Alterations in Neurologic Alterations in Neurologic FunctionFunction

Ball & BindlerBall & Bindler

Donna Hills APN EdD Donna Hills APN EdD

Pediatric DifferencesPediatric Differenceshead is large:neck musc underdevelopedhead is large:neck musc underdeveloped– prone to HI with fallsprone to HI with falls

unfused sutures < 18mounfused sutures < 18mo– prone to fractureprone to fracture

highly vascular brain;less CSF to cushionhighly vascular brain;less CSF to cushion– brain prone to hemorrhage and traumabrain prone to hemorrhage and trauma

cervical spine immature: incr mobilitycervical spine immature: incr mobility– higher risk for C1-C2 injuryhigher risk for C1-C2 injury

Pediatric Differences (cont.)Pediatric Differences (cont.)

ossification of vertebral bodies ossification of vertebral bodies incompleteincomplete– greater risk for compression fxs of greater risk for compression fxs of

vertebrae with fallsvertebrae with falls

myelination, responsible for smooth myelination, responsible for smooth motor movements, incomplete at motor movements, incomplete at birthbirth– proceeds in cephalocaudal directionproceeds in cephalocaudal direction– usually complete by 4-5yrs of age.usually complete by 4-5yrs of age.

Level of Consciousness:LOCLevel of Consciousness:LOC

most important indicator of neurologic most important indicator of neurologic dysfunctiondysfunction

if neurologic insult continues, pt will if neurologic insult continues, pt will progress from alert thru stages to coma:progress from alert thru stages to coma:– confusion:where am I?confusion:where am I?– Delirium: fear, anxiety, agitationDelirium: fear, anxiety, agitation– obtunded: limited response, falls asleepobtunded: limited response, falls asleep– stupor: resp to vigorous stim onlystupor: resp to vigorous stim only– coma: even painful stim will not arousecoma: even painful stim will not arouse

Increased ICP: intracranial Increased ICP: intracranial pressurepressure

ICP: the force exerted by brain tissue, ICP: the force exerted by brain tissue, csf, and blood within cranial vaultcsf, and blood within cranial vault

decline in loc follows a sequential decline in loc follows a sequential pattern of deteriorationpattern of deterioration

initial changes may be subtleinitial changes may be subtle

severe: posturingsevere: posturing– decordicate: rigid flexiondecordicate: rigid flexion– decerebrate: rigid extensiondecerebrate: rigid extension

Clinical Manifestations of Clinical Manifestations of Increased ICP (child/adol)Increased ICP (child/adol)

HA, n, v, visual disturbancesHA, n, v, visual disturbances

pupils sluggishpupils sluggish

sunsetting eyessunsetting eyes

seizuresseizures

slight change in LOCslight change in LOC

Clinical Manifestations of Incr Clinical Manifestations of Incr ICP (in infant)ICP (in infant)

above signs plus:above signs plus:

bulging fontanelbulging fontanel

wide sutures: incr head circwide sutures: incr head circ

dilated scalp veinsdilated scalp veins

high-pitched cry: catlike cryhigh-pitched cry: catlike cry

Late Signs of Incr ICPLate Signs of Incr ICP

significant decrease in LOCsignificant decrease in LOC

Cushing’s Triad:Cushing’s Triad:– incr syst BPincr syst BP– widening pulse pressurewidening pulse pressure– bradycardia (typo in book)bradycardia (typo in book)– irregular respirationsirregular respirations

fixed and dilated pupilsfixed and dilated pupils

B&B (pg 1302 Table 33-1)B&B (pg 1302 Table 33-1)

Clinical TherapyClinical Therapy

assess for recent trauma, infection, assess for recent trauma, infection, ingestioningestion

has a shunt, tumor or other medical has a shunt, tumor or other medical condition that could affect LOCcondition that could affect LOC

determine child’s baseline from determine child’s baseline from someone who knows him/her.someone who knows him/her.

Work up: labs, LP, EEG, CT, and/or Work up: labs, LP, EEG, CT, and/or MRI.MRI.

Glascow Coma Scale:GCSGlascow Coma Scale:GCS

fairly objective tool that attempts to fairly objective tool that attempts to quantify LOC and functioningquantify LOC and functioning

part of VS of any child with altered part of VS of any child with altered neuro state =NVSneuro state =NVS

don’t need a doctor’s order to start don’t need a doctor’s order to start themthem

B&B pg 1303 Table 33-2: adaptation B&B pg 1303 Table 33-2: adaptation to pedi. with developmentally approp to pedi. with developmentally approp response.response.

Treatment for Child with Altered Treatment for Child with Altered LOCLOC

goal: optimized cerebral perfusiongoal: optimized cerebral perfusion

O2 to keep sats > 95%O2 to keep sats > 95%

correction of fluid/electrolyte, acid/base correction of fluid/electrolyte, acid/base or any other metabolic distrubanceor any other metabolic distrubance

antibiotics administered AFTER cultures antibiotics administered AFTER cultures obtained.obtained.

If incr ICP is severe, ventricles may be If incr ICP is severe, ventricles may be tapped or a VP shunt may be tapped or a VP shunt may be externalized.externalized.

Nursing Care of Child with Nursing Care of Child with Altered LOCAltered LOC

What abnormal vital sign findings should What abnormal vital sign findings should be reported to the physician?be reported to the physician?

What emergency equipment should be What emergency equipment should be kept at the bedside?kept at the bedside?

If the corneal reflex is absent, what is If the corneal reflex is absent, what is your most appropriate nursing action?your most appropriate nursing action?

What is the appropriate interval for vital What is the appropriate interval for vital signs in a pt with altered LOC?signs in a pt with altered LOC?

Approp action for pt w/o gag reflex? Approp action for pt w/o gag reflex?

HeadachesHeadachesFour major types of headaches:Four major types of headaches:– Migraine (vascular)Migraine (vascular)– Tension (muscular)Tension (muscular)– Medication overuse (caffeine,aceto,nsaids)Medication overuse (caffeine,aceto,nsaids)– Inflammatory(sinusitis/dental)Inflammatory(sinusitis/dental)– Structural (space occupying lesion)Structural (space occupying lesion)

each type of HA has specific clinical each type of HA has specific clinical manifestations and treatmentmanifestations and treatment

B&B pg 1323 B&B pg 1323

Clinical Management of HA in Clinical Management of HA in Children/AdolChildren/Adol

good history to determine the clinical good history to determine the clinical manifestationsmanifestations

headache journal can be helpful to headache journal can be helpful to clarify characteristics, associations clarify characteristics, associations (with food, time, activity, medications), (with food, time, activity, medications), duration, and what helps.duration, and what helps.

assess for abnormal neurologic signs assess for abnormal neurologic signs assoc with a HAassoc with a HA

determine strategies to relieve them.determine strategies to relieve them.

Seizure DisordersSeizure Disorders

common in children (2-4% of pedi common in children (2-4% of pedi pop)pop)

most common in infancy (1 in 1,000 most common in infancy (1 in 1,000 infantsinfants))

incidence decreases with ageincidence decreases with age

Epilepsy: chronic seizure disorder Epilepsy: chronic seizure disorder (1:100 (1:100 peoplepeople).).

Clinical Manifestations of Sz.Clinical Manifestations of Sz.types of seizures B&B pg 1306-7types of seizures B&B pg 1306-7

focal seizures are isolated and focal seizures are isolated and manifestation related to the cortical area manifestation related to the cortical area affectedaffected– unilateral and specificunilateral and specific

generalized seizures results from diffuse generalized seizures results from diffuse electrical activity: tonic/clonicelectrical activity: tonic/clonic– assoc with paleness, cyanosis, hypoxia, assoc with paleness, cyanosis, hypoxia,

hypoglycemia, incr metabolic demandshypoglycemia, incr metabolic demands– bilateral and symmetricbilateral and symmetric

Clinical Manifestations of Sz Clinical Manifestations of Sz (cont.)(cont.)

postictal period: phase following a sz postictal period: phase following a sz characterized by decreased LOC.characterized by decreased LOC.– difficult to arousedifficult to arouse– length in children is variablelength in children is variable– spontaneous breathing is intact.spontaneous breathing is intact.

visual or olfactory auras may precede visual or olfactory auras may precede the sz.the sz.

febrile sz: sudden rise in temp; may febrile sz: sudden rise in temp; may be familial; no other cause.be familial; no other cause.

Clinical TherapyClinical Therapyhistory: determine desc and length of sz, history: determine desc and length of sz, if child lost consciousness and if it was if child lost consciousness and if it was preceded by an aura (see Box 33-4 p. preceded by an aura (see Box 33-4 p. 1308)1308)

PE, neuro exam, labs, diagnostic tests are PE, neuro exam, labs, diagnostic tests are ordered.ordered.

if taking anticonvulsant(s), levels should if taking anticonvulsant(s), levels should be orderedbe ordered

maintain airway, ensure safety, admin maintain airway, ensure safety, admin meds and provide emotional support.meds and provide emotional support.

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

Status EpilepticusStatus Epilepticus

a continuous sz lasting more than 30 a continuous sz lasting more than 30 min or a series of sz between which min or a series of sz between which consciousness is not regained.consciousness is not regained.

monitor for electrolytes, glucose, blood monitor for electrolytes, glucose, blood gases, temp, VS incl BP, O2 sat and cap gases, temp, VS incl BP, O2 sat and cap refill to assess perfusion.refill to assess perfusion.

often give Diastat rectally (Diazepam)often give Diastat rectally (Diazepam)

be prepared to assist if airway is lostbe prepared to assist if airway is lost– RN’s resp to provide approp equipmentRN’s resp to provide approp equipment

AnticonvulsantsAnticonvulsants

list of meds B&B( p 1310)list of meds B&B( p 1310)

know generic and brand names of know generic and brand names of emergency and first line meds if not emergency and first line meds if not already familiar.already familiar.

should witness all anticonvulsants should witness all anticonvulsants taken by the patienttaken by the patient

regular dental care is impt d/t the regular dental care is impt d/t the effect of some anti-sz meds on the effect of some anti-sz meds on the gingiva.gingiva.

AnticonvulsantsAnticonvulsants

DiazepamDiazepam

PhenobarbitalPhenobarbital

PhenytoinPhenytoin

CarbamazepineCarbamazepine

Valproic AcidValproic Acid

ClonazepamClonazepam

Ketogenic DietKetogenic Diet

used for children with myoclonic and used for children with myoclonic and absence seizuresabsence seizures

high fat/ low (no) carbohydrate, low high fat/ low (no) carbohydrate, low proteinprotein

stay on diet 2-3yrs to try to decrease stay on diet 2-3yrs to try to decrease or irradicate szor irradicate sz

child and family motivation must be child and family motivation must be highhigh

Nursing considerations of caring Nursing considerations of caring for a child on a ketogenic dietfor a child on a ketogenic diet

the child’s metabolism is forced into the child’s metabolism is forced into ketosis by dietary managementketosis by dietary management– urine checked Q void; UA Q day; finger urine checked Q void; UA Q day; finger

sticks Q 6hr; lytes and CO2 Q day.sticks Q 6hr; lytes and CO2 Q day.

ketones are measured in both the ketones are measured in both the urine and the bloodurine and the blood

all products and meds need to be all products and meds need to be evaluated for their CHO contentevaluated for their CHO content

assess for sx of hypoglyc + acidosisassess for sx of hypoglyc + acidosis

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

Nursing care of the child having Nursing care of the child having a seizurea seizure

make note of the time sz started, the make note of the time sz started, the type of movements, whether they type of movements, whether they changed/progressed, LOCchanged/progressed, LOC

prevent harm; don’t hold down. Position prevent harm; don’t hold down. Position of comfort (as long as airway is open)of comfort (as long as airway is open)

jaw thrust if needed; O2 blow by if sat jaw thrust if needed; O2 blow by if sat <95<95

call for help/physician; check ID band for call for help/physician; check ID band for allergiesallergies

ABOVE ALLABOVE ALL

remain calm and remain calm and reassure family.reassure family.

Care of the child with a Sx Care of the child with a Sx disorder at homedisorder at home

(good practical common sense for any (good practical common sense for any child)child)

children are at increased risk for death children are at increased risk for death due to drowningdue to drowning

don’t leave in the bathtub alone; use don’t leave in the bathtub alone; use the showerthe shower

lifesaver when swimminglifesaver when swimming

life vest when boatinglife vest when boating

avoid fall risksavoid fall risks

Infectious DiseasesInfectious Diseases

Bacterial MeningitisBacterial Meningitis

Viral (aseptic) MeningitisViral (aseptic) Meningitis

EncephalitisEncephalitis

Reye SyndromeReye Syndrome

Guillain-Barre SyndromeGuillain-Barre Syndrome

Bacterial MeningitisBacterial Meningitis

bacterial etiology high M&Mbacterial etiology high M&M

infants at greatest risk; 70% of children infants at greatest risk; 70% of children with Bacterial Meningitis are <5yrwith Bacterial Meningitis are <5yr

may occur secondary to: OM, sinusitis, may occur secondary to: OM, sinusitis, pharyngitis pharyngitis

may occur after head trauma or may occur after head trauma or neurosurg interventionneurosurg intervention

3 common organisms: HIB, PCV, 3 common organisms: HIB, PCV, Neisseria MeningitidisNeisseria Meningitidis

Effects of ImmunizationsEffects of Immunizations

rates of HIB meningitis and rates of HIB meningitis and pneumococcal have declined with pneumococcal have declined with increased use of the HIB and PCV increased use of the HIB and PCV vaccines.vaccines.

Neisseria Meningitidis may show a Neisseria Meningitidis may show a rise in incidence.rise in incidence.

Meningococcal Meningitis has incr Meningococcal Meningitis has incr incidence in the college age incidence in the college age population.population.

Effects of Immuniz (cont)Effects of Immuniz (cont)

Meningococcal vaccine Meningococcal vaccine recommended for those living in recommended for those living in dorms or highly populated livingdorms or highly populated living

Some schools now require it.Some schools now require it.

Teaching point:Teaching point:– It only prevents meningitis from It only prevents meningitis from

meningococcal infectionmeningococcal infection

Clinical Manifestations:BMClinical Manifestations:BM

onset usually abrupt but may also be onset usually abrupt but may also be insidious over about a week.insidious over about a week.

infant: fever, change in feeding, v/d, infant: fever, change in feeding, v/d, ant fontanel flat or bulging, alert, ant fontanel flat or bulging, alert, restless, lethargic or irritable. restless, lethargic or irritable.

However, if irritable, the child can However, if irritable, the child can not be consoled by their caregiver: not be consoled by their caregiver: what usually works no longer works what usually works no longer works to calm the infant.to calm the infant.

Clinical Manifestations: BMClinical Manifestations: BMolder child: fever, irritable, lethargic, older child: fever, irritable, lethargic, confused, combative or change in confused, combative or change in personality.personality.

c/o muscle or joint pain, back/neck pain, c/o muscle or joint pain, back/neck pain, HA, photophobia, esotropia, nuchal HA, photophobia, esotropia, nuchal rigidity.rigidity.

rash: petechae, purpura, necrotic patches rash: petechae, purpura, necrotic patches (assoc with meningococcal meningitis)(assoc with meningococcal meningitis)

positive Kernig and/or Brudzinski sxpositive Kernig and/or Brudzinski sx

Kernig SignKernig 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.

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

Opisthotonis:Opisthotonis:hyperextension of the head and neckhyperextension of the head and neck

Clinical Therapy:BMClinical Therapy:BM

Hx, PE, labs (CBC with diff, Bld cult, Hx, PE, labs (CBC with diff, Bld cult, lytes and osmolality, clotting factors.lytes and osmolality, clotting factors.

LP to evaluate opening pressure, LP to evaluate opening pressure, WBC’s, protein and glucose levels in WBC’s, protein and glucose levels in CSF.CSF.

Gram stain and culture on the CSF, bld Gram stain and culture on the CSF, bld cx.cx.

A/B admin as soon as all culture A/B admin as soon as all culture specimens are obtained.specimens are obtained.

Common antibiotics usedCommon antibiotics used

AmpicillinAmpicillin

AminoglycosidesAminoglycosides– GentamicinGentamicin

CeftriaxoneCeftriaxone

Cefotaxime.Cefotaxime.

Sequelae of Bacterial MeningitisSequelae of Bacterial Meningitis

neurologic damageneurologic damage

cranial nerves at risk, esp VIII (Aucoustic cranial nerves at risk, esp VIII (Aucoustic or Vestibulocochlear) results in hearing or Vestibulocochlear) results in hearing lossloss

seizures, hydrocephalus in the infant.seizures, hydrocephalus in the infant.

DD: cognitive soft signs; LDDD: cognitive soft signs; LD

SIADH:hypersecretion of ADHSIADH:hypersecretion of ADH

meningococcal septicemia with meningococcal septicemia with DIC,organ failure.DIC,organ failure.

Nursing Care of Pt with BMNursing Care of Pt with BM

see NCP in B&B (1317-19).see NCP in B&B (1317-19).

Viral (aseptic) MeningitisViral (aseptic) Meningitis

inflammatory processinflammatory process

increased number of WBC and increased number of WBC and protein in CSFprotein in CSF

culture will not grow any bacterialculture will not grow any bacterial

gram stain will be negativegram stain will be negative

does not appear as illdoes not appear as ill

are treated aggressively until 48hr are treated aggressively until 48hr cultures are negativecultures are negative

EncephalitisEncephalitisinflammation of the braininflammation of the brain

usually caused by virusesusually caused by viruses

Herpes Simplex Type I most common cause Herpes Simplex Type I most common cause in newborn period: assoc with high M&Min newborn period: assoc with high M&M

high fever, irritability, vomiting, high fever, irritability, vomiting, disoriented, confuseddisoriented, confused

sx of meningeal irritation uncommon: sx of meningeal irritation uncommon: nucchal rigidity, photophobia, Kernigs and nucchal rigidity, photophobia, Kernigs and BrudzinskiBrudzinski

Reye SyndromeReye Syndrome

acute encephalopathy: cerebral acute encephalopathy: cerebral dysfunction caused by a toxin, injury, dysfunction caused by a toxin, injury, inflammatory or anoxic insultinflammatory or anoxic insult

may result in permanent may result in permanent damage;dysfunction may improve damage;dysfunction may improve over timeover time

associated with hepatic dysfunctionassociated with hepatic dysfunction

mortality highmortality high

Clinical Manifestations of Reye Clinical Manifestations of Reye SyndromeSyndrome

n/v, mental status changes, seizures n/v, mental status changes, seizures and progressive unresponsiveness.and progressive unresponsiveness.

5 stages that outline progressive 5 stages that outline progressive neurologic deterioration: neurologic deterioration: hyperreflexivity, followed by hyperreflexivity, followed by decorticate rigidity then posturing, decorticate rigidity then posturing, decerebrate rigidity, then posturing, decerebrate rigidity, then posturing, coma with flaccidity and eventual coma with flaccidity and eventual arrest.arrest.

Decerebrate PosturingDecerebrate Posturing

Decerebrate posturing, distinguished by rigid extension, is associated with lesions of the brainstem.

FIGURE 33–3A (continued)FIGURE 33–3A (continued)

Decorticate PosturingDecorticate PosturingDecorticate PosturingDecorticate Posturing

FIGURE 33–3A Decorticate posturing, characterized by rigid flexion, is associated with lesions

above the brainstem in the corticospinal tracts.

Etiology of Reye SyndromeEtiology of Reye SyndromeUnclearUnclear assoc with viral illness and use of assoc with viral illness and use of ASA.ASA.now rare with acetominophen and now rare with acetominophen and nsaids.nsaids.

Because of assoc of Reye with use of Because of assoc of Reye with use of ASA post viral syndrome, counsel ASA post viral syndrome, counsel parents preventively.parents preventively.

Guillain-Barre SyndromeGuillain-Barre SyndromePostinfectious PolyneuritisPostinfectious Polyneuritis

acute inflammatory demyelinating acute inflammatory demyelinating polyneuropathypolyneuropathy

deteriorating motor function and deteriorating motor function and paralysis in paralysis in ascendingascending pattern pattern

immune response to an infectious immune response to an infectious organism: GI or resp 2-3 wks priororganism: GI or resp 2-3 wks prior

respiratory diffic may require ventilationrespiratory diffic may require ventilation

rarely fatal but rapidly debilitatingrarely fatal but rapidly debilitating

Clinical Management of GBSClinical Management of GBS

LP: incr protein levels LP: incr protein levels

EMG: abnormal nerve conductionEMG: abnormal nerve conduction

hx and PE consistent with progressive hx and PE consistent with progressive motor weakness; weak or areflexia motor weakness; weak or areflexia LE>UE.LE>UE.

Rx: IgG or plasmaphoresis if unable to Rx: IgG or plasmaphoresis if unable to ambulate.ambulate.

Autonomic nerv sx dysf linked to fatal Autonomic nerv sx dysf linked to fatal arrhythmias; nurs assessement crucial arrhythmias; nurs assessement crucial

Structural DefectsStructural Defects

HydrocephalusHydrocephalus

Spina BifidaSpina Bifida

CraniosynostosisCraniosynostosis

HydrocephalusHydrocephalus FIGURE 33–10FIGURE 33–10 AA, Normal size of ventricle. , Normal size of ventricle. BB, Enlarged ventricles, characteristic of hydrocephalus, Enlarged ventricles, characteristic of hydrocephalus

HydrocephalusHydrocephalus

imbalance of production and imbalance of production and absorption of CSFabsorption of CSF

communicating communicating – blockage of flow or absorption of CSF in blockage of flow or absorption of CSF in

subarachnoid space or villisubarachnoid space or villi– acquired from postinfectious meningitis acquired from postinfectious meningitis

or IVHor IVH– congenital: sm amt cases d/t x-linkedcongenital: sm amt cases d/t x-linked– or unknown etiologyor unknown etiology

Hydrocephalus (cont.)Hydrocephalus (cont.)

non-communicatingnon-communicating– responsible for majority of cases;usually a responsible for majority of cases;usually a

developmental defectsdevelopmental defects– blockage in ventricles preventing flow blockage in ventricles preventing flow

CSFCSF– caused by infection (toxoplasmosis, or caused by infection (toxoplasmosis, or

CMV) hemorrhage, tumor or structural CMV) hemorrhage, tumor or structural deformitydeformity

– often associated with myelomeningocele often associated with myelomeningocele (spina bifida)(spina bifida)

Clinical Manifestations of Clinical Manifestations of Hydrocephalus:infantsHydrocephalus:infants

first sign in infancy is bulging fontanels, first sign in infancy is bulging fontanels, then head enlargement, sutures become then head enlargement, sutures become palpably separated to produce the “crack-palpably separated to produce the “crack-pot sound” (Macewen Sx) when pot sound” (Macewen Sx) when percussed.percussed.

Frontal protrusion or bossingFrontal protrusion or bossing

eyes depressed downward: setting sun eyes depressed downward: setting sun sign (sclera visible above pupil).sign (sclera visible above pupil).

Pupils may be sluggish with unequal Pupils may be sluggish with unequal response to light.response to light.

Clinical Manifestations of Clinical Manifestations of Hydrocephalus: older childrenHydrocephalus: older childrensx of presentation are different than sx of presentation are different than infants after closure of the cranial suturesinfants after closure of the cranial sutures

children present with sx of incr ICP and sx children present with sx of incr ICP and sx related to the focal lesions.related to the focal lesions.

space occupying lesions: HA(upon space occupying lesions: HA(upon wakening with improvement following wakening with improvement following emesis or upright position). Papilledema, emesis or upright position). Papilledema, strabismus and extrapyramidal tract sx strabismus and extrapyramidal tract sx (ataxia). Irrtitable, lethargic, confused.(ataxia). Irrtitable, lethargic, confused.

Arnold-Chiari MalformationsArnold-Chiari Malformations

Type II seen exclusively with Type II seen exclusively with meningomyelocelemeningomyelocele

herniation of a small cerebellum, herniation of a small cerebellum, medulla, pons and fourth ventricle medulla, pons and fourth ventricle into the spinal canal through an into the spinal canal through an enlarged foramen magnum. enlarged foramen magnum.

The resulting obstruction of CSF flow The resulting obstruction of CSF flow causes hydrocephaluscauses hydrocephalus

Ventriculoperitoneal(VP) ShuntVentriculoperitoneal(VP) Shunt

a pathway to divert excess fluid from a pathway to divert excess fluid from ventricles to peritoneumventricles to peritoneum

replaced as child growsreplaced as child grows

can become blocked, kinked or infectedcan become blocked, kinked or infected

shunt malfunction causes recurrent sx shunt malfunction causes recurrent sx of hydrocephalus, and incr ICPof hydrocephalus, and incr ICP

infection is most serious complicationinfection is most serious complication

if severe, may need to externalized.if severe, may need to externalized.

FIGURE 33–12FIGURE 33–12 The tubing drains the excess cerebrospinal fluid from the ventricles to the The tubing drains the excess cerebrospinal fluid from the ventricles to the abdomen. The main goal of treatment is to reduce the intracranial pressure and to preserve central abdomen. The main goal of treatment is to reduce the intracranial pressure and to preserve central

nervous system function.nervous system function.

Spina Bifida: MeningomyeloceleSpina Bifida: Meningomyelocelecongenital neural tube defect anywhere congenital neural tube defect anywhere along the spinealong the spine

cause unknown but environmental and cause unknown but environmental and genetic factors suspectedgenetic factors suspected– maternal valproic acid use, insulin maternal valproic acid use, insulin

dependency, folic acid deficiencydependency, folic acid deficiency

higher the defect, the greater the higher the defect, the greater the neurologic dysfunctionneurologic dysfunction

LE paralysis, ortho prob, bowel and renal.LE paralysis, ortho prob, bowel and renal.

Clinical Management of Spina Clinical Management of Spina BifidaBifida

early surgical closure (24-48 hrs)early surgical closure (24-48 hrs)

cover sac with sterile saline gauzecover sac with sterile saline gauze

place child prone, hips flexed and place child prone, hips flexed and knees abductedknees abducted

observe latex sensitivity precautionsobserve latex sensitivity precautions

observe for sx incr ICP, before and observe for sx incr ICP, before and after correction.after correction.

MeningomyeloceleMeningomyelocele

External viewExternal view

CraniosynostosisCraniosynostosis

premature closure of the cranial premature closure of the cranial suturessutures

can cause deformity of the skullcan cause deformity of the skull

can palpate over riding of the suturescan palpate over riding of the sutures

reconstructive surgery before age reconstructive surgery before age 1yr has a better outcome1yr has a better outcome

PlagiocephalyPlagiocephaly

flat occiput in healthy newbornflat occiput in healthy newborn

due to placing child supine to sleep due to placing child supine to sleep to avoid risk of SIDSto avoid risk of SIDS

helmet device can be worn to remold helmet device can be worn to remold the skullthe skull– 4 hrs /day brings results in 4 months4 hrs /day brings results in 4 months

Cerebral PalsyCerebral Palsynon-progressive motor and posture non-progressive motor and posture dysfunctiondysfunction

secondary to CNS insults: congenital, secondary to CNS insults: congenital, hypoxic, ischemic or traumatic originhypoxic, ischemic or traumatic origin

prenatal, perinatal or postnatal (up to 2 prenatal, perinatal or postnatal (up to 2 yrs)yrs)

most common chronic disorder is childhoodmost common chronic disorder is childhood

four types of motor dysfunction: spastic, four types of motor dysfunction: spastic, dyskinetic, ataxic and mixeddyskinetic, ataxic and mixed

Clinical Manifestations of CPClinical Manifestations of CPspastic type: persistent hypertonia, spastic type: persistent hypertonia, neonatal reflexes, rigidity, incr DTR’s, neonatal reflexes, rigidity, incr DTR’s, contractures, abnormal curve of the contractures, abnormal curve of the spinespine

dyskinetic: impairment of voluntary dyskinetic: impairment of voluntary muscle control, twisting movements, muscle control, twisting movements, tremors, diffic with fine and purposeful tremors, diffic with fine and purposeful movements, exaggerated posturing, movements, exaggerated posturing, inconsistent muscle tone.inconsistent muscle tone.

ataxic:abnl bal and gait, hypotonia.ataxic:abnl bal and gait, hypotonia.

Clinical Manifestations(cont.)Clinical Manifestations(cont.)

wide variety of symptoms wide variety of symptoms

frequently have other problems: DD, frequently have other problems: DD, strabismus, nystagmus, refractory strabismus, nystagmus, refractory errors, hearing loss, language delay, errors, hearing loss, language delay, speech impediments, seizures, speech impediments, seizures, and/or mental retardation. and/or mental retardation.

May have altered nutrition d/t diffic May have altered nutrition d/t diffic chewing and swallowing; risk for chewing and swallowing; risk for aspir.aspir.

Clinical TherapyClinical Therapyany child with DD and poor suck should any child with DD and poor suck should be referred for eval.be referred for eval.

Focus is on child reaching his/her Focus is on child reaching his/her maximum potentialmaximum potential

referrals to PT,OT, speech, special ed, EI, referrals to PT,OT, speech, special ed, EI, ortho (as needed) and hearing and ortho (as needed) and hearing and vision.vision.

Psych and Social Work referral should be Psych and Social Work referral should be an integrated part of the family’s care.an integrated part of the family’s care.

Nursing care of the child with Nursing care of the child with CPCP

see NCP B& B pg. 1341-2.see NCP B& B pg. 1341-2.

Traumatic Brain InjuryTraumatic Brain Injury

30,000 children and adolescents under 30,000 children and adolescents under 19yrs of age develop a permanent 19yrs of age develop a permanent disability from a moderate or severe disability from a moderate or severe brain injury (ie) epilepsy, cognitive brain injury (ie) epilepsy, cognitive impairment, learning problems and impairment, learning problems and behavioral or emotional problems.behavioral or emotional problems.

Occurs from falls, abuse, poor Occurs from falls, abuse, poor judgement errors, MVA, sports related, judgement errors, MVA, sports related, risk taking behaviors.risk taking behaviors.

Types of traumatic brain injuriesTypes of traumatic brain injuries

concussionconcussion

skull fracturesskull fractures

hematomas: subdural, epidural, hematomas: subdural, epidural, intracerebralintracerebral

coup(direct blow) or contrecoup coup(direct blow) or contrecoup injury(accel/decel)injury(accel/decel)

cerebral contusioncerebral contusion

penetrating injuriespenetrating injuries

ConcussionsConcussions

grade of severity 1,2,3.grade of severity 1,2,3.– Grade1: mental status changes <15 minGrade1: mental status changes <15 min– Grade 2: MSC > 15 min.Grade 2: MSC > 15 min.– Grade 3: LOC.Grade 3: LOC.

Pediatric concussive synd: stunned, no Pediatric concussive synd: stunned, no LOC. Later become pale, clammy, LOC. Later become pale, clammy, lethargic, may vomit. Admit for obsv.lethargic, may vomit. Admit for obsv.

Postconcussive synd:HA, dizzy, vertigo, Postconcussive synd:HA, dizzy, vertigo, CMS, photophobia, poor conc/memoryCMS, photophobia, poor conc/memory

Clinical Management of Clinical Management of ConcussionsConcussions

parental teaching for parameters to follow parental teaching for parameters to follow up. up.

Limited activity until return to normal Limited activity until return to normal mentationmentation

risk of falls and poor judgementrisk of falls and poor judgement

athletes should be protected from second athletes should be protected from second impact syndrome: cumulative effects of impact syndrome: cumulative effects of second concussion, could cause cerebral second concussion, could cause cerebral edema, cognitive deficits or sudden death edema, cognitive deficits or sudden death

Skull fracturesSkull fractures

linear: no sx, superficial hematomalinear: no sx, superficial hematoma

depressed: assoc intracranial depressed: assoc intracranial injury/epilepsyinjury/epilepsy

compound:depressed and/or compound:depressed and/or penetrating fx:incr risk of infectionpenetrating fx:incr risk of infection

basilar:fx of base of the skull: assoc basilar:fx of base of the skull: assoc with CSF leak, dura tear.with CSF leak, dura tear.– Bld behind TM, raccoon eyes, battle sign, Bld behind TM, raccoon eyes, battle sign,

cranial nerve damage (hearing loss).cranial nerve damage (hearing loss).

Depressed Skull FxDepressed Skull Fx

Intracranial hematomasIntracranial hematomas

Epidural:extradural: between the Epidural:extradural: between the cranium and the duracranium and the dura– bleeding is usually arterialbleeding is usually arterial– momentary unconsciousness followed momentary unconsciousness followed

by normal period, then rapid by normal period, then rapid deteriorationdeterioration

– uncommon in children <4yrs.uncommon in children <4yrs.– If undiagnosed, herniation and death will If undiagnosed, herniation and death will

resultresult

Subdural hematomasSubdural hematomas

subdural;between the dura and the subdural;between the dura and the cortexcortex– bleeding is usually venousbleeding is usually venous– more common than epidurals and freq more common than epidurals and freq

occur in infancyoccur in infancy– develop slowly(48-72 hr post injury)develop slowly(48-72 hr post injury)– more than half die: 25% develop szmore than half die: 25% develop sz– assoc with child abuse;esp Shaken Baby assoc with child abuse;esp Shaken Baby

SyndromeSyndrome

Contracoup Injury: Contracoup Injury: subdural hematomasubdural hematoma

Intracerebral HematomaIntracerebral Hematoma

result of deep contusionresult of deep contusion

surgical treatment not indicatedsurgical treatment not indicated– usually self absorbs over timeusually self absorbs over time

neuro deficits depends upon size and neuro deficits depends upon size and location of the lesionlocation of the lesion

Usually with altered consciousnessUsually with altered consciousness

may result in hemiplegia or visual may result in hemiplegia or visual loss.loss.

Penetrating InjuriesPenetrating Injuries

gun shot woundsgun shot wounds– high or low velocityhigh or low velocity– approx 50% dieapprox 50% die– survivors have high risk for multiple survivors have high risk for multiple

deiecits and seizuresdeiecits and seizures

impaled objects: must be left in place impaled objects: must be left in place and removed by neurosurgeon in OR and removed by neurosurgeon in OR– high risk for focal injuries, seizures and high risk for focal injuries, seizures and

infection.infection.

Clinical Manifestations of Clinical Manifestations of Traumatic Brain InjuriesTraumatic Brain Injuries

changes in LOCchanges in LOC

changes in respiratory statuschanges in respiratory status

headacheheadache

vomitingvomiting

lethargylethargy

retinal hemorrhages (65-90% with retinal hemorrhages (65-90% with HI)HI)

Cushing’s Triad: Cushing’s Triad:

incr ICPincr ICP

HTNHTN

incr systolic pressure incr systolic pressure

widening pulse pressure widening pulse pressure

bradycaradiabradycaradia

irregular respirations irregular respirations

Clinical Therapy:Eval.Clinical Therapy:Eval.

thorough history and PE, observation, thorough history and PE, observation, determine LOC and/or vomiting at determine LOC and/or vomiting at time of the injury, child’s memory of time of the injury, child’s memory of event.event.

VS and use of Glascow Coma ScaleVS and use of Glascow Coma Scale

Labs, including toxicology, probable Labs, including toxicology, probable CT and MRICT and MRI

consider cervical spine injuryconsider cervical spine injury

Cervical Spine InjuryCervical Spine InjuryIf MOI indicates possible injury to cervical If MOI indicates possible injury to cervical spine, a hard cervical collar will be applied spine, a hard cervical collar will be applied in the ER AND LEFT ON until the patient is in the ER AND LEFT ON until the patient is conscious.conscious.Pt must have a normal cervial spine xray Pt must have a normal cervial spine xray series AND be able to verbally reassure series AND be able to verbally reassure the Neurosurgeons that there is no the Neurosurgeons that there is no cervical pain/involvement.cervical pain/involvement.DO NOT REMOVE A CERVICAL COLLAR DO NOT REMOVE A CERVICAL COLLAR WITHOUT AN ORDER FROM THE NEURO OR WITHOUT AN ORDER FROM THE NEURO OR TRAUMA TEAMTRAUMA TEAM

Clinical Management: Clinical Management: Traumatic Brain InjuryTraumatic Brain Injury

ABC;s supported as neededABC;s supported as needed

perfusion to brain priority: keep bed perfusion to brain priority: keep bed flat until this is assuredflat until this is assured

shock is treated aggressively with shock is treated aggressively with fluid bolusesfluid boluses

Cerebral EdemaCerebral Edema

incr in intracellular and extracellular incr in intracellular and extracellular fluid in brainfluid in brain– results from anoxia, vasodilation or vascular results from anoxia, vasodilation or vascular

stasisstasis

treated with Mannitol and furosemidetreated with Mannitol and furosemide

goal is to prevent hypoxia and goal is to prevent hypoxia and hypercapnia since they cause (cerebral) hypercapnia since they cause (cerebral) vasodilation and incr ICP.vasodilation and incr ICP.

Long term effect can’t be eval until 1 yr.Long term effect can’t be eval until 1 yr.