-imaging)
    • CT Scan
  • 6 Truths about Epilepsy
    • Not to be called epileptic but a person with a seizure disorders
    • In epilepsy there might be seldom brain damage, brain function is disturb by seizure
    • Difference level of Intelligence
    • Violence does not follow epilepsy
    • Non usually inherited – cause is unknown and usually associated with environmental causes
    • Epilepsy is not a curse, it is a medical condition
  • Nursing Diagnoses
    • Fear related to the ever-present possibility of having seizures
    • Ineffective coping related to stresses imposed by epilepsy
    • Knowledge deficit about epilepsy and its control
    • High risk for injury during seizures
    • Goals:
    • Short Term Goals:
    • Maintenance of control of seizures
    • Achievement of a satisfactory psychosocial adjustment
    • Acquisition of knowledge and understanding about the condition
    • Long Term Goals:
    • To achieve a satisfactory life adjustment
    • To prevent or manage episodes of status epilepticus
    • Nursing Interventions:
    • Seizure Control
    • Improved Coping Mechanisms
    • Patient Education
  • STATUS EPILEPTICUS
    • (ACUTE PROLONGED SEIZURE ACTIVITY)
    • IS A SERIES OF GENERALIZED SEIZURE THAT OCCUR WITHOUT FULL RECOVERY OF CONSCIOUSNESS BETWEEN ATTACKS
    • THE TERM HAS BEEN BROADENED TO INCLUDE CONTINUOUS CLINICAL OR ELECTRICAL SEIZURES LASTING AT LEAST 30 MINUTES, EVEN WITHOUT IMPAIRMENT OF CONSCIOUSNESS.
    • Happens when there is an abrupt cessation of anticonvulsant drugs/ethanol
    • A seizure is a sudden disruption of the brain's normal electrical activity, which can cause a loss of consciousness and make the body twitch and jerk. This condition is a medical emergency.
  • CAUSES
    • Not taking anticonvulsant medication
    • Also caused by an underlying condition, such as meningitis, sepsis, encephalitis, brain tumor, head trauma, extremely high fever, low glucose levels, or exposure to toxins.
  • Symptoms
    • seizures occurring so frequently that they appear to be one continuous seizure.
    • These seizures include severe muscle contractions and difficulty breathing . Permanent damage can occur to the brain and heart if treatment is not immediate.
    • A person's symptoms can range from simply appearing dazed to the more serious muscle contractions, spasms, and loss of consciousness.
    • The specific symptoms depend on the underlying type of seizure.
  • TWO CATEGORIES OF STATUS EPILEPTICUS
    • CONVULSIVE
    • Epilepsia partialis continua is a variant it involve an hour, day or even week-long jerking. It is a consequence of vascular disease, tumor or encephalitis and drug resistant.
    • NONCONVULSIVE
    • Complex Partial Status Epilepticus CPSE and absence status epilepticus are rare forms of the condition which are marked by nonconvulsive seizures.
    • The seizure is confined to a small area of the brain, normally the temporal lobe. But the latter, status epilepticus, is marked by a generalised seizure affecting the whole brain, and an EEG is needed to differentiate between the two conditions.
    • This results in episodes characterized by a long-lasting stupor, staring and unresponsiveness.
  • NURSING DIAGNOSIS
    • High Risk for Injury r/t Seizure Activity
    • Individual Coping r/t perceive social stigma, potential changes in employment
  • HOW IT IS DIAGNOSED?
    • Status epilepticus is diagnosed according to its characteristics symptoms. The doctor will order test to look for the cause of the seizures. This may include:
    • Blood test
    • ECG to check for an abnormal heart rhythm
    • EEG to check electrical activity in the brain
    • MRI or CT scan to check for braing tumors or signs of damage to the brain tissue.
  • MEDICATIONS
    • Diazepam (Valium) this will stop motor movement
    • Phenytoin (Dilatin)
    • Phenobarbital (Barbita)
    • Paraldehyde
    • Thiopenthal sodium (Pentotal sodium)
    • General anesthesia may also be used as a treatment of last resort to stop seizure activity
  • NURSING INTERVENTIONS
    • PREVENTING INJURY
    • REDUCING FEARS OF SEIZURE
    • IMPROVING COPING MECHANISMS
    • PROVIDING PATIENT AND FAMILY
    • EDUCATION
    • MONITORING AND MANAGING POTENTIAL COMPLICATIONS
    • TEACHING PATIENTS SELF-CARE
  • PREVENTING INJURY
    • Injury prevention for the patient with seizure is a PRIORITY.
      • patient should be placed on the floor and remove any obstructive items
      • patient should never be forced into a position
      • pad side rails
      • do not attempt to try to open jaws that are clenched in a spasm to insert anything.
      • if possible place the patient on one side with head flexed forward
  • PATIENT EDUCATION
    • TAKE MEDICATION AT REGULAR BASIS
    • AVOID ALCOHOL. Lowers seizure threshold
    • ADEQUATE REST
    • WELL-BALANCED DIET
    • AVOID DRIVING, OPERATING MACHINES, SWIMMING UNTIL SEIZURES ARE WELL CONTROLLED.
    • LIVE AN ACTIVE LIFE
  • REDUCING FEARS OF SEIZURE
    • Fear that a seizure may occur unexpectedly can be reduced
    • by the patients adherence to the prescribed treatment regimen.
    • Cooperation of the patient and family and their trust in the prescribed regimen are essential for control of seizures.
    • Periodic monitoring is necessary to ensure the adequacy of the treatment regimen and to prevent the side effects. .
  • IMPROVING COPING MECHANISMS
    • It has been noted that the social, psychological, and behavioral problems frequently accompanying the attack can be more handicap than the actual seizure.
    • Counselling assists the individual and family to understand the condition and the limitations imposed by it.
    • Social and recreational opportunities are good for mental health .
    • Nurses can improve the quality of life for patients with the disorder by educating them and their family about the symptom and also the management.
  • PROVIDING PATIENT AND FAMILY EDUCATION
    • Ongoing education and encouragement should be given to patients to enable them to overcome these feelings.
    • The patient and family should be educated about the medications as well as care during a seizure.
    • Perhaps the most valuable facets are education and efforts to modify the attitudes of the patient and family toward the disorder.
  • MONITORING AND MANAGING POTENTIAL COMPLICATIONS
    • Patients should have plan to have serum drug levels drawn at regular intervals.
    • The patient and family are instructed about the side effects and are given specific guidelines to assess and report signs and symptoms indicating medication overdose.
  • Anticonvulsant drugs – phenytoin (Dilantin)
    • A loading dose is needed to reach therapeutic levels more quickly.
    • When given through IV route, mix the drug with saline solution ONLY. Dextrose causes an insoluble precipitate to form
    • Therapeutic Level:
      • 10-20 mg/dl
    • Given 1 hr before or 2 hrs after meal (like NGT feeding)
    • Nutritional supplements like vitamins, milk products and alcohol interfere absorption of the drug
    • Adverse effect:
      • Sedation
      • Drowsiness
      • Gingival hyperplasia
      • Blood dyscrasia
      • Toxicity
        • Confusion and ataxia
  • TEACHING PATIENTS SELF CARE
    • Like thorough oral hygiene after each meal, gum massage, daily flossing, and regular dental care.
    • The patient is also instructed to inform all health care providers of the medication being taken because of the possibility of drug interactions. An individualized comprehensive teaching plan is needed to assist the patient and family to adjust to this chronic disorder.
  • Autonomic Dysreflexia/ Hyperreflexia
  • Definition
    • A sudden nervous system response to a condition that irritates the body
    • It can happen to people with a spinal cord injury at the thoracic (T) 6 level or higher
    • common
    • It is a MEDICAL EMERGENCY that raises the blood pressure so high, that it can cause death if not taken care of right away
    • AKA Autonomic hyperreflexia, dysreflexia, A/D
  • Causes
    • Full bladder
    • Full bowel or constipation
    • Bladder infection or bladder stones
    • Tests done on the bladder
    • Pressure sores
    • Ingrown toenails
    • Labour and delivery
    • Genital stimulation (or pressure)
    • Ejaculation
    • Tight clothing or shoes
    • Severe menstrual cramps
    • Fractures bones (traumatic pain)
  • Causes
    • Abdominal medical problems
      • Gall stones
      • Appendicitis
      • Kidney stomes
      • ulcers
    • Hot and cold temperatures
    • Sunburn
    • Some drugs
      • e.g. digoxin
  • Common Symptoms
    • Sudden severe rise in blood pressure
    • Pounding headache
    • Change in heart rate
    • Flushed skin above level of injury
    • Sweating above or below level of injury
    • An “aura”
    • Anxious feeling
    • Blurred vision
    • Stuffy nose
    • Shivering above level of injury
    • Goose bumps below level of injury
    • Pale skin below level of injury
  • Wallet Sized Card Autonomic Dysreflexia (AD) AD is a potentially life threatening complication of spinal cord injury above T7 level. It is caused by an unopposed sympathetic nervous system response to noxious stimulation below the level of the injury. Blood pressure may rise dangerously. The most typical cause of AD is distended bladder. Other causes could be distended bowel, pressure sore, in-grown toenail, etc.
    • Autonomic Dysreflexia Management
    • Raise the head of the bed by 90  or sit person upright.
    • Monitor BP every 5 minutes.
    • Check for sources of AD: drain bladder first, consider using topical anesthetic jelly for lubrication of catheter.
    • Check rectum for stool. Apply anesthetic jelly to rectal wall before manipulation. Use digital stimulation to promote reflex defecation.
    • Check for other sources of AD such as ulcer, fracture, in-grown toenail, etc.
    • If SBP is above 150 mmHg after above checks, give captopril 25 mg sublingually x1. Advise patient to avoid swallowing until tablet dissolved.
    • If SBP still greater than 150 mmHG at 30 minutes post-captropril then give immediate release nifedipine 5 mg capsule via the bite and wallow method.
    • ****ONLY IN A HOSPITAL SETTING****
    • Repeat nifedipine 5 mg bite and swallow 15 minutes after the initial nifedipine dose if SBP still greater than 150 mmHg.
    • Consider intravenous agents for hypertension if hypertension is refractory.
    • Symptoms may include:
    • elevated blood pressure
    • Headache
    • Sweating
    • flushed face
    • Anxiety
    • bradycardia.
    • Treatment is to remove the cause. Once the cause is removed the BP will return to normal immediately.
  • Nursing Interventions
    • Sit up if lying down – this will decrease our blood pressure
    • Find and remove the cause – it usually will NOT go away until the cause is removed or corrected
    • Loosen tight clothing, legbag straps, shoes
    • Check for BLADDER problems
      • empty bladder with in/out catheter
      • check for kinks in tubing
      • check for full legbag
      • change foley catheter
    • Check for BOWEL problems
      • Do rectal check: if there is stool, remove it gently.
      • Use xylocaine gel to decrease potential stimulation which could cause BP to increase even more
    • Check for SKIN problems
      • Do a thorough check of the skin from top to bottom, front to back
      • Check buttocks, feet, toenails, etc
      • Use a mirror and/or get help from someone
  • Run Down on Autonomic Dysreflexia
  • Autonomic Dysreflexia/hyperreflexia
    • Seen commonly in spinal cord injury above T6
    • An exaggerated response by the autonomic system resulting from various stimuli most commonly distended bladder, impacted feces, pain, skin irritation
  • Autonomic Dysreflexia/hyperreflexia
    • Clinical MANIFESTATIONS
    • 1. Hypertension
    • 2. Bradycardia
    • 3. Severe pounding headache
    • 4. Diaphoresis
    • 5. Nausea
    • 6. Nasal congestion
  • Autonomic Dysreflexia/hyperreflexia
    • NURSING INTERVENTIONS
    • 1. Elevate the head of the bed immediately
    • 2. Check for bladder distention and empty bladder with urinary catheter
    • 3. Check for Fecal impaction and other triggering factors like skin irritation, pressure ulcer
    • 4. Administer antihypertensive medications- usually hydralazine
  • Infection and Inflammation
    • Meningitis
    • Encephalitis
    • Brain abscess
    • Guillain-Barré
    • Neurosyphilis
    • Poliomyelitis
    • Rabies
    • Tetanus
    • Botulism
    • AIDS
  • Meningitis
  • Meningitis
    • Acute infection of the meninges
    • Viral or bacterial
    • Almost any bacteria entering the body can cause meningitis
  • PATHOPHYSIOLOGY
    • Invasion may occur at choroid plexus or directly thru an opening in the dura
    • Organisms colonize in the CSF, leading to inflammation of the meninges that contains it
    • Exudate forms, meninges then become thickened, and adhesions form, leading to hydrocephalus.
    • Arteries supplying the subarachnoid space maybe inflamed, leading to rupture or thrombosis of these vessels.
    • Severe cases, lead to cerebral edema and IICP, vasculitis and cerebral infarction
  • Manifestations
    • Classical signs:
      • Nuchal rigidity
      • Brudzinski’s sign
      • Kernig’s sign
      • Photophobia
  • Manifestations:
    • Other s/sx:
      • Headache
      • Fever
      • Tachycardia
      • N * V
  • Meningitis-Medical Management
    • Diagnosed by LP
    • Medications
    • Respiratory isolation
    • Cool, dark quiet room
    • Maintain hydration
    • Prevent injury
  • Ideal Medical Management Diagnostic Evaluation
    • Complete blood count (CBC) with differential
      • detect an elevated leukocyte count in bacterial and viral meningitis
    • Lumbar puncture
      • elevated CSF pressure
      • cloudy or milky white CSF
      • high protein level
      • positive Gram stain and culture that usually identifies the infecting organism unless it's a virus
      • depressed CSF glucose concentration)
    • CSF evaluation for pressure, leukocytes, protein, glucose
    • MRI/CT scan
      • with and without contrast rules out cerebral hematoma, hemorrhage, or tumor
      • CT scan with contrast - to detect abscesses.
    • Low CD4+ counts indicate immunosuppression in HIV-positive patients and other patients with immunosuppressive disorders.
    • Latex agglutination may be positive for antigens in meningitis.
    • Chest X-rays
      • may reveal pneumonitis or lung abscess, tubercular lesions, or granulomas secondary to fungal infection
    • Lumbar puncture is essential
    • Cornerstone in the diagnosis
    • should be performed in all cases whenever the diagnosis of meningitis is known or suspected on the basis of clinical signs
    • Contraindications to doing a lumbar tap
    • 1. presence of significant cardio-pulmonary compromise and shock
    • 2. signs of increased ICP
    • 3. suspected case of space occupying lesion
    • 4. infection in the area that the spinal needle will traverse to obtain CSF
    • 5. hematologic problems
    Laboratory Diagnosis of Bacterial Meningitis
  • CSF Findings in Bacterial Meningitis
    • CSF pressure - usually elevated
    • CSF cells count and chemistry
    • leukocytosis- >1000/cu mm
    • % PMN - 90%
    • Glucose- <40 mg/dl
    • CSF blood to glucose ratio <0.40
    • Protein 50-500 mg/dl
    • c. stained smears of CSF
    • gram stain - (+) for bacteria
    • AFB smear - (-)
    • India ink - (-)
    • d. CSF culture
    • *a negative culture does rule out meningitis
  • Treatment
    • Team effort:
      • Nursing
      • infectious diseases specialists
      • Neurology
      • internal medicine
      • otolaryngology specialists
      • laboratory and diagnostic staff
    • Antibiotic therapy and vigorous supportive care
      • I.V. antibiotics are given for at least 2 weeks, followed by oral antibiotics ampicillin, cefotaxime, ceftriaxone, and nafcillin
    • Dexamethasone (Decadron) - as adjunctive therapy, to prevent deafness among young children
    • Mannitol - to decrease cerebral edema
    • Anticonvulsant (usually given I.V.) or a sedative - to reduce restlessness
    • Aspirin or acetaminophen - to relieve headache and fever
    • Supportive measures consist of:
      • bed rest
      • hypothermia, and
      • fluid therapy to prevent dehydration
    • Isolation - if nasal cultures are positive
    • Therapy for any coexisting conditions, such as endocarditis or pneumonia
    • Temozolomide (Temodar) - neoplastic meningitis
    • Cochlear implantation rehabilitation - deafness caused by meningitis
    • Therapy for S. aureus and gram-negative bacilli - If meningitis is suspected after neurosurgical procedures, potential I.V. line bacteremia, CSF leak, or immunosuppression
    • Antifungal agents - for cryptococcal meningitis
    • Empiric antituberculosis drugs must be initiated if infection by Mycobacterium tuberculosis is suspected
  • Nursing Management :
    • Nursing Assessment
      • Obtain a history of recent infections such as upper respiratory infection, and exposure to causative agents
      • Assess neurologic status and vital signs
      • Evaluate for signs of meningeal irritation
      • Assess sensorineural hearing loss (vision and hearing), cranial nerve damage (eg, facial nerve palsy), and diminished cognitive function.
  • Nursing Diagnoses
    • Acute pain related to meningeal irritation
    • Anxiety
    • Hyperthermia related to the infectious process and cerebral edema
    • Impaired gas exchange
    • Impaired Physical Mobility related to prolonged bed rest
    • Ineffective Tissue Perfusion (cerebral) related to infectious process and cerebral edema
    • Risk for deficient fluid volume related to fever and decreased intake
    • Risk for impaired skin integrity
  • Key outcomes:
    • The patient will:
      • express feelings of comfort and relief of pain
      • identify strategies to reduce anxiety
      • exhibit temperature within normal range
      • maintain adequate ventilation and oxygenation
      • maintain fluid volume within normal range
      • Have skin integrity remain intact
  • Nursing Interventions
    • Reducing Fever
      • Administer antimicrobial agents on time to maintain optimal blood levels.
      • Monitor temperature frequently or continuously, and administer antipyretics as ordered.
      • Institute other cooling measures, such as a hypothermia blanket, as indicated.
    • Maintaining Fluid Balance
      • Prevent I.V. fluid overload, which may worsen cerebral edema.
      • Monitor intake and output closely.
      • Monitor CVP frequently.
    • Enhancing Cerebral Perfusion
      • Assess LOC, vital signs, and neurologic parameters frequently. Observe for signs and symptoms of ICP (eg, decreased LOC, dilated pupils, widening pulse pressure).
      • Maintain a quiet, calm environment to prevent agitation, which may cause an increased ICP.
      • Prepare patient for a lumbar puncture for CSF evaluation, and repeat spinal tap, if indicated. Lumbar puncture typically precedes neuroimaging
      • Notify the health care provider of signs of deterioration: increasing temperature, decreasing LOC, seizure activity, or altered respirations.
    • Reducing Pain
      • Administer analgesics as ordered; monitor for response and adverse reactions. Avoid opioids, which may mask a decreasing LOC.
      • Darken the room if photophobia is present.
      • Assist with position of comfort for neck stiffness, and turn patient slowly and carefully with head and neck in alignment.
      • Elevate the head of the bed to decrease ICP and reduce pain.
    Nursing Interventions
  • Nursing Interventions
    • Promoting Return to Optimal Level of Functioning
      • Implement rehabilitation interventions after admission (eg, turning, positioning).
      • Progress from passive to active exercises based on the patient's neurologic status
  • Patient Education and Health Maintenance
    • Advice close contacts of the patient with meningitis that prophylactic treatment may be indicated; they should check with their health care providers or the local public health department.
    • To help prevent the development of meningitis, teach patients with chronic sinusitis or other chronic infections the importance of proper medical treatment.
    • Encourage the patient to follow medication regimen as directed to fully eradicate the infectious agent.
    • Encourage follow-up and prompt attention to infections in future.
    • Inform patients who have children about the importance of vaccination with measles, mumps, rubella vaccine, H. influenzae type B vaccine, and pneumococcal vaccine as a preventive measure. Vaccination is recommended for children younger than school age.
  • Expected Outcomes
    • Afebrile
    • Adequate urine output;
    • CVP in normal range
    • Alert LOC;
    • normal vital signs
    • Pain controlled
    • Optimal level of functioning after resolution
  • Encephalitis
  • Encephalitis
    • Inflammatory process of CNS with altered function of brain and spinal cord
    • Variety of causative organisms—viral most frequent
    • Vector reservoir : mosquitoes and ticks
  • Encephalitis
    • 2 forms:
    • Primary
      • Occurs when a virus invades and replicates within the brain
    • Postinfectious (parainfectious)
      • Brain inflammation that develops in combination with other viral illness or ff admin of vaccines such as measles, mumps and rubella –due to hypersensitivity reaction that leads to demyelination of nerves
  • Clinical Manifestations of Encephalitis: Onset Sudden or Gradual
    • Malaise
    • Fever
    • Headache/dizziness
    • Stiff neck
    • Nausea/vomiting
    • Ataxia
    • Speech difficulties
  • Clinical Manifestations of Severe Encephalitis
    • High fever
    • Disorientation/stupor/coma
    • Seizures/spasticity
    • Ocular palsies
    • Paralysis
    • IICP
  • Encephalitis
    • Diagnostic evaluation
      • CSF analysis
      • EEG
      • MRI
      • PET
  • Medical Management
    • Prescribed diuretics – mannitol
      • Decrease edema
    • Antibiotics – acyclovir (Zovirax)
      • for herpes encephalities
    • Risk for ineffective airway clearance r/y unresponsiveness and inability to clear secretions.
    • Ineffective airway clearance
    • Altered thought process r/t increased in ICP
    Nursing Diagnoses
  • Nursing Intervention
    • Maintain a patent airway
      • Assess pupil size and reaction, LOC, strength and motion of the extremities, response to noxious stimuli
      • Endotracheal intubation, oxygen therapy and mechanical ventilation
      • Ongoing neurological assessment
      • Document changes in the pt’s condition and initiates proper care immediately.
      • Turn, cough and deep breathe every 2 hours
  • Nursing Intervention
    • Maintain airway, breathing and circulation
      • Foremost concern
    • Maintain an open airway with suctioning as needed
      • Primary nursing responsibility
    • Limit the effects of immobility such as skin care, ROM, turning and positioning schedule
    • Note effect of position changes on ICP and space activities as necessary.
    • Reorient pt to time, place and person as needed.
    • Keep familiar objects or pictures around the pt
    • Allow visitation of significant others
    • Establish alternate means of communication if unable to maintain verbal contact (pt who needs intubation)
  • Brain Abscess
  • CNS ABSCESSES
    • Focal pyogenic infections of the central nervous system
    • Exert their effects mainly by:
      • Direct involvement & destruction of the brain or spinal cord
      • Compression of parenchyma
      • Elevation of intracranial pressure
      • Interfering with blood &/or CSF flow
    • Include: Brain abscess, subdural empyema, intracranial epidural abscess, spinal epidural abscess, spinal cord abscess
  • PATHOPHYSIOLOGY
    • Begins as localized cerebritis (1-2 wks)
    • Evolves into a collection of pus surrounded by a well-vascularized capsule (3-4 wks)
    • Lesion evolution:
      • Days 1-3: “early cerebritis stage”
      • Days 4-9: “late cerebritis stage”
      • Days 10-14: “early capsule stage”
      • > day14: “late capsule stage”
  • PATHOGENESIS Etiologies:
    • Direct spread from contiguous foci (40-50%)
    • Hematogenous (25-35%)
    • Penetrating trauma/surgery (10%)
    • Cryptogenic (15-20%)
  • DIRECT SPREAD (from contiguous foci)
    • Occurs by:
      • Direct extension through infected bone
      • Spread through emissary veins, diploic veins, local lymphatics
    • The contiguous foci include :
        • Otitis media/mastoiditis
        • Sinusitis
        • Dental infection (<10%), typically with molar infections
        • Meningitis rarely complicated by brain abscess (more common in neonates with Citrobacter diversus meningitis, of whom 70% develop brain abscess)
  • HEMATOGENOUS SPREAD (from remote foci)
    • Sources:
      • Empyema, lung abscess, bronchiectasis, endocarditis, wound infections, pelvic infections, intra-abdominal source, etc…
      • may be facilitated by cyanotic HD, AVM.
    • Results in brain abscess(es) at middle cerebral artery distribution
    • Often multiple
  • CLINICAL MANIFESTATIONS
    • Non-specific symptoms
    • Mainly due to the presence of a space-occupying lesion
        • N/V, lethargy, focal neuro signs , seizures
    • Signs/symptoms influenced by
        • Location
        • Size
        • Virulence of organism
        • Presence of underlying condition
  • CLINICAL MANIFESTATIONS
        • Headache
        • Often dull, poorly localized, non-specific
          • Abrupt, extremely severe H/A
          • Sudden worsening H/A with rupture of brain abscess into ventricle (often fatal)
  • LOCATION & CLINICAL FEATURES
    • FRONTAL LOBE : H/A, drowsiness, inattention, hemiparesis, motor speech disorder
    • TEMPORAL LOBE : Ipsilateral H/A, aphasia, visual field defect
    • PARIETAL LOBE : H/A, visual field defects, endocrine disturbances
    • CEREBELLUM : Nystagmus, ataxia, vomiting, dysmetria
  • DIAGNOSIS
    • High index of suspicion
    • Contrast CT or MRI
    • Drainage/biopsy
  • IMAGING STUDIES
    • MRI
      • more sensitive for early cerebritis, satellite lesions, necrosis, ring, edema, especially posterior fossa & brain stem
    • CT scan
    • 99m Tc brain scan
      • very sensitive; useful where CT or MRI not available
    • Skull x-ray : insensitive,
      • if air seen, consider possibility of brain abscess
    • LABORATORY TESTS
    • BRAIN ABSCESS
    • Aspirate: Gram/AFB/fungal stains & cultures, cytopathology (+/-PCR for TB)
    • WBC Normal in 40% ( only moderate leukocytosis in ~ 50%
        • & only 10% have WBC >20,000)
    • ESR Usually moderately elevated
    • LP Contraindicated in patients with known/suspected brain abscess
            • Risk of herniation 15-30%
        • If done, m ay have normal CSF findings, but:
    • Usually elevated CSF protein & cell count (lymphs)
      • Unremarkable glucose & CSF cultures rarely positive
  • TREATMENT
    • Combined medical & surgical
        • Aspiration or excision
        • empirical abx
    • Empirical antibiotics are selected based on:
        • Likely pathogen (consider primary source, underlying condition, & geography)
    • Modify abx based on stains
    • Duration: usually 6-8 wks
        • after surgical excision, a shorter course may suffice
  • Guillain-Barré – Polyneuritis – Acute Idiopathic Polyneuritis
  • Guillain-Barré – Polyneuritis
    • An uncommon, acute, rapidly progressing and potentially fatal polyneuritis
    • The immune system destroys the myelin sheath
    • Exact etiology:
      • unknown
      • research suggest cell-mediated immunologic reaction
    • Often associated with:
      • history of acute respiratory or GI illness
      • Surgery
      • Trauma
      • immunization 1-8 weeks before the onset of the disorder
    • Women between 30-50 years are more susceptible
    • Respiratory failure is serious complication
  • Manifestations:
      • Symmetrical ascending weakness of the lower extremities
      • Paresthesia
      • Paralysis
      • Decrease in muscle tone
      • Decrease or absent deep tendon reflexes
      • Hypertension
      • Bradycardia
      • Orthostatic hypotension
      • Absent bowel and bladder function
      • Facial weakness
      • Dysphagia
      • Extraocular eye movements
      • Pain – generally worse at night
      • Difficulty communicating
    • Diagnostic Tests
      • Complete history and physical exam
      • CSF analysis
      • Electromyography (EMG)
      • Nerve conduction studies
      • Respiratory function studies
  • Nursing Interventions:
    • Promote optimal airway exchange
    • Monitor arterial blood gases
    • Maintain emergency intubation equipment at the bedside
    • Provide oxygen, suctioning and chest physiotherapy as needed.
    • Monitor the client for dysphagia and implement dysphagia interventions as appropriate.
    • Administer prescribed analgesics
    • Implement communication interventions
    • Provide emotional support
    • Prevent complications of physical immobility
    • Assist with plasmapheresis as appropriate.
  • Guillain-Barré - Polyneuritis
    • Peripheral nerve disease
    • Prior infection; autoimmune response
    • Weakness and paralysis, begins in extremities and works up
    • Respiratory failure may occur
  • Rabies
  • RABIES 2 kinds: Etiology: A.K.A.: Vital facts: Hydrophobia, Lyssa Rabies virus (A rhabdovirus of the genus lyssavirus) Urban/ Canine rabies and Sylvatic rabies Urban/ Canine Rabies: Transmitted by dogs Sylvatic Rabies: Transmitted by bats Didn’t you know? The Philippines has one of the highest prevalence rates of rabies in the world
  • RABIES Is man to man transmission possible? Can it be introduced thru breaks in the skin? MOT: Vital facts: Bite from a rabid animal Very rare Yes How about organ transplants? Yes. (Corneal transplant) Incubation period: R-a-b-i-e-s (6 weeks/ 2-8 weeks) Communicability period: 3 days before onset until the whole disease duration
  • RABIES CNS Sx (Site of bite): CNS Sx (early): Hydrophobia: Signs and symptoms: Spasms of muscles of deglutition Headache, apprehension, fever Sensory changes CNS Sx (late): Paralysis, delirium, convulsions Usual lifespan of victim w/o medical intervention: 2-6 days Usual cause of death: Respiratory paralysis
  • RABIES If it dies or shows signs of rabies, behead it and bring to doctor Submit for immunization while waiting for results If dog is not available: submit for immunization Observe the dog for 14 days, do not kill it yet. Patient may be given antibiotics/ tetanus immune globulin Wash the wound with antiseptics/ soap & water Management: Sequence of actions
  • RABIES Responsible pet ownership: Immunization of pets after 3 months of age and yearly thereafter Never allow pets to roam the streets Take good care of pets: bathe, feed, clean sleeping quarters Your pet’s action is your responsibility
  • Rabies
    • Rhabovirus infection of CNS transmitted by infected saliva that enters the body through bite or open wound
    • Critical illness almost always fatal
    • Source = bite of infected domestic or wild animal
    • Incubation is 10 days to years
  • Manifestations occur in stages:
    • Prodromal:
    • wound is painful
    • various paresthesias
    • general signs of infection
    • increased sensitivity to light, sound,
    • skin temperature changes
    • Excitement stage:
    • periods of excitement and quiet
    • develops laryngospasm
    • afraid to drink (hydrophobia)
    • Convulsions
    • muscle spasms and
    • death usually due to respiratory failure
  • Rabies
    • Collaborative Care
    • Animal that bit person is held under observation for 7 – 10 days to detect rabies
    • Sick animal are killed and their brains are tests for presence of rabies virus
    • Blood of client may be tested for rabies antibodies
  • Rabies
    • Post-exposure treatment
    • Rabies immune globulin (RIG) is administered for passive immunization
    • Client often has local and mild systemic reaction; treatment is over 30 days
    • Treatment of client with rabies:
    • involves intensive care treatment
    • Health Promotion
    • Vaccination of pets
    • Avoid wild animals, especially those appearing ill
    • Follow up care for any bites
    Rabies
  • Tetanus (lockjaw)
  • Tetanus (lockjaw)
    • Disorder of nervous system caused by neurotoxin
    • Etiology:
      • Clostridium tetani , anaerobic bacillus present in the soil
    • Contract disease from:
      • open wound contaminated with dirt, debris
      • Traumatic wound like gunshot
      • Compound fracture
      • Dental infection, animal bite
      • Dirty/contaminated needles during illegal drug use
    • Has high mortality rate
    • Incubation period range from 7-21days, ave 7 days
    • tetanus is generalized, affecting skeletal muscles throughout the body.
    • However, tetanus is sometimes localized to muscles near an entry wound.
    Tetanus (lockjaw)
  • Pathophysiology
    • Manifestations of tetanus are caused by an exotoxin (tetanospasmin).
    • The toxin may enter the CNS along the peripheral motor nerves or may be bloodborne to nervous tissue.
    • Tetanospasmin binds irreversibly to the ganglioside membranes of nerve synapses, blocking release of inhibitory transmitter from nerve terminals and thereby causing a generalized tonic spasticity, usually with superimposed intermittent tonic seizures.
    • Disinhibition of autonomic neurons and loss of control of adrenal catecholamine release cause autonomic instability and a hypersympathetic state. Once bound, the toxin cannot be neutralized.
  • Manifestations
    • hypertonic muscle contraction
    • Stiffness of jaw
    • Stiff neck
    • Opisthotonos (severe arching of the back)
    • Retraction of the head
    • Laryngeal or respiratory spasms
    • Diaphoresis
    • Tachycardia
    • Dysphagia
    • Spasms of jaw and facial muscles
    • Develops generalized seizures
    • painful body muscle spasms
    • Late stage:
      • Difficulty opening the jaw (trismus)
      • Fluctuation of heart rate and BP
    • Death occurs from respiratory and cardiac complications
    • Risus Sardonicus
      • Facial muscle spasm produces a characteristic expression with a fixed smile and elevated eyebrows
    • Distinguishing signs:
      • intact sensorium
      • normal CSF, and
      • muscle spasms
  • Opisthotonus
  • Tetanus neonatorum:
    • Tetanus in neonates is usually generalized and frequently fatal.
    • It often begins in inadequately cleansed umbilical stumps in children born of inadequately immunized mothers.
    • Onset during the first 2 wk of life is characterized by rigidity, spasms, and poor feeding. Bilateral deafness may occur in surviving children.
  • Tetanus (lockjaw)
    • Diagnosis is made on clinical manifestations
    • Treatment:
      • Antibiotics (doxycycline, metronidazole, penicillin G)
      • Chlorpromazine (Thorazine)
      • Diazepam (Valium ) for muscles spasms, seizure
      • Benzodiazepines to control rigidity and spasm.
  • 3 Guiding Principles for treatment:
    • Prevent further toxin release by debriding the wound and giving an antibiotic (see below);
    • Neutralize toxin outside the CNS with human tetanus immune globulin and tetanus toxoid, taking care to inject into different body sites and thus avoid neutralizing the antitoxin; and
    • Minimize the effect of toxin already in the CNS.
  • Health Promotion
    • Active immunization with boosters given at time of exposure
    • Passive immunization is given to persons who are not adequately immunized
  • Nursing Interventions:
    • Monitor CBC, serum electrolytes, arterial blood gases, glucose, clotting factors and albumin
    • Place the client in a dark, quiet room away from noise
    • Administer prescribed sedation
    • Avoid unnecessary touching of the client
    • When touching the client is necessary, use a firm touch
    • Maintain a warmer than normal temperature
    • Avoid covering the client with bed linens
    • Priority is to ensure tetanus prophylaxis by antitoxin
    • Wash the wound with warm soapy water to decrease incidence of tetanus
  • Supportive care:
    • Intubation (moderate/severe cases)
    • Mechanical ventilation is essential when neuromuscular blockade is required to control muscle spasms that impair respirations.
    • Stool softener (constipation)
    • A rectal tube may control distention.
    • Bladder catheterization is required if urinary retention occurs.
    • Chest physiotherapy,
    • frequent turning, and forced coughing are essential to prevent pneumonia.
    • Analgesia with opioids is often needed.
  • Botulism
  • Botulism
    • Food poisoning caused by ingestion of food contaminated with toxin
    • Etiology:
      • Clostridium botulinum , anaerobic bacteria found in soil
    • Contracted by eating contaminated foods usually improperly canned or cooked
    • Incubation period: 18-36 hrs
    • Untreated death rate is high
  • Pathophysiology:
    • Bacteria produce a toxin, which blocks release of acetylcholine from nerve endings causing respiratory failure by paralysis of muscles
  • Botulism
    • Manifestations:
    • Visual disturbances
      • diplopia
    • Gastrointestinal symptoms
      • Dysphagia
      • Paralytic ileus
      • Constipation
      • Abdominal pain
    • Paralysis of all muscle groups
      • Dysarthria
      • Weakness
    • Respiratory failure
    • Diagnosis
    • Complete pt history
    • Stool culture for Clostridium botulinum
    • CBC
    • Testing the suspected food
  • Botulism
    • Treatment
    • Administration of antitoxin
    • Supportive treatment including mechanical ventilation and systemic support in intensive care unit
  • Nursing Interventions:
    • Administer prescribed botulism antitoxin after the client is tested for hypersensitivity and immediately after the diagnosis is made.
    • Lavage the stomach or administer laxatives
    • Monitor the client for respiratory paralysis
    • Implement tracheostomy and mechanical ventilation interventions as appropriate
    • Report the disorder to CDC
    • Primary prevention should be the goal
    • Instruct clients on proper canning of home foods, particularly those wuth a low-acid content.
      • Boil foods for 10 minutes
      • Remove bad spots from all fruits and vegetables before canning
      • Ensure canning jar is airtight
      • Store canned foods in a cool location
      • Discard ant canned container that swells or looks bad when opened.
    Nursing Interventions:
  • CVA
  • CEREBROVASCULAR ACCIDENTS
    • An umbrella term that refers to any functional abnormality of the CNS related to disrupted blood supply
  • CEREBROVASCULAR ACCIDENTS
    • Can be divided into two major categories
    • 1. Ischemic stroke-
      • Caused
        • Thrombus – associated with atherosclerosis
        • Embolus – breaking off and travels to the cerebral/carotid arteries
    • 2. Hemorrhagic stroke
      • caused commonly by hypertensive bleeding
    • Transient ischemic attack (TIA)/
      • Referred as “silent stroke”
      • Temporary loss of neurological function often lasting less than 15 minutes and no more than 24 hrs
    • Reversible ischemic neurological deficit (RIND)
      • Temporary loss of neurological function lasting more than 24 hrs but less than 1 week
      • Indications of progressing cerebrovascular disease
  •  
  •  
  • CEREBROVASCULAR ACCIDENTS
    • The stroke continuum
    • 1. TIA- transient ischemic attack, temporary neurologic loss less than 24 hours duration
    • 2. Reversible Neurologic deficits
    • 3. Stroke in evolution
    • 4. Completed stroke
  • General manifestations
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • There is disruption of the cerebral blood flow due to obstruction by embolus or thrombus
  • RISKS FACTORS
    • Non-modifiable
    • Advanced age
    • Gender
    • Race
    • Modifiable
    • Hypertension
    • Cardio disease
    • Obesity
    • Smoking
    • Diabetes mellitus
    • Hypercholesterolemia
    • Atrial fibrillation
  • Pathophysiology of ischemic stroke
    • Disruption of blood supply
    • Anaerobic metabolism ensues
    • Decreased ATP production leads to impaired membrane function
    • Cellular injury and death can occur
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • CLINICAL MANIFESTATIONS
    • 1. Numbness or weakness
    • 2. Confusion or change of LOC
    • 3. Motor and speech difficulties
    • 4. Visual disturbance
    • 5. Severe headache
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • Motor Loss
    • Hemiplegia - one-sided paralysis
    • Hemiparesis - weakness
    • Neglect - unaware of weakness on one side of the body
    • Ptosis – drooping of eyelid
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • Communication loss
    • Dysarthria= difficulty in speaking
    • Aphasia= Loss of speech
      • Expressive =difficulty in ability to write/speak
      • Receptive = difficulty with verbalization of sounds & words
      • Global = impairment of all verbal and understanding of communication
    • Apraxia= inability to perform a previously learned action
    • Alexia = difficulty reading
    • Agraphia = difficulty writing
    • Agnosia = inability to read, write or understand material
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • Perceptual disturbances
    • Amaurosis fugax = temporary period of blindness in one eye
    • Hemianopsia – blindness in 1 side of the visual field
      • Homonymous hemianopsia – loss of visual field on the nasal side and the opposite temporal side due to damage of the optic nerve
    • Sensory loss
    • Paresthesia (numbness)
  • Medications
    • Diuretic drugs
      • Mannitol and furosemide to decrease cerebral edema
    • Anticoagulant
      • Heparin and warfarin (Coumadin)
    • Platelet inhibitors – prevent thromboembolic
      • Ticlopidine (Ticlid), clopidogrel (Plavix) dipyridamole (Persantine)
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • DIAGNOSTIC test
    • 1. CT scan
    • 2. MRI
    • 3. Angiography
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • Improve Mobility and prevent joint deformities
    • Correctly position patient to prevent contractures
      • Place pillow under axilla
      • Hand is placed in slight supination- “C”
      • Change position every 2 hours
      • Arm sling to prevent shoulder subluxation
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 2. Enhance self-care
    • Carry out activities on the unaffected side
    • Prevent unilateral neglect
    • Keep environment organized
    • Use large mirror
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 3. Manage sensory-perceptual difficulties
    • Approach patient on the Unaffected side
    • Encourage to turn the head to the affected side to compensate for visual loss
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 4. Manage dysphagia
    • Place food on the UNAFFECTED side
    • Provide smaller bolus of food
    • Manage tube feedings if prescribed
    • Thickened liquid – to prevent aspiration during stroke evolution
    • Before feeding, check for presence of gag reflex
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 5. Help patient attain bowel and bladder control
    • Intermittent catheterization is done in the acute stage
    • Offer bedpan on a regular schedule
    • High fiber diet and prescribed fluid intake
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 6. Improve thought processes
    • Support patient and capitalize on the remaining strengths
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 7. Improve communication
    • Anticipate the needs of the patient
    • Offer support
    • Provide time to complete the sentence
    • Provide a written copy of scheduled activities
    • Use of communication board
    • Give one instruction at a time
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 8. Maintain skin integrity
    • Use of specialty bed
    • Regular turning and positioning
    • Keep skin dry and massage NON-reddened areas
    • Provide adequate nutrition
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 9. Promote continuing care
    • Referral to other health care providers
  • CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
    • NURSING INTERVENTIONS
    • 10. Improve family coping
    • 11. Help patient cope with sexual dysfunction
  • CVA: Hemorrhagic Stroke
    • Normal brain metabolism is impaired by interruption of blood supply, compression and increased ICP
    • Interruption of vessel wall integrity accounting for a bleed into the brain tissues as a result of:
      • Hypertension
      • Aneurysm (weakening or ballooning of an artery)
      • Subarachnoid hemorrhage
      • Arteriovenous malformation (embryonic abnormality resulting in a conglomeration of spaghetti-like tangles and thin walled dilated vessels prone to rupture)
  • CVA: Hemorrhagic Stroke
    • Sudden and severe headache
    • Same neurologic deficits as ischemic stroke
    • Loss of consciousness
    • Meningeal irritation
    • Visual disturbances
  • CVA: Hemorrhagic Stroke
    • DIAGNOSTIC TESTS
    • 1. CT scan
    • 2. MRI
    • 3. Lumbar puncture (only if with no increased ICP)
  • CVA: Hemorrhagic Stroke
    • NURSING INTERVENTIONS
    • 1. Optimize cerebral tissue perfusion
    • 2. Relieve Sensory deprivation and anxiety
    • 3. Monitor and manage potential complications
  • Generalized Nursing Interventions:
    • Primary prevention:
      • Instruct clients and families on reducing modifiable risk factors as the priority
  • Acute Stroke Management
    • Maintain airway, breathing and circulation
    • Assess the client’s LOC
    • Perform cranial nerve assessment
    • Administer prescribed antihypertensive drugs
    • Monitor fluid and electrolytes
    • Elevate the head of the bed 30o
    • Monitor for IICP
    • Administer prescribed analgesics
    • Administer prescribed diuretics – mannitol and furosemide to decrease cerebral edema
    • Insert a foley catheter
    • Administer prescribed anticoagulants such as heparin and warfarin (Coumadin)
    • Administer prescribed platelet inhibitors such as ticlopidine (Ticlid), clopidogrel (Plavix), and dipyridamole (Persantine)
  • Intermediate Stroke Management
    • Maintain patent airway
    • Assess for dysphagia
    • Maintain upright position for 30 minutes after eating
    • Thicken fluids as appropriate
    • Maintain hemostasis, preventing fluid overload
    • Monitor v/s frequently
    • Administer prescribed low-molecular weight heparin (Lovenox) to prevent deep vein thrombosis
    • Prevent complications of immobility
    • Perform active range of motion
    • Administer good skin care
    • Initiate a bladder retraining program
    • Increase fiber and fluids in the diet to prevent constipation
    • Offer emotional support
    • Approach the client from unaffected side
    • Implement aphasia interventions
      • Avoid environmental distractions
      • Talk directly to the patient
      • Avoid letting family members answer for the client
      • Allow plenty of time for the client to answer
      • Ask simple “yes” or “no” questions
      • Avoid unnecessary communication when the client is fatigued
      • Encourage gestures or pointing at items to facilitate communication
      • Honestly tell the client if he is not understood.
      • Speak to the client in a normal tone and volume.
      • Attempt to communicate one idea at a time
  • Rehabilitative Nursing Interventions
    • Encourage participation in care
    • Encourage the client to participate in occupational therapy
    • Encourage the client to participate in speech therapy
    • Assess the client for rehabilitative aids
    • Instruct the client on medications
    • Encourage importance of scheduled follow-up with health care provider
    • Instruct the client on the importance of frequent blood pressure checks.
  •  
  • RUN DOWN on CVA
  • Cerebrovascular Accident (CVA)
    • Ischemia of brain tissue
      • Thrombus – associate with atherosclerotic
      • Embolus – results from an emboli breaking off and traveling to the cerebral or carotid arteries.
    • All ages, but usually elderly
  • CVA – Contributing Factors
    • Atherosclerosis
    • Heart disease
    • Kidney disease
    • Hypertension
    • Obesity
    • High cholesterol
    • Cigarette smoking
    • Stress
    • Sedentary
    • Diabetes
    • Oral contraceptives
    • Cocaine
  • Cerebral Thrombosis
    • Most common cause of CVA
    • Most often:
        • Atheroclerosis
        • Thrombus
        • CVA
  • Cerebral Embolism
    • 2nd most common cause of CVA
    • Most often:
      • Heart disease
      • Thrombus
      • Embolus
      • CVA
  • Cerebral Hemorrhage
    • 3rd most common cause of CVA
    • Most often:
      • Hypertension
      • Ruptured cerebral blood vessel
      • CVA
  • Transient Ischemic Attack
    • Cerebrovascular insufficiency
    • Causes – same as CVA
    • Warning sign of impending CVA
  • CVA - Assessment
    • Motor changes
      • Opposite side
      • Balance, coordination, gait, proprioception
      • Glasgow Coma Scale
  • CVA Assessment
    • Sensory Changes
      • Aphasia =can’t speak or write
      • Agnosia =can’t recognize familiar objects/people
      • Apraxia =can’t perform purposeful acts or use objects properly
      • Neglect Syndrome
      • Visual problems, including hemianopsia
  • CVA Assessment
    • Cognitive changes
      • denial
      • impaired memory, judgment
      • can’t concentrate
      • disoriented
      • slow and cautious versus impulsive
      • depressed, anxious versus euphoric
      • angers quickly versus constantly smiling
  • CVA - Testing
    • CT or MRI
    • Cerebral angiogram
    • CBC, PT, PTT, electrolytes
  • CVA – Medical Management
    • Thrombolytic (“clot buster”)
    • Anticoagulants
    • Antiplatelet drugs
    • Aneurysm repair
    • Carotid endarterectomy
  • CVA-Nursing Care
    • Assess LOC
    • IV, NG, Foley, Vent.
    • Nutrition
    • Encourage perform ADLs
    • Bladder and bowel training
    • ROM
    • Teaching and emotional support
  • INTRACRANIAL ANEURYSM
  • Intracranial Aneurysm
    • Ballooning of blood vessel
    • Most remain asymptomatic until they rupture and cause a subarachnoid hemorrhage.
    • Some of them grow to a large size and compress the neighborhood nerves and present with neuropathies.
    • Saccular/berry type generally composed only of tunica intima and adventitia.
    • 85% of all spontaneous hemorrhages into the sabarachnoid space.
    • Develop during the course of life
    • Commonly located in the anterior circulation, at the junction of the internal carotid artery.
    • More common in intracranial arteries compared with their extracranial counterparts, intracranial arteries have an attenuated tunica media and lack an external elastic lamina
    • Frequency of  intracranial aneurysms:   
    • 1. Internal carotid 38%   
    • 2. Anterior cerebral system 36%   
    • 3. Middle cerebral system 21%   
    • 4. Vertebro basilar system 5%
    Intracranial Aneurysm
    • Risk Factors:
      • Smoking
      • Hypertension
      • Atherosclerosis
      • Alcohol abuse
      • Stimulant drug abuse
      • Aging process
    forms a neck with a dome cause increased strain in the more elastic portions of the vessel wall. intimal layer becomes inelastic earliest stage in the formation of aneurysms local thickening of the intimal layer ( ‘intimal pads') in the arterial wall Arterial internal elastic lamina disappears at the base of the neck. Media thins Connective tissues replaces smooth muscle cells Tear allows bleeding – 7mm in diameter Vasospasm 4-14 days after hemorrhage Ischemia & infarction DEATH PATHOPHYSIOLOGY
  • Manifestations during bleeding
    • “ worst headache of my life”
    • Vomiting
    • Generalized seizure
    • Altered LOC
    • Signs of meningeal irritations (blood in SA space
    • Depend on the site of aneurysm
  • Goal of Management:
    • Prevent rebleeding
    • Maintaining cerebral perfusion pressure
    • Controlling ICP
    • Minimizing the effects of vasospasm
    • Managing hydrocephalus
    • Managing cardiac dysrhythmias
  • Nursing Management:
    • Prevent rebleeding
    • Keep the client quiet and comfortable
    • Reducing hypertension (may minimize rebleeding)
    • Ongoing neurologic assessment
    • Monitor cardiac and respiratory function
    • Continuous ECG monitoring – to identify life threatening dysrhythmias
    • Prevent Vasospasm
    • use of liberal isotonic fluids
    • If needed, volume expansion is added to promote cerebral perfusion.
    • Presence of Vasospasm
    • Induce hypertension and hypervolemia – increase cerebral blood flow/perfusion – but may develop cardiopulmonary crisis.
  • Arteriovenous Malformation (AVM)
  • AVM
    • ETIOLOGY
    • Congenital lack of capillaries
    • Tangled array of arteries and veins form
    • Common in brain particularly on cerebral hemisphere and spinal cord
    • Common <40 y.o.
    • Manifestations are related to anatomy of malformation and the vessels involved and occur as the result of weakening of the vessels and of the shunting of blood.
  • PATHOPHYSIOLOGY Lack of capillary bed Blood shunted directly from the artery - vein High pressure arterial system to lower pressure venous system Hemorrhage
    • Common s/sx:
      • Headache
      • Seizures
      • Focal deficits
    As AVM expands, its vessel dilates Stealing blood/divert blood flow Result to hypoperfusion and hypoxia on adjacent tissue
  • MANAGEMENT
    • Similar to intracranial aneurysm
  • CRANIAL NERVE DISORDERS
    • TRIGEMINAL NEURALGIA
    • BELL’S PALSY
    • GBS
  • Trigeminal neuralgia (tic douloureux)
  • Description
    • Chronic disease of trigeminal nerve (cranial nerve V) causing severe facial pain
    • Occuring in 50-70 y.o, females more than males
    • Trigeminal nerve’s 3 divisions
      • Ophthalmic division
      • Maxillary division = common
      • Mandibular division = common
    • Disease may occur in any 1 or more of the divisions.
    • Usually on the right side of the face
    • Cause:
      • INTRINSIC LESIONS
        • lesions on the nerve itself
        • like gross abnormalities of axon or myelin – multiple sclerosis
      • EXTRINSIC LESIONS
        • Mechanical compression by tumors, vascular anomalies, dental abscesses or jaw malformation
  • Trigeminal neuralgia/ Tic Douloureux
    • Intermittent episodes of sudden onset of intense pain that makes the client ponders suicide
    • Rarely relieved by analgesic
    • Triggering factors:
      • Tactile stimulation – touch & facial hygiene, talking
  • Ophthalmic Maxillary Mandibular
  • Manifestations
    • Severe facial pain occurring for brief seconds to minutes, hundreds of times a day, several times a year
    • Usually occurs unilaterally in area of mouth and rises toward ear and eye
    • Wincing or grimacing in response to the pain
    • Trigger areas on the face may initiate the pain
    • Sensory contact or eating, swallowing, talking may set off the pain
    • Often there is spontaneous remission after years, and then condition recurs with dull ache in between pain episodes
  • Diagnosis
    • In-depth history with attention paid to triggering stimuli, nature and site of pain
    • DIAGNOSTIC TESTS
    • Skull x-ray or CT scan
  • Medications
    • Anticonvulsants – dampen the reactivity of neurons
      • carbamazepine (Tegretol)
      • phenytoin (Dilantin)
      • gabapentin (Neurotin)
    • Baclofen (Lioresal)
  • Surgery
    • Intractable pain may be treated by severing the nerve root: rhizotomy through craniotomy
      • Complications: facial weakness and paresthesia
    • Client may have lost facial sensation and have loss of corneal reflex
    • Temporary treatments:
    • Nerve block with alcohol and glycerol
    • Peripheral neurectomy
    • Percutaneous radiofrequency wave form – create lesions that alter the pain transmission
  • Trigeminal neuralgia
    • ASSESSMENT
    • 1. Pain history
    • 2. Searing or burning jabs of pain lasting from 1-15 minutes in an area innervated by the trigeminal nerve
  • Trigeminal neuralgia
    • NURSING INTERVENTIONS
    • Provide emotional support
    • Encourage to express feelings
    • Provide adequate nutrition in small frequent meals at room temperature
    • Help clients use and improve any pain control strategies they have developed.
    • Monitor liver enzymes before and during carbamazepine and phenytoin – cause liver impairment
    • When feeding, check the temperature of the food before putting it into the mouth
    • Instruct to chew on the unaffected side and inspect mucous membrane for irritation
    • Use water jet device instead of toothbrush for dental hygiene
    • Advise them to visit their dentist as soon as possible after surgery.
    • Teach client on eye care if corneal reflex has been impaired.
  • Nursing Care
    • Teaching client self-management of pain
    • Maintaining daily nutrition needs
    • Oral hygiene
    • Preventing injury
  • Bell’s Palsy (U nilateral Facial Paralysis)
  • Description
    • Disorder that affect the motor part of 7 th cranial nerve (facial nerve) and causes unilateral facial paralysis (muscle of expression)
    • Most common type of peripheral facial paralysis
    • Occurs between age of 20 – 40 equally in males and females
    • Cause unknown, but thought to be related to herpes virus
  • BELL’S PALSY
    • Causes
    • 1. infection
    • 2. hemorrhage
    • 3. tumor
    • 4. local traumatic injury
  •  
    • Paralysis may be
      • Central
        • upper motor neuron paralysis
        • Client can’t show his teeth on the paralyzed side but with emotional stimulation – causing a smile/laughter = voluntary emotional dissociation
      • Peripheral
    BELL’S PALSY
    • TYPICAL MANIFESTATIONS:
      • Upward movement of the eyeball on closing the eye (Bell’s phenomenon)
      • Drooping of the mouth
      • Flattening of the nasolabial fold
      • Widening of the palpebral fissure
      • Slight lag in closing the eye
      • Eating may be difficult
    BELL’S PALSY
  • BELL’S PALSY
    • OTHER MANIFESTATIONS
    • Unilateral facial weakness
    • Distorted taste perception
    • Smooth forehead
    • Inability to close eyelid on the affected side
    • Incomplete eye closure
    • Excessive tearing when attempting to close the eyes
    • Inability to raise eyebrows, puff out the cheek
  • Prognosis
    • Majority of person recover fully in few weeks to months
    • Some persons have residual paralysis
  • BELL’S palsy
    • Diagnostic tests
      • EMG
    • Based on physical examination
    • Medical management
    • Corticosteroid like Prednisone – decrease nerve tissue edema
    • Artificial tears
    • Acyclovir
    • Physical therapy with moist heat, gentle massage and stimulation of facial nerve
    • Use of artificial tears, sunglasses, eye patch at night and periodic gentle closure of the eye.
    BELL’S palsy
  • BELL’S palsy
    • Nursing Interventions
    • Apply moist heat to reduce pain
    • Massage the face to maintain muscle tone
    • Give frequent mouth care
    • Protect the eye with an eye patch.
    • Eyelid can be taped at night
    • Instruct to chew on unaffected side
  • Nursing Care
    • Teaching client self-care: prevent injury and maintain nutrition
    • Soft diet that can be chewed easily, small frequent meals
  • Client with Guillain-Barre Syndrome
  • Guillian-Barre’ Syndrome
    • An auto-immune attack of the peripheral nerve myelin
    • Acute, rapid segmental demyelination of peripheral nerves and some cranial nerves
  • Guillian-Barre’ Syndrome
    • CAUSE: post-infectious polyneuritis of unknown origin commonly follows viral infection
  • Description
    • Acute inflammatory demyelinating disorder of peripheral nervous system characterized by acute onset of motor paralysis (usually ascending)
    • Cause is unknown but precipitating events include GI or respiratory infection prior, surgery, or viral immunizations
    • 80 – 90% of clients have spontaneous recovery with little or no disabilities
    • 4 – 6% mortality rate, and up to 10% have permanent disabling weakness
    • Characterized by progressive ascending flaccid paralysis of extremities with paresthesia and numbness
    • 20 % require mechanical ventilation due to respiratory involvement
  • Guillian-Barre’ Syndrome
    • PATHOPHYSIOLOGY
      • Cell-mediated imune attack to the myelin sheath of the peripheral nerves
      • Infectious agent may elicit antibody production that can also destroy the myelin sheath
  • Pathophysiology
    • Destruction of myelin sheath covering peripheral nerves as result of immunologic response
    • Demyelinization causes sudden muscle weakness and loss of reflex response
  •  
  • Manifestations
    • Most clients have symmetric weakness beginning in lower extremities
    • Ascends body to include upper extremities, torso, and cranial nerves
    • Sensory involvement causes severe pain, paresthesia and numbness
    • Client cannot close eyes
    • Paralysis of intercostals and diaphragmatic muscle can result in respiratory failure
    • Autonomic nervous system involvement: blood pressure fluctuations, cardiac dysrhythmias, paralytic illness, SIADH, urinary retention
    • Weakness usually plateaus or starts to improve in the fourth week with slow return of muscle strength
  • Guillian-Barre’ Syndrome
    • CLINICAL MANIFESTATIONS
    • 1. Ascending weakness and paralysis
    • 2. diminished reflexes of the lower extremities
    • 3. paresthesia
    • 4. potential respiratory failure
  • Collaborative Care
    • Ensuring adequate respiration and oxygenation
    • Preventing complications due to immobility
  • Diagnostic Tests
    • diagnosis made thorough history and clinical examination; there is no specific test
    • CSF analysis: increased protein
    • EMG: decrease nerve conduction
    • Pulmonary function test reflect degree of respiratory involvement
  • Surgery
    • may need tracheostomy, if prolonged ventilator support
  • Guillian-Barre’ Syndrome
    • MEDICAL MANAGEMENT
    • ICU admission
    • Mechanical Ventilation
    • TPN and IVF
    • PLASMAPHERESIS
    • IV IMMUNOGLOBULIN
  • Medications
    • supportive and prophylactic care
    • Antibiotics
    • Morphine for pain control
    • Anticoagulation to prevent thromboembolic complications
    • Vasopressors as needed
  • Plasmapheresis
    • may be helpful, if used early in the course of disease
  • Dietary Management
    • usually requires enteral feeding or total parenteral nutrition
  • Physical and Occupational Therapy
    • usually require long-term rehabilitation to regain maximum muscle strength
  • Nursing Diagnoses
    • Acute Pain
    • Risk for Impaired Skin Integrity
    • Impaired Communication
  • Guillian-Barre’ Syndrome
    • NURSING INTERVENTIONS
    • Maintain respiratory function
    • Chest physiotherapy and incentive spirometry
    • Mechanical ventilator
  • Guillian-Barre’ Syndrome
    • NURSING INTERVENTIONS
    • 2. Enhance physical mobility
      • Support paralyzed extremities
      • Provide passive range of motion exercise
      • Prevent DVT and pulmonary embolism
      • Padding over bony prominences
  • Guillian-Barre’ Syndrome
    • NURSING INTERVENTIONS
    • 3. Provide adequate nutrition
      • IVF
      • Parenteral nutrition
      • Assess frequently return o gag refelx
  • Guillian-Barre’ Syndrome
    • NURSING INTERVENTIONS
    • 4. Improve communication
      • Use other means of communication
  • Guillian-Barre’ Syndrome
    • NURSING INTERVENTIONS
    • 5. Decrease fear and anxiety
      • Provide Referrals
      • Answer questions
      • Provide diversional activities
    • 6. Monitor and manage complications
      • DVT, Urinary retention, pulmonary embolism, respiratory failure
  • Home Care
    • Clients will usually require hospitalization, rehabilitation, and eventually discharge to home
    • Client and family will need support; support groups
  • PERIPHERAL NERVE IMPULSE DISORDERS
    • MULTIPLE SCLEROSIS
    • PARKINSON’S DISEASE
    • MYSTHANIA GRAVIS
    • AMYOTROPHIC LATERAL SCLEROSIS
    • HUNTINGTON’S DISEASE
  • MULTIPLE SCLEROSIS
  • Myelin Sheath
    • axon is electrically conductive
    • Myelin sheath has the ability to increase the speed at which impulses propagate along the myelinated fiber
    • Essential for the proper functioning of the nervous system
    • Myelin inhibits charge leakage through the membrane
    • Thus, action potentials &quot;hop&quot; along the axon, by which process they travel faster than they would otherwise
    • Oligodendrocyte is responsible for producing the protective myelin sheath surrounding the axon in the CNS
  • MULTIPLE SCLEROSIS
    • An auto-immune mediated progressive demyelinating disease of the CNS
    • The myelin sheath is destroyed and replaced by sclerotic tissue (sclerosis)
    • Causing slowing of nerve conduction
  • MULTIPLE SCLEROSIS
    • CAUSE- unknown
    • Multiple predisposing factors-
      • viral infection –Epstein-Barr virus
      • environmental factors
        • If an individual lives in an area with low incidence of MS until age 15 years, that person's risk is low
        • However, if an individual lives in an area with a high incidence until age 15 years, the risk of developing MS is high.
      • geographic location – nonequatorial regions
      • Race – White people
      • genetic predisposition – alters body’s immune response to viral infection
      • Physical injury
      • Pregnancy – (pregnancy-related exacerbation occur 3 mos postpartum
      • Emotional stress
      • Fatigue
    • Common in WOMEN ages 20-40
  • Multiple Sclerosis
    • Description
    • Initial onset followed by total remission making diagnosis difficult
    • With periods of exacerbations and remissions
    • Progression= leads to increasing loss of function
    • More common in temperate climates
    • Occurs mainly in Caucasians
  •  
  •  
  • MULTIPLE SCLEROSIS
    • PATHOPHYSIOLOGY
    • Sensitized T cells will enter the brain and promote antibody production that damages the myelin sheath
    • Plaques of sclerotic tissues appear on the demyelinated axons interrupting the neuronal transmission
  • PATHOPHYSIOLOGY
    • Multiple factors
    • viral infection
    • environmental factors
    • geographic location – North America, other climate area
    • Race – White people
    • genetic predisposition
    BLOOD BRAIN BARRIER BREAKDOWN N = no passage of antibodies Leak = immune cells infiltrate (Helper T cells) Interleukin (protein) differentiate naïve T cells to inflammatory T cells. OVER PRODUCTION - interleukin Increased inflammation T cells attack CNS Triggers inflammatory process Stimulate other immune cells, cytokines and antibodies Demyelination Repair process = remyelination Symptoms tend to decrease/disappear Plaques of sclerotic tissues appear
  • Inflammation destroys myelin leading to axon dysfunction Myelin sheaths of nerves destroyed in patches called plaque ( white matter of spinal cord, brain, optic ) Demyelination slows and distorts nerve conduction resulting in absence of impulse transmission Recurrent demyelination and plaque formation result in scarring of glia and degeneration of axons Disease follows different courses, most common is the relapsing-remitting type Stressors trigger MS: febrile states, pregnancy, physical exertion and fatigue
  • MULTIPLE SCLEROSIS
    • The most common areas affected are
      • Optic nerves and chiasm
      • Cerebrum
      • Cerebellum
      • Spinal cord
    • Early symptoms and signs vary in duration and severity from one individual to the other and at different times in the same individual.
    • The most recurrent are:
    • walking difficulties
    • the sensation of having a weak or numb limb
    • cold or tingling feet
    • facial pain (Neuralgia)
    • blurred vision
    • Less common MS early symptoms include:
    • lack of coordination
    • cognitive difficulties
    • slurred speech
    • sudden onset of paralysis
    • As the disease progresses other symptoms can appear.
  • Types of MS pain:
    • Neuralgia
      • which is a stabbing pain in the face; it is usually treated with anticonvulsants.
    • Dysesthesias
      • which is a burning, aching body pain; it is usually treated with anticonvulsants and sometimes with antidepressants which act on the nervous central system.
    • Lhermitte sign
      • which is a brief, electric shock like sensation that runs down the spine and is caused by bending the neck forward or backward. It is controlled by means of a soft collar.
    • A chronic sensation of ‘pins and needles’
      • which is treated similarly to acute Dysesthesias.
    • Muscle spasm and cramps
      • which are treated with anti-inflammatory drugs.
    • Back and skeleton pains
      • which are treated with heat, massage and physical therapy.
    • The most common MS symptoms and signs include:
    • Ataxia = coordination and balance problems such as a gross lack of coordination of muscle movements or difficulty in moving
    • bladder problems (incontinence)
    • bowel problems
    • memory and cognitive difficulties
    • depression and emotional symptoms such as mood swings
    • muscle stiffness, weakness and spasms
    • acute and chronic pain
    • Fatigue
    • Sensory symptoms which include:
    • Hypoesthesia = changes in sensation such as a reduced sense of touch and partial loss of sensitivity
    • Paresthesia = sensations of tingling, pricking, and numbness of the skin like the sensation of a limb being ‘asleep’ or the feeling of ‘pins and needles’
  • CLINICAL MANIFESTATIONS
    • And also:
    • erectile dysfunction and other sexual difficulties
    • speech difficulties (Dysarthria)
    • swallowing difficulties (Dysphagia)
    • tremors
    • Vision problems which can include:
    • a particular form of involuntary eye movement (Nystagmus)
    • an inflammation of the optic nerve (Optic Neuritis)
    • the simultaneous perception of two images of the same object (Double Vision)
    • Other more rare MS symptoms include:
    • Epilepsy
    • Psychosis
    • A language disorder characterized by an impairment of speech and comprehension of speech (Aphasia)
  • MULTIPLE SCLEROSIS
    • DIAGNOSTIC TESTS
    • MRI- primary diagnostic study;
      • determine the presence of MS plaque
    • 2. CSF Immunoglobulin G
  • Diagnostic Tests
    • Neurological exam, careful history
    • Lumbar puncture with CSF analysis:
      • increased number of T lymphocytes; elevated level of immunoglobulin G (IgG)
    • Cerebral, spinal optic nerve MRI:
      • shows multifocal lesions
    • CT scan of brain
    • PET: measures brain activity
    • Evoked response testing of visual, auditory, somatosensory impulses show delayed conduction
  • MULTIPLE SCLEROSIS
    • MEDICAL MANAGEMENT
    • Pharmacotherapy
      • Interferons
      • Immunomodulators
      • Corticosteroids -
      • BACLOFEN for muscle spasms
      • NSAIDS for pain
  • Management of exacerbations
    •   Relapse,
      • an attack has to last at least 24 hours and happen at least a month after the last exacerbation.
      • most relapses last several days, or even weeks or months.
    • TX: with high doses of intravenous corticosteroids
      • to reduce the inflammation & leave fewer lasting disabilities on the MS patient.
    • Side effect:
      • affect the memory
      • cause osteoporosis, which is a bone disease leading to bone fragility and an increased risk of fracture.
  • Interferon
    • routine therapy used to treat acute relapses & exacerbations
    • reducing the frequency of the attacks and the progression to disability
    • effective for slowing disease progression and activity in relapsing-remitting
    • several side effects, which include:
    • irritation at the injection site
    • Lipoatrophy – a localised loss of fat tissue – can develop with time at the injection site
    • influenza-like symptoms
    • sometimes serious liver damage
  • Interferon
    • Betaseron
      • Used for ambulatory clients with relapsing-remitting type
      • Antiviral and immunoregulatory properties
      • Reduce the number of exacerbations
      • SQ route given every other day
    • Avonex
      • Used for relapsing form type
      • Provide delay in disability.
    • Copaxone (not an interferon)
      • Mimicking the myelin basic protein and interrupting the inflammatory cascade to prevent damage to myelin
      • SE:
        • Face flushing
        • Chest tightness
        • SOB less than 15mins
  • Medications
    • Adrenocorticotropic hormone (ACTH) = increase corticosteroid production in adrenal cortex
    • Immunosuppressants
      • azathioprine (Imuran),
      • cyclophosphamide (Cytoxan)
    • Antispasmodics to treat muscle spasms
    • Medications to deal with bladder problems: anticholinergics (bladder spasticity) or cholinergics (urinary retention) depending on problem experienced by client
  • Symptomatic Tx
    • Bladder dysfunction
      • Oxybutynin, propantheline
    • Constipation
      • Bisacodyl pills or suppositories
    • Fatigue
      • Amantidine, modafinil
    • Spasticity
      • Baclofen, diazepam, dantrolene
    • Tremor
      • Propanolol, phenobarbital, clonazepam
    • Dysesthesias
      • Carbamazepine, phenytoin, amitriptyline
      • Transcutaneous electrical nerve stimulation (TENS)
  • Collaborative Care
    • Focus is on retaining optimum functioning, limiting disability
  • Rehabilitation
    • Physical therapy to maintain abilities and deal with spasticity
    • occupational therapists
    • speech/language pathologists
    • cognitive remediation specialists
    • The therapy is tailored according to the specific symptoms of the patient.
  • MULTIPLE SCLEROSIS
    • NURSING INTERVENTIONS
    • 1. Promote physical mobility to maintain ability to perform ADL
    • Exercise
    • Schedule activity and rest periods
    • Warm packs over the spastic area
    • Swimming and cycling are very useful
  • MULTIPLE SCLEROSIS
    • NURSING INTERVENTIONS
    • 2. Prevent injuries
    • Wide stance walking
    • Use of walking aids
    • Wheelchair
  • MULTIPLE SCLEROSIS
    • 3. Enhance bladder and bowel control
    • Set a voiding schedule
    • Intermittent bladder catheterization
    • Use of condom catheter
    • Adequate fluids, dietary fibers and bowel training program
  • MULTIPLE SCLEROSIS
    • 4 . Manage speech and swallowing difficulties
    • Careful feeding, proper positioning, suction machine availability
    • Speech therapist
  • MULTIPLE SCLEROSIS
    • 5. Improve Sensory and Cognitive function
    • Vision- use eye patch for diplopia
    • Obtain large printed reading materials
    • Offer emotional support
    • Involve the family in the care
  • MULTIPLE SCLEROSIS
    • 6. Strengthen coping mechanism
    • Alleviate the stress
    • Referral to the appropriate agencies
  • MULTIPLE SCLEROSIS
    • 7. improve self-care abilities
    • Modify activities according to physical strength
    • Provide assistive devices
  • MULTIPLE SCLEROSIS
    • 8. promote sexual functioning
    • Refer to sexual counselor
  • Health Promotion
    • Client needs to develop strategies to deal with fatigue, exacerbations
    • Prevention of respiratory and urinary tract infections
  • Home Care
    • Education
    • Referral to support group and resources
    • Referral to home health agencies when condition requires
  • RUN DOWN on MULTIPLE SCLEROSIS
  • Multiple Sclerosis
    • Common degenerative neurological disease.
    • Myelin sheath is destroyed.
    • Symptoms vary.
    • Relapsing/remitting.
    • Usually ages 20-40.
  • Multiple Sclerosis - Symptoms
    • Subjective:
      • Shakiness, difficulty walking
      • Fatigue, muscle weakness
      • Numbness, tingling
      • Tinnitus
      • Visual problems
      • Difficulty chewing and speaking
      • Incontinent; impotent
  • Multiple Sclerosis - Symptoms
    • Objective:
      • Ataxia
      • Changes in behavior & emotions
      • Nystagmus
      • Spasticity, tremors, dysphagia, facial palsy, speech impaired, fatigue
      • Incontinence
      • Impaired judgment
    • Intention tremors
      • Tremor occuring with activity
    • Dysmetria
      • Immobility to direct or limit movement
    • Disdiadochokinesia
      • Inability to stop one motor movement and substitute another
    Multiple Sclerosis - Symptoms
  • Multiple Sclerosis - Tests
    • CSF
    • CT scan
    • MRI
  • Multiple Sclerosis-Treatment
    • Meds:
      • Interferon
      • Anti inflammatory
        • ACTH, Solu Medrol, Prednisone
      • Immuno Modifiers
        • Avonex, Betaseron, Capoxone, Imuran
      • Muscle Relaxants
        • Valium
  • Multiple Sclerosis-Nursing Interventions
    • Nutrition
    • Skin Care
    • Activity
    • Control of environment
    • Emotional support
    • Patient teaching
  • PARKINSON’S DISEASE James Parkinson “An Essay on the Shaking Palsy”
  • Dopamine – a neurotransmitter
    • acts to facilitate release of inhibition
    • high levels of dopamine= promote motor activity/control fine motor movements
    • low levels of dopamine function, such as occur in PD, demand greater exertions of effort for any given movement.
    • Thus the net effect of dopamine depletion is to produce hypokinesias/bradykinesias, an overall reduction in motor output
  • Acetylcholine
    • In peripheral nervous system:
      • acetylcholine activates muscles contraction (skeletal)
  • PARKINSON’s Disease
    • A slowly progressing neurologic movement disorder
    • The degenerative idiopathic form is the most common form
    • There is degenerative changes in substantia nigra (part of the brain), which produces dopamine, that enables people to move normally and smoothly
  • Progressive, degenerative neurological disease
    • characterized by hand tremor at rest, muscle rigidity and akinesia (poor movement), difficulties with gait and balance
    • Affects older adults mostly, mean age 60 with males more often than females
    • Parkinson-like syndrome can occur with:
      • Some medications ( long-term use of phenothiazines)
      • Encephalitis
      • Toxins (carbon monoxide and mercury/manganese poisoning);
      • Traumatic injury to the midbrain.
  • PARKINSON’s Disease
    • CAUSATIVE FACTORS: unknown
    • Potential factors
      • Genetics
      • Atherosclerosis
      • Free radical stress
      • Viral infection
      • Head trauma
      • Environmental factors
  •  
  • PARKINSON’s Disease
    • Pathophysiology
    • Decreased levels of dopamine due to destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia
    • Clinical symptoms do not appear until 80% of the neurons have disappeared
  •  
  • Pathophysiology
    • Neurons in cerebral cortex atrophy and dopamine receptors in basal ganglia decrease
    • Decrease in dopamine, which is neurotransmitter involved with motor function
    • Disturbance between balance of dopamine and acetylcholine
    • Balance needed for smooth coordinated movement
  • PARKINSON’S Disease
    • CLINICAL MANIFESTATIONS
    • 1. Tremor at rest on one side = 1 st sign
      • Coarse pill-rolling of thumbs against the fingers
      • Intention tremors = tremor during voluntary movement
    • 2. Rigidity- cog-wheel, lead-pipe
      • Increased tone and stiffness in the muscles
    • 3. Bradykinesia- abnormally slow movement
      • Fine movements become clumsy
    • 4. Flexed posture of neck, trunk and limbs = advance stage
    • 5. Loss of postural reflexes
    • 6. Freezing movement
    • 7. Dementia, depression, sleep disturbances and hallucinations
    • 8. Excessive sweating, paroxysmal flushing, orthostatic hypotension
    • 9. Stiff, mask-like and without expression
  • Manifestations
    • Tremor at rest with pill rolling motion of thumb and fingers
      • Lessens with purposeful movement
      • Worsens with stress and anxiety
      • Progressive impairment affecting ability to write and eat
    • Rigidity
    • Involuntary contraction of skeletal muscles
    • Cogwheel rigidity: jerky motion
  • Manifestations
    • Akinesia = absence of movements
    • Slowed or delayed movement that affects chewing, speaking, eating
    • May freeze: loss of voluntary movement
    • Bradykinesia: slowed movement
    • Abnormal posture
    • Involuntary flexion of head and shoulders, stooped leaning forward position
    • Equilibrium problems causing falls, and short, accelerated steps
  • Manifestations
    • Autonomic nervous system
    • Constipation and urinary hesitation or frequency
    • Orthostatic hypotension, dizziness with position change
    • Eczema, seborrhea
    • Depression and dementia; confusion, disorientation, memory loss, slowed thinking
    • Inability to change position while sleeping, sleep disturbance
  • Manifestations
    • Micrographia – small, cramped handwriting
  •  
  • Complications
    • Parkinsonian Crisis
      • Due to emotional trauma or sudden withdrawal of anti-parkinsonian drugs
      • s/sx: severe exacerbation
        • Tremor
        • Rigidity and bradykinesia
        • Acute anxiety
        • Sweating
        • Tachycardia
        • Hyperpnea
        • Mgt:
          • Respiratory and cardiac support
          • Placed in quiet roo,
          • Barbiturates and anti-park drugs
    • Oculogyric crisis (fixed lateral and upward gaze)
    • Impaired communication
    • Falls
    • Infection related to immobility and pneumonia
    • Malnutrition related to dysphagia
    • Skin breakdown
    • Depression and isolation
  • Diagnostic Tests: No specific test for disease
    • Drug screens to determine medications or toxins causing parkinsonism
    • EEG: slowed and disorganized pattern
  • Prognosis
    • Slow progressive degeneration
    • Eventual debilitation
  • PARKINSON’s Disease
    • Medical management
    • 1. Anti-parkinsonian drugs- Levodopa, Carbidopa (Sinemet)
    • 2. Anti-cholinergic therapy- Artane and Cogentin– reduce tremor
    • 3. Antiviral therapy- Amantadine
    • 4. Dopamine Agonists- bromocriptine and Pergolide, Ropirinole & Pramipexole
      • Pronounced stage
  • PARKINSON’s Disease
    • Medical management
    • 5. MAOI = to block 1 pathway in the breakdown of dopamine
      • selegiline
    • 6. Anti-depressants
    • 7. Antihistamine
  • Medications
    • Initially selegiline (Carbex), amantadine (Symmetrel), anticholinergics
    • Combination carbidopa-levodopa (Sinemet)
    • Bromocriptine (Parlodel) pergolide (Permax) inhibit dopamine breakdown
    • Medications may lose their efficacy; response to drugs fluctuates: “on-off” effect
  • Treatments
    • Electrical stimulation for tremor suppression
    • Surgery has sometimes been done
    • Pallidotomy: destruction of involved tissue
  • Rehabilitation
    • Physical therapy
    • Occupational therapy
    • Speech therapy
  • Nursing Diagnoses
    • Impaired Physical Mobility
    • Impaired Verbal Communication
    • Impaired Nutrition: Less than body requirements
    • Disturbed Sleep Patterns
  • Nursing Care
    • Education and support to client and family
    • Maintain functioning
    • Referral to home care, community resources
  • PARKINSON’s Disease
    • NURSING INTERVENTIONS
    • 1. Improve mobility
    • 2. Enhance Self- care activities
    • 3. Improve bowel elimination
    • 4. Improve nutrition
    • 5. Enhance swallowing
    • 6. Encourage the use of assistive devices
  • PARKINSON’s Disease
    • NURSING INTERVENTIONS
    • 7. improve communication
    • 8. Support coping abilities
    • Administer prescribed dopaminergics such as carbidopa/levodopa (Sinemet) to treat rigidity
    • Administer prescribed anticholinergic such as trihexyphenidyl (Artane) and benztropine (Cogentin) to treat tremor.
    • Bromocriptine mesylate (Parlodel) maybe administered to increase dopaminergic receptors.
    • MAO inhibitors such as selegiline (Eldepryl) to inhibit the release of levodopa
    • Encourage to participate in physical, occupational and speech therapies
    • Instruct to perform breathing exercises to prevent respiratory problems
    • Encourage to wear elastic stockings for orthostatic hypotension
    • Encourage to provide self-care activities
    • Monitor intake and output
    • Assess the client for dysphagia
    • Provide the client with an upright chair with arms and legs at the side when sitting
    • Place elevated toilet seat
  • Home Care
    • Medication education
    • Adaptation of home environment
    • Gait training and exercises
    • Nutritional teaching
  • RUN DOWN on PARKINSON’S DISEASE
  • Parkinson’s Disease
    • Unknown cause
    • Lack of dopamine.
    • Parkinsonism: encephalitis, toxic chemicals, meds, drugs
  • Parkinson’s
    • Symptoms include:
      • Muscular tremors and rigidity
      • Emotional instability
      • Judgment defects
      • Heat intolerance
      • Mask-like facial appearance
      • Dysphagia and drooling
  • Parkinson’s Testing
      • No specific test to diagnose Parkinson’s
      • Diagnosis based on symptoms
  • Parkinson’s – Medical Treatment
    • Medications
      • Sinemet, Symmetrol, Levodopa or Cogentin
      • Less effective over time
    • Surgery
    • Experimental
  • Parkinson’s – Nursing Care
    • Prevent injury (fall or aspiration)
    • Prevent urinary retention and constipation
    • Patient teaching about medication
    • Patient and family support
  • Client with Myasthenia gravis (MG)
  • Myasthenia gravis
    • A sporadic, but progressive weakness and abnormal fatigability of striated muscles which are exacerbated by exercise and repetitive movements
    • Chronic autoimmune neuromuscular disorder involving a fluctuating weakness of the skeletal muscles in which the antibodies attack the number and effectiveness of acetylcholine at the neuromuscular junction.
  • Description
    • Chronic neuromuscular disorder characterized by fatigue and severe weakness of skeletal muscles
    • Occurs with remissions and exacerbations
    • Believed to be autoimmune in origin
    • Occurs more frequently in females, with onset between ages 20 – 30
  • Myasthenia gravis
    • ETIOLOGY
    • Autoimmune disease
    • Women suffer at an earlier age and are more affected
  • Myasthenia gravis
    • Pathophysiology:
    • 1. Acetylcholine receptor antibodies interfere with impulse transmission
    • 2. Follows an unpredictable course of periodic exacerbations and remissions
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  • Pathophysiology
    • Antibodies destroy or block neuromuscular junction receptor sites, resulting in decreased number of acetylcholine receptors
    • Causes decrease in muscle’s ability to contract, despite sufficient acetylcholine
    • Majority of clients have hyperplasia of thymus gland which is usually inactive after puberty; believed that thymus is source of autoantigen causing MG
    • Associated in some clients with other autoimmune conditions
  • Manifestations
    • Seen in the muscles that are affected
    • Ptosis (drooping of eyelids), diplopia (double vision)
    • Weakness in mouth muscles resulting in dysarthria and dysplagia
    • Weak voice, smile appears as snarl
    • Head juts forward
    • Muscles are weak
    • Weakness and fatigue exacerbated by stress, fever, overexertion, exposure to heat; improved with rest
    • Weakness that worsens during the day
  • Complications
    • Pneumonia
    • Myasthenic Crisis
    • Sudden exacerbation of motor weakness putting client at risk for respiratory failure and aspiration
    • Precipitated by: infection, sudden withdrawal of anticholinesterase drugs, and may occur spontaneously
    • Manifestations:
      • Tachycardia
      • Tachypnea
      • Respiratory distress
      • Dysphasia
      • Endotracheal intubation and mechanical ventilation if increase dosage of drugs does not improve
  • Complications
    • Cholinergic Crisis
    • Occurs with overdosage of medications (anticholinesterase drugs) used to treat MG
      • Develops GI symptoms (abdominal cramps, diarrhea)
      • severe muscle weakness
      • Vertigo
      • Respiratory distress (excessive pulmonary secretions, bronchial spasm)
    • Both crises often require ventilation assistance
    • Differentiation is by administration of (edrophonium chloride) Tensilon, which will improve the muscle weakness in myasthenic crisis and be ineffective with cholinergic crisis
  • Diagnostic Tests
    • Physical examination and history
    • Tensilon Test:
      • Edrophonium chloride (Tensilon) administered and client with myasthenia will show significant improvement lasting 5 minutes
    • EMG
      • reduced action potential
    • Antiacetylcholine receptor antibody serum levels:
      • increased in 80% MG clients; used to follow course of treatment
    • Serum assay of circulating acetylcholine receptor antibodies:
      • if increased is diagnostic of MG
  • Myasthenia gravis
    • DIAGNOSTIC TESTS
    • 1. TENSILON TEST
    • 2. EMG
    • 3. CT scan
    • 4. Serum anti-AchReceptor antibodies
  • Medications
    • Anticholinesterase medications, which act at neuromuscular junction, allowing acetylcholine to concentrate at receptor sites and promote muscle contraction; most commonly used medication is
      • pyridostigmine (Mestinon)
    • Immunsuppression medications
      • glucocorticoids
    • Cyclosporine or azathioprine (Imuran)
  • Myasthenia gravis
    • MEDICAL THERAPY
    • Anticholinesterase drugs- pyridostigmine and neostigmine
    • Corticosteroids
    • Immunosuppresants
    • Plasmapheresis
    • Thymectomy
  • Surgery
    • Thymectomy is recommended in clients <60
    • Remission occurs in 40 % of clients, but may takes several years to occur
  • Plasmapheresis
    • Used to remove antibodies
    • Often done before planned surgery, or when respiratory involvement has occurred
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  • Nursing Diagnoses
    • Ineffective Airway Clearance
    • Impaired Swallowing: plan to take medication to assist with chewing activity
  • Nursing Care
    • Teaching interventions to deal with fatigue
    • Importance of following medication therapy
  • Myasthenia gravis
    • NURSING INTERVENTIONS
    • 1. Administer prescribed medication as scheduled
    • 2. Prevent problems with chewing and swallowing
    • 3. Promote respiratory function
    • 4. Encourage adjustments in lifestyle to prevent fatigue
    • 5.maximize functional abilities
  • Myasthenia gravis
    • 6. Prepare for complications like myasthenic crisis and cholinergic crisis
    • 7. prevent problems associated with impaired vision resulting from ptosis of eyelids
    • 8. provide client teaching
    • 9. promote client and family coping
  • Home Care
    • Avoid fatigue and stress
    • Plan for future with treatment options
    • Keep medications available
    • Carry medical identification
    • Referral to support group, community resources
  • RUN DOWN on MYASTHENIA GRAVIS
  • Myasthenia Gravis
    • Autoimmune disorder
    • Myoneural junction problem causing muscle weakness
    • Symptoms:
      • ptosis, diplopia,
      • weakness, dysarthria, dysphagia, difficulty sitting up, respiratory distress
  • Myasthenia Gravis - Treatment
    • Medication
      • to improve impulse transmission (Mestinon)
      • to suppress immune system (steroids, Cytoxan)
      • Pyridostigmine and neostigmine
    • Plasmapheresis
    • Respiratory support
    • Safety
  • Client with Amyotrophic Lateral Sclerosis (ALS) Lou Gehrig’s Disease Charcot’s disease
  • Description
    • Progressive, degenerative neurologic disease characterized by weakness and wasting of muscles without sensory or cognitive changes
    • Involve the motor system characterized by atrophy of the hands, forearms, and legs that lead to paralysis and death.
    • Several types of disease including a familial type;
    • onset is usually between age of 40 – 60;
    • higher incidence in males at earlier ages but equally post menopause
    • Most common of the motor neuron diseases, age-dependent, fatal paralytic disorder
    • Physiologic problems involve swallowing, managing secretions, communication, respiratory muscle dysfunction
    • 50% of clients die within 2 – 5 years of diagnosis, often from respiratory failure or aspiration pneumonia
    • Cause: unknown
    • Sensory system and cognition are not affected.
    Description
  • Pathophysiology
    • Degeneration and demyelination of motor neurons in anterior horn of spinal cord, brain stem and cerebral cortex
    • Involves upper and lower motor neurons
    • Reinnervation occurs in the early course of disease, but fails as disease progresses
    • Weakness begins in the upper extremities (upper arm and shoulder)
    • Followed by the neck and throat.
    • Lower extremities and trunk are usually not affected until late in the disease.
    • When intercostal muscles and diaphragm involved, respiration becomes shallow and coughing is ineffective.
    • Cognition, bowel and bladder sphincters remain intact even during the advance stage.
    • Bulbar ALS = when weakness begins in the brain stem causing dysarthria and dysphagia
    • Lower motor neurons:
      • Weakness
      • Atrophy
      • Cramps
      • Fasciculation (irregular twitching of muscle fibers/bundles)
    • Upper motor neurons:
      • Spasticity
      • Hyperreflexia
    Manifestations
    • Corticobulbar tracts:
      • Dysphagia
      • Dysarthria
      • Risk for suboptimal caloric and fluid intake
      • Worsening of muscle atrophy
      • Weakness
      • Fatigue
    Manifestations
    • Atrophy of tongue and facial muscles result in dysphagia and dysarthria; emotional lability and loss of control occur
    • Sign of pending respiratory insufficiency is when there is SOB while eating.
    • Pt usually are admitted to facilities only 2x.
      • 1 st during diagnosis
      • 2 nd during the final stage of debilitation
    Manifestations
  • Diagnostic Test
    • Testing rules out other conditions that may mimic early ALS such as hyperthyroidism, compression of spinal cord, infections, neoplasms
    • EMG to differentiate neuropathy from myopathy
    • Muscle biopsy shows atrophy and loss of muscle fiber
    • Serum creatine kinase is elevated (non-specific)
    • Pulmonary function tests: to determine degree of respiratory involvement
  • Medications
    • antiglutamate : Rilutek (Riluzole)
      • To slow disease progression;
      • Prescribed to slow muscle degeneration
    • Requires monitoring of liver function, blood count, chemistries, alkaline phosphatase
  • Nursing Diagnoses
    • Risk for Disuse Syndrome
    • Ineffective Breathing Pattern: may require mechanical ventilation and tracheostomy
  • Nursing Interventions
    • Aimed at conserving energy.
    • Activities should be spaced during the day
    • Muscle stress, strenuous activity, and extremes of hot and cold should be avoided .
    • Use of leg braces, canes and walkers prolong independence on ambulation
    • Use of hand braces, special utensils and adaptive devices can help with dressing and self-feeding
    • Gather information from the client and family on the position best for respiration, handling secretions, eating and turning routines.
    • Encourage fluid intake regularly, when the client is not fatigued.
    • Proper positioning is imperative
    • Providing a cup with spout may prevent liquid from running out of the corners of the mouth
    • Give liquids by using a large syringe with short tubing on the tip. Tube should be place on the anterior portion of the tongue and gentle force is used to deliver small amount of liquid.
    • Encourage small frequent feeding , high nutrient feedings.
    • Sit upright, with head slightly flexed forward while eating.
    • Papase tablet may be used . Placed under the tongue 10 minutes before meals can make thick saliva less sticky.
    • Allow plenty of time for eating, and pt should not attempt to speak while food is in the mouth
    • Suction equipment should be available during meals to reduce the risk for aspiration of food and secretions.
    • Use of soft cervical collar to stabilize the head
    • Percutaneous endoscopic gastrostomy (PEG) should be considered as an alternative route for oral nutrition if dysphagia progresses.
    • When verbal communication is not possible, writing may be encouraged.
    • Advance stage, speech pathologies can provide communication devices such as alphabet boards and portable memo writers.
    • Pulmonary function test should be done to regularly assess ventilatory status
    • Help client and family deal with current health problems
    • Prevent complications of immobility
    • Implement aspiration precaution
    • Implement pain relief intervention
  • Home Care
    • Education regarding disease, community resources for health care assistance and dealing with disabilities
  • Amyotrophic Lateral Sclerosis ALS – Lou Gehrig’s disease
    • Motor neurons in brain stem and spinal cord degenerate
    • Brain’s messages don’t reach the muscles
    • Symptoms – weakness, dysarthria, dysphagia
    • No loss of cognitive function
    • No cure, death occurs in 2-6 years
  • Manifestations
    • Fatigue
    • Muscle atrophy
    • muscle flaccidity/weakness
      • usually involves hands, shoulders, upper arms, and then legs
    • Dysarthria
    • Dysphagia
    • fasciculations (twitching of involved muscles);
  • Client with Huntington’s Disease (chorea)
  • Progressive, degenerative inherited neurologic disease
    • An autosomal-dominant degenerative neurologic disease = offspring of affected person has 50% chance of inheriting the disease.
    • It does not skip generations, offspring who have not inherited the disease will not pass it on to their offspring.
    • Characterized by intellectual decline, emotional disturbance and chorea (rapid, jerky involuntary movements)
    • Abnormal gene has been isolated on chromosome 4.
    • Usually asymptomatic until age of 30 – 40
    • Both sexes are equally affected.
    • Disease is progressive, leading to disabilities and death within 15-20 yrs.
    • Cause unknown
    • No cure
    • Death occur as a result of:
      • respiratory tract complications caused by aspiration
      • Infection (pneumonia)
      • Injuries r/t fall or other complications
  • Pathophysiology
    • involves destruction of the striatum (caudate and putamen) cells in basal ganglia and other brain areas such as the cortex and cerebellum.
    • Loss of neurons and an increased number of glial cells (gliosis).
    • The degeneration of caudate nucleus leads to reduction in several neurotransmitters such as
      • GABA
      • Acetylcholine
      • Substance P
      • Metenkephalin
      • This leads to increase in other neurotransmitter like dopamine and norepinephrine.
      • Leads to excessive movement (excess dopamine) compared to PD’s lack of movement.
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  • Manifestations
    • Emotional disturbance
      • Negative
      • Suspicious
      • Irritable
      • Depression
      • Psychosis
      • Temper outburst
      • Sexual promiscuity
      • Severe mood swings are common
    • Mental deterioration
      • Cognitive decline
      • Dementia
      • Incontinent
      • Completely unable to do self-care
  • Manifestations
    • Abnormal movement subtle at first
    • Appear restless or fidgety.
    • Pt may aware of these movements, trying to mask the movement as if they are part of intentional movements = head scratching or leg crossing.
    • As disease progresses, the rapid, jerky choreiform movements become more pronounced and involve all muscles.
    • Pt is in constant motion except during sleep.
    • Stress, emotional situations and attempt to perform voluntary movement can aggravate the abnormal movements
    • Most dangerous and common problem is DYSPHAGIA
  • Diagnostic Tests
    • genetic testing of blood
    • MRI/CT scan = atrophy of the head of the caudate but not confirmatory
  • Medications
    • Antipsychotic (phenothiazines and butyrophenones) to restore neurotransmitters
    • Antidepressants
    • Anxiolytic drugs
      • Diazepam = lower anxiety = thereby aiding in control of movements
    • Haloperidol, a dopamine-blocker
      • To control abnormal movements and some behavioral manifestations
  • Collaborative Care
    • almost always requires long-term care
  • Nursing Care
    • Very challenging: physiological, psychosocial and ethical problems
    • Genetic counseling
  • Nursing Diagnoses
    • Risk for Aspiration
    • Imbalanced Nutrition: Less than body requirements
    • Impaired Skin Integrity
    • Impaired Verbal Communication
  • Nursing Interventions
    • Mealtime should be free from stress and have an unhurried atmosphere.
    • Use of adaptive eating utensils to encourage and extend independence in eating.
    • Diet = foods that are easily swallowed and form a bolus in the mouth (canned peaches, chopped meat in gravy and mashed potatoes, custards)
    • Intake of 5000 calories a day without gaining weight (due to excessive movements)
    • Small frequent meals containing high calorie foods
    • Sit upright during meal.
    • While swallowing, pt should keep chin down toward chest.
    • Should be trained to hold their breath before swallowing and cough after each mouthful is swallowed to clear the throat of any residual food.
    • High risk for dehydration = require large fluid intake esp. during hot weather.
    • Advance stage, feeding tube maybe necessary
    • Provide information on the types, risks, benefits and long-term effects of artificial feeding methods.
    • Use of communication devices when communication is difficult
  • Home Care
    • Referral to agencies to assist client and family, support group and organization
  • RUN DOWN on HUNTINGTON’S DISEASE
  • Huntington’s Disease Chorea
    • Genetic
    • Onset at age 30-40
    • Excessive involuntary movements
    • Death in 15-20 years
    • No cure
  • Manifestations
    • Early signs are personality change with severe depression, memory loss; mood swings, signs of dementia
    • Abnormal movement and progressive dementia
    • Increasing restlessness, worsened by environmental stimuli and emotional stress; arms and face and entire body develops choreiform movements, lurching gait; difficulty swallowing, chewing, speaking
    • Slow progressive debilitation and total dependence
    • Death usually results from aspiration pneumonia or another infectious process
  • Huntington’s Disease
    • Nursing interventions are palliative
      • Give meds
      • Provide for safety
      • Provide adequate diet
    • Emotional support
    • Genetic counseling
  • ALZHEIMER’S DISEASE
  • Client with Alzheimer’s Disease
    • Form of dementia characterized by progressive, irreversible deterioration of general intellectual functioning
    • Begins with memory loss, initially subtle until progresses to being more noticeable; course includes deteriorating cognition and judgment with eventual physical decline and total inability to perform ADL
  • Alzheimer’s
    • Unknown cause, but genetic link
    • Very common; risk increases with age
    • Brain changes:
      • plaques
      • tangled neurons
      • blood vessel degeneration
      • chemical changes
  • Risk factors
    • older age
    • female
    • family history
    • Exact cause is unknown; theories include loss of transmitter stimulation, genetic defects, viral and autoimmune cases
  • Warning signs include
    • Memory loss affecting ability to function in job
    • Difficulty with familiar tasks
    • Problems with language, abstract thinking
    • Disorientation, changes in mood and personality
  • Types and Changes in brain
    • Familial (follows inheritance pattern) and sporadic
    • Early-onset (<65)
    • Older-onset (>65)
    • Loss of nerve cells and presence of neurofibrillary tangles and amyloid plaques
    • Progressive brain atrophy
  • Alzheimer’s - Symptoms
    • 1st– memory lapses, difficult word finding, decreased attention span
    • 2nd – increased memory problems, disoriented to time, loses things, confabulates
    • 3rd – total disorientation, apraxia, wanders
    • 4th – severe impairment
  • Manifestations : Stage I
    • Appears healthy and alert
    • Cognitive deficits are undetected
    • Subtle memory lapses, personality changes
    • Seems restless, forgetful, uncoordinated
  • Stage II
    • Memory deficits more apparent
    • Less able to behave spontaneously
    • Wandering behavior, deterioration in orientation to time and place
    • Changes in sleeping patterns, agitation, stress
    • Trouble with simple decisions
    • Sundowning: increased agitation, wandering, disorientation in afternoon and evening hours
    • Echolalia, scanning speech, total aphasia at times, apraxia, astereognosis, inability to write
    • Becomes frustrated and depressed
  • Stage III
    • Increasing dependence with inability to communicate, loss of continence
    • Progressive loss of cognitive abilities, falls, delusion, paranoid reactions
    • Average life expectancy is 7 years from diagnosis to death, often from pneumonia, secondary to aspiration
  • Collaborative Care
    • No cure
    • Supportive care for client and family
  • Diagnostic Tests
    • Diagnosis by ruling out other conditions including depression, hypothyroidism, infection, stroke
    • EEG shows slow pattern in later stages of disease
    • MRI and CT scan: shrinkage of hippocanthus
    • Positron emission tomography (PET):visualizes brain activity and interactions
    • Folstein Mini-Mental Status: instrument reflecting loss of memory and cognitive skills
  • Alzheimer’s - Testing
    • No definitive test
    • Family history
    • Diagnosis: autopsy
  • Alzheimer’s – Medical Management
    • Medication to treat symptoms
      • Memory:Cognex, Aricept
      • Agitation: Mellaril, Haldol
    • Supplements
      • Folic Acid & Vitamin B12
      • Low fat diet
      • NSAIDS
  • Medications
    • Cholinesterase inhibitors used to treat mild to moderate dementia
    • Tacrine hydrochloride (Cognex)
    • Donepezil hydrochloride (Aricept)
    • Rivastigmine (Exelon)
    • Medications to treat depressions
    • Tranquilizers for severe agitation
    • Thioridazine (Mellaril)
    • Haloperidol (Haldol)
    • Antioxidants: vitamin E, anti-inflammatory agents, estrogen replacement therapy in women
  • Complementary Therapy
    • Massage, herbs, ginko biloba, Coenzyme Q10
    • Art therapy, music, dance
  • Nursing Care & Health Promotion
    • Intensive, supportive nursing interventions directed at physical and psychosocial responses to illness
    • Maintain functional abilities
    • Maintain safety of client and caregiver
  • Nursing Diagnoses
    • Impaired Memory
    • Include written or verbal reminders
    • Use cues to deal with memory loss
    • Chronic Confusion
    • Anxiety
    • Hopelessness
    • Caregiver Role Strain
  • Home Care
    • Education regarding disease, anticipation of needs, use of memory cues, support groups and peer counseling
    • Refer to home health agencies, family support, group support
  • Alzheimer’s – Nursing Care
    • 2 key points for all care:
      • Prevent overstimulation
      • Provide structured, orderly environment
    • Other concerns
      • Communication
      • Family support and education
  • RUN DOWN on ALZHEIMER’S DISEASE
  • ALZHEIMER’S disease
    • A progressive neurologic disorder that affects the brain resulting in cognitive impairments
  • ALZHEIMER’S disease
    • CAUSES:
    • Unknown
    • Potential factors- Amyloid plaques in the brain, Oxidative stress, neurochemical deficiencies
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  • ALZHEIMER’S disease
    • CLINCAL MANIFESTATIONS
    • 1. Forgetfulness
    • 2. Recent memory loss
    • 3. Difficulty learning
    • 4. Deterioration in personal hygiene
    • 5. Inability to concentrate
  • ALZHEIMER’S disease
    • LATE CLINICAL MANIFESTATIONS
    • 6. Difficulty in abstract thinking
    • 7. Difficulty communicating
    • 8. Severe deterioration in memory, language and motor function
    • 9. repetitive action- perseveration
    • 10. personality changes
  • ALZHEIMER’S disease
    • DIAGNOSTIC TEST
    • Neurologic examination
    • PET scan
    • EEG, CT and MRI
    • Other tests to rule out Vit B deficiencies and hypothyroidism
    • Autopsy is the most definitive
  • ALZHEIMER’S disease
    • Drug therapy
    • 1. drugs to treat behavioral symptoms- antipsychotics
    • 2. anxiolytics
    • 3. Donepezil
    • 4. Tacrine
  • ALZHEIMER’S disease
    • Nursing Interventions
    • 1. Support patient’s abilities
    • 2. Provide emotional support
  • ALZHEIMER’S disease
    • Nursing Interventions
    • 3. Establish an effective communication system with the patient and family
    • Use short simple sentences, words and gestures
    • Maintain a calm and consistent approach
    • Attempt to analyze behavior for meaning
  • ALZHEIMER’S disease
    • 4. protect the patient from injury
    • Provide a safe and structured environment
    • Requests a family member to accompany client if he wanders around
    • Keep bed in low position
    • Provide adequate lightning
    • Assign consistent caregivers
  • ALZHEIMER’S disease
    • 5. Encourage exercise to maintain mobility
  • SPINAL CORD INJURY
  • Spinal cord injury
    • The most frequent vertebrae C1-2, C4-6, T11-L2 as they are mobile, thereby most easily injured.
    • Cause:
      • Trauma – most common
        • Vehicular accidents, gunshot/knife wounds, falls & sports mishaps
        • Male, 16-30
      • Cervical spondylosis
        • Spinal canal narrowing with progressive injury to the cord and roots)
      • Myelitis
        • Infective/noninfective
      • Osteoporosis causing vertebral compression fractures
      • Tumors
      • Vascular disease = infarction and hemorrhage
  • Pattern of Cervical Injury: Flexion-Rotation, Dislocation and Fracture-Dislocation Injuries
    • Flexion injury = most common SCI
    • When head strikes the steering wheel/windshield, the spine is forced into acute hyperflexion.
    • Rupture of the posterior ligaments results.
    • Nutrient blood vessels may be damaged, leading to ischemia of the spinal cord
    • C5-C6, most common affected by flexion injury.
    • T12-L1, common type affected on thoracic and lumbar
  • Hyperextension Injuries
    • Result after fall where chin hits an object and the head is thrown back.
    • Anterior ligament is ruptured with fracture of the posterior elements of the vertebral body.
    • Hyperextension of the cord against the ligamentum flavum can lead to dorsal column contusion and posterior dislocation of the vertebrae.
    • Complete transection of the cord can follow a hyperextension injury.
    • Complete lesions of the cord result in loss of all voluntary movement and sensation below the lesion and loss of reflex function in isolated segments of the cord.
  • Compression Injuries
    • Caused by falls/jumps in which the person lands directly on the head, sacrum or feet.
    • The force of impact fractures the vertebrae and the fragments compress the cord.
    • Lumbar and lower thoracic vertebra commonly injured after a compression impact when the person lands on the feet.
    • Cervical spine will be injured if they land on the head.
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  • PATHOPHYSIOLOGY
      • CAUSES:
    • Trauma
    • Cervical spondylosis
    • Myelitis
    • Osteoporosis Tumors
    • Vascular disease
    Result to acceleration, deceleration/compression Microscopic bleeding primarily in gray matter 1 st hr, presence of edema, spreads along segments of the spinal cord Arachidonic acid and its metabolites (prostaglandin, thromboxanes, leukotrienes) causes the edema Edema peaks 2-3 days, subside within 7 days after injury Temporary loss of sensation & function Fragmentation of the axonal covering and loss of myelin Phagocytic cells injure the surviving axon
  • Fragmentation of the axonal covering and loss of myelin Chemotactic & inflammatory mediators causes tissue necrosis Macrophages engulf the spinal cord tissue causing central cavity = post traumatic syringomyelia develop 9 days after the injury Cord injury leads to rapid loss of axonal conduction Due to increase in extracellular potassium and influx of calcium into the cell. Free radicals are produced Free radicals usually controlled by antioxidant enzyme but too much of it, causes tissue damage
  • Physiologic changes
    • Sympathetic nervous system stress response results in reduced perfusion of GIT and reduce production of gastric mucus to protect the lining.
    • Ulceration and bleeding occur.
    • After SCI, the brain can no longer influence reflex movement thru the spinal cord.
    • The lower part of the cord, using spinal reflex arcs begins to work automatically such as:
      • Flexor withdrawal reflex and reflex emptying of the bladder and bowel.
    • During recovery, flexor responses are combined with extensor spasm and the limbs spasm into extension with movement.
  • Clinical manifestations
    • Altered LOC, sensory and motor function
    • Bradycardia
    • Hypotension
    • Poikilothermism (the body has a decreased ability to sweat and shiver below the level of injury)
    • Hypoventilation
    • Urinary retention
    • Paralytic ileus
    • Neurogenic bowel
    • Skin breakdown
    • Loss of body weight
    • DVT
    • Gastric distention
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  • DIAGNOSTIC TEST
    • Complete hx and physical assessment
    • Spinal x-ray
    • CT scan
    • MRI
  • Complications:
    • Spinal Shock
    • Occurs immediately following the injury
    • The sudden depression of reflex activity in the spinal cord below the level of injury
    • Characterized by:
      • Decreased or loss of reflexes
      • Loss of skeletal muscle function, sensation
      • Loss of bladder and bowel tone
      • Loss of sexual function
      • flaccid paralysis below the site of injury
    • Lasts 1 to 6 weeks
    • Indication of recovery:
      • Return of reflexes
      • Development of hyperreflexia
      • Return of reflex emptying of the bladder
  • Complications:
    • Neurogenic Shock
    • The loss of vasomotor tone results from the injury.
    • Characterized by:
      • Hypotension
      • Bradycardia
      • Dry warm extremities
    • Generally occurs with a cervical or high thoracic injury
  • Complications:
    • Autonomic Dysreflexia
    • A response to visceral stimulation after resolution of spinal shock
    • Occurs in injury that occurs at T6 or above
    • Most common cause is an overdistended bladder or bowel
    • Characterized by:
      • severe hypertension (systolic greater than 300mmHg),
      • Bradycardia
      • Diaphoresis
      • Flushed above the site of injury
      • Throbbing headache
      • Blurred vision
  • Spinal cord injury
    • EMERGENCY MANAGEMENT
    • A-B-C
    • Immobilization
    • Immediate transfer to tertiary facility
  • Activity
    • Do a library research and make a ppt presentation on the following topics with their assessment, pathophysiology, s/sx, management.
    • Central cord syndrome
    • Anterior cord syndrome
    • Posterior cord syndrome
    • Brown-Sequard syndrome
    • Conus medullaris syndrome
    • Cauda equina syndrome
    • Different tractions for SCI
    • Presentation of output will be presented tomorrow.
  • Spinal cord injury
    • NURSING INTERVENTION
    • 1. Promote adequate breathing and airway clearance
    • 2. Improve mobility and proper body alignment
    • 3. Promote adaptation to sensory and perceptual alterations
    • 4. Maintain skin integrity
  • Spinal cord injury
    • 5. Maintain urinary elimination
    • 6. Improve bowel function
    • 7. Provide Comfort measures
    • 8. Monitor and manage complications
      • Thromboplebhitis
      • Orthostaic hypotension
      • Spinal shock
      • Autonomic dysreflexia
  • Spinal cord injury
    • 9. Assists with surgical reduction and stabilization of cervical vertebral column
  • Spinal Shock
    • Nursing Interventions
    • 1. Assist in chest physical therapy
    • 2. Manage potential complication- DVT
  • Cognitive Impairment
    • Nursing Interventions
    • Assist or encourage the patient to use eyeglass, hearing aid or assistive devices
    • Reorient the patient by calling his name frequently
    • Provide background information as to date, time, place, environment
  • Cognitive Impairment
    • Nursing Interventions
    • 4. Use large signs as visual cues
    • 5. Post patient's photo on the door
    • 6. Encourage family members to bring personal articles and place them in the same area
  • Bowel and Bladder incontinence
    • Establish a regular pattern for bowel care
    • Maintain a dietary intake. Avoid foods that can cause excessive gas production
  • CONGENITAL DISORDERS
    • HYDROCEPHALUS
    • SPINAL CORD DEFECT
  • CONGENITAL DISORDERS: Hydrocephalus
    • Excessive CSF accumulation in the brain’s ventricular system
    • In infants, head enlarges
    • In children and adults- brain compression
  • CONGENITAL DISORDERS: Hydrocephalus
    • Non-communicating hydrocephalus results from CSF outflow obstruction
    • Communicating hydrocephalus results from faulty absorption or increased CSF production
  • CONGENITAL DISORDERS: Hydrocephalus
    • Assessment
    • 1. irritability
    • 2. change in LOC
    • 3. infants- enlargement of the head, thin scalp skin
    • 4. sunset eyes
  • CONGENITAL DISORDERS: Hydrocephalus
    • DIAGNOSTIC TESTS
    • 1. Skull x-ray
    • 2. ventriculography
  • Ventriculo-Peritoneal Shunt
  • CONGENITAL DISORDERS: Hydrocephalus
    • Nursing Intervention
    • 1. monitor neurologic status
    • 2. teach parents to watch for signs of shunt malfunction, and periodic surgery to lengthen the shunt as child grows
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  • CONGENITAL DISORDER- Spinal cord defects
    • 1. Spina bifida occulta- incomplete closure of one or more vertebrae without protrusion of the spinal cord or meninges
    • 2. Spina bifida with meningocele- a sac contains meninges and CSF
    • 3. Spina bifida with meningomyelocele- a sac contains spinal cord substance, meninges and CSF
  • CONGENITAL DISORDER: Spinal cord defects
    • Causes
    • 1. environmental factors
    • 2. radiation
    • 3. folic acid deficiency in a pregnant woman
    • 4. possibly genetic
  • CONGENITAL DISORDER: Spinal cord defects
    • ASSESSMENT
    • 1. a dimple or tuft of hair in the vertebral area
    • 2. external sac
    • DIAGNOSIS
    • 1. Spinal x-ray
    • 2. myelography
  • CONGENITAL DISORDER: Spinal cord defects
    • NURSING INTERVENTION
    • 1. cover the defect with sterile dressing moistened with sterile saline
    • 2. position the patient on prone or side to protect the fragile sac
    • 3. place a diaper under the infant and change it often
  • CONGENITAL DISORDER: Spinal cord defects
    • NURSING INTERVENTION
    • 4. avoid the use of lotion
    • 5. avoid frequent handling
    • 6. Measure the child’s head circumference daily
    • 7. check anal reflex
    • 8. support family members
    • 9. prepare the parents for the possible outcome of eh defect
  • CONGENITAL DISORDER: Spinal cord defects
    • NURSING INTERVENTION
    • 10. Post-operative care
    • Position on abdomen
    • Check post-operative dressings
    • Place infant’s hips in abduction and feet in neutral position
    • Monitor intake and output
    • Check for urine retention
    • Asess infant frequently as he recovers from the surgery