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Pediatric Nursing (Neurology)


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Pediatric Nursing (Neurology)

  1. 1. HYDROCEPHALUS IN CHILDREN Ketan Thummar 3rd B.Sc Nursing RN:40
  2. 2. DEFINITION Diverse group of conditions characterised by excessive CSF in the brain. Thus: 1. Impaired flow 2. Decreased reabsorbtion 3. Increased production
  3. 3. FLOW OF CSF
  4. 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. 5. ETIOLOGY NON COMMUNICATING( obstructive) 1. Meningitis with thick purulent exudates- s. Pneumoniae, mycobacterium tuberculosis. 2. Subarachnoid hemorrhage 3. Leukemic infiltrates
  6. 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
  8. 8. CLINICAL FEATURES SYMPTOMS: Irritability Big head Poor feed Lethargy Vomiting In older patients: Headache  Changes in personality  Academic deterioration 
  9. 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. 10. Child with hydrocephalus
  11. 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. 12. THERAPY MULTIDISCIPLINARY Medical: Acetazolamide Furosemide Surgical: main stay V-p shunt placement Extraventricular drainage
  14. 14. ©2007, National League for Nursing
  15. 15. Ketan Thummar-Hydrochephalus in children Patient Report: Assessments Vital Signs 144-36-88/60-37.6 C (99 F) Pain, irritable
  16. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 32. PROGNOSIS Visual problems: Strabismus Visuospatial abnormalities Decreased visual acuity Visual field defects Patients require long term follow up (multidisciplinary)
  33. 33. Ketan Thummar 3rd BSc.(N) RN:40
  34. 34. Definition Meningitis is the inflammation of the membranes surrounding the brain & spinal cord, including the dura, arachinoid & pia matter.
  35. 35. 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.
  36. 36. 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.
  37. 37. Routes of Infection Nasopharynx Blood stream Direct spread (skull fracture, meningo and encephalocele) Middle ear infection Infected Ventriculoperitoneal shunts. Congenital defects Sinusitis
  38. 38. 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
  39. 39. 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
  40. 40. Types Bacterial Viral (aseptic) Fungal Parasitic Non-infectious
  41. 41. 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
  42. 42. 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).
  43. 43. 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.
  44. 44. 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)
  45. 45. 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.
  46. 46. 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
  47. 47. 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)
  48. 48. Tuberculous meningitis It’s a complication of Childhood tuberculosis & common cause of prolonged morbidity, handicap & death. Children below 5 years are specially prone.
  49. 49. 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
  50. 50. 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
  51. 51. TERMINAL PHASE Child is characteristically comatose with opisthotonus, & multiple focal paresis. Cranial nerve palsies are present. High grade fever often occurs terminally.
  52. 52. 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.
  53. 53. 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.
  54. 54. 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.
  55. 55. 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)
  56. 56. 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).
  57. 57. 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
  58. 58. Diagnostic Tests CSF picture is quite diagnostic of the kind of meningitis present.
  59. 59. 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
  60. 60. Treatment Supportive therapy: Maintain fluid & electrolyte balance as required Transfuse whole blood,or platelets as required. Maintain temperature control
  61. 61. 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.
  62. 62. Treatment Initial till results of Ampicillin Probable/Proved Penicillins C/S are known Meningococci 300mg/kg/day+ Chloramphenicol 2-5 lac units /kg/day
  63. 63. 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
  64. 64. Treatment Probable group B streptococci Penicillin 50,000i.u/kgI.V/4 hourly.
  65. 65. Other Drugs available Anti-microbials Ceftriaxone Cefotaxime Penicillin G Vancomycin Ampicillin Gentamicin Anti-Virals Acyclovir Ganciclovir (>3mths) Anti-fungals Amphotericin B Fluconazole
  66. 66. 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)
  67. 67. 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.
  68. 68. 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.
  69. 69. 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.
  70. 70. 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.
  71. 71. 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.
  72. 72. 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.
  73. 73. Cont; Maintaining fluid balance Prevent IV fluid overload, which may worsen cerebral edema. Monitor intake and output closely. Monitor CVP frequently.
  74. 74. 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
  75. 75. 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.
  76. 76. 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.
  77. 77. 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.
  78. 78. 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.
  79. 79. 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.
  80. 80. 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.
  81. 81. 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.
  82. 82. CAUSES OF CONVULSION NEONATAL PERIOD : • • • • asphyxia & injury Hypoglycemia & hypocalcemia Narcotic & anesthetic drug Septicemia, meningitis Birth, tetanus , kernicterus • Congenital malformation • Intra uterine infection
  83. 83. SIGNS & SYMPTOMS Twiching of limb Tongue bite Discharge from the mouth Pale face sucking movement Tremors
  84. 84. Infant & young children Febrile convulsion CNS infection Accidental & non accidental injury Metabolic disturbance Drug & poison
  85. 85. 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
  86. 86. 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.
  87. 87. 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.
  88. 88. MEDICAL MANAGEMENT Anticonvulsive drug : Diazepam 0.3mg/kg iv Phemobarbital 5mg/kg Antipyratic drug : Paracetamol Mefanamic acid
  89. 89. NURSING MANAGEMENT Tapid sponge bath. Clearing the airway % oxygen therapy. Provide Rest , comfortable position . Explanation & emotional support. 
  90. 90. 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.
  91. 91. 1 GENERALIZED SEIZURES Tonic – clonic seizures absence seizures : - typical : - atypical  Atopic seizures  Myoclonic seizures  
  93. 93. CLINICAL MENIFESTATION An Aura: 1. Dizzines 2. Convulsion  Tonic spasm phase 1. Body become stiff 2. Pale face 3. Eye fixe one position
  94. 94. 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
  95. 95. 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
  96. 96. ABSENCE SEIZURE (PETIT MAL) 1. Staring appearance 2. Discontinue activity suddenly 3. Duration: 5 to 10 sec 4. Fatigue 5. Stress situation
  97. 97. STATUS EPILEPTICUS 1. Ataxia 2. Aphasia 3. Cardiopulmonary arrest 4. Aspiration of vomitus 5. Duration: 30 min
  98. 98. MYOCLONIC SEIZURE 1. Mental retardation 2. Cerebral abnormality 3. Contraction of muscles of trunk, neck, extremities 4. Duration: less than 1min
  99. 99. PARTIAL SEIZURES SIMPLE PARTIAL SEIZURES with motor sing  with somato-sensory or special sensory  with autonomic manifestation  COMPLEX PARTIAL SEIZURES Impaired consciousness
  100. 100. 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
  101. 101. 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
  102. 102. 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 &
  103. 103. 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
  105. 105. 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.
  106. 106. 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
  107. 107. 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
  108. 108. Diagnostic test Physical & neurological examination Examination of blood, urin , CSF EEG X-RAY of skull CT SCAN MRI
  109. 109. 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.
  110. 110. 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
  111. 111. CONCUSSION OF BRAIN Concussion is reversible neurological dysfunction Transient loss of consciousness & loss of memory Injury at occipital area & shearing srain at brain stem
  112. 112. 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
  113. 113. EXTRADURAL HEMATOMA It occurs mostly in temporal or frontal lobe. Blood may be collected due to bleeding from fracture line.
  114. 114. 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.
  115. 115. BRAIN SWELLING It may be occur due to vascular congestion, may be due to neurogenic vasoparalysis & increase blood flow.
  116. 116. SIGNS & SYMPTOMS Loss of consciousness Respiratory obstruction Increase icp Headache Vommiting Convulsion Loss of memory Bladder bowel dysfunction
  117. 117. DIAGNOSTIC STUDY Physical examination Glasgow coma scale Neurological examination CT SCAN X – RAY EEG ABG Lumber puncture
  118. 118. NURSING MANAGEMENT Maintain the airway Establishment of breathing Assessment of neurological status Maintain nutritional status Prevent infection & related complication