chapter 45 cerebral dysfunction all elsevier items and derived items 2014, 2010, 2006, 2002, mosby,...

Chapter 45

Cerebral Dysfunction

All Elsevier items and derived items © 2014, 2010, 2006, 2002, Mosby, Inc., an imprint of Elsevier Inc.

The brain is well protected but vulnerable to pressure that may accumulate within the cranium

As pressure increases, signs and symptoms become more pronounced, and level of consciousness (LOC) deteriorates

Early signs and symptoms may be subtle

Increased Intracranial Pressure (ICP)

2All Elsevier items and derived items © 2014, 2010, 2006, 2002, Mosby, Inc., an imprint of Elsevier Inc.

Increased Intracranial Pressure (ICP) (Cont.)


Irritability, poor feeding High-pitched cry, difficult to soothe Fontanels: tense, bulging Cranial sutures: separated Eyes: setting-sun sign Scalp veins: distended

Clinical Manifestations of Increased ICP in Infants


Headache Forceful vomiting Seizures Drowsiness, lethargy Diminished physical activity Inability to follow simple commands

Clinical Manifestations of Increased ICP in Children


Bradycardia Decreased motor response to command Decreased sensory response to painful stimuli Alterations in pupil size and reactivity Extension or flexion posturing Decreased consciousness Coma

Late Signs of Increasing ICP


In descending order Full consciousness Confusion: impaired decision making Disorientation: to time and place Lethargy: sluggish speech

Levels of Consciousness


Obtundation: arouses with stimulation Stupor: responds only to vigorous and repeated

stimulation Coma: no motor or verbal response to noxious

stimuli Persistent vegetative state: permanent loss of

function of cerebral cortex

Levels of Consciousness (Cont.)


Pediatric Glasgow Coma Scale Three-part assessment

• Eye opening• Verbal response• Motor response

Score of 15: unaltered LOC Score of 8 or below: coma Score of 3: extremely decreased LOC (worst possible

score on the scale)

Coma Assessment


Coma Assessment (Cont.)


Vital signs Skin Eyes Motor function Posturing Reflexes

Neurologic Examination


Neurologic Examination (Cont.)


Laboratory tests Electroencephalography (EEG) Lumbar puncture Assessment of evoked potentials (auditory and

visual) Imaging

Radiography (rule out skull fractures, dislocations; evaluate degenerative changes, suture lines)

Computed tomographic (CT) scan Magnetic resonance imaging (MRI)

Special Diagnostic Procedures for Increased ICP


Outcome and recovery of unconscious child may depend on level of nursing care and observational skills

Emergency management Airway Reduction of ICP Treatment of shock

Nursing Care of the Unconscious Child


LOC Pupillary reaction Vital signs Frequency of assessment: depends on

condition; ranges from every 15 minutes to every 2 hours

Assessment Parameters for Increased ICP


Requires astute nursing observation Signs of pain

Increased agitation and rigidity ICP increased by pain Alterations in vital signs

Usually increase in heart rate, respiratory rate, and blood pressure and decrease in oxygen saturation

Pain Assessmentin the Comatose Child


Opioids: controversial Fentanyl + midazolam + vecuronium Acetaminophen and codeine Adequate dosage and regular administration Comfort measures Quiet, dimly lit environment

Pain Management in the Comatose Child


Airway management is primary concern Cerebral hypoxia lasting >4 minutes may cause

irreversible brain damage CO2 retention causes vasodilation, increased

cerebral blood flow, and increased ICP Gag and cough reflexes may be minimal Risk of aspiration of secretions is increased

Respiratory Management in the Comatose Child


Indications for ICP monitoring Glasgow Coma Scale score of less than 8 Traumatic brain injury with abnormal CT scan Deteriorating neurologic condition Subjective judgment regarding clinical appearance

and response

ICP Monitoring


Intraventricular catheter Subarachnoid bolt (Richmond screw) Epidural sensor Anterior fontanel pressure monitor

Types of ICP Monitors


Patient positioning Avoid neck vein compression Provide alternating-pressure mattress Elevate head of the bed 30 degrees

Avoiding activities that may increase ICP Eliminating or minimizing environmental noise Suctioning issues

Nursing Activities for Increased ICP


Intravenous administration of fluids and parenteral nutrition

Avoidance of overhydration Later: gastric feedings via nasogastric or

gastrostomy tube Continued monitoring for aspiration

Nutrition and Hydration for Increased ICP


Syndrome of inappropriate antidiuretic hormone and diabetes insipidus may accompany central nervous system (CNS) diseases

Altered pituitary secretion may result from hypothalamic dysfunction

Fluid replacement, electrolyte balance, medications specific to disorder should be provided

Diabetes insipidus should be addressed

Altered Pituitary Secretion


Antibiotics for infectious processes Corticosteroids for inflammation and edema Sedatives or antiepileptics Sedation or amnesic anxiolytics Barbiturates (controversial) Paralytic agents

Medications (As Indicated) for Increased ICP


Thermoregulation Elimination Hygienic care Positioning and exercise Stimulation Family support

Care Management of Increased ICP


Head injury Three major causes of brain damage in childhood

• Falls• Motor vehicle injuries• Bicycle- or sports-related injuries

Cerebral Trauma


Force of intracranial contents cannot be absorbed by the skull and musculoligamentous support of the head

The head is especially vulnerable to acceleration-deceleration injuries

A child’s response is different because of larger head size in relation to body and because of insufficient musculoskeletal support

Pathophysiology of Head Injury


Injuries that occur at a time of physical trauma Skull fracture Contusions Intracranial hematoma Diffuse injury

Primary Head Injuries


Primary Head Injuries (Cont.)


An alteration in neurologic or cognitive function with or without loss of consciousness

Transient and reversible Results from trauma to the head Generally followed by amnesia and confusion

Concussion


Contusion: visible bruising Laceration: tearing of tissue Coup: bruising at point of impact Contrecoup: bruising at a site far removed from

point of impact Possibility of multiple sites of injury

Contusion and Laceration


Because of flexibility, the immature skull can withstand a greater increase in deformities before fracture

To produce skull fracture in infant, force must be extreme

Skull Fractures in Children


Linear Depressed Comminuted Basilar Open Growing

Types of Skull Fractures


Epidural hemorrhage Bleeding between the skull and the dura

Subdural hemorrhage Bleeding between the dura and the arachnoid

membrane Cerebral edema

Associated with traumatic brain injury Increased ICP with herniation

Complications of Head Trauma


Complications of Head Trauma (Cont.)


Detailed history Assessment of airway, breathing, and circulation Evaluation for shock Neurologic examination, LOC assessment Assessment of vital signs Special tests: CT scan, MRI, behavioral

assessment

Diagnostic Evaluation of Head Trauma


Postconcussion syndrome Posttraumatic seizures Structural complications such as hydrocephalus Duration of manifestations from several days to

months

Posttraumatic Syndromes


Care in hospital if severe injuries, LOC for several minutes, prolonged or continued seizures

Nothing administered orally at first Surgical therapy Prognosis

Therapeutic Management of Head Trauma


Assess frequently: vital signs, neurologic status, and LOC

Provide analgesia and sedation Perform careful observation and recording Provide family support Arrange for rehabilitation Teach prevention

Care Management of Head Trauma


A major cause of accidental death in children Can occur with even small quantity of water

(even as small as a pail of water) Near drowning: survival for at least 24 hours

after submersion

Submersion Injury (Near Drowning)


Hypoxia Pulmonary edema Atelectasis Airway spasm

Aspiration Hypothermia

Increased risk because of the largeness of surface area in comparison with body mass

Pathophysiology of Drowning


Emergency resuscitative efforts at the scene Management: based on degree of cerebral insult Aspiration pneumonia: frequent complication Hospitalization for observation Prognosis: best predictor is the length of

submersion

Therapeutic Management of Drowning


Care depends on condition of the child Help parents cope with feelings of guilt Parental anxiety is related to prognosis Teach prevention of submersion injuries

Nursing Care Management of Drowning


Brain tumors and neuroblastoma are derived from neural tissue

CNS tumors account for approximately 20% of childhood cancers

CNS tumors are difficult to treat, and survival rates are poor

Nervous System Tumors


Brain tumors are the most common solid tumors in children

They can arise from any cell in the brain or spinal cord

Infratentorial tumors involve the cerebellum and brainstem

Supratentorial tumors occur mainly in the cerebrum

Brain Tumors


Signs and symptoms: related to anatomic location, size, and child’s age

Presenting clinical signs Lumbar puncture MRI, CT scan, EEG Definitive diagnosis based upon specimens

obtained during surgery

Diagnostic Evaluation of Nervous System Tumors


Depends on type of tumor Surgery Radiotherapy Chemotherapy Combination of modalities Prognosis

Variable

Therapeutic Management of Nervous System Tumors


Prepare child and family for diagnostic and operative procedures

Consider how disease affects child’s body image Prevent postoperative complications Support child and family Promote return to optimum functioning

Care Management of Nervous System Tumors


Neuroblastoma is the most common malignant extracranial solid tumor of childhood

Majority of tumors develop in adrenal gland or retroperitoneal sympathetic chain

Other sites include the head, neck, chest, and pelvis

Metastasis may have already occurred before diagnosis is made

Neuroblastoma


Objective: to locate primary site and sites of metastasis

Signs and symptoms: depend on location and stage of disease

Skeletal survey Radiologic studies, bone marrow evaluation Intravenous pyelography to evaluate renal

involvement

Diagnostic Evaluation of Neuroblastoma


Clinical staging to establish treatment plan Surgery to remove tumor and obtain biopsy

samples Radiation, chemotherapy Bone marrow transplantation Stem cell rescue

Therapeutic Management of Neuroblastoma


95% survival at 5 years for low-risk disease 30% survival at 5 years for high-risk disease In general, the younger the patient is at

diagnosis, the better the prognosis Tumor may regress spontaneously as embryonic

cells mature and with development of active immune system

Prognosis for Neuroblastoma


CNS has limited response to injury Difficult to determine cause from clinical

manifestations Laboratory studies required to identify causative

agent Inflammation: can affect meninges, brain, or

spinal cord

Intracranial Infections


Acute inflammation of the meninges and cerebrospinal fluid (CSF)

Decreased incidence since introduction of “Hib” vaccine in 1990

Can be caused by various bacterial agents Streptococcus pneumoniae Neisseria meningitis Group β streptococci Staphylococcus aureus Escherichia coli

Bacterial Meningitis


Droplet infection from nasopharyngeal secretions

Appears as extension of other bacterial infection through vascular dissemination

Organisms then spread through CSF Increased risk with the number of contacts Seasonal variation: late winter and early spring

Transmission of Bacterial Meningitis


Diagnostics: lumbar puncture is definitive diagnostic test

Therapeutic management Isolation precautions Antimicrobial therapy Restricted hydration Maintenance of systemic shock Maintenance of ventilation Control of seizures and temperature

Therapeutic Management of Bacterial Meningitis


Causative agents are principally viruses Arbovirus, herpes simplex virus, cytomegalovirus,

human immunodeficiency virus, and adenovirus Diagnosis is based upon CSF findings Onset is abrupt or gradual Manifestations include headache, fever, malaise Treatment is primarily symptomatic

Nonbacterial Meningitis(Aseptic Meningitis)


Inflammatory process of CNS with altered function of brain and spinal cord

Variety of causative organisms Direct invasion of the CNS by a virus Postinfectious involvement of the CNS after a viral

disease Vector reservoir in United States: mosquitoes

and ticks

Encephalitis


Malaise Fever Headache/dizziness Stiff neck Nausea/vomiting Ataxia Speech difficulties

Clinical Manifestations of Encephalitis


High fever Stupor/seizures Disorientation/spasticity Coma Ocular palsies Paralysis

Clinical Manifestations of Severe Encephalitis


Hospitalization for observation Supportive treatment ICP monitoring: may be required Follow-up care with reevaluation and

rehabilitation In very young children, possibility of increased

neurologic disability

Therapeutic Management of Encephalitis


Rabies is an acute infection of the CNS It is caused by virus transmitted by saliva of

infected animal (skunks, raccoons, bats) Virus multiplies in muscles, and infection is fatal

if untreated Incidence in humans is highest among those

<15 years old

Rabies


Inactivated rabies vaccines Globulins Thorough cleansing of the wound Passive immunization with human rabies

immunoglobulin as soon as possible After exposure: human diploid cell rabies

vaccine

Therapeutic Management of Rabies


A disorder defined as toxic encephalopathy associated with other characteristic organ involvement

Characterized by fever, profoundly impaired consciousness, and disordered hepatic function

Reye Syndrome


Cause is not well understood Most cases follow common viral illness

Influenza Varicella

Potential association exists between aspirin therapy for fever and development of Reye’s syndrome

Reye’s Syndrome (Cont.)


Diagnostic evaluation Liver biopsy

Therapeutic management Early diagnosis and aggressive therapy

Prognosis Recovery: good, in view of the gravity of the disease

Reye’s Syndrome (Cont.)


Caused by excessive and disorderly neuronal discharges in the brain

Determined by site of origin Most common neurologic dysfunction

in children Symptom of an underlying disease process

Seizure Disorders


Two or more unprovoked seizures Caused by a variety of pathologic processes in

the brain Optimal treatment and prognosis: require an

accurate diagnosis and determination of cause

Epilepsy


Acute symptomatic Head trauma or meningitis

Remote symptomatic Prior brain injury such as encephalitis or stroke

Cryptogenic No clear cause

Idiopathic Genetic in origin

Causes of Seizures


Partial Local onset and involves a relatively small location of

the brain Generalized

Involves both hemispheres without local onset Unclassified

Seizure Classification


Goal: to control seizures or reduce the frequency and severity

Discovery and correction of the cause Management

Drug therapy Ketogenic diet Vagus nerve stimulation Surgical therapy

Therapeutic Management of Seizure Disorders


Status epilepticus Prognosis Long-term care Triggering factors Treatment goal: living as normal a life as

possible

Therapeutic Management of Seizure Disorders (Cont.)


Transient disorder of childhood Affect approximately 2%-5% of children Usually occur between ages 6 months and 3

years Rare after age 5 years Twice as frequent in boys Cause: uncertain

Viral infection

Febrile Seizures


Suture and fontanel ossification 8 weeks of age: posterior fontanel closed 6 months of age: fibrous suture lines and interlocking

of serrated edges 18 months of age: anterior fontanel closed After 12 years of age: sutures unable to be separated

by increased ICP

Cranial Deformities


Caused by an imbalance in the production and absorption of CSF

Pathophysiology Impaired absorption of CSF within the subarachnoid

space Obstruction through the ventricular system Communicating and noncommunicating

hydrocephalus

Hydrocephalus


Hydrocephalus (Cont.)


Result of developmental defects Usually apparent in early infancy Other causes include neoplasms, infection, and

trauma Often associated with myelomeningocele

Causes of Hydrocephalus


Relief of hydrocephalus Treatment of complications Assessment of problems related to the effects of

motor development Treatment: most often surgical

Ventriculoperitoneal shunt

Therapeutic Management of Hydrocephalus


Therapeutic Management of Hydrocephalus (Cont.)


Period of greatest risk is 1 to 2 months after shunt placement

Infections Septicemia Bacterial endocarditis Wound infection Shunt nephritis Meningitis

Treatment: massive-dose antibiotics or shunt removal

Shunt Infection


When caring for an unconscious child, an appropriate nursing intervention is to

A. Change the child’s position infrequently to minimize the chance of increased ICP

B. Avoid using narcotics or sedatives to provide comfort and pain relief

C. Monitor fluid intake and output carefully to avoid fluid overload and cerebral edema

D. Give tepid sponge baths to reduce fever because antipyretics are contraindicated

Question


chapter 45 cerebral dysfunction all elsevier items and derived items 2014, 2010, 2006, 2002, mosby,...

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