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.

1. HYDROCEPHALUS IN
CHILDREN
Ketan Thummar
3rd B.Sc Nursing
RN:40

2. DEFINITION
Diverse group of conditions characterised by excessive CSF
in the brain. Thus:
1. Impaired flow
2. Decreased reabsorbtion
3. Increased production

3. FLOW OF CSF

4. ETIOLOGY
COMMUNICATING (non obstructive)
1. AQUEDUCTAL STENOSIS: genetic(sex linked
recessive), neurofibromatosis, mumps
2. AQUEDUCTAL GLIOSIS: meningitis, intraventicular
hemorrhage
3. AQUEDUCTAL COMPRESSION: malformations of
the great vein of galen
4.Dandy walker
5.Posterior fossa tumors

5. ETIOLOGY
NON COMMUNICATING( obstructive)
1. Meningitis with thick purulent exudates- s.
Pneumoniae, mycobacterium tuberculosis.
2. Subarachnoid hemorrhage
3. Leukemic infiltrates

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

7. PATHOPHYSIOLOGY

8. CLINICAL FEATURES
SYMPTOMS:
Irritability
Big head
Poor feed
Lethargy
Vomiting
In older patients:
Headache
 Changes in personality
 Academic deterioration


9. CLINICAL FEATURES
SIGNS:
Anterior fontanel wide open and bulging, increased
head circ.
Dilated scalp veins
Setting sun sign
Brisk tendon reflexes, spasticity
Clonus, babinsky
Macewen sign “cracked pot”
Prominent occiput (dandy-walker)

10. Child with hydrocephalus

11. IMAGING STUDIES
X-ray plain films:
Separation of sutures
Erosion of posterior clinoids
Increased convolutional markings (beaten silver
appeareance)
Ultrasound
CT SCAN
MRI

12. THERAPY
MULTIDISCIPLINARY
Medical:
Acetazolamide
Furosemide
Surgical: main stay
V-p shunt placement
Extraventricular drainage

13. VENTRICULOPERITONEAL SHUNT

14. ©2007, National League for Nursing

15. Ketan Thummar-Hydrochephalus in children
Patient Report: Assessments
Vital Signs
144-36-88/60-37.6 C (99 F)
Pain, irritable

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.

32. PROGNOSIS
Visual problems:
Strabismus
Visuospatial abnormalities
Decreased visual acuity
Visual field defects
Patients require long term follow up
(multidisciplinary)

34. Ketan Thummar
3rd BSc.(N)
RN:40

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.

38. Routes of Infection
Nasopharynx
Blood stream
Direct spread (skull fracture, meningo and
encephalocele)
Middle ear infection
Infected Ventriculoperitoneal shunts.
Congenital defects
Sinusitis

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

41. Types
Bacterial
Viral (aseptic)
Fungal
Parasitic
Non-infectious

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).

60. Investigations
CBC
Blood culture
Gram staining
LP- D/r, C/s (color, leukocyte count, differential, glucose,
protein)
Electrolytes
PCR
Coagulation profile
liver and kidney function
Chest X-ray
CT/ MRI
Blood gases
EEG
ECG

61. Diagnostic Tests
CSF picture is quite diagnostic of the kind of
meningitis present.

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

63. Treatment
Supportive therapy:
Maintain fluid & electrolyte balance as required
Transfuse whole blood,or platelets as required.
Maintain temperature control

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

66. Treatment
Probable H.Influenzae
Ampicillin +
Probable E.Coli
 Ampicillin +
chloramphenicol or
3rd generation
cephalosporin
(cefotaxime
200mg/kg/day)
gentamycin
200mg/kg+2.5-4 mg/kg IV
12hrly

67. Treatment
Probable group B
streptococci
Penicillin
50,000i.u/kgI.V/4
hourly.

68. Other Drugs available
Anti-microbials
Ceftriaxone
Cefotaxime
Penicillin G
Vancomycin
Ampicillin
Gentamicin
Anti-Virals
Acyclovir
Ganciclovir (>3mths)
Anti-fungals
Amphotericin B
Fluconazole

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.

76. Cont;
Maintaining fluid balance
Prevent IV fluid overload, which may worsen
cerebral edema.
Monitor intake and output closely.
Monitor CVP frequently.

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.

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.

93. MEDICAL MANAGEMENT
Anticonvulsive drug :
Diazepam 0.3mg/kg iv
Phemobarbital 5mg/kg
Antipyratic drug :
Paracetamol
Mefanamic acid

94. NURSING MANAGEMENT
Tapid sponge bath.
Clearing the airway % oxygen
therapy.
Provide Rest , comfortable
position .
Explanation & emotional support.


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.

98. 1 GENERALIZED SEIZURES
Tonic – clonic seizures
absence seizures : - typical
: - atypical

Atopic seizures

Myoclonic seizures



99. TONIC-CLONIC SEIZURES
 PHASES
A. AN AURA
B. TONIC SPASM PHASE
C. CLONIC PHASE
D. POSTICTAL OR POST
CONVULSIVE PHASE

101. CLINICAL MENIFESTATION
An Aura:
1. Dizzines
2. Convulsion
 Tonic spasm phase
1. Body become stiff
2. Pale face
3. Eye fixe one position

102. 4. Unconciouness
5. Discharge from the mouth
6. Breathing difficulty & cynosis
7. Muscular spasm
8. Pulse mazy be weak
 CLONIC PHASE
1. Jerky movement
2. Contraction of muscle
3. Tongue bite

103. 4. Involunantry pass stool & urine
5.
6.
7
8.
Jerky movement
Contraction of muscle
Tongue bite
Involunantry pass stool & urine
POSTICAL STAGE
1. Become sleepy
2. Confused
3. Headache

104. ABSENCE SEIZURE
(PETIT MAL)
1. Staring appearance
2. Discontinue activity suddenly
3. Duration: 5 to 10 sec
4. Fatigue
5. Stress situation

105. STATUS EPILEPTICUS
1. Ataxia
2. Aphasia
3. Cardiopulmonary arrest
4. Aspiration of vomitus
5. Duration: 30 min

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

112. HEAD INJURY
(CARCINO CEREBRAL
TRAUMA)

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

115. TYPES OF INJURY
1.
2.
3.
4.
5.
6.
7.
Fracture of skull
Intracranial hemorrhage
Concussion of brain
Cerebral contusion
Extradural hematoma
Acute subdural hematoma
Brain swelling

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

121. EXTRADURAL
HEMATOMA
It occurs mostly in temporal or
frontal lobe.
Blood may be collected due to
bleeding from fracture line.

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

125. DIAGNOSTIC STUDY
Physical examination
Glasgow coma scale
Neurological examination
CT SCAN
X – RAY
EEG
ABG
Lumber puncture

126. NURSING MANAGEMENT
Maintain the airway
Establishment of breathing
Assessment of neurological status
Maintain nutritional status
Prevent infection & related
complication