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  • 1. ALTERED LEVEL OF CONSCIOUSNESS
  • 2. Definition:
    • Is Apparent in patient who is not oriented, does not follow commands, or needs persistent stimuli to achieve state of alertness.
    • Level of consciousness is gauged as a continuum with a normal state of alertness and full cognition( consciousness) on one end or coma on the other end.
  • 3. COMA > is a clinical state of unconsciousness in which the patient is unaware of self or the environment for prolonged periods. AKINETIC MUTISM > a state of unresponsiveness to the environment which the patient makes no movement or sounds but sometimes opens the eyes. PERSISTENT VEGETATIVE STATE > is a condition which the patient is described as wakeful but devoid of conscious content, without cognitive or affective mental function.
  • 4. PATHOPHYSIOLOGY :
    • Altered LOC is not a disorder itself: but it is a function and a symptom of multiple of physiologic phenomena.
    • The underlying cause of neurologic dysfunction in cells of nervous system, neurotransmitters, or brain anatomy.
    • A disruption in the basic functional units or neurotransmitters results in a faulty impulse transmission impending communication within the brain or from the brain to the other parts of the body.
    • The brain stems contains areas that control the heart, respiration and blood pressure.
    • Disruptions of the anatomic structures are caused by trauma, edema, pressure from tumors as well as other mechanisms such as increased or decreased in blood in CSF circulation.
  • 5. LEVEL OF CONSCIOUSNESS : LEVEL I- CONSCIOUS > normal awareness oriented to time, person, and place. LEVEL II- LETHARGY SOMNOLENCE DROWSINESS OR OBSTUNDATION > responds with confusion alone, falls alone to sleep; responds briefly to stimuli. LEVEL III- STUPOR > physical and mental activity is minimal. > Reflexes and sphincter actions are not changed. > Patient awareness by vigorous stimulation. LEVEL IV- SEMI-COMA > no spontaneous movement, withdrawal from painful stimuli and verbal response are limited to groaning. > vomiting. > reflex activities. COMA OR DEEP COMA > no spontaneous movement.  
  • 6. ASSESSMENT AND DIAGNOSTIC FINDINGS:
    • Glasgow Coma Scale
    • evaluation of mental status
    • cranial nerve functional
    • reflexes
    • motor and sensory functional
  • 7. LABORATORY TESTS INCLUDE :
    • analysis of blood glucose
    • electrolytes
    • serum ammonia
    • blood urea nitrogen level
    • serum osmolality
    • calcium level
    • partial thromboplastin and prothrombin times
    • serum ketone and alcohol
    • drug levels
    • arterial blood gas level
  • 8. COMPLICATIONS:
    • respiratory failure
    • pneumonia
    • pressure ulcers
    • aspirations from GI tract
    • MEDICAL MANAGEMENT:
    • maintain patent airway
    • patient may be orally and nasally intubated
    • tracheotomy
    • mechanical ventilator- maintain adequate oxygenation
    • intravenous catheter
    • nutritional support > feeding tube; gastrostomy
  • 9. NURSING INTERVENTIONS :
    • maintaining the airway
    • protecting the patient
    • maintaining the fluid and balance monitoring
    • providing mouth care
    • maintaining skin and joint integrity
    • preserving corneal integrity
    • achieving thermoregulation
    • promoting bowel functional
    • providing sensory stimulation
    • meeting family needs
    • monitoring and managing potential complications
  • 10. GLASGOW COMA SCALE
  • 11. DEFINITION:
    • evaluates level of consciousness
    • objective measurement of level of consciousness sometimes called quick neuro check
  • 12. MOTOR RESPONSE POINTS:
    • 6 = obeys simple response
    • 5 = localized painful stimuli
    • 4 = normal flexion ( withdrawal)
    • 3 = abnormal flexion ( decortication)
    • 2 = extensor response ( decerebration)
    • 1 = no response
  • 13. VERBAL RESPONSE:
    • 5 = oriented
    • 4 = confused conversation
    • 3 = inappropriate word
    • 2 = response with comprehensible sounds
    • 1 = no verbal response
  • 14. EYE OPENING POINTS:
    • 4 = spontaneous
    • 3 = in response to sound
    • 2 = response to pain
    • 1 = no response event to painful stimuli
    •  
  • 15. INTERPRETATIONS:
    • 15 – 14 = conscious
    • 13 – 11 = lethargy
    • 10 – 8 = stupor
    • 7= semi- coma
    • 3= deep coma
  • 16. TEST OF MEMORY:
    • SHORT TERM MEMORY
    • positive result mean anterograde amnesia and damage to temporal lobe.
    • Ask most recent activity .
    • LONG TERM ACTIVITY
    • positive result mean retrograde amnesia and damage to limbic system.
    • Consider educational background .
  • 17. INCREASED INTRACRANIAL PRESSURE (ICP)
  • 18.
    • an increased ICP caused by trauma, hemorrhage, growth of tumors, hydrocephalus, edema or inflammation.
    • Can impede circulation to the brain, impede the absorption of CSF, affect the functioning of nerve cells, and lead to brain stem compression and death.
  • 19. PATHOPHYSIOLOGY:
    • increased in ICP is a syndrome that affect many patients with acute neurologic conditions.
    • An elevated ICP most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, toxic and viral encelophaties.
    • Increase ICP from any cause decreased cerebral perfusion, stimulates further swelling and shifts brain tissue through openings in they rigid dura, resulting in herniation.
  • 20. CLINICAL MANIFESTATIONS :
    • any sudden change in patient's condition, such as restlessness without apparent cause, confusion or increasing drowsiness, has neurogic significance.
    • Comprehension of the brain due to swelling from hemorrhage or edema.
    • Expanding intra cranial lesion.
    • As ICP increase, patient becomes stuporous.
    • As neurologic function deteriorates, patient becomes comatose and exhibits abnormal motor response in the form of decortication, decerebration or flaccidity.
  • 21. ASSESSMENT:
    • assess LOC, which is the most sensitive and earliest indication of increasing ICP.
    • Declining LOC from restlessness to confusion and coma.
    • Headache
    • abnormal respirations
    • increase in BP with widening pulse
    • slowing of pulse
    • elevated temperature
    • pupil changes
    • change in motor functions from weakness to hemiplegia, a positive Babinski reflex, decorticate, decerebrate posturing and seizures.
    • Late signs of increase ICP include increased systolic BP widened pulse pressure and slowed heart rate
  • 22. COMPLICATIONS:
    • brain stem herniation- results in increase ICP
    • Diabetes Insipidus
    • Syndrome of Innapropriate Antidiuretic Hormone (SIADH)- results in over secretion of antidiuretic hormone.
    •   excessive urine output and hyperosmolality results.
  • 23. MEDICATIONS AND MANAGEMENT:
    • MONITORING ICP > to quantify the degree of evaluation, to initiate appropriate treatment- VENTRICULOSTOMY, SUBARACHNOID BOLT, EPIDURAL or SUBDURAL CATHETER.
    • MANNITOL (OSMITROL ) > Hyperosmotic agent; increased intravascular pressure by drawing fluid from the interstitial spaces and from the brain cells.
    • CORTICOSTEROIDS > stabilizes the cell membrane and reduce the leakiness in the blood-brain barrier.
    • > A histamine blocker may be administered to counteract the excess gastric secretion that occurs with corticosteroid.
    • > client must be withdrawn slowly from corticosteroid therapy to reduce the risk of adrenal crisis.
  • 24. BLOOD PRESSURE MEDICATION > required to maintain cerebral perfusion at a normal level. > notify the physician if the BP range is below 100 or above 150mm Hg systolic. ANTIPYERETIC AND MUSCLE RELAXANTS > temperature reduction decreases metabolism, cerebral blood flow, and thus ICP. > prevents shivering. ANTICONVULSANTS > may be given prophylactic ally to prevent seizures. > seizures increase metabolic requirements and cerebral blood flow and volume and increase ICP. IV FLUIDS > administration via infusion pump to control the amount of IV fluid treatment. > Hypertonic IV solutions are avoided because of the risk of promoting additional cerebral edema.  
  • 25. INTERVERNTIONS:
    • elevate the head of the bed 30 to 40 degrees as prescribed .
    • Avoid trendeleburg position
    • prevent flexion of neck and lips.
    • Monitor respiratory status and prevent hypoxia
    • maintain mechanical ventilations as prescribed, maintaining PaCO2 at 30 to 35 mm Hg, which will result in vasoconstriction of cerebral blood vessels, decreased blood flow and therefore decrease ICP.
    • Maintain body temperature.
  • 26. SEIZURES
  • 27. TYPES OF SEIZURE:
    • GENRALIZED SEIZURE:
    • TONIC CLONIC ( GRAND MAL )
    • > may begin with an aura.
    • > this phase may be involves the stiffening or rigidity of the muscles of the arms and legs usually lasts 10 to 20 seconds followed by loss of consciousness.
    • > this phase consists of hyperventilation and jerking of the extremities and usually lasts about 30 seconds.
    • > full recovery from seizures may take several hours.
    • ABSENCE
    • > brief seizures lasts seconds and the individual may or may not lose of consciousness.
    • > no loss or change in muscle tone occurs.
    • > seizure may occur several times a day.
    • >Victim appears to daydreaming.
    • > this type of seizure is more common in children.
  • 28. MYOCLONIC >a seizure that presence as a brief generalized jerking or stiffening of extremities. > the victim may fall to ground as a result of seizure. ATONIC OR AKINETIC ( DROP ATAACKS ) > a sudden momentary loss of muscle tone. > The victim may fall to ground as a result of the seizure. PARTIAL SEIZURE : SIMPLE PARTIAL > produces sensory symptoms accompanied by motor that are localized or confined to a specific area. > client remains conscious and report an aura > with autonomic symptoms > with special sensory and somatosensory symptoms. COMPLEX PARTIAL > with impairment of consciousness only. > a psycho motor seizure. > characterized by periods of altered behavior that the client is not aware of. >the client loses of consciousness for a few seconds.  
  • 29. ASSESSMENT:
    • seizure history
    • type of seizure
    • occurrence before, during, before and after seizure.
    • Prodomal signs, such as mood changes, irritability, insomnia.
    • Aura, a sensation that warns the client of the impeding seizure.
    • Loss of motor activity, or bowel and bladder function, or loss of consciousness, during the seizure.
    • NURSING MANAGEMENT:
    • document events leading to an occurring during the seizure and to prevent complications.
    • Patient risk for hypoxia, vomiting, and pulmonary aspiration. To prevent complications, patient is placed on side-lying position to facilitate drainage or oral secretions and is suctioned.
    • Maintain patent airway.
    • Bed placed in low position and side rails up.
    •  
  • 30. PATHOPHYSIOLOGY:
    • massages the body are carried by the neuron of the brain by means of discharges of electrochemical energy that swept along them.
    • During the period of unwanted discharges, parts of the body controlled by the errant cells may perform erratically.
    • When these uncontrolled, abnormal discharges occur repeatedly, a person is said to have an epileptic syndrome.
    • People with epilepsy without other brain or nervous system disabilities fall within the same intelligence ranges as the overall population.
  • 31. MEDICAL MANAGEMENT:
    • CARBAMAZEPINE (TEGRETOL )
    • > drug of choice for treatment of partial seizures
    • > also been used for treatment of tonic-clonic seizures and trigeminal neuralgia.
    • GABAPENTIN (NEURONTIN)
    • >used as adjunctive therapy in treatment of focal seizures.
    • LAMOTRIGINE(LAMICTAL)
    • >for focal seizures.
    • > toxic effects is Steven-Johnson syndrome.
    • TIAGABINE (GABITRIL)
    • > which is relatively a new drug that is used as adjunctive therapy of partial seizure.
    •  
  • 32. INTERVENTIONS:
    • maintain patent AIRWAY
    • administer oxygen
    • prepare to suction
    • turn the clients head to side.
    • Prevent injury during the seizure
    • remain with the client
    • loosen restrictive clothing
    • monitor for incontinence
    • document the character of the seizure
    • instruct the client to avoid alcohol, excessive stress and fatigue.
  • 33. HEADACHE
  • 34. DEFINITION:
    • headache or cephalgia; one of the most common of all human physical complaints.
    • Headache is a symptom rather a disease entity.
    • It may indicate organic disease (neurologic or other disease), a stress response, vasodilatation( migraine), skeletal muscle tension, (tension headache) or a combination of factors.
  • 35.
    • I.PRIMARY HEADACHE
    • > one for which no organic cause can be identified. Types of headache include migraine, tension-type, and cluster headache.
    • MIGRAINE > a vascular disturbance that occurs more commonly in woman.
    • > a symptom complex characteristics periods and recurrent attacks of severe headaches.
    • TENSION HEADACHE > more chronic than severe and are probably the most common type of headache.
    • CLUSTER HEADACHE > are severe form of vascular headache.
    • > seen five times more frequently in men than in women.
    • CRANIAL ARTERITIS > cause of headache in the older population, reaching its greatest incidence in those older than 70 years old of age.
  • 36.
    • II. SECONDARY HEADACHE > a symptom associated with an organic cause, such as brain tumor, or an aneurysm.
    • > serious disorders related to headaches include brain tumor, subarrachnoid hemorrhage, stroke, severe hypertension, meningitis or head injury.
    • ASSESSMENT:
    • detailed history
    • physical assessment of head and neck and a complete neurologic examination.
    • May manifest differently within an individual over the course of a lifetime of headache may present differently from patient to patient.
    • Sleep patter and level of stress.
    • Recreational interests and appetite
    • emotional problems
    • family stressors
    • headache's frequency, location and duration
    • type of pain
  • 37.
    • DIAGNOSTIC TESTS:
    • CT scan
    • cerebral angiography
    • MRI
    • Electromyography
    • LABORATORY TESTS:
    • CBC
    • erythrocyte sedimentation rate
    • electrolytes
    • glucose
    • creatinine
    • thyroid hormone levels
  • 38.
    • PHATOPHYSIOLOGY:
    • the cerebral signs and symptoms of migraine may result from dysfunction of the brain stem pathways that normally modulate sensory input.
    • Headache is preceded by risk in plasma serotonin, which dilates the cerebral vessels, but migraines are more than just vascular headaches.
    • Migraines can be triggered by menstrual cycles, bright lights, stress, depression, sleep deprivation, fatigue, overuse of certain glutamate, nitrates or milk products.
    • Emotional or physical stress may cause contraction of the muscles in the neck and scalp, resulting in tension headache.
    • Cranial arteritis is thought to represent an immune vasculitis in which immune complexes are deposited within the walls of the affected blood vessels.
  • 39. CLINICAL MANIFESTATIONS: I.MIGRAINE PRODOME PHASE : depression, irritability, feeling cold, food cravings, anorexia, change in activity level, increase urination, diarrhea, constipation. AURA PHASE : characterize by focal neurologic symptoms, visual disturbances, numbness and tingling of face and lips, hand, mild confusion, slight weakness of extremity, drowsiness, dizziness. HEADACHE PHASE: a vasodilatation and a decline in serotonin level occur, a throbbing headache over several hours. Severe anticipating; associated with photo phobia, nausea and vomiting. RECOVERY PHASE : pain gradually subsides; muscle in the neck and scalp; muscle ache, localized tenderness, exhaustion and mood changes.
  • 40. II.TENSION PHASE: ·steady, constant feeling of pressure that usually begins in forehead, temple or back of the neck.     III. CLUSTER HEADACHE: ·are unilateral and come in clusters of one to 8 daily with excruciating pain localized to eye and orbit radiating to the facial temporal regions. ·Pain accompanied by watering eye and nasal congestion.   IV. CRANIAL ARTERITIS ·fatigue, malaise, weight lose and fever ·inflammation usually are present ·sometimes a tender swollen or nodular temporal artery is visible.  
  • 41. PREVENTION: · avoid specific triggers · medication therapy · avoid alcohols, nitrates, vasodilators, histamines. · Prophylactic medication therapy  
    • NURSING MANAGEMENT:
    • ·  relieving pain
    • · comfort measures such as quiet, dark environment, elevation of head of bed to 30 degrees
    • · treatment of antiemetics
    • · application of local heat or massage
  • 42.
    • MEDICAL MANAGEMENT:
    • DIHYDROERGOTAMINE (MIGRANOL)
    • >which can be used in the IM or IV form, or as a nasal spray.
    • ERGOTAMINE
    • > mainstay of migraine headache.
    • > administered sublingually for rapid absorption.
    • CAFERGOT
    • >very popular oral form, combines ergotamine with caffeine to increase absorption from GI tract.
    • METHYSERGIDE( SANSERT)
    • >which is not used for acute attacks but to prevent attacks or to decrease the intensity and frequency of attacks.
    • TRYPTANS, SEROTONIN RECEPTOR ANTAGONIST
    • >cause vasoconstriction, reduce inflammation and may reduce pain transmission.
    •  
  • 43. Anthony Toledo, MD, RN