The document discusses hydrocephalus in children, defining it as a condition characterized by excessive cerebrospinal fluid in the brain. It covers the etiology, pathophysiology, clinical features, imaging studies, and treatment of hydrocephalus, noting that the mainstay of treatment is surgical placement of a ventriculoperitoneal shunt to drain excess cerebrospinal fluid from the brain to the abdomen. Complications of hydrocephalus and hydrocephalus treatment are also reviewed.
2. DEFINITION
Diverse group of conditions characterised by excessive CSF
in the brain. Thus:
1. Impaired flow
2. Decreased reabsorbtion
3. Increased production
6. PATHOPHYSIOLOGY
Accumulation of fluid leads to increased pressure in
the proximal part of pathway and progessive
dilatation.
Pressure effect on the surrounding nervous pathways
and delicate portions of brain: pyramidal tracts,
cortex, tectum
16. Ketan Thummar-Hydrochephalus in children
Patient Report: Assessments
Neurological/behavioral
Pupils sluggish L>R
Irritable, crying
VS: WNL
History:
• Sunsetting eyes
• Projectile vomiting
• Irritability
• Full fontanel
• Slightly separated
sutures
• Floppy
• Lethargic
Labs:
• LP - elevated pressure
• No RBCs or WBC’s
• CT scan/serial
transilluminations
demonstrate fluid/
no
signs of trauma, swelling,
or bleeding
17. Ketan Thummar-Hydrochephalus in children
Patient Report: Assessments
Hydration
Skin turgor: Skin supple
Weight: WNL
I&O: diaper dry
VS: WNL
History:
Last void 8 hours ago
Vomiting: 30-60 cc q 1h
Labs:
Elevated specific gravity
Normal blood glucose
18. Ketan Thummar-Hydrochephalus in children
Patient Report: Assessments
Nutrition
Well developed, floppy
Lethargic
Weight: Weight WNL
I&O: Intake = Output
Vs: WNL
History:
Last void 8 hours ago
Vomiting
19. Ketan Thummar-Hydrochephalus in children
Patient Report: Assessments
Family
Parental anxiety
Lack of primary, well child care
Poor eye contact
Mother’s comments
History:
Labs:
Family signs of stress
No signs of trauma
20. Ketan Thummar-Hydrochephalus in children
Patient Report: Assessments
Developmental
Patient has met age-appropriate milestones
Patient is alert, crying, irritable
Patient able to roll and sit with support
Developmental Milestones
• Overall development
Gross and fine motor
Language
Cognitive
Social skills
• Social and Emotional Development
• Speech and Language Development
21. Ketan Thummar-Hydrochephalus in children
Patient Priority: Safety/Developmental Care
Nursing Actions
Provide developmentally-appropriate
safety measures
Siderails
Name band
Allergy bracelet
Provide developmentally-appropriate
toys and stimulation
22. Ketan Thummar-Hydrochephalus in children
Patient Priority:
Hydration
Nursing Actions
Principles of IV therapy
IV therapy - replace for losses
(bolus)
Restrict fluids as indicated
for IICP
Assess and maintain IV site
23. Ketan Thummar-Hydrochephalus in children
Patient Priority:
Care of the patient related to surgery
Nursing Actions
Consents, teaching, preparation, sedation
Assessments: prep for the operating room
Post-operative care:
Incision assessment
Advancing diet and
activity as tolerated
Pumping of shunt
as ordered
Assess for infections
Pulmonary care
24. Ketan Thummar-Hydrochephalus in children
Patient Priority: Family-centered care
Nursing Actions
Ensure patient safety
Family-oriented teaching and explanations
Include family in care
Adapt family orientation for specific family needs
Family support, counseling, and referral
25. Ketan Thummar-Hydrochephalus in children
Patient Priority: Pain assessment and
management/meeting comfort needs
Nursing Actions
Pain assessment across the lifespan -
Using behavioral signs/vital signs/parental report
Non-pharmacological measures Positioning, music, contact, comfort measures
Pharmacological measures - Fentanyl (Duragesic) or
acetaminophen with codeine (Tylenol #3 )
Assessing response to pain interventions
Documentation
26. Ketan Thummar-Hydrochephalus in children
Complications:
Signs of increased intracranial pressure (IICP)
The night before surgery the patient
demonstrates signs of IICP
Monitor for Symptoms:
• Increased systolic
blood pressure
• Decreased HR and RR
• Irritability
• Sluggish pupils
• Vomiting
• Decreased level of
consciousness
Nursing Actions:
• Providae oxygen
• Encourage ventilation
to blow off CO2
• Diuretics to decrease ICP mannitol (Osmitrol)
• Surgery
• Monitor
27. Ketan Thummar-Hydrocephalus in children
Complications: Hypothermia
Following surgery, during frequent vital sign while in
the PACU, the nurse assesses the child’s temperature.
The electronic thermometer reads 35.8 C (96.5 F).
Nursing Actions:
Monitor for Symptoms:
• Warming blankets
• Warmed blankets
• Warmed intravenous
fluids
• Frequent assessments
• Body temperature
• Signs of vasoconstriction
• Decreased level of
consciousness
28. Ketan Thummar-Hydrocephalus in children
Complications: Seizures
Patient has a seizure upon transfer to the patient care unit.
The child becomes mildly cyanotic around the lips, has
rapid eye movements, demonstrates tonic/clonic
movements of upper and lower extremities.
Monitor for Symptoms:
Aura, seizure activity (tonic/clonic movement, random muscle
movement,eye movement, cyanosis)
Nursing Actions:
Maintain patent airway, seizure precautions, padded siderail,
loosen clothing, oxygen, suction at bedside, safety, monitor
timing and characteristics of seizure activity,
Anticonvulsants: phenytoin (Dilantin); status epilepticus
diazepam (Valium)
29. Ketan Thummar-Hydrochephalus in children
Complications: Infection
Two days after the insertion of the VP shunt,
the patient develops signs of a shunt infection.
Temperature at 1600 39.4 C (103 F).
Child demonstrating behaviors consistent with IICP.
Monitor for Symptoms:
• Temperature
• Pain and tenderness
• Irritability
• Incisional changes,
abdominal distension/ pain
assess for meningitis
(nuchal pain, etc.)
Nursing Actions:
• Culture wound (+S. Aureus)
• CSF (from LP)
• Provide antipyretics
acetaminophen [Tylenol]or
ibuprofen [Advil]
• Administer antibiotics
cefuroxine [Ceftin])
• Comfort
30. Ketan Thummar-Hydrochephalus in children
Complications: Family Stress
During the post-operative period, the unit nurses note
the interactions are strained between the mother and
father. The father interacts little with the infant but visits
frequently. Both parents express concern about cost of
hospitalization and missed work.
Monitor for Symptoms:
Nursing Actions:
• Body language
• Family support,
counseling, and referral
• Family aspects
• Role as mandatory
(family communication,
boundaries, dynamics,
reporters
and decision-making)
• Referral to resources/
• History
social service consult
• Stress levels
• Assess for cardinal signs of abuse
31. PROGNOSIS
Increased risk for developmental disabilities
Mean IQ is reduced compared to general population
Abnormalities in memory
Some patients show aggressive or delinquent
behavior.
35. Definition
Meningitis is the inflammation of the membranes
surrounding the brain & spinal cord, including the
dura, arachinoid & pia matter.
36. Incidence
Meningitis can occur at all ages but it is commonest
in infancy. While 95% of the cases take place between
1 month- 5 years of age.
It is more common in males than females.
37. Transmission
The bacteria are transmitted from person to
person through droplets of respiratory or throat
secretions.
Close and prolonged contact (e.g. sneezing and
coughing on someone, living in close quarters or
dormitories (military recruits, students), sharing
eating or drinking utensils, etc.)
The incubation period ranges between 2 -10 days.
39. Signs & Symptoms
The symptoms of meningitis vary and depend on the age of the
child and cause of the infection. Common symptoms are:
Flu-like symptoms
fever
lethargy
Altered consciousness
irritability
headache
photophobia
stiff neck
Brudzinski sign
Kernig sign
skin rashes
seizures
40. Symptoms
Other symptoms of meningitis in Neonates/infants
can include:
Apnea
jaundice
neck rigidity
Abnormal temperature (hypo/hyperthermia)
poor feeding /weak sucking
a high-pitched cry
bulging fontanelles
Poor reflexes
42. Pyogenic Meningitis
ETIOLOGY
‘Meningococcal’ meningitis- N. meningitidis. A, B, C and W135) are
recognized to cause epidemics
The commonest organisms according to age groups are:
0-2 months
E.Coli, Group B streptococci, S.Aureus, Listeria
Monotocytogenes
2 months- 2yrs H.Influenzae type b, S.Pneumoniae,
N.Meningitides.
2 yrs – 15+yrs
N.Meningitides (serotypes A,B,C, Y & W135)
S.Pneumoniae (serotypes 1,3, 6,7)
H.Influenzae
43. Bacterial Meningitis
Pathogenesis:
Entry of organism through blood brain barrier
release of cell wall & membrane products
Outpouring of polymorphs & fibrin
cytokines & chemokines
Inflammatory mediators
Inflamed meninges covered with exudate (most
marked in pneumoccocal meningitis).
44. Pathogenesis
Meningeal irritation signs: inflammation of the spinal nerves &
roots.
Hydrocephalus: Adhesive thickening of the arachinoid in basal
cistern or fibrosis of aqueduct or Foramina of Lushka or
Magendie
Cerebral atrophy: thrombosis of small cortical veins resulting in
necrosis of the cerebral cortex.
Seizures: depolarisation of neuronal membranes as a result of
cellular electrolyte imbalance.
Hypoglycorhachia: decreased transport of glucose across
inflammed choroid plexus & increased usage by host.
45. Viral meningitis
Viral meningitis comprises most aseptic
meningitis syndromes. The viral agents for aseptic
meningitis include the following:
Enterovirus (polio virus, Echovirus,
Coxsackievirus )
Herpesvirus (Hsv-1,2, Varicella.Z,EBV )
Paramyxovirus (Mumps, Measles)
Togavirus (Rubella)
Rhabdovirus (Rabies)
Retrovirus (HIV)
46. Fungal Meningitis
It’s rare in healthy people, but is a higher risk in those
who have AIDS, other forms of immunodeficiency or
immunosuppression.
The most common agents are Cryptococcus
neoformans, Candida, H capsulatum.
47. Parasitic Meningitis
Infection with free-living amoebas is an infrequent
but often life-threatening human illness.
It’s more common in underdeveloped countries
and usually is caused by parasites found in
contaminated water, food, and soil.
The most common causative agents are:
Free-living amoebas (ie, Acanthamoeba, Balamuthia,
Naegleria)
Helminthic eosinophilic meningitis
48. Non-infectious meningitis
Rarely, meningitis can be caused by exposure to certain
medications, such as the following:
Immune globulin
Levamisole
Metronidazole
Mumps and rubella vaccines
Nonsteroidal anti-inflammatory drugs (e.g., ibuprofen,
diclofenac, naproxen)
49. Tuberculous meningitis
It’s a complication of Childhood
tuberculosis & common cause of
prolonged morbidity, handicap &
death.
Children below 5 years are specially
prone.
50. CLINICAL FEATURES
Always sec. to primary tuberculosis.
First Phase: Vague symptoms.
Child doesn’t play, is irritable, restless or drowsy.
Anorexia & vomiting may be present
Older child may complain of headache.
Possibly preceding history of Measles or another illness
with incompletely recovery
51. SECOND PHASE:
Child is drowsy with neck stiffness, &
rigidity.
Kernig & Brudzinski sign may become
positive, anterior fontanels bulges
Twitching of muscles, convulsions, raised
temperature.
strabismus, nystagmus, and papilloedema
may be present.
Fundoscopy: Choroidal TB may be seen
52. TERMINAL PHASE
Child is characteristically comatose
with opisthotonus, & multiple focal
paresis.
Cranial nerve palsies are present.
High grade fever often occurs
terminally.
53. Diagnostic Tests
Lumbar Puncture: pressure usually raised,
10-500 PMNs early but later lymphocytes
predominate
Protein- 100-500,raised
Glucose less than 50mg/dl in most cases
Culture for tubercle bacilli.
Presence of tuberculous focus elsewhere in the
body is strong supportive diagnosis.
Chest X-Ray.
Tuberculin skin test.
54. Treatment
Antituberculous Therapy:
Includes simultaneous administration of 4 drugs
(Isoniazid, rifampicin,streptomycin , pyrazinamide) for
first 3 months, followed by 2 drugs for another 15 months
usually Rifampicin & INH.
Total period: 18 months.
55. Treatment
STEROIDS: to reduce cerebral edema and to prevent
subsequent fibrosis & subsequent obstruction to CSF
2mg/kg/24 hours of prednisolone for 6-8 weeks at the start
of treatment starting 3 days after initiation of anti
tuberculous therapy.
56. Examination
General physical- Check for Consciousness level according to GCS
scoring, jaundice or irritability.
Resuscitation: incase of septic shock, or DIC.
Vitals: temperature , HR, B.P., R/R.
Signs of Increased ICP- Bulging fontanelle, headache, nausea,
vomiting, ocular palsies, altered level of consciousness, and
papilledema
Fundus: papilloedema
CN palsies: (esp. occulomotor, facial, and auditory)
57. Examination
Meningismus - check for nuchal rigidity with passive
neck flexion (gives 'involuntary resistance).
Brudzinski sign (hip & knee flexion with neck
movement)
Kernig sign (extend knee with hip flexed)
Hemiparesis.
Rash: petechial or purpuric rash (not only in
meningococcal but also pneumococcal bacteremia).
62. Diagnostic Tests
Latex particle agglutination: detects presence of
bacterial antigen in the spinal fluid. useful for detection
of H.influenzae type b, S.Pnemoniae, N.Meningitidis,
E.Coli
Concurrent immuno-electrophoresis (CIE)-used for
rapid detection of H.influenza, S.pneumoniae &
N.meningitides.
Smears: taken from purpuric spots may show
meningococci in Meningococcaemia
DNA sequences : are helpful in identifying bacteria
64. Treatment
Steroids:
Dexamethasone useful for H.influenzae type b, First
dose should be given 1 hr prior to starting
antibiotics.
Antibiotics IV.
Duration:1-3 weeks depending on age & type of
organisms.
65. Treatment
Initial till results of
Ampicillin
Probable/Proved
Penicillins
C/S are known
Meningococci
300mg/kg/day+
Chloramphenicol
75-100mg.kg/day
2-5 lac units /kg/day
69. Prevention
The vaccines against Hib, measles, mumps, polio,
meningococcus, and pneumococcus can protect against
meningitis
Hib vaccine: all infants should receive at 2,4,6 months of
age & booster 1 year later.
After 1 year 1 dose is given till the age of 5 years.
Pneumococcal vaccine: 0.5 ml is given IM (<2 yrs)
70. Prevention
High-risk children should also be immunized routinely.
Vaccination before travelling to an endemic area
Chemoprophylaxis for susceptible individuals or close
contacts:
H influenzae type b : Rifampin(20 mg/kg/d) for 4 days
N meningitidis: Rifampin (600 mg PO q12h) for 2 days upto
10weeks
Ceftriaxone (250 mg IM) single dose or
Ciprofloxacin(500-750 mg) single dose.
71. Complications
Bacterial meningitis may result in
Cranial nerve palsies
Subdural empyema
Brain abscess
Hearing loss
Obstructive hydrocephalus
Brain parenchymal damage: Learning disability, seizures,
Mental retardation.
Septic shock
Ataxia
Stroke
SIADH (Na+ <130 mE/l), puffiness of face, dec UO.
72. Treatment of Complications:
Convulsions: Diazepam I.V, Can be
repeated q4 hours as required.
Cerebral edema: *I.V Mannitol 1g/kg in 20-
30 mins 6-8 hourly given for first few days.
IV Dexamethasone can then be used 6 hourly.
73. Subdural effusion:
Aspirate subdural effusion if large.
Shock: Treat with IV Fluids, maintanence of BP.
SIADH: Increase body weight, decreased serum
osmolality, hyponatremia.
Prevented by fluid restriction to 800-1000ml/m2/24
hours.
Hyperpyrexia: Tepid sponging, correction of
dehydration.
74. Nursing care
Obtain a history of recent infections such as
upper respiratory infection, and exposure to
causative agents
Assess neurologic status and vital signs,signs of
meningeal irritation
Assess sensorineural hearing loss (vision and
cranial nerve damage.
(eg, facial nerve d diminished cognitive function.
75. Cont;
Reducing Fever
Administer antimicrobial agents on time to
maintain optimal blood levels.
Monitor temperature frequently or continuously,
and administer antipyretics as ordered.
Institute other cooling measures, such as a
hypothermia blanket, as indicated.
77. Cont;
Enhancing Cerebral Perfusion
Assess LOC, vital signs, and neurologic parameters
frequently. Observe for signs and symptoms of ICP (eg,
decreased LOC, dilated pupils, widening pulse
pressure).
Maintain a quiet, calm environment to prevent
agitation, which may cause an increased ICP.
Prepare patient for a lumbar puncture for CSF
evaluation, and repeat spinal tap, if indicated. Lumbar
puncture typically precedes neuroimaging
Notify the health care provider of signs of deterioration:
increasing temperature. decreasing LOC. seizure
78. Cont;
Redusing Pain
Administer analgesics as ordered; monitor for
response and adverse reactions. Avoid opioids which
may mask a decreasing LOC.
Darken the room if photophobia is present.
Assist with position of comfort for neck stiffness, and
turn patient slowly and carefully with head and neck
in alignment.
Elevate the head of the bed to decrease ICP and
reduce pain.
79. Cont;
Promoting Return to Optimal Level of Functioning
Implement rehabilitation interventions after admission
(eg, turning, positioning).
Progress from passive to active exercises based on the
patient's neurologic status.
Patient Education and Health Maintenance
Advice close contacts of the patient with meningitis
that prophylactic treatment may be indicated: they
should check with their health care providers or the
local public health department.
80. Cont;
To help prevent the development of meningitis,
teach patients with chronic sinusitis or other
chronic infections the importance of proper
medical treatment.
Encourage the patient to follow medication
regimen as directed to fully eradicate the
infectious agent.
Encourage follow-up and prompt attention to
infections in future.
81. Cont;
Inform patient who have children about
the importance of vaccination with measles,
mumps, rubella vaccine, H. influenzae type
B vaccine, pneumocococcal vaccine as a
preventive measure. Vaccination is
recommended for children younger than
school age.
82. Prognosis
It depends on the age of the patient, the duration of the
illness, complications, micro-organism & immune status.
Patients with viral meningitis usually have a good
prognosis for recovery.
The prognosis is worse for patients at the extremes of age
(ie, <2 y, >60 y) and those with significant comorbidities
and underlying immunodeficiency.
Patients presenting with an impaired level of
consciousness are at increased risk for developing
neurologic sequelae or dying.
83. Prognosis
A seizure during an episode of meningitis also is a
risk factor for mortality or neurologic sequelae.
Acute bacterial meningitis is a medical emergency
and delays in instituting effective antimicrobial
therapy result in increased morbidity and
mortality.
The prognosis of meningitis caused by
opportunistic pathogens depends on the
underlying immune function of the host as may
require lifelong suppressive therapy.
84.
85.
86. DEFINITION
Convulsion is involuntary contraction or
series of contraction of voluntary muscle.
It occur due to disturbance of brain
function resulting from abnormal
excessive electrical discharge from brain.
It may be associated with alteration of
level of consciousness.
Convulsion is also termed as SEIZURE.
87. CAUSES OF CONVULSION
NEONATAL PERIOD :
•
•
•
•
asphyxia & injury
Hypoglycemia & hypocalcemia
Narcotic & anesthetic drug
Septicemia, meningitis Birth, tetanus ,
kernicterus
• Congenital malformation
• Intra uterine infection
88. SIGNS & SYMPTOMS
Twiching of limb
Tongue bite
Discharge from the mouth
Pale face
sucking movement
Tremors
89. Infant & young children
Febrile convulsion
CNS infection
Accidental & non accidental
injury
Metabolic disturbance
Drug & poison
90. Febrile convulsion
It refers to the seizures
associated with fever but
excluding those related to CNS
infection.
It is related to increase in body
temperature rather than degree of
91. Types
Typical febrile
convulsion :-
• it is usually found in children between 6 month
& 5 years of age.
• The fits occur within 24 hours of the onset of
fever.
• Higher incidence occur in twins & genetic
predisposition or immature neuronal membrane.
92. ATYPICAL FEBRILE
CONVULSION
There may have abnormal EEG
for 2 weeks after attack.
The children may have focal
convulsion of more than 20
minutes duration even without
significant fever.
97. EPILEPSY
Epilepsy is recurrent episodic
paroxysmal transient disturbance of
brain function due to abnormal
electrical activity of neurons.
It is manifested as abnormal motor
sensory or psychomotor phenomena &
loss of consciousness.
106. MYOCLONIC SEIZURE
1. Mental retardation
2. Cerebral abnormality
3. Contraction of muscles of trunk,
neck, extremities
4. Duration: less than 1min
107. PARTIAL SEIZURES
SIMPLE PARTIAL SEIZURES
with motor sing
with somato-sensory or special
sensory
with autonomic manifestation
COMPLEX PARTIAL SEIZURES
Impaired consciousness
108. MEDICAL MANAGEMENT
Phenoberbital
: 3 to 5mg/kg/day
Diphenylhydantoin : 10 to
20mg/kg/day
Carbamazepin
: 10 to
20mg/kg/day
Sodium valproate : 15 to
20mg/kg/day
Ethosuximide
: 10 to
109. NURSING MANAGEMENT
Ensuring safety during seizures
protect child from injury
side rail of bed
oxygen therapy should be given
close observation & monitoring child
condition for vital sign & airway
110. Preventive respiratory arrest &
aspiration
loosen the clothing around neck &
placing the child flat
Do not give anything between teeth
or in mouth when teeth are
clenched
during convulsion
Clear airway, remove secretion &
111. Providing health teaching
Continuation of medication, care during convulsion &
diet therapy, restricted activities.
DIET THERAPY
Ketogenic diet should be given.
Protien & fat amount should be calculated.
Child should not be given IV fluid with dextrose.
Strict fluid restriction
113. Head injury includes any
injury including scalp,
skull, meninges or any
portion of the brain caused
by external forces.
It is one of the important
cause of childhood
mortality & morbidity.
One third of all head
injury cases are children.
114. CAUSES
NEONATES - birth injury
instrumental delivery
TODDLER - fall from height
hits on head by hard object
OLDER
CHILDREN
- automobile accident
road traffic accident
sports injury
116. Diagnostic test
Physical & neurological examination
Examination of blood, urin , CSF
EEG
X-RAY of skull
CT SCAN
MRI
117. Fracture of the skull
A typical “ping-pong” fracture may
occur due to elasticity of bone.
The fracture may be fissured or
depressed type.
Older children may have comminuted
fracture with dural tear & laceration
with brain damage.
118. INTRACRANIAL
HEMORRHAGE
Excessive moulding of skull bone
Rupture of delicate surface veins
leads to acute subdural
hemorrhage
About 20 to 25 % neonatal death
due to intracranial hemorrhage
119. CONCUSSION OF BRAIN
Concussion is reversible neurological
dysfunction
Transient loss of consciousness &
loss of memory
Injury at occipital area & shearing
srain at brain stem
120. CEREBRAL CONTUSION
It is bruising or petechial
hemorrhage in brain tissue
It consist of hemorrhagic brain
necrosis & infraction
Contusion at frontal & temporal
lobe are common
122. ACUTE SUBDURAL HEMATOMA
It results from any severe injury.
It is an accumulation of fluid, blood within potential
subdural space between dura & arachnoid.
When sutures are not fused, the hematoma can grow
slowly.
123. BRAIN SWELLING
It may be occur due to
vascular congestion, may be
due to neurogenic vasoparalysis
& increase blood flow.
124. SIGNS & SYMPTOMS
Loss of consciousness
Respiratory obstruction
Increase icp
Headache
Vommiting
Convulsion
Loss of memory
Bladder bowel dysfunction
126. NURSING MANAGEMENT
Maintain the airway
Establishment of breathing
Assessment of neurological status
Maintain nutritional status
Prevent infection & related
complication
Notas del editor
Image of a child with hydrocephalus and suspected child abuse