Pediatric Neuro – Flashcards

Status of the brain is obtained by indirect measurements Looking for: -Increased ICP -alterations in LOC

Volume in cranium: brain 80%, CSF 10%, Blood 10% Changes in one of these components must be followed by a compensatory change in another. *Children with open fontanels compensate by skull expansion and widened sutures Increase in ICP caused by: -tumors, accumulation of fluid within ventricular system, bleeding, edema of cerebral tissues When body can no longer compensate for changes, any further increase in craniums volume results in rapid rise in ICP. Children: -early S/S of increased ICP are subtle -as pressure increases, s/s more pronounce-> LOC deteriorates dramatically Normal ICP: < 20 mm Hg Cerberal Perfusion Pressure: MAP- ICP -is brain getting perfused?

Infants: -taught, bulging fontanels -widened cranial sutures -Macewen (Cracked pot) sign -irritability and restlessness, high-pitched cry -drowsiness, increased sleeping -increased OFC -distended scalp veins -POOR FEEDING -Sun-setting sign (Late-sign) Kids: -HA, projectile vomiting without nausea -Diplopia(double vision), blurred vision -Seizures -Drowsiness, increased sleeping -decline in school & physical activity performance -inability to follow commands -lethargy (late sign) Late Signs in Infants and Children: -Bradycardia, Cheyne-stokes respirations(irregular) -Widening pulse pressure -decreased motor response to command, sensory response to painful stimuli, consciousness - flexion or extension posturing -Alterations in pupil size and reactivity (fixed, slow) -Papilledema (optic nerve swelling) -Coma

2 Components of consciousness -Alertness and cognitive power (ability to process, verbal and motor responses) Unconsiousness: depressed cerebral fxn, inability to respond to sensory stimuli Coma: state of unconsciousness which pt. cannot be aroused seven with powerful stimuli *Assessment of LOC remains the earliest indicator of improvement or deterioration in neruo status. -For children: utilize parent to help elicit desired response b/c kids may not respond to unfamiliar person. -Child >3yo: can give name, not necessarily place and time. Glasgow Coma Scale: eye opening, verbal response, motor response. A decrease indicates a deterioration of pts. condition. Lowest score 3: can be in a coma or dead.

Irritable but consolable> Irritable and inconsolable> Lethargic when left alone> Needs more stimulation to wake up> No response to touch> No response to pain (coma, death)

Establish baseline! Vital Signs: autonomic activity is disturbed if deep coma or brainstem lesions - Temp: Elevated temp for intracranial bleeding, infx, hypothalmic involement -Pulse: variable -BP: for children don't often should cushing's triad, more important are the CHANGES in pulse and BP rather than the direction -Respirations: Hyperventilation: metabolic acidosis, abnormal stimulation of Medulla caused by hepatic coma, or Reyes syndrome Irregualr breathing is ominous sign of brainstem dysfunction. Pupils: pipoint pupils- opiate poisoning, brainstem dysfunction. Dilated and fixed: NEURO EMERGENCY: paralysis of CN III r/t pressure from herniation of brain. Fixed > 5min, brainstem damage. (hypothermia, anoxia, drug poisoning) Unilateral fixed pupil: lesion on same side Doll's Head maneuver: elicited by rotating head from ne side to another. Normal: both eyes together move opposite direction to rotation. Absence = brainstem dysfunction or CN III. Motor Function: observe asymmetric movements Posturing: Flexion: decorticate or Extension: decerebrate- elicit by painful or noxious stimuli

Infants: primarily reflexes -Health infant: Moro, tonic neck and withdraw reflexes -delays in milestones helps identify high-risk children. -persistence or reappearance of reflexes that normally disappear indicate a pathologic condition. -need to understand child's pregnancy and delivery history: IUGR, maternal infix, tobacco or alcohol, drugs Coma: -corneal, pupillary, muscle-stretch, superficial and plantar reflexes tend to be absent. -absence of corneal reflex and tonic neck reflex are associate with severe brain damage. -Positive Babinski in child > 18 months: pyramidal tract lesion.

Outcomes for the unconscious child: -early and complete recovery -death within a few hours or days -persistent and permanent unconsciousness -recovery with varying degrees of residual mental or physical disability Emergency Measures: Airway, breathing, circulation, stabilizing spine when indicated, treating shock, reducing ICP if present. Assessmnets: frequent depending on cause of unconsciousness. VS: hypothalamic and brainstem disorders effect thermoregulation Pain Management: monitor responses to pain, motor reactions, facial changes, physiological reactions (HR, RR, HTN, diaphoresis); document assessment of pain intervention effectiveness. -unrelived pain activates stress response-> increase ICP -use of opiod analgesics, sedatives, and some paralyzing agents (fentanyl, midazolam, vecuronium) -When opioids are used: monitor BM, give stool softeners Respiratory managmenet ICP monitoring Nutrition/ Hydration Medications

Airway: always priority -Resp. obstruction-> compromise-> cardiac arrest. CO2 is a potent vasodilator-> increase cerebral blood flow-> increase ICP Cerebral hypoxia > 4 minutes = irreversible brain damage Deep coma: at risk for aspiration and unable to handle secretions. Interventions: -Positioned to prevent aspiration and stomach emptying (HOB up) -Oral airway: for temporary LOC: seizure, contusion, anesthesia -OT, NT, ET intubation: for unconsciousness for longer time; ET if GCS resp. alkalosis -CXR daily -Position change q2hr to prevent pulmonary complications

Indication for inserting ICP monitor: -GCS evaluation drain too fast-> cause bleeding and pain If ICP high ( > 20 to 25) Interventions: -Osmotic diuretics: excrete water ad Na+ -Mannitol: IV if low Na+ used for rapid reduction and can lower ICP in 1-5 minutes. Usually slow admin unless emergency of impending herniation or herniation. -Hypertonic solutions: 3% NS reduce ICP by its osmotic force and beneficial to hypovolemia and hypotensive pts (volume). PaCO2: maintained at 25-30 mm HG to produce vasoconstriction-> reducing CSF -> decrease ICP

Nursing Interventions: -fall precautions, seizure precautions -careful positioning -alternating pressure mattress -HOB at 30 degrees or reverse trendelenburg and head midline to promote venous drainage and avoid jugular vein compression.(no kinks in neck) -decreased IV fluid maintenance volume if increased ICP; prevent cerebral edema -NPO; NG or GT tube -DVT prophylaxis -gentle ROM -minimize environmental stimuli -stool softeners -avoid non therapeutic touch -gentle auditory stimulation, soft music, thoughtful speech -NO suction: only if necessary-> increase ICP -Monitor Na+ and glucose -Hyperthermia: external cooling blankets, antipyretics usually ineffective -I&O: catheter or diapers (weigh) -Mouth care: AM/PM, toothettes if intubated, lip care -Artificial tears or eye oinmentL due to incomplete close of eyes.

altered ability to handle fluid loads is attributed to SIADH (inappropriate antidiuretic hormone secretion) and Diabetes Insipidus d/t hypothalmic dysfxn. -SIADH accompanies CNS diseases (head inj. meningitis, encephalitis brain abscess, tumor, and subarachnoid hemorrhage.) -over secretion of ADH-> low UP, high retained volume -hyponatremia and hyposmolality: dilution, overhydration -Hyperkalemia? **Looks like dehydration d/t low UP but requires further investigation Treatment: restrict fluids until serum lutes and osmolality return to normal Diabetes Insipidus: hypo function of post. pituitary-> under secretion of ADH-> uncontrolled diuresis -d/t Intracranial trauma Tx: Adequate replacement of fluids -detect s/s of hypernatremia and hyperosmolality -IV Vasopressin (ADH)

depends on cause for unconsciousness: infix, seizures, edema, etc. Meds for specifics. Sedation + Paralytic = decreases ICP and allows for treatment of cerebral edema -Morhpine, midazolam and pancuronium. Warning: long term use of proposal in kids = risk metabolic acidosis Barbituates: decreases cerebral metabolic rate for O2 and protect brain during times of reduced cerebral perfusion pressure. -extensive monitoring, CV and reps. support, ICP monitoring. Paralyzing agents for diagnostic procedures maybe necessary.

may demonstrate: guilt, fear, hostility, and anxiety faced with uncertain outcome of childs cerebral dysfunction Fear of death, intellectual disability or other permanent disability. Family of a child whom may never regain consciousness will have prolonged grief and search for signs of hope. May face decision of whether to remove child from life-support if severely damaged. -Have and open and honest dialogue about child's conditions and prognosis

Meningitis: inflammation/ infxn of meninges Cause by: 1. Bacterial: pus forming bacteria -Meningococci (Neisseria) -Streptococcus pneumoniae -Haemophilus organisms (Hib) *considered much more serious: can be severe include: shock, coma, seizures, hearing/vision loss, death 2. Viral (aseptic): *short lived, self-limiting; usually followed by complete recovery 3, Tuberculosus: tuberculin bacteria Encephalitis: inflammation of the brain

acute inflammation of meninges and CSF Medical EMERGENCY 95% cases in children > 2m Infants blood supply-> CSF-> subarachnoid space. -inflammation, exudate layer over brain and CSF, WBCs, varying tissue damage Diagnosed by Lumbar Puncture: -do not due if high ICP: will increased ICP: BAD! -if suspicion on Increased ICP: Head CT before LP -LP should delay if recent sz, deteriorating LOC< brainstem signs -Elevated WBC, culture/sens., low CSF glucose(normal in viral), CSF protein increased. *after LP: supine for several hours to prevent HA

Children: -abrupt onset -Flu-like symptoms: fever, chills, vomiting -SEVERE HA -Stiff neck, back pain -Dislike bright light, irritable, agitation, drowsiness, -stupor, coma -Seizures (often initial sign) -Hyperactivity w/ varying reflex response. Brudzinski sign (stiff neck: flex neck-> bend knees and hips flex) Infants and Child < 2yo: Difficult to dx -fever, vomiting -poor feeding, marked irritability -seizures, high pitched cry, weak cry bulging fontanel S/S peculiar to individual organisms: -Petechial rash= meningococcal infxn, -joint involvement: menigococcal, Hib -poor tone, lack of movement: neonates

Emergency Priorities: -Early recognition of S/S -Isolation precautions (droplet, contact): respiratory for at least 24 hours after abx admin -Maintenance of ventilaiton -management of systemic shock IVs in -STAT ABX and corticosteroids -Reduce increased ICP: may receive corticosteroid -restrict hydration initially (2/3): monitor electrolytes -control seizures -control temp -tx complications: treat DIC, SIADH, hearing loss is common Nursing Interventions: -reduce environmental stimuli: sensitive to noise, bright lights -HOb slightly elevated, -side-lying position for neck stiffness, avoid lifting child's head -pain management -Assess: VS, neuro, LOC, UO, signs of complications Follow up: hearing test 6 mo post, exam for lingering neuro damage or hydrocephalus in infants

caused by: arbovirus, Herpes Simplex Virus, cytomegaloviirus, adenovirus and HIV: Enteroviruses are most common cause elf viral meningitis. Meningeal symptoms, fever and increased WBC without bacterial growth from CSF cultures. -most common in young children. S/S same as bacterial: fever, HA, photophobia, neck stiffness. -can also have skin manifestations of Enterovirus: hand, foot, mouth syndrome, rash. Clinical course is shorter and usually without any significant complications. Diagnosis: LP - no bacterial growth, normal CSF glucose Treatment: Sympomatic -acetaminophen for HA, muscle pain, fever -maintenance hydration -position for comfort -until definitive dx is made: ABX admin. and isolation until r/o of bacterial origin. -Acyclovir: antivirals

From the Meninococcal infxn -Pts can present with meningococcemia w/ meningitis or w/o meningitis Can cause DIC: inappropriate clotting in vessels and surrounding tissue to bleed Clotting factors are exhausted-> bleeding, hemorrhage-> Petechia/ Pupera: pin pricks or looks like huge rash (blood) under skin Non-blanchable -need to treat with fluids, vasopressors if in shock, clotting, blood admin

Inflammation of the brain Most often caused by viral infection: HSV Clinicanl Manifestations: Onset: -Malaise, fever, HA, lethargy, neck stiffenss Severe: -high fever, stupor, seizures, disorientation, N/V, Ataxia, Tremors, hyperactivity, Mutism, spaciitu, paralysis, coma-> death Dx: Head CT, labs, EEG (distinct findings) Treatment is supportive and the sam with a ny child with decreased LOC or meningitis -Acylovir -Monitor for Increased ICP -frequent neuro checks -Nutritional support -Strict I&Os *Approx: 2/3 children with HSV Enceph> will have residual neuro deficits.

acute encephalopathy associated with other characteristic organ involvement. -fever, profoundly impaired consciousness, hepatic dysfunction Most cases follow a viral illness: influenza or varicella. Characterized by cerebral edema and fatty changes in the liver. Onset: profuse effortless vomiting and varying degrees of neurological impairment: personality changes, seizures, and coma, that lead to increase ICP, herniation, and death. Caused by abnormal mitochondrial function induced by various viruses, drugs, exogenous toxins, and genetic factors. Elevated ammonia levers tend to correlate with the clinical manifestations and prognosis. Definitive Dx: liver biopsy: staging based on liver fxn an neuro signs Association between Aspirin for treatment of fever in child with Varicella or influenza and RS.

Early dx and aggressive support therapy Rapid progression to coma and high peak ammonia concentrations = more serious prognosis Cerebral edema= most serious problem Nursing care for child with altered state of consciousness and Increasing ICP Strict I&Os to prevent dehydration and cerebral edema. Impaired Liver fxn: labs to monitor Coags (prolonged bleeding time) Prevention: check all medicines to be administered to children during the flu and chickenpox for " hidden" salicylates. (Pepto-Bismol) Prognosis: rapid recovery usually without sequelae if the dx is early and therapy is initiated promptly.

most common peds neuro disorder Types: -Partial (simple or complex): local onset -Generalized( tonic-clonic or absence): immediate loss of consciousness, stiffens in generalized symmetric tonic contraction of entire body, apenic, violent jerking movements maybe inconinent -Akinetic: drop attack -Atonic: loss of tone child falls to flow, unable to break fall by putting out hand Epilepsy is diagnose with two or more unprovoked sz -Hallmark signs during generalized seizure: tachycardia, HTN, hyperglycemia, hypoxemia Dx: EEG confirms presence of electrical activity and sz type. Stimulation maybe required

Sudden loud noise Fatigue Dehydration Infection Flashes of light/ rapid changes in light to dark -Strobe lights, driving through trees Extreme/ abrupt temperature canoes Hyperventilation: hypocapneia: Respiratory Alkalosis If it is not child's first seizure: parents know what is normal for their child. Trauma Metabolic process

Medical management: often multi drug tx, ketogenic diet Antiepileptic: serves to raise the threshold and prevent sz. -blood cell counts, urinalysis, and live function tests: meds can effect organ function. -titrate up to toxicity: then back down -hoping for 1 drug to treat -Monitor therapeutic levels -Increase dosage as child grows -avoid abrupt discontinuation: gradual dose reduction -Rectal Diazepam if seizures lasting longer than 5 minutes then ale to hospital. Ketogenic diet: high-fat, low-carbohydrate and adequate protein diet -forces odd to shift using glucose as a primary source to using fat= develop a state of ketosis -deficient of vitamins and mineral= take vitamin Vagal Nerve Stimulation: implantable device that reduces seizures. Use magnet to activate device in chest that stimulates the Vagus nerve. Surgical therapy: if sz caused by hematoma, tumor or cerebral lesion.Focal resection: removal of epileoptogenic sone.

continuous seizure that last more than 30 mins or series of seizure from which child does not regain premorbid LOC. Treatment: support and maintenance of vital functions, ABCs of life support, administering oxygen, and gaining IV access Immediate admin of anti epileptic meds -Hospital : IV diazepam or Lorazepam(Ativan) -home: Rectal Diazepam(Diastat) with them at all times. -SE: respiratory depression

Observe seizure episode and document. Seizure precautions Stay with the child and prevent harm Ease child to the floor if standing, assume side lying side rails padded and up Aspiration risk Suctioning maybe necessary after convulsions DO not move or forcefully destain child during tonic clonic seizure and do not place objects between teeth. Reintegrate child to environment as soon as possible It is not necessary to send a child with chronic seizure disorder home from school after sz. Parent teaching: medications regularly on time. Meds continued until child has been sz free for 2 years. During illness; threshold lower and increased risk for sz. Frequent sz disorder children should avoid skating, skateboarding, and bike riding and always wear a helmet. At higher risk for submersion injury: do not levee alone in bathtub. Encourage to shower and should never swim unsupervised.

occur bewteen 6 mo- 3yo Simple febrile: no hx of neuro impairment: general tonic-clonic seizure that occurs with a fever > 38C and resolves within 15 minutes with a return to alert mental status after sz and no further sz in 24 hours. Complex: hx of neuro impairment, prolonged sz and can reoccur within 24 hours. Treatment: (if still occurring at hospital) -Pt will be given IV or Rectal diazepam -Acetaminophen to reduce temp. -Antipyretics will not prevent a seizure. Family teaching: -febrile seizures are scary but benign -if seizure lasts more than 5 minutes call 911 -safety: do not place child who is actively having seizure in the car.

condition caused by imbalance in the production and absorption of CSF in ventricular system. Productiong> absorption -> increased ICP Cause: impaired absorption within spaces and malfunction(communicating between ventricles still) or obstructive (noncommunicating) -Ventricles become dilated (Ventriculomegaly) and compress the brain against cranium. -if prior to fusion of sutures, causes enlargement of skull and dilation of ventricles. Obstructive: usually developmental malformation, apparent in early infancy S/S: Infancy: abnormally rapid head growth, bulging fontanels(tense, non pulsating), separated sutures,thinning of skull bones, irritable, cries when being moved Later sings: frontal enlargement, sunset eyes, pupils sluggish and unequal response to light. Child: HA, improvement after emesis or upright posture, papilledema, irritability, Ataxia, confusion, incoherence, vomiting Dx: head circumference, head CT and MRI>

Treatment: surgical -direct removal of an obstruction or placement of a shunt that provides primary drainage of the CSF from the ventricle: Venticuloperitoneal shunt (VP) or ventricular catheter. Major complications of VP shunts are: malfunction and infection. -Malfunction: can get obstructed, can cause worsening neuro status and increased ICP. -Infection: septicemia, bacterial endocarditis, wound infection, shunt nephritis, meningitis and ventriclitis. Treated with abx IV for 7-10 days. If persistent infection, switch to EVD. Nurisng Mgmt: -measure OCF daily, palpate sutures, fontanels, -identify s/s of increased ICP -post op assessment, evaluate shunt -sedation required for CT and MRI: hold still. Postop care: -monitor neuro -positioned on nonop side. Keep child flat. -Acetominophen for pain. -If increased ICP: MD orders to raise HOB and facilitate drainage of csf -abdominal distention-> peritonitis or postop ileus.

group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non progressive disturbances that occurred in the developing fetal or infant brain. -Motor disorders: abnormal muscle tone and coordination -disturbances in sensation, perception, communication, cognition and behavior, Seizures Non progressive disorder Cause: Congenital development, Birth trauma (asphyxia), Postnatal: meningitis, child abuse, etc. DX: If suspected brain abnormality: MRI or CT Hard to detect motor impairment in infants b/c voluntary control is usually not apparent until after 2-4 months. Dx cannot be confirmed until 2 yo b/c motor abnormalities may indicate another neuromuscular illness. Presistence of primitive reflexes: tonic neck, moro reflex, crossed extensor reflex

Mild to Severe Spastic (Pyramidal) -persistent primitive reflexes, + Babinski reflex, ankle clonus, exaggerated stretch reflexes, eventual development of contractors -Most cases, all extremities affected, diaplegia, tertaplegia, monoplegia, Hemiplegia -Hypertonicity with poor control of posture, balance, coordination; impaired fine/gross motor skills Dyskinetic (Nonspastic, Extrapyramidal) -Athetoid: Chorea: involuntary, irreg, jerky movements): slow wormlike movements of the extremities, trunk, neck, tongue -Dystonic: slow, twisting, laryngeal and oral muscles causing drooling and imperfect speech Ataxia (Nonspastic, Extrapyramidal) -Wide-based gait, rapid repetitive movements performed poorly, disintegration of movements of upper ex. when child reaches for object Mixed Type: Spastic and dyskinetic

Goal: early recognition and promoting of optimal development to enable affected child to again normalization and their potential within limits of existing health problems. Ankle-Foot orthoses: braces to help reduce/prevent deformity, increase efficacy of gait, control align. Wheelchairs, mobilization devices Ortho Surgery to correct contracture or spastic deformities (tendon lengthening, release spastic muscles, correct hip dislocation, Spinal fusion for scoliosis) Management for muscle spasms: Baclofen(Lioresal) pump, PO, GT and Diazepam(Valium) effective in reducing overall spasticity. Side Effects: diaphoresis, constipation, fatigue, muscle weakness. Botox to reduce spasticity in target muscles: prevents muscle movement-> preventing muscle contractors usually on LE. SE: pain and temporary weakness. Pain Management Antiepileptics if seizures; Levodopa for Dystonia Dental Hygiene: decreased oral intake leads to tartar build up Elimination: risk for constipation, incontinence Respiratory: aspiration risk, PNA, GERD, abnormal muscle tone and immobility Skin: immobility, altered positioning, poor nutrition. PT , OT, Speech pathology

Parent education: Home care Multidisciplinary team plan reinforcement CP children expend so much energy to accomplish ADLs: allow frequent rest periods. GT feedings: if unable to meet requirements PO and to ensure adequate weigh gain Safety precautions: helmets, safe environment, fall risk Immunizations to prevent illness, protect resp. tract Routine dental care Transportation: CP children with pro neck control should remain in rear facing care seat for as long as possible. Education: mild to moderate cognitive impairment: school with special help

failure of neural tube closure: may involve entire tube or restricted area Anencephaly: both cerebral hemispheres are absent; incompatible with life, most stillborn. Spina bifida Occulta: defect not visible externally. -outer part of vertebrae not completely joined. missing the bone) Spinal cord and covering meninges not damaged but exposed w/o bony protection. Hair or small dimple often at site of defect. Meningocele: outer part of vertebrae split, Spinal cord in normal place, Meninges and CSF damaged and pushed out through opening. Myelomeningocele: outer part of vertebrae split. Spinal cord, meninges damaged and pushed out through opening. Possible hydrocephalus. Etiology: drugs, radiation, maternal malnutrition, chemically, pregnancy obesity, GDM, low folate, -> abnormal development Dx: Prenatal Detection via ultrasound, elevated maternal levels of MS-AFP in amniotic fluid-> anencephaly or myekimeningocele. Performed at 16-18 weeks.

Multidisiplinary team: neurology, peds, uerology, ortho, rehab, PT, OT, social servises. Early surgical closure of the myelomeningocele sac through fetal surgery Infancy: newborn care involves preventing infection, neuro assess, early closure better outcomes, Broad spectrum ABX, Passive ROM, positioning and stretching-> prevent contractures Ortho: prevent joint contractures, correction of existing deformities, prevent and minimize motor deficits, prevent skin breakdown, best possible fxn of lower extremities. The status of the neurologic deficit remains the most important factor in determining the child's ultimate functional abilities. Neurogenic bladder dysfunction: goal of tx to preserve renal function. Urinary incontinence is chronic, UTI, vesicoureteral reflux, and renal insufficiency. -Prompt tx of UTI, bladder emptying schedule, self in and out cath, meds to improve bladder storage and continence (Ditropan), surgical vesicostomy: Bowel Control: prevent constipation. Fiber supp. laxatives, enemas, Antegrade continence enema procedure, toileting schedule.

Infant in incubator to maintain temp. without clothing that cover lesion. Sterile NS moistened dressing over defect to keep from dehydrating/drying. Dressing change q2-4hrs Inspect sac closely for leaks, abrasions, irritation and s/s of infxn. (temp. instability, irritability, lethargy) and for signs increased ICP-> hydroceph. Carefully classed if becomes soiled. Positioning: kept in prone position: hips flexed with soft pads. Areas of sensory and motor impairment: at risk for skin breakdown

Postop care: VS, I&Os, pain management Care of operative site: observe signs of CSF leakage Prone position to side lying to reduce pressure sores and facilitated feeding after anesthesia has subsided. Teach parents: positioning, feeding, skin care, ROM exercises -Signs of complications, urinary, neuro, ortho Development of Latex allergy: high risk d/t repeated exposure to latex products during surgery and procedures. -SB child should not be exposed to latex products from birth onward to minimize occurrence of latex hypersensitivity. Rxn: urticaria, wheezing, watery eyes, rashes to anaphylactic shock. -Latex free environment. -Allergic rxn to tropical fruits?