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CNS infections

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Cns infections
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CNS infections

  1. 1. Central Nervous System Infections Dr. Wassihun T. ( MD ) 05/21/18 1
  2. 2. Outline • Introduction • Acute bacterial meningitis – Definition – Etiology – Risk factors – Pathology and pathogenesis – Clinical manifestations – Diagnosis – Management – Complication – Prognosis – Prevention 2
  3. 3. CNS Infections • Most common cause of fever associated with signs and symptoms of CNS disease • Viral > bacterial > fungal and parasitic infections • Regardless of etiology, most patients with CNS infection have similar clinical manifestations 3
  4. 4. Cont… 1. Diffuse  Meningitis  Encephalitis  Meningoencephalitis 2. Focal  Brain abscess  Parameningeal abscess  subdural empyema,  spinal epidural abscess 4
  5. 5. SS
  6. 6. Acute Bacterial Meningitis • Definition-Inflammation of the leptominges surrounding the brain and spinal cord: pia, arachnoid and subarachnoid matter • Occurs at all ages but is commonest during infancy (greatest risk 6-12 months) 6
  7. 7. Con…... • Bacterial meningitis is one of the most potentially serious infections occurring in infants and older children. • This infection is associated with a high rate of acute complications and risk of long-term morbidity. • The incidence of bacterial meningitis is sufficiently high in febrile infants that it should be included in the differential diagnosis of those with altered mental status and other evidence of neurologic dysfunction
  8. 8. SS
  9. 9. ETIOLOGY Neonatal period • Groups B streptococci • Gram-negative enteric bacilli (E. coli, Klebsiella), and • Listeria monocytogenes 9
  10. 10. ETIOLOGY….. Children 2 mo to 12 yr of age • N. meningitidis • H. influenzae type b • S. pneumoniae 10
  11. 11. Etiology… • Alterations of host defense – Pseudomonas aeruginosa – Staphylococcus aureus, Coagulase- negative staphylococci – Salmonella spp – L. monocytogenes 11
  12. 12. EPIDEMIOLOGY Predisposing Factors Major risk –Lack of immunity to specific pathogens associated with young age Additional risk factors • Recent colonization with pathogenic bacteria • Close contact with patients having invasive disease caused by N. meningitidis and H. influenzae type b, • Crowding • Poverty • Male sex  Person to person contact through respiratory secretions or droplets. 12
  13. 13. Risk factors … Congenital or acquired CSF leak  Middle ear or inner ear fistulas  Basal skull fracture into the cribriform plate or increased risk of pneumococcal meningitis. • Lumbosacral dermal sinus and meningomyelocele: staphylococcal and gram-negative enteric meningitis. 13
  14. 14. Streptococcus pneumonia • Commonly occurs during the first 2yrs of life • Peak 6-12 months • Highest in children with • HIV- infection • Anatomic or functional asplenia • Other risk factors include • Otitis media • Sinusitis • Pneumonia • CSF otorrhea or rhinorrhea 14
  15. 15. Neisseria Meningitides Occurs • Sporadically or as epidemics • Serogroups A,B,C,Y, W-135,X are responsible • Contact infection • Epidemics is defined as the occurrence of 3 cases in 3 months time with attack rate of 10 cases per 100,000 population in the same community • Epidemics is usually caused by serogrup A 15
  16. 16. Haemophilus influenza type B • Primarily occurs in infants 2month to 2 yrs • 50% of cases occur in the 1st year of life • Peak at 6-9 months of age • Risk increased among family or day care center contacts of patients with HIB disease. unvaccinated and those with blunted immunologic responses to vaccine ( HIV- Infection) 16
  17. 17. Pathogenesis Routes of infection • Hematogenous dissemination of micro-organisms from a distant site of infection-Most common route. • Direct invasion of the CNS from  contiguous focus of infection: otitis media, mastoditis, sinusitis,osteomyelitis (cranial,vertebral) through anatomic abnormalities head trauma neurosurgical procedures 18
  18. 18. Pathogenesis • Bacterial colonization of the nasopharynx • Hematogenous dissemination • Bacteremia • Prior or concurrent viral upper respiratory tract infection may enhance the pathogenicity of bacteria producing meningitis
  19. 19. Pathogenesis….. • Bacteria gain entry to the CSF • Multiply rapidly and incite local inflammatory response, with polymorphonuclear cell infiltration. • Marked inflammatory response with local production of TNF, IL-1, and other cytokines • Inflammatory response in characterized by – Neutrophilic infiltration – Altered BBB – Increased vascular permeability – Vascular thrombosis and vasculitis • Inflammation of spinal nerves and roots produces meningeal signs • Inflammation of the cranial nerves produces cranial neuropathies 20
  20. 20. Nasopharyngeal colonization Local invasion Bacteremia Meningeal invasion Bacterial replication in the subarachnoid space Release of bacterial components (cell wall, LOS) Cerebral microvascular endothelium Macrophages, neutrophils, other CNS Cells Cytokines Subarachnoid space inflammation Cerebral vasculitis Increased CSF outflow resistance Hydrocephalus Interstitial edema Increased intracranial pressure Decreased cerebral blood flow and loss of cerebrovascular autoregulation Cytotoxic edema Cerebral infarction Increased BBB permeability Vasogenic edema 21
  21. 21. Clinical manifestations Infants • Fever • Poor feeding • Projectile Vomiting • Altered level of consciousness • Convulsions • Neck stiffness ( hyper extension) • Bulging fontanel • Rash (Purpuric) • Meningeal signs are not consistently present 22
  22. 22. Clinical manifestations….. Older children • Classic signs are preceded upper respiratory or GIT symptoms • Fever • Headache • Projectile Vomiting • Poor feeding • Seizures are common-20-30% of patients before or during the first 3 days after diagnosis 23
  23. 23. P/E • Neck stiffness • Positive Kerning’s sign • Positive Brudzinski’s sign • Altered state of consciousness • CN palsies • Meningococcal meningitis -generalized purpuric rash -Peripheral cyanosis -Toxic and comatose -Tachycardia, Hypotension - DIC 24
  24. 24. • Alterations of mental status – Irritability, lethargy to coma may be due to: • Increased ICP • Cerebritis • Hypotension • Factors that lead to Death or Brain Damage in Meningitis – SIADH secretion With resultant Hyponatremia – Brain edema → Acute Brainstem Compression – Subdural Effusion/Empyema/Brain Abscess – Seizures 25
  25. 25. Kerning Vs Brudzinski signs 26
  26. 26. Diagnosis Lumbar Puncture- CSF analysis • Leukocyte count (>1000/mm3 ) with neutrophilic predominance (75–95%). • Turbid CSF when WBC count is >200–400/mm3 . – <250/mm3 in as many as 20% of patients – pleocytosis may be absent in severe overwhelming sepsis and meningitis and is a poor prognostic sign – lymphocyte predominance may be present during the early stage • Elevated protein  Gram stain-positive in 70–90% of untreated patients • Culture 27
  27. 27. Conditions Pressure (mmH2O) Leukocyte (mm3) Protein (mg/dl) Glucose (mg/dl) Normal 50-80 <5, ≥75% Lymphocytes 20-45 >50 (or 75% Serum Glucose) Acute Bacterial Usually elevated (100 -300) >100-10,000 ; usually 300-2,000; PMNs Usually 100-500 usually <40 (or <50% serum glucose) Partially Rxed Bact. Normal or elevated 5-10,000; PMNs early/Mon dominate most of the course Usually 100-500 Normal or decreased Viral Normal/slight ly (80-150) Rarely >1,000, Mon predominate Usually 50- 200 Generally normal; but mumps Tuberculou s Usually elevated 10–500;lymp predominate through most of the 100-3,000; may be higher <50 in most cases 28
  28. 28. Diagnosis…… • CBC- Leukocytosis, with polymorph predominance • Blood culture- reveals organisms in ~80-90% of cases » CXR if pneumonia or TB is suspected 29
  29. 29. Contra-indications for Lumbar Puncture • Elevated ICP and focal Neurologic deficit • Severe cardio respiratory compromise – postpone LP • Infection of the overlying skin • Thrombocytopenia ( relative) 30
  30. 30. DDX • Aseptic meningitis • Tuberculous meningitis • Cerebral malaria • Brain abscess • Brain tumor 31
  31. 31. Management I. Supportive Measures  Vital Signs _ 15-30 min.  Frequent Neurologic assessment -Follow patient with neurosign chart – Level of consciousness(GCS) – Pupillary size and reactivity – Pattern of breathing – Posture – Occulocephalic reflex – Seizure – Cranial nerve palsies or focal Neurologic deficits – Daily HC measurement –for children<18 months 32
  32. 32. Management…..  Strict input/output recording  Serum electrolytes  Body weight  Antipyretics ,Cold sponging • Fluid restriction to 2/3rd maintenance for fear of syndrome of inappropriate ADH secretion - fluid restriction should be avoided in the presence of hypotension • Coma care- bowel, bladder, skin, air way • Seizure control – Active SZ –arrest with diazepam 0.1 -0.3 mg/kg/IV or PR – Prevention of recurrence of seizure » Phenytoin- 20mg/kg loading then 5mg/kg/ 24 hrs – bid – Phenobarbitone can be added for refractory SZ 33
  33. 33. Management….. II. Specific Measures • Shock – in meningo coccemia or due to vomiting – IV NS/RL /Plasma • Antibiotic therapy 34
  34. 34. Antibiotic therapy Empirical treatment • Cyst.pencillin plus • Chloramphenicol or • Ceftriaxone 100mg/kg/24hrs Bid • Vancomycin – penicillin/ceftriaxone resistant S.pneumoniae • According to culture and sensitivity result 35
  35. 35. Antibiotics • Duration of therapy – 5-7 days for meningococcal meningitis – 7-10 days for H. influenzae meningitis – 10-14 days for pneumococcal meningitis – Gram-negative meningitis should be treated for 3 wk or for at least 2 wk after CSF sterilization 36
  36. 36. Corticosteroids • Corticosteroid: – decrease ICP by decreasing meningeal inflammation and brain water content – modulate the production Of cytokines, lessens the meningeal inflammatory response – decrease incidence of sensorineural hearing loss or other neurologic complications • Dexamthasone • 0.15 mg/kg/dose Qid for 2 days before the 1st dose of antibiotic for those older than 6wks 37
  37. 37. Complications Increased Intracranial pressure(ICP)- • Common acute complication 1. Increase ICP is due to:- – Cytotoxic cerebral edema- due to cell swelling→cell death – Vasogenic cerebral edema- due to cytokine induced increased capillary vascular permeability – Interstitial cerebral edema- increased hydrostatic pressure after impaired reabsorption or obstruction of CSF flow (Hydrocephalus) 38
  38. 38. Management of Increased ICP – Elevating head by 300 – 20%Manitol 0.5-1g/kg/dose over 30min, Q6hrs or Frusemide 1mg/kg or hypertonic saline(3% Saline) – Dexamethasone 0.25 -0.5mg/kg QID – Endotracheal intubation and hyperventilation (Pco2 25-30mmHG) – Treat fever aggressively 39
  39. 39. 2 .Hydrocephalus • Communicating – Ocurrs most commonly – due to adhesive thickening of arachnoid villi around the cisterns - impaired CSF reabsorption • Obstructive – Less often – due to fibrosis and gliosis of the aqueduct of sylvius 40
  40. 40. 3 .Subdural effusion • 10-30% of cases • Highest in infants ,and H.influenzae meningitis(45% of cases) • 85-90% are asymptomatic • C/Fs o bulging fontanel o diastasis of sutures o enlarging HC o Persistence /recurrence of emesis o Persistent/focal seizures o persistence of fever • Symptomatic - subdural tap 41
  41. 41. Complications….. 4 . Cranial nerve palsies – Inflammation of cranial nerves results cranial neuropathies of Optic ,Oculomotor, Facial ,Auditory Nerves – Increased ICP Produces oculomotor and abducens nerve palsies 5. Seizure – focal or generalized – 20–30% of patients – occurs due to cerebritis, infarction, or electrolyte disturbances _ on presentation or within the 1st 4 days of onset is usually of no prognostic significance 42
  42. 42. Complications….. 6 .Syndrome of inappropriate ADH secretion 7 .Cerebral herniation 8 .Stroke 43
  43. 43. chronic complications • Sensorineural hearing loss– mainly cochlear injury • Ataxia • Hemiparesis/Quadriparesis • Epilepsy • Spinal cord infarction • Cortical blindness - Optic arachnoiditis • Diabetes insipidus • Intellectual deficits 44
  44. 44. Prognosis Poor prognostic factors 1. Infants <6 months 2. Delayed/Late presentation 3. >106 CFU/ml of CSF 4. Seizure that persist after 4 days of illness and difficult to treat/control 5. Coma or focal Neurologic signs at presentation. 6. Delayed sterilization of CSF 45
  45. 45. Prevention Chemoprophylaxis /vaccination Neisseria meningitides Chemoprophylaxis • All close contacts regardless of age & immunization • Meningococcal quadrivalent vaccine ( Serogroups A,C,Y,W-135) 46
  46. 46. Prevention… H. Influenza – Rifampin 20mg/kg/daily for 4 day for all close contacts if any close family member younger than 48 mo has not been fully immunized or if an immunocompromised person, of any age, resides in the household – HIB vaccine - Prevents development of HIB Infection – If given for all < 2yrs Pneumococcal • Conjugate vaccine against S.pneumoniae ( PCV10) for all younger than 2 yrs. 47
  47. 47. References • Nelson Text book of pediatrics, 20th ed • UpTodate 21.4 48
  48. 48. 49

Hinweis der Redaktion

  • Most infections of children are acquired from a contact in a daycare facility, a colonized adult family member, or an ill patient with meningococcal disease.
  • BBB (arachnoid membrane, choroid plexus epithelium, and cerebral microvascular endothelium)
  • A household contact is one who lives in the residence of the index case or who has spent a minimum of 4 hr with the index case for at least 5 of the 7 days preceding the patient&amp;apos;s hospitalization

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