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 http://www.youtube.com/watch?v=8tf5VewEfGs
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