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Cerebral.dysf.peds

NP5 Peds Test 3 SFC

QuestionAnswer
Changes in _______ are the earliest sign of neurological worsening or improvement LOC
Slow, deep & irregular respirations occur after ______/______. seizure/infection.
Slow and shallow respirations occur after _________ ingestion opioid ingestion.
Deep and rapid respirations (kussemal's) occur with _________ _________. metabolic acidosis
If Blood pressure variable of <HR, > BP, seen in child with cerebral dysfunction it is a _______ sign late
Pupillary changes are often a _____ sign late
Pinpoint pupils = opioids
Fixed and dilated pupils > 5” indicates brainstem dysfunction or hypothermia
Decorticate posture indicates cerebral cortex dysfunction
Decerebrate posture indicates midbrain dysfunction
Brudzinski sign ask child to flex head. Pain or involuntary flexion of knees & hips is abnormal
Kernig sign have child flex leg at hip & knee. Pain or resistance on extension is abnormal. Not as accurate on children
Brudzinski & Kernig sign test for meningeal irritation
Meningitis Acute infection and inflammation of the meninges
Meningitis categorized as 1. Aseptic aka viral requiring supportive care (no puss involved) 2. Bacterial, most serious
Bacterial Meningitis Etiology 0-3 mos. = GBS & E-coli Most common. Older infants Pneumococcal and Neisseria Meningitides(meningococcal).
Risk Factors for bacterial meningitis include Neonatal infections:URI, OM, UTI. Head Trauma, Neurosurgery, Neoplastic diseases, Immunodeficiency,Sickle Cell Disease
Pathophysiology of bacterial meningitis Infection and inflammatory changes = brain becoming covered with exudates that compromise circ blood flow & reabsorption of CSF. Ventricles enlarge & the brain becomes hyperemic & edematous. ICP increases leading to tissue damage, destruction & death
Clinical Manifestations of bacterial meningitis in Neonates low grade temperature or sub-normal, pallor, lethargy,poor suck or feeding,vomiting, diarrhea, bulging font. > head circ.,seizures, opisthotonus (marked archery of back)
Clinical manifestations of Infants and younger children with bacterial meningitis Fever, lethargy,irritability, pallor, high pitched cry, insists on being held, bulging fontanel, increased head circ (<2), seizures, nuchal rigidity positive Kernig and Brudzinski. Can lead to Sepsis, shock and death.
Clinical manifestations of bacterial meningitis for School Age and Adolescents Fever, headache,nausea, vomiting, irritability,photophobia,diplopia, spinal and nuchal rigidity, positive Kernig and Brudzinski, confusion,seizures,petechiae (w/ neisseria meng.), sepsis >shock >DIC
How does bacterial meningitis usually spread? vascular dissemination
Lumbar puncture results for bacterial meningitis includes WBC’s- incr.Protein- incr. Glucose- decr. w/viral
Urine osmolarity increases with bacterial meningitis bc of increased presence of ADH
Therapeutic Management for bacterial meningitis Goal: Eradicate cause and prevent complications. 24 hour isolation. Immediately obtain labs and cultures. Secure IV at 2/3 maint. and start broad spectrum antibiotics STAT.
Preventative Measures for bacterial meningitis includes H. influenza type b (Hib) vaccine, Pneumococcal vaccine (Prevnar),Meningococcal vaccine for dorm bound college students
A pt. with bacterial meningitis will be on what precautions? Droplet & Seizure precautions
Complications of bacterial meningitis includes Seizures,Hydrocephalus (d/t CSF flow being blocked by thickened meninges),Cranial nerve damage. Learning Disabilities includes perceptual deficits,cognitive impairment, behavioral changes.Motor dysfunction such as CP (cerebral palsy)
Etiology of SIADH in bacterial meningitis patient Pressure on posterior pituitary gland cause abn Release of ADH. Decrease U.O d/t Na and H2O is reabsorbed
What happens to serum osmo in a pt with SIADH? decreased (less concentrated)
What happens to urine osmo in a pt with SIADH? increased (more concentrated)
Tx for SIADH in bacterial meningitis pt includes ½ maintenance fluids ordered and underlying problem treated
DIC (Disseminated Intravascular Coagulation)is a Life threatening complication caused from sepsis leads to the gram neg Neisseria releasing endotoxins that trigger massive changes in clotting system. Platelets are consumed along with the deposite of fibrin clots in microcirculation leading to both hemorrhaging & clotting simultaneously
Etiology of Encephalitis an inflammatory process in the brain primarily r/t viral inf.
Encephalitis Symptoms can be mild and similar to aseptic meningitis or life threatening as is the case with herpes encephalitis.
In severe cases of Encephalitis infection can lead to cerebral edema, >ICP and herniation of brain.
Another infectious source of encephalitis is via arthropod vectors including ticks and mosquitoes
Prevention of encephalitis includes avoiding dawn and dusk outside activities and or wear appropriate attire, eliminate standing H2O and use DEET
Reye Syndrome Defined as a toxic encephalopathy with fatty infiltration of the liver which typically follows an acute viral illness like influenza B, varicella, or acute gastroenteritis.
Reye Syndrome is linked to what use of medication in children? ASA
Is Reye syndrome contaious? Not contagious
Diagnosis of Reye Syndrome is determined by 1. History of previousillness 2. Labs: Increased NH3 (ammonia, Liver enzymes,PTT, PT 3. Clinical presentation Prognosis
Management of Reye Syndrome includes ICU w/ ICP monitoring, Airway Management,Medications to reduce ICP (drug induced coma),HOB ^ 15-30 degrees, midline,air mattress. Strict I&O, watch VS, espec temp. QUIET…environment with min stim, Seizure control
Goal with Reye Syndrome includes maintain stable ICP
“Spina Bifida” is defined as Embryonic developmental failure of the spinal cord’s protective sheath of bone and meninges to close anywhere along the neural tract
Causes of spina bifida are multi-factorial and include folic acid deficiency, post maternal infections and genetics
Spina Bifida Myelomeningocele is classified as the Hernial protrusion of a sac containing meninges, CSF and part of spinal cord and associated nerves
80% of spina bifida occur in the LS area primarily because that is the last part to close, but can occur anywhere
Neurological Dysfunction of spina bifida is Related to level of defect for example L-2 and above = wheelchair verses at sacrum = ankle bracing
________ is common with spina bifida Hydrocephalus 75% require shunt
Spina Bifida Occulta is defined as Failure of the spinous processes to join in the lumbosacral area (L5-S1), meninges and neural tissue are not exposed at skin surface
Spina Bifida Meningocele is defined as Saclike cyst of meninges and CSF protrude through unfused vertebral arches without spinal cord involvement.
Management of Spina Bifida Myelomeningocele Pre-operatively NPO,(surgery in first 12-18 hrs), Prevent infection by protecting fragile sac
Primary Complications of Spina Bifida Myelomeningocele includes Meningitis, Hydrocephalus, Neurogenic Bladder (UTI),Musculoskeletal Problems (scoliosis),Latex Allergy Precautions!
Hydrocephalus is Defined as excessive accumulation of CSF in the brain resulting in dilatation of ventricles and increased ICP
Hydrocephalus is Diagnosed by CT or MRI
Symptoms of Hydrocephalus in Early infancy include enlarged skull, widening sutures, thin bones, dilated veins, bulging fontanels, irritability
Symptoms of Hydrocephalus in Late infancy include irritability, feeding difficulty,frontal bossing and setting sun sign
Symptoms of Hydrocephalus in Childhood are related to increased ICP
Ventricular-peritoneal Shunt is used to Provide drainage of excess CSF to the peritoneal cavity
Complications of VP shunt include infections, mechanical problems like kinking, separating or becoming obstructed and becoming displaced d/t child’s growth
Seizure is defined as a “Short circuit” in brain wave activity caused by excessive and disorderly discharge of electrical impulses by neuronal tissue
Convulsion is defined as an Involuntary muscular contraction and relaxation
Epilepsy is defined as a Chronic disorder characterized by repeated and non-provoked seizures requiring treatment
Etiology of seizure d/o includes Idiopathic: “unknown” genetics plays a part. Acquired: Perinatal brain injury, Trauma, Tumors, Infections, & other
Developmental Connection with seizure disorders in NB anoxia, hemorrhage, congenital anomaly
Developmental Connection with seizure disorders in Late infancy and early childhood CNS infections, fever, and trauma
Developmental connection with seizures and 3 yrs. – adolescence idiopathic
Pathophysiology of seizure disorders is described as Neuro cells are stimulated by stress, fatigue, F&E imbal etc. to discharge electrical impulses from a focal point in brain(epileptogenic focus)Stimulated cells may remain localized to a part of the cortex or become generalized.
Partial Seizures Present with an aura and originate in frontal,temporal or parietal lobes. EEG changes are unilateral and present with spikes
Simple partial (focal)seizure is defined as No loss of consciousness, localized motor symptoms, eyes/head deviate from side of focus,
Partial complex seizure is defined as Aura, appears dazed, unable to respond,automatisms like lip smacking, picking at clothes, harder to diagnose and treat
Generalized Seizures “Grand Mal” Symptoms are often abrupt, without warning,with immediate loss of consciousness and classic movements Tonic: eyes back, arms flex, body extends and possibly apnea. Clonic: violent jerking, foaming @ mouth,incontinence
Generalized seizures "Grand Mal" May follow a partial seizure that spreads giving some “warning”
If generalized seizure "grand mal" lasts longer than 29 minutes = Status Epilepticus, a medical emergency
Generalized Seizures can present as Absence Seizures “petit mal” which is defined as an abrupt arrest of activity with brief loss of consciousness for 5-10 seconds, slight loss of muscle tone with mild motor movement
Regardless of what type of generalized seizure, there is a post-ictal period when pt is semiconscious, confused, sore and may have delayed gag
One of the most common neurological disturbances of childhood is _______ ______ Febrile Seizures
Highest incidence of febrile seizures is 6 mos-3yrs and are self limiting
Rapid temperature increases a factor for febrile seizures
Febrile seizures Treatment when needed is **Valium or Ativan
Management for a Generalized Seizure includes Maintain Seizure Precautions, Protect patient, Describe seizure, noting time started
Management of Status Epilepticus includes Protect airway, suction, ambu and O2 IV access or rectal valium ATIVAN is preferred over phenobarb and Dilantin
When to Notify EMS about seizure activity 1ST Seizure or if unknown, Evidence of ingestion, Diabetic, Pregnant, Lasts > 5 minutes, Cannot arouse, Occurs in water
Anti Epileptic Drugs “AED’s” Common se with all is motor and cognitive slowing
Anti Epileptic Older drugs more likely metabolized by liver i.e., Carbamazipine, Dilantin, and Valproic Acid
Anti Epileptic Newer drugs generally excreted by kidneys i.e., gabapentin (Neurontin), lamotrigine (Lamictal),topiramate (Topomax), and levetiracetam (Keppra)
Cerebral Palsy is defined as A non-progressive motor function disorder characterized by impaired movement and posture.
Cerebral Palsy Etiology Pre-natal – 44% - majority of cases not r/t problems in the delivery room! L&D – 19% Perinatal – 8% Childhood – 5% Not obvious – 24%
Cerebral Palsy Pathophysiology Variable, caused by abnormal CNS development or r/t injuries occurring in the prenatal, perinatal or post natal period leading to motor dysfunction.
Pre-maturity is assoc with what type of cerebral palsy? > spastic type
Kernicterus is assoc with what type of cerebral palsy? > dyskinetic type
Spastic cerebral palsy Affects fine & gross motor movement. Uni or bilateral, hypertonic,hyper reflexive, poor control of posture and balance, scissor gait
Dyskinetic/athetoid cerebral palsy Normal movements thwarted by involuntary jerking, writhing worm like movements of extremities, trunk, neck facial muscles and tongue, more cognitive impairment
Ataxic cerebral palsy wide unsteady gait, rapid repetitive movements performed poorly
Mixed cerebral palsy consists of spastic and dyskinetic (affects fine & gross motor mvmt. uni or bilateral,hypertonic,hyper reflexive,poor control or posture & balance,scissor gait,in addition to normal mvmts thwarted by involuntary mvmts of extremities,trunk,neck,facial muscles & tongue
Physiological and Developmental Variables of cerebral palsy Delayed motor function universal sign,Abnormal motor performance,Alteration in muscle tone,Abn posture at rest,Reflexes persist beyond expected time,Intellectual impairment, Seizure d/o,Sensory impairment,Ortho problems,FTT,ADD/ADHD
Simple Screening Tool for cerebral palsy in infants over 6 months placelight blanket over face normally pulls blanket off with both hands. If baby only uses one hand, may want to further assess
Diagnostic Evaluation for cerebral palsy includes H&P,EEG,CT, MRI
Therapeutic Goals for cerebral palsy includes Est. locomotion, communication, self care. Enhanced appearance and motor function. Repair defects. Provide appropriate educational/social outlets.
Conservative therapy for cerebral palsy includes mobilizing devices such as braces, orthotics, wheelchairs and/or scooters.Medications to reduce spasticity:Baclofen (pump),Dantrium, Botox.Anticonvulsants. ADD/ADHD meds: Dexadrine
Invasive Approaches for cerebral palsy includes Osteotomy: slice of bone removed to change alignment and shift weight bearing in pts. with deformity and pain.Tendon heel cord lengthening with casting (noted for painful post-op course).Dorsal Rhizotomy:if center is available
AAMR defines retardation as Significant sub-average general intellectual functioning existing concurrently with deficits in adaptive behavior and manifested during the developmental period
Adaptive behavior is the degree with which the child is able to meet standards of personal independence and social responsibility
Handicap is A condition or barrier imposed by society, the environment or self.
Disability is Functional limitation that interferes with abilities to fx. i.e… walk, talk learn
Cognitive impairment Etiology Most common cause of mild retardation is familial, social and environmental deprivation.More severe forms often r/t genetics,pre-natal toxin exposure, infection,trauma, hypothyroidism or metabolic disorders
Down Syndrome is Most common syndrome r/t chromosomal abnormality with variable causes.
Downs syndrome is caused by extra chromosome on 21ST pair, hence Trisomy 21. Risk for increases with age in both parents.
Clinical Findings of Down syndrome Facial features include microcephaly,hypoplastic mandible so mouth breather, epicanthal eye folds, small nose and dental problems. Musculoskeletal features include hypotonia, hyperflexion, and atlantoaxial instability. short & thick fingers & toes
Pt with Down syndrome have an Increased Risk for Various Disorders such as Congenital heart disease, Hypothyroidism, ltered Immune System (URI’s),Leukemia, Hirshsprungs
Downs syndrome Diagnosis Clinical manifestations may make diagnosis straightforward (unless mosaic),Chromosomal analysis essential toidentify specific defect. Prenatal diagnosis: low maternal serum AFP, chorionic villous sampling and amniocentesis, esp. in high risk cases
Prognosis of down syndrome Generally shortened life span, Depends upon associated problems
Created by: stilsl