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Lauren Walker, RN, BSN Georgetown University

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1 Lauren Walker, RN, BSN Georgetown University
Cerebral Dysfunction Lauren Walker, RN, BSN Georgetown University

2 Overview Topics Increased Intracranial Pressure Level of Consciousness
Cerebral Abnormalities Nervous System Tumors Infections

3 Pediatric Cerebral Dysfunction General Information
Children under the age of 2 require special evaluation for neurologic function Observation of fine and motor reflexes Pregnancy and delivery history General Assessment Family History Health History Physical Evaluation Children under the age of 2 require special evaluation for neurologic function: -Infants are primarily reflexive- responses are gradually replaced by meaningful movement with development Info about infants and children are gained by observation: watch spontaneous/elicited reflexes as they develop -A delay or deviation from milestones helps identify high-risk children -Persistent reappearance of reflexes that normally disappear may indicate a pathologic condition -Obtain a pregnancy/delivery history: impact of intrauterine influences that affect the CNS (maternal infections, chemicals, trauma) Fam History: clues for possible genetic disorders Health History: cause of dysfunction: (injury, febrile illness, encounter with animal/insect, injection of chemical, past illness) Physical Eval of Pt

4 Abnormal neurologic physical evaluations of infants
Size and shape of head Sensory responses Spontaneous activity Symmetry in extremity movement Frequent movement of extremities Skin and hair texture Distinctive facial features High-pitched, piercing cry Abnormal eye movements Inability to suck or swallow Lip smacking Asymmetric facial movements Yawning Muscular activity and coordination Level of development

5 Increased Intracranial Pressure
Brain is enclosed in the solid bony cranium Cranium’s total volume: Brain: 80% Cerebrospinal fluid (CSF): 10% Blood: 10% Volume must remain approximately the same at all times Brain is terrible at compensation! Normal ICP 5-10 ICP Video Brain is well protected but highly vulnerable to pressure that may accumulate inside Increased ICP- caused by tumors or other space occupying lesions, accumulation of fluid in ventricles, bleeding, edema of brain tissue Once compensation is exhausted- an increase of volume = rapid increased ICP

6 Clinical s/s of Increased ICP
Infants Children Tense and/or bulging fontanel Separated cranial sutures Irritable High-pitched cry Increased occipital circumference Distended scalp veins Changes in feeding Crying when disturbed Setting-sun sign Headache Nausea Vomiting Diplopia, blurred vision Seizures setting-sun sign  downward deviation of the eyes so that each iris appears to “set” beneath the lower lid, with white sclera exposed between it and the upper lid; indicative of increased intracranial pressure or irritation of the brain stem. Box 28-1, Chapter 28 Wong

7 Clinical s/s of Increased ICP
Personality and behavioral signs Late signs Irritability, restlessness Indifference, drowsiness Decline in school performance Diminished physical activity and motor performance Increased sleeping Memory loss Inability to follow simple commands Lethargy and drowsiness Bradycardia Lowered level of consciousness Decreased motor response to commands Decreased sensory response to painful stimuli Alterations in pupil size and reactivity to light Flexion and extension posturing Cheyne-stokes respirations Papilledema Coma Box 28-1, Chapter 28 Wong

8 Level of Consciousness
Earliest indicator of improvement or deterioration Determined by observations Physical Assessment Motor activity, reflexes, vital signs Observations: responses to environment

9 15 points- highest score, unaltered LOC
Three part assessment to interpret the depressed loc (eyes, verbal, motor) With kids- helpful to have parents interact to initiate a proper response- may not be response to someone unfamiliar Below 8- typically in coma 15 points- highest score, unaltered LOC 3 points- lowest score, deep coma

10 Nursing Management of ICP
Positioning Alternating mattresses Avoid causing pain Cluster care Minimize environmental noise Closely monitor nutrition and hydration Positioning: avoid neck vein compression- may further increase ICP by interfering with venous return to heart Mattress: prolong pressure Pain- may increase ICP, assess frequently Nutrition: difficult, don’t want to fluid overload a pt with increased ICP, may be supplied by iv initially, then feeding tube (examine skin and mucous membranes)

11 Nursing Management of Increased ICP
Indications for inserting a monitor: GCS of 8 or below Deterioration Judgment from clinical appearance and response Monitors: Intraventricular catheter Subarachnoid bolt Epidural sensor Anterior fontanel pressure monitor Catheters can provide drainage to reduce pressure Bolt- connected to a monitor Mannitol- administered IV for rapid reduction in ICP

12 Medications for Altered ICP
What is the cause? Corticosteroids: inflammation Antibiotics: infectious process Diuretics: edema Antiepileptic: seizure activity Sedation: combativeness Barbiturates: deep coma Steroids: decrease inflammation Barbiturates: decreased metabolic rate for oxygen, protects brain (respiratory support, cv monitoring)

13 Cerebral Malformations
Newborn cranial sutures are separated by membranous seams Sutures: Soft areas: -Sagittal -Anterior fontanel -Coronal -Posterior fontanel -Lambdoidal Cranial bones are highly mobile- allows them to mold and slide to adjust and accommodate to the changing shape and character of the birth canal Various types of cranial deformities are encountered with early infancy Can occur in prenatal development Occur with growth Eight weeks: Posterior fontanel closed Six Months: union of suture lines Eighteen Months: Anterior fontanel closed After 12 years: sutures unable to be separated by increased ICP

14 Hydrocephalus “water on the brain”
Imbalance in the production and absorption of CSF in the ventricular system Causes: Impaired absorption of CSF fluid Obstruction of flow through ventricle Brain structures become compressed Most cases are from developmental defects Production of CSF > than absorption CSF accumulates in the ventricular system- increased pressure- passive dilation of the ventricles Impaired absorption: nonobstructive or communicative hydrocephalus Obstruction: obstructive or noncommunicative hydrocephalus- can occur at any point (infections, trauma) Defects: Arnold-Chiari malformation, aqueduct stenosis…) from birth to 2 yrs Intrauterine infections Older kids- lesions, intracranial infections, hemorrhage Imbalance of fluid in brain causes an increased accumulation of CSF in the ventricles- become dilated (ventriculomegaly) and compress the brain substance around the bony cranium -before fusion of cranial sutures- enlargement of the skull and dilation of ventricles -younger than partially closed suture lines- may become opened

15 Diagnosing Hydrocephalus
Time of onset and preexisting lesions Infants: Head circumferences and neuro signs CT MRI Infancy: before closure of sutures, they will have an enlarged head- daily head circumferences (abnormal/rapid head growth) Older infants: neurologic signs through pressure on the adjacent structure

16 Clinical Manifestations of Hydrocephalus
Infancy (early) Infancy (later) Infancy (general) Childhood Abnormal rapid head growth Frontal enlargement Irritable Headache on awakening Bulging fontanels Depressed eyes Lethargy Papilledema Dilated scalp veins Sun-setting sign Cries when picked up or rocked strabismus Separated sutures Pupils sluggish Infantile reflexes persist Macewen sign Change in LOC Thinning of skull bones Lower extremity spasticity Confusion/ incoherence Difficult suck and feeding vomiting Anterior bulging fontanel Macewen sign- cracked pot sound on perfusion Box 28-13, chapter 28, Wong

17 Management of Hydrocephalus
Direct removal of obstruction Placement of shunt Ventriculoperitoneal shunt (VP shunt) Associated with infection and malfunction High success rate with surgically treatment Vp shunt: drainage of the CSF from the ventricles to an extracranial compartment, ie peritoneum Catheter is threaded beneath the skin Placed to relieve csf obstruction- revisions are needed when signs of malfunction appear -initally very successful, associated with complications that interfere with continued shunt function or threaten a child’s life -infection**, malfunctions (kinking, plugging, separation of tubing) obstruction of tissue thrombosis- growth -s/s of increased ICP, declining neurologic status Surgical treatment with monitored medical management- 80% survival rate Mortality in first yr of treatment ½ have neurologic disabilities

18 Shunting Shunting Video
Shunting Video

19 Family Support Coping is difficult with patents Feel guilty, anxious
Uncertain outcome Continue to educate family Include family in patient care Possibility of long term rehabilitation Survival of cerebral insult: may have physical or mental limitations- long term rehab process

20 Nervous System Tumors CNS tumors account for 20% of all childhood cancers 3.3 cases per 100,000 occur in kids under 15 years old Difficult to treat No dramatic advancements or improvements seen vs other childhood cancers

21 Brain Tumors Most common solid tumors in children Infratentorial (60%)
Primairly in brain stem or cerebellum Usually see increased ICP (medulloblastoma, cerebellar astrocytoma, brainstem glioma) Supratentorial Mainly cerebrum (astrocytoma, hypothalamic tumors, optic pathway tumors)

22 Brain Tumor Diagnostics
s/s are related to: Location Size of tumor Child’s age Most common signs: Headache, vomiting s/s are vague and can be overlooked Detected by: MRI CT scan Official diagnosis with biopsy from surgery Infants with open sutures- no early signs will develop Obstruction Vomiting: increased icp compresses the brainstem- directly stimulates the vomiting center in medulla MRI: location and extent of tumor Ct

23 Treatment of Brain Tumors
Treatment of choice = total removal of tumor without neurologic damage Surgery, radiotherapy, chemotherapy Prognosis: Depends on size, tumor type, extent of disease Radiotherapy- shrink tumor before surgery Chemo- rec for kids under 3, recurrent tumors, nonresectable tumors Prognosis: advances in surgery, radiation, use of chemo has increased the long-term survival rates in kids

24 Nursing Management of Brain Tumors
Establish a baseline assessment Vital signs Look for sudden variations Frequent neurologic assessments Headache? Vomiting? Seizures? Child’s behavior positioning Postoperatively check muscle strength when awake Neuro assessment: pupil responses, LOC, sleep patterns, response to stimuli HA? Vom? Seiz? How long, time of day, aggravating factors Positioning depends on where the tumor is- check with MD, prevent sudden movements Facing away from light, non engaging in play

25 Intracranial Infections
Nervous system is limited in ways to respond to an infection Inflammatory process in brain affects: Meninges (meningitis) Brain (encephalitis) Meningitis has many origins bacteria, virus, or tuberculosis

26 Bacterial Meningitis Definition: acute inflammation of the meninges and CSF 10-15% of cases are fatal Caused by many bacterial agents H. Influenzae type b, S. pneumoniae, Neisseria Meningitidis Vascular dissemination or direct implantation Infective Process E. Coli in infancy Gets from vascular dissemination- organism in nasopharynx invades the underlying blood vessels and enters blood supply Direct implantation: penetration of wounds, skull fractures- opening in the skin- organism will spread to CSF  subarachnoid space Infective process: inflammation, exudation, WBC accumulation, tissue damage -brain edema, covered in purulent exudate -as infection extends to ventricles, pus, fibrin, or adhesions occlude passages and obstruct CSF flow

27 Clinical Manifestations of Bacterial Meningitis
Infants and Young Children Children and Adolescents (Classic picture) Fever Poor feeding Vomiting Irritable Frequent seizures Bulging fontanel Difficult to evaluate in this age group Abrupt onset, rash Fever, chills, headache Alteration in senses Seizures* Irritability/agitation Nuchal rigidity Positive Kernig & Brudzinski signs Kernig’s: pt supine, hip flexed 90 degees, knee cant be fully extended Brudzinski: passive flexion of neck causes flexion of both legs and thighs Box 28-5, Chapter 28 Wong

28 Clinical Manifestations of Bacterial Meningitis
Neonates: Specific Signs Neonates: Nonspecific Signs Very hard to diagnose Well at birth- behaves poorly a few days later Refuses feeds Poor sucking Vomiting/diarrhea Poor tone Lack of movement Weak cry Supple neck Hypothermia/fever Jaundice Irritable Drowsiness Seizures Respiratory irregulations cyanosis Box 28-5, Chapter 28 Wong

29 Diagnostic and Therapeutic Management of Bacterial Meningitis
Lumbar Puncture Elevated WBC count Decreased Glucose level Considered a medical emergency! Initial management: Isolation, iv antibiotics, fluids, monitored, treatment of complications LP: Fluid pressure is measured, samples are sent for culture (organism), gram stain, blood cell count, protein and glucose content. Emergency: early recognition and immediate implementation of therapy to prevent death or residual disabilities Drugs: initially give steriods to decrease ICP and herniation- not good for long-term use antibiotics

30 Management of Bacterial Meningitis
Hydration Quiet, decreased stimulation Side lying position Correct electrolyte imbalance Measure for s/s increased ICP Monitor for complications Prevention: Vaccines for children starting at 2 months Maintain fluid deficit then restrict to prevent cerebral edema Electrolytes- assoc with poor neuro outcome later Complications: DIC, shock, seizures, hearing loss Vaccines: A, C, Y and W-135 meningococci and H. Influenzae type b.

31 Nonbacterial (aseptic) Meningitis
Caused by many viruses! Abrupt or gradual onset Symptoms develop 1-2days after onset s/s vague Diagnosis is based on pt assessment and CSF findings Systematic treatment Nursing care similar to bacterial meningitis Vague: thought to be associated with a minor illness Treatment: tylenol for HA and pain, fluids

32 Encephalitis Definition: inflammatory process of the CNS which is caused by a variety of organisms Virus invades CNS or postinfection after a viral disease Cause in typically unknown Bacteria, spirocytes, fungi, protozoa, viruses**


34 Clinical Findings of Encephalitis
Initial findings are nonspecific Evolve to demonstrate neuro s/s Seizures, abnormal CSF Mild s/s for a few days, rapid recovery, to fulminating encephalitis with CNS involvement Onset Severe Cases Malaise Fever Headache/Dizziness Lethargy Neck Stiffness Nausea/Vomiting Tremors Speech Difficulties Altered Mental Status High Fever Stupor Seizures Disorientation Spasticity Coma Paralysis Initially- fever, altered mental status Sudden or gradual onset

35 Diagnosis and Management of Encephalitis
Based on clinical findings CT in late stages Some viruses are found in CSF Hospitalized for observation with supportive treatment Prognosis depends on age, organism, neurologic damage CT in late stages can show hemorrhagic areas in the frontotemporal region Herpes, mumps, measles, enteroviruses found in CSF Support symptoms: control of cerebral manifestations, adequate nutrition and hydration Can cause devastating neurologic injury Kids under 2 years- may have increased disability, learning, seizure disorders


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