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Alterations in Neurologic Function

Alterations in Neurologic Function. Ball & Bindler Donna Hills APN EdD . Pediatric Differences. head is large:neck musc underdeveloped prone to HI with falls unfused sutures < 18mo prone to fracture highly vascular brain;less CSF to cushion brain prone to hemorrhage and trauma

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Alterations in Neurologic Function

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  1. Alterations in Neurologic Function Ball & Bindler Donna Hills APN EdD

  2. Pediatric Differences • head is large:neck musc underdeveloped • prone to HI with falls • unfused sutures < 18mo • prone to fracture • highly vascular brain;less CSF to cushion • brain prone to hemorrhage and trauma • cervical spine immature: incr mobility • higher risk for C1-C2 injury

  3. Pediatric Differences (cont.) • ossification of vertebral bodies incomplete • greater risk for compression fxs of vertebrae with falls • myelination, responsible for smooth motor movements, incomplete at birth • proceeds in cephalocaudal direction • usually complete by 4-5yrs of age.

  4. Level of Consciousness:LOC • most important indicator of neurologic dysfunction • if neurologic insult continues, pt will progress from alert thru stages to coma: • confusion:where am I? • Delirium: fear, anxiety, agitation • obtunded: limited response, falls asleep • stupor: resp to vigorous stim only • coma: even painful stim will not arouse

  5. Increased ICP: intracranial pressure • ICP: the force exerted by brain tissue, csf, and blood within cranial vault • decline in loc follows a sequential pattern of deterioration • initial changes may be subtle • severe: posturing • decordicate: rigid flexion • decerebrate: rigid extension

  6. Clinical Manifestations of Increased ICP (child/adol) • HA, n, v, visual disturbances • pupils sluggish • sunsetting eyes • seizures • slight change in LOC

  7. Clinical Manifestations of Incr ICP (in infant) • above signs plus: • bulging fontanel • wide sutures: incr head circ • dilated scalp veins • high-pitched cry: catlike cry

  8. Late Signs of Incr ICP • significant decrease in LOC • Cushing’s Triad: • incr syst BP • widening pulse pressure • bradycardia (typo in book) • irregular respirations • fixed and dilated pupils • B&B (pg 1302 Table 33-1)

  9. Clinical Therapy • assess for recent trauma, infection, ingestion • has a shunt, tumor or other medical condition that could affect LOC • determine child’s baseline from someone who knows him/her. • Work up: labs, LP, EEG, CT, and/or MRI.

  10. Glascow Coma Scale:GCS • fairly objective tool that attempts to quantify LOC and functioning • part of VS of any child with altered neuro state =NVS • don’t need a doctor’s order to start them • B&B pg 1303 Table 33-2: adaptation to pedi. with developmentally approp response.

  11. Treatment for Child with Altered LOC • goal: optimized cerebral perfusion • O2 to keep sats > 95% • correction of fluid/electrolyte, acid/base or any other metabolic distrubance • antibiotics administered AFTER cultures obtained. • If incr ICP is severe, ventricles may be tapped or a VP shunt may be externalized.

  12. Nursing Care of Child with Altered LOC • What abnormal vital sign findings should be reported to the physician? • What emergency equipment should be kept at the bedside? • If the corneal reflex is absent, what is your most appropriate nursing action? • What is the appropriate interval for vital signs in a pt with altered LOC? • Approp action for pt w/o gag reflex?

  13. Headaches • Four major types of headaches: • Migraine (vascular) • Tension (muscular) • Medication overuse (caffeine,aceto,nsaids) • Inflammatory(sinusitis/dental) • Structural (space occupying lesion) • each type of HA has specific clinical manifestations and treatment • B&B pg 1323

  14. Clinical Management of HA in Children/Adol • good history to determine the clinical manifestations • headache journal can be helpful to clarify characteristics, associations (with food, time, activity, medications), duration, and what helps. • assess for abnormal neurologic signs assoc with a HA • determine strategies to relieve them.

  15. Seizure Disorders • common in children (2-4% of pedi pop) • most common in infancy (1 in 1,000 infants) • incidence decreases with age • Epilepsy: chronic seizure disorder (1:100 people).

  16. Clinical Manifestations of Sz. • types of seizures B&B pg 1306-7 • focal seizures are isolated and manifestation related to the cortical area affected • unilateral and specific • generalized seizures results from diffuse electrical activity: tonic/clonic • assoc with paleness, cyanosis, hypoxia, hypoglycemia, incr metabolic demands • bilateral and symmetric

  17. Clinical Manifestations of Sz (cont.) • postictal period: phase following a sz characterized by decreased LOC. • difficult to arouse • length in children is variable • spontaneous breathing is intact. • visual or olfactory auras may precede the sz. • febrile sz: sudden rise in temp; may be familial; no other cause.

  18. Clinical Therapy • history: determine desc and length of sz, if child lost consciousness and if it was preceded by an aura (see Box 33-4 p. 1308) • PE, neuro exam, labs, diagnostic tests are ordered. • if taking anticonvulsant(s), levels should be ordered • maintain airway, ensure safety, admin meds and provide emotional support.

  19. FIGURE 33–6 A child who has a seizure when standing should be gently assisted to the floor and placed in a side-lying position. Clear the area of any objects that might cause harm to the child.

  20. Status Epilepticus • a continuous sz lasting more than 30 min or a series of sz between which consciousness is not regained. • monitor for electrolytes, glucose, blood gases, temp, VS incl BP, O2 sat and cap refill to assess perfusion. • often give Diastat rectally (Diazepam) • be prepared to assist if airway is lost • RN’s resp to provide approp equipment

  21. Anticonvulsants • list of meds B&B( p 1310) • know generic and brand names of emergency and first line meds if not already familiar. • should witness all anticonvulsants taken by the patient • regular dental care is impt d/t the effect of some anti-sz meds on the gingiva.

  22. Anticonvulsants • Diazepam • Phenobarbital • Phenytoin • Carbamazepine • Valproic Acid • Clonazepam

  23. Ketogenic Diet • used for children with myoclonic and absence seizures • high fat/ low (no) carbohydrate, low protein • stay on diet 2-3yrs to try to decrease or irradicate sz • child and family motivation must be high

  24. Nursing considerations of caring for a child on a ketogenic diet • the child’s metabolism is forced into ketosis by dietary management • urine checked Q void; UA Q day; finger sticks Q 6hr; lytes and CO2 Q day. • ketones are measured in both the urine and the blood • all products and meds need to be evaluated for their CHO content • assess for sx of hypoglyc + acidosis

  25. Ketogenic DietFIGURE 33–5 The family must make an effort to make the high-fat diet appealing to the child on a ketogenic diet, despite their personal feelings about eating large amounts of food such as mayonnaise, as this child is doing

  26. Nursing care of the child having a seizure • make note of the time sz started, the type of movements, whether they changed/progressed, LOC • prevent harm; don’t hold down. Position of comfort (as long as airway is open) • jaw thrust if needed; O2 blow by if sat <95 • call for help/physician; check ID band for allergies

  27. ABOVE ALL • remain calm and reassure family.

  28. Care of the child with a Sx disorder at home • (good practical common sense for any child) • children are at increased risk for death due to drowning • don’t leave in the bathtub alone; use the shower • lifesaver when swimming • life vest when boating • avoid fall risks

  29. Infectious Diseases • Bacterial Meningitis • Viral (aseptic) Meningitis • Encephalitis • Reye Syndrome • Guillain-Barre Syndrome

  30. Bacterial Meningitis • bacterial etiology high M&M • infants at greatest risk; 70% of children with Bacterial Meningitis are <5yr • may occur secondary to: OM, sinusitis, pharyngitis • may occur after head trauma or neurosurg intervention • 3 common organisms: HIB, PCV, Neisseria Meningitidis

  31. Effects of Immunizations • rates of HIB meningitis and pneumococcal have declined with increased use of the HIB and PCV vaccines. • Neisseria Meningitidis may show a rise in incidence. • Meningococcal Meningitis has incr incidence in the college age population.

  32. Effects of Immuniz (cont) • Meningococcal vaccine recommended for those living in dorms or highly populated living • Some schools now require it. • Teaching point: • It only prevents meningitis from meningococcal infection

  33. Clinical Manifestations:BM • onset usually abrupt but may also be insidious over about a week. • infant: fever, change in feeding, v/d, ant fontanel flat or bulging, alert, restless, lethargic or irritable. • However, if irritable, the child can not be consoled by their caregiver: what usually works no longer works to calm the infant.

  34. Clinical Manifestations: BM • older child: fever, irritable, lethargic, confused, combative or change in personality. • c/o muscle or joint pain, back/neck pain, HA, photophobia, esotropia, nuchal rigidity. • rash: petechae, purpura, necrotic patches (assoc with meningococcal meningitis) • positive Kernig and/or Brudzinski sx

  35. Kernig Sign To test forKernig sign, raise the child’s leg with the knee flexed. Then extend the child’s leg at the knee. If any resistance is noted or pain is felt, the result is a positive Kernig sign. This is a common finding inmeningitis.

  36. Brudzinski Sign • To test Brudzinski sign, flex the child’s head while in a supine position. If this action makes the knees or hips flex involuntarily, a positive Brudzinski sign is present. This is a common sign in meningitis.

  37. Opisthotonis: • hyperextension of the head and neck

  38. Clinical Therapy:BM • Hx, PE, labs (CBC with diff, Bld cult, lytes and osmolality, clotting factors. • LP to evaluate opening pressure, WBC’s, protein and glucose levels in CSF. • Gram stain and culture on the CSF, bld cx. • A/B admin as soon as all culture specimens are obtained.

  39. Common antibiotics used • Ampicillin • Aminoglycosides • Gentamicin • Ceftriaxone • Cefotaxime.

  40. Sequelae of Bacterial Meningitis • neurologic damage • cranial nerves at risk, esp VIII (Aucoustic or Vestibulocochlear) results in hearing loss • seizures, hydrocephalus in the infant. • DD: cognitive soft signs; LD • SIADH:hypersecretion of ADH • meningococcal septicemia with DIC,organ failure.

  41. Nursing Care of Pt with BM • see NCP in B&B (1317-19).

  42. Viral (aseptic) Meningitis • inflammatory process • increased number of WBC and protein in CSF • culture will not grow any bacterial • gram stain will be negative • does not appear as ill • are treated aggressively until 48hr cultures are negative

  43. Encephalitis • inflammation of the brain • usually caused by viruses • Herpes Simplex Type I most common cause in newborn period: assoc with high M&M • high fever, irritability, vomiting, disoriented, confused • sx of meningeal irritation uncommon: nucchal rigidity, photophobia, Kernigs and Brudzinski

  44. Reye Syndrome • acute encephalopathy: cerebral dysfunction caused by a toxin, injury, inflammatory or anoxic insult • may result in permanent damage;dysfunction may improve over time • associated with hepatic dysfunction • mortality high

  45. Clinical Manifestations of Reye Syndrome • n/v, mental status changes, seizures and progressive unresponsiveness. • 5 stages that outline progressive neurologic deterioration: hyperreflexivity, followed by decorticate rigidity then posturing, decerebrate rigidity, then posturing, coma with flaccidity and eventual arrest.

  46. Decerebrate Posturing Decerebrate posturing, distinguished by rigid extension, is associated with lesions of the brainstem. FIGURE 33–3A (continued)

  47. Decorticate Posturing Decorticate Posturing FIGURE 33–3ADecorticate posturing, characterized by rigid flexion, is associated with lesions above the brainstem in the corticospinal tracts.

  48. Etiology of Reye Syndrome • Unclear • assoc with viral illness and use of ASA. • now rare with acetominophen and nsaids. • Because of assoc of Reye with use of ASA post viral syndrome, counsel parents preventively.

  49. Guillain-Barre Syndrome • Postinfectious Polyneuritis • acute inflammatory demyelinating polyneuropathy • deteriorating motor function and paralysis in ascending pattern • immune response to an infectious organism: GI or resp 2-3 wks prior • respiratory diffic may require ventilation • rarely fatal but rapidly debilitating

  50. Clinical Management of GBS • LP: incr protein levels • EMG: abnormal nerve conduction • hx and PE consistent with progressive motor weakness; weak or areflexia LE>UE. • Rx: IgG or plasmaphoresis if unable to ambulate. • Autonomic nerv sx dysf linked to fatal arrhythmias; nurs assessement crucial

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