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Meningitis class lecture note medicine pdf
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- 2. What is meningitis?…… •Inflammation of the meninges • And meninges?
- 3. The meninges &CSF…… • The meninges is the connective tissue layers covering brain and spinal cord • The meninges collectively constitute the blood-brain barrier • The meninges is made up of the pia mater (closest to the Brain) the arachnoid mater the dura mater (farthest from the Brain)= LEPTOMENINGES = PIA + ARACCHNOID PACHYMENINGES = DURA • Meninges contain cerebrospinal fluid (CSF) = subarachnoid space
- 5. The meninges &CSF…… • Meningitis is an inflammation of the meninges • Often the inflammation of the leptomeninges -Inflammation of the subarachnoid space with meningeal involvement • May involve inflammation of the pachymeninges
- 6. Types of meningitis •Non-infective – Cancer – Trauma to head or spine – Foreign bodies – SLE – Chemicals and drugs • Infective – Bacterial – Viral – Fungal – Parasitic
- 7. CNS INFECTIONS 1. Meningitis:Infection of the meninges 2. Encephalitis :Inflammation of brain 3. Meningoencephalitis : Inflammation of brain with meningeal involvement 4. Brain Abscess: Complication of other CNS Infections, Abscess collection, Pathogens may be bacterial, TB, viral, fungal, or parasitic
- 8. Classification of InfectiveMeningitis 1. Taxonomic Classification of Agents 2. Disease Progression Acute Meningitis- symptoms evolving rapidly over 1-24 hours, Sub-acute Meningitis- symptoms evolving over 1-7days, Chronic Meningitis- symptoms evolving over more than 1 week 3. CSF Cytology & Chemistry Septic Meningitis Aseptic Meningitis 4. Anatomic Leptomeningitis - inflammation of the leptomeninges Pachymeningitis - inflammation of the pachymeninges
- 9. Classification of InfectiveMeningitis 5. Host/Syndromes Neonatal Meningitis Post-operative Meningitis 6. Origin Community Acquired Hospital Acquired 7. Epidemiology Epidemic Non-epidemic (Sporadic)
- 10. Etiology of InfectiveMeningitis • Bacteria • Viruses • Parasites • Fungi
- 11. Bacterial Aetiology • Varywith patient age, • 3 bacteria types commonest • Accounts for ˃ ¾ of all cases • They include: Neisseria meningitidis (meningococcus) Haemophilus influenzae (in young and unvaccinated) Streptococcus pneumoniae ( pneumococcus)
- 12. Bacterial Aetiology inNeonates & Infants (2-3 Months) • Escherichia coli • ß-haemolytic streptococci particularly GBS • Staphylococcus aureus • Staphylococcus epidermidis • Listeria monocytogenes
- 13. Bacterial Etiology – Elderlyand immunocompromised • Listeria monocytogenes • Gram negative bacteria – Hospital-acquired infections • Klebsiella • Escherichia coli • Pseudomonas • Staphylococcus aureus
- 14. Bacterial Etiology • Themost common organisms in Neonates and infants under the age of 2months • Escherichia coli • Pseudomonas • Group B Streptococcus • Staphylococcus aureus
- 15. Bacterial Etiology • Childrenover 2 months – Haemophilus influenzae type b – Neisseria meningitidis – Streptococcus pneumoniae • Children over 12 years – Neisseria meningitidis – Streptococcus pneumoniae
- 16. Routes of CNSinfections • Blood: Septicaemia/ Bacteraemia (main route) • Direct extension from nearby focus (mastoiditis, sinusitis), uncommon • Direct invasion (dermoid sinus tract, head trauma, meningo-myelocele), very rare
- 17. ORGANISM ROUTE/SITE OFENTERY Neisseria meningitidis Nasopharynx Streptococcus pneumoniae Nasopharynx or direct extension across skull fracture Listeria monocytogenes GI tract, placenta Haemophilus influenzae Nasopharynx Staphylococcus aureus Bacteremia, skin, or foreign body Staphylococcus epidermidis Skin or foreign body ORGANISM ASSOCIATED ROUTE OF ENTRY
- 18. Pathogenesis • CNS Susceptibilityto bacterial infection in children – 1. Immaturity of immune systems • Nonspecific immunity – Immaturity of BBB (Blood-brain barrier) – Immaturity of complement system/activity – Sub-optimal chemotaxis of neutrophils – Sub-optimal functioning of monocyte-macrophage system – Diminished Blood levels of interferon (INF) –γ and interleukin - 8 ( IL-8 )
- 19. Pathogenesis • Specific immunity –Immaturity of both the cellular immune systems – Immaturity of both the humoral immune systems » Insufficient antibody-mediated protection » Diminished immunologic response 2. Bacterial virulence • Host immunity evasion techniques
- 20. Pathogenesis • Offending bacteriumfrom blood invades the leptomeninges. • Bacterial toxins and Inflammatory mediators are released. • Bacterial toxins • Lipopolysaccharide, LPS • Teichoic acid • Peptidoglycan • Inflammatory mediators • Tumor necrosis factor, TNF • Interleukin-1, IL-1 • Prostaglandin E2, PGE2
- 21. Pathogenesis • Bacterial toxinsand inflammatory mediators cause suppurative inflammation. – Inflammatory infiltrates – Increased Vascular permeability – Tissue edema – Blood-brain barrier destroyed – Thrombosis
- 22. Nasopharyngeal colonization Local invasion Bacteremia Meningealinvasion 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
- 23. Pathology • Diffuse bacterialinfections involve the leptomeninges, arachnoid membrane and superficial cortical structures, and brain parenchyma is also inflamed. • Meningeal exudate of varying thickness is found. • There is purulent material around veins and venous sinuses, over the convexity of the brain, in the depths of the sulci, within the basal cisterns, and around the cerebellum, and spinal cord may be encased in pus. • Ventriculitis (purulent material within the ventricles) has been observed repeatedly in children who have died of their disease.
- 24. Pathology • Invasion ofthe ventricular wall with perivascular collections of purulent material, loss of ependymal lining, and subependymal gliosis may be noted. • Subdural empyema may occur. • Hydrocephalus is an common complication of meningitis. – Obstructive hydrocephalus – Communicating hydrocephalus
- 25. Pathology • Blood vesselwalls may be infiltrated by inflammatory cells. – Endothelial cell injury – Vessel stenosis – Secondary ischemia and infarction • Ventricle dilatation which ensues may be associated with necrosis of cerebral tissue due to the inflammatory process itself or to occlusion of cerebral veins or arteries.
- 26. Pathology • Inflammatory processmay result in cerebral edema and damage of the cerebral cortex. – Altered Consciousness – Convulsion – Motor disturbance – Sensory disturbance • Meningeal irritation sign is found because the spinal nerve root is irritated. • Cranial nerve may be damaged
- 27. Meningitis and Septicaemia Meningitisand Septicaemia often occur together: • Meningitis – Inflammation of meninges – Pathogen enters the blood stream and travel to the meninges and cause inflammation. • Septicaemia – Pathogen’s presence in the blood stream accompanied with rapid multiplication and release toxins. – The rash associated with meningitis of meningococcus is due to septicaemia
- 28. Meningitis and Septicemia Meningitisand meningococcaemia is not always easy to detect. In early stages, the symptoms can be similar to flu. They may develop over one or two days, but sometimes develop in a matter of hours. It is important to remember that symptoms do not appear in any particular order and some may not appear at all.
- 29. Symptoms for meningitisand meningococcal septicaemia: :Young Children -High temperature, fever, possibly with cold hands and feet -Vomiting or refusing feeds -High pitched moaning, whimpering cry -Blank, staring expression -Pale, blotchy complexion -Stiff neck -Arched back -Baby may be floppy, may dislike being handled, be fretful -Difficult to wake or lethargic -The fontanelle (soft spot on babies heads) may be tense or bulging.
- 31. Older Children andAdults -High temperature, fever, possibly with cold hands and feet. -Vomiting, sometimes diarrhoea. -Severe headache. -Joint or muscle pains, sometimes stomach cramps. -Neck stiffness (unable to touch the chin to the chest) -Dislike of bright lights. -Drowsiness. The patient may be confused or disorientated. Fitting may also be seen. A rash may develop.
- 33. One of thephysically demonstrable sign of meningitis is Kernig's sign. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
- 34. Another physically demonstrable signof meningitis is Brudzinski's sign. Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed.
- 35. In the earlystages, signs and symptoms can be similar to many other more common illnesses, for example flu. Early symptoms can include fever, headache, nausea (feeling sick), vomiting and general tiredness. The common signs and symptoms of meningitis and septicaemia (See Diagram). Others can include rapid breathing, diarrhoea and stomach cramps. In babies, check if the soft spot (fontanelle) on the top of the head is tense or bulging.
- 36. One sign ofmeningococcal septicaemia is a rash that does not fade under pressure (see ‘Glass test’) -This rash is caused by blood leaking under the skin. It starts anywhere on the body. It can spread quickly to look like fresh bruises. -This rash is more difficult to see in dark skinned.
- 37. ‘Glass Test’ A rashthat does not fade under pressure will still be visible when the side of a clear drinking glass is pressed firmly against the skin. If someone is ill or obviously getting worse, do not wait for a rash. It may appear late or not at all. A fever with a rash that does not fade under pressure is a medical emergency.
- 38. Clinical manifestation • ToxicPatient – Hyperpyrexia – Headache – Photophobia – Painful eye movement – Fatigued and weak – Malaise, myalgia, anorexia, – Vomiting, diarrhea and abdominal pain – Cutaneous rash – Petechiae, purpura
- 39. Clinical manifestation • Increasedintracranial pressure • Headache • Projectile vomiting • Hypertension • Bradycardia • Bulging fontanel • Cranial sutures diastasis • Coma • Decerebrate rigidity • Cerebral hernia
- 40. Clinical manifestation • Seizures •Seizures occur in about 20%-30% of children with bacterial meningitis. • Seizures is often found in Haemophilus influenzae and pneumococal infection. • Seizures is correlative with the inflammation of brain parenchyma, cerebral infarction and electrolyte disturbances.
- 41. Clinical manifestation • Consciousdisturbance • Drowsiness • Altered consciousness • Coma • Psychiatric symptom – Irritation – Dysphoria – dullness
- 42. Clinical manifestation • Meningealirritation sign • Neck stiffness • Positive Kernig’s sign • Positive Brudzinski’s sign
- 43. Clinical manifestation – Transientor permanent paralysis of cranial nerves and limbs may be noted. – Deafness or disturbances in vestibular function are relatively common. – Involvement of the optic nerve, with blindness, is rare. – Paralysis of the 6th cranial nerve, usually transient, is noted frequently early in the course.
- 44. Clinical manifestation – Insome children, particularly young infants under the age of 3 months, symptom and signs of meningeal inflammation may be minimal. – Fever is generally present, but its absence or hypothermia in a infant with meningeal inflammation is common. – Only irritability, restlessness, dullness, vomiting, poor feeding, cyanosis, dyspnea, jaundice, seizures, shock and coma may be noted. – Bulging fontanel may be found, but there is not meningeal irritation sign.
- 45. Complication • Subdural effusion –Subdural effusions occur in about 10%-30% of children with bacterial meningitis. – Subdural effusions appear to be more frequent in the children under the age of 1 year and in haemophilus influenzae and pneumococal infection. – Clinical manifestations are enlargement in head circumference, bulging fontanel, cranial sutures diastasis and abnormal transillumination of the skull. – Subdural effusions may be diagnosed by the examination of CT or MRI and subdural pricking.
- 46. Complication • Ependymitis – Neonateor infant with meningitis – Gram-negative bacterial infection – Clinical manifestation • Persistent hyperpyrexia, • Frequent convulsion • Acute respiratory failure • Bulging fontanel • Ventriculomegaly (CT) • Cerebrospinal fluid by ventricular puncture – WBC>50×109 /L – Glucose<1.6mmol/L – Protein>o.4g/L
- 47. Complication • Cerebullar hyponatremia –Syndromeof inappropriate secretion of antidiuretic hormone (SIADH) • Hyponatremia • Degrade of blood osmotic pressure • Aggravated cerebral edema • Frequent convulsion • Aggravated conscious disturbance
- 48. Complication • Hydrocephalus – Increasedintracranial pressure – Bulging fontanel – Augmentation of head circumference – Brain function disorder • Other complication – Deafness or blindness – Epilepsy – Paralysis – Mental retardation – Behavior disorder
- 49. Laboratory Findings • Peripheralhemogram –Total WBC count • 20×109 /L ～ 40×109 /L WBC • Decreased WBC count in severe infection –Leukocyte differential count • 80% ～ 90% Neutrophils
- 50. Laboratory Findings • Examinationof cerebrospinal fluid (CSF) – Increased pressure of cerebrospinal fluid – Cloudiness – Increased total WBC count (>1000×109 /L) – Increased neutrophils in leukocyte differential count – Decreased glucose (<1.1mmol/l) – Increased protein level – Decreased or normal chloride – CSF film preparation or cultivation : positive result
- 51. Laboratory Findings • Specialexamination of CSF –Specific bacterial antigen test • Countercurrent immuno-electrophoresis • Latex agglutination • Immunofluorescent test – Neisseria meningitidis (meningococcus) – Haemophilus influenzae – Streptococcus pneumoniae ( pneumococcus) – Group B streptococcus
- 52. Laboratory Findings • specialexamination of CSF –Other test of CSF • LDH • Lactic acid • CRP • TNF and Ig • Neuron specific enolase (NSE)
- 53. Laboratory Findings • Otherbacterial test – Blood cultivation – Film preparation of skin petechiae and purpura – Secretion culture of local lesion • Imageology examination
- 54. Diagnosis • Diagnostic methods –Acareful evaluation of history –A careful evaluation of infant’s signs and symptoms –A careful evaluation of information on longitudinal changes in vital signs and laboratory indicators • Rout examination of cerebrospinal fluid (CSF)
- 55. Differential diagnosis • Clinicalmanifestation of bacterial meningitis is similar to clinical manifestation of viral, tuberculous , fungal and aseptic meningitis. • Differentiation of these disorders depends upon careful examination of cerebrospinal fluid obtained by lumbar puncture and additional immunologic, roentgenographic, and isotope studies.
- 56. Characteristics of CSFon common disease in CNS BM TM VW FM TE Pressure ↑ ↑ － or↑ ↑↑ ↑ Cloudiness ＋＋ or ＋＋＋ ＋ － ± － Pandy T ＋＋ or ＋＋＋ ＋ or ＋＋＋ ±or ＋＋ ＋ or ＋＋＋ － WBC ↑↑↑ N ↑ L － or↑L ↑ M － Protein ↑ ↑ ↑ ↑ ↑ ↑ － or↑ ↑ ↑ － or ± Glucos ↓ ↓ ↓ ↓ ↓ － ↓ ↓ － Chloridate － or ↓ ↓ ↓ ↓ － ↓ ↓ － Cultivation Bacterium TB Viral Fungus －
- 57. Treatment Antibiotic Therapy • Therapeuticprinciple – Good permeability for Blood-brain barrier – Drug combination – Intravenous drip – Full dosage – Full course of treatment
- 58. Antibiotic Therapy • Selectionof antibiotic – know exact cause: Bacterium • Community-acquired bacterial infection • Nosocomial infection acquired in a hospital • Broad-spectrum antibiotic coverage as noted below – Children under age 3 months » Cefotaxime and ampicillin » Ceftriaxone and ampicillin (children over age 1months) – Children over 3 months » Cefotaxime or Ceftriaxone or ampicillin and chloramphenicol
- 59. Antibiotic Therapy • CertainlyBacterium – Once the pathogen has been identified and the antibiotic sensitivities determined, the most appropriate drugs should selected. • N meningitidis : penicillin, tert- cephalosporin • S pneumoniae: penicillin, tert- cephalosporin, vancomycin • H influenzae: ampicillin, tert- cephalosporin • S aureus: penicillin, nefcillin, vancomycin • E coli: ampicillin, chloramphenicol, tert- cephalosporin
- 60. Antibiotic Therapy • Courseof treatment – 7 days for meningococcal infection – 10 ～ 14 days for H influenzae or S pneumoniae infection – More than 21 days for S aureus or E coli infection – 14 ～ 21 days for other organisms
- 61. Treatment General and SupportiveMeasures • Monitor of vital sign • Correcting metabolic imbalances – Supplying sufficient heat quantity – Correcting hypoglycemia – Correcting metabolic acidemia – Correcting fluids and electrolytes disorder • Application of cortical hormone – Lessening inflammatory reaction – Lessening toxic symptom – lessening cerebral edema
- 62. General and SupportiveMeasures • Treatment of hyperpyrexia and seizures – Pyretolysis by physiotherapy and/or drug – Convulsive management • Diazepam • Phenobarbital – Subhibernation therapy • Treatment of increased intracranial pressure – Dehydration therapy • 20%Mannitol 5ml/kg vi q6h • Lasix 1-2mg/kg vi
- 63. General and SupportiveMeasures –Treatment of septic shock and DIC • Volume expansion • Dopamine • Corticosteroids • Heparin • Fresh frozen plasma • Platelet transfusions
- 64. Treatment Complication Measures • Subduraleffusions – Subduaral pricking • Draw-off effusions on one side is 20-30ml/time. • Once daily or every other day is requested. • Time cell of pricking may be prolonged after 2 weeks. • Ependymitis – Ventricular puncture — drainage • Pressure in ventricle be depressed. • Ventricular puncture may give ventricle an injection of antibiotic.
- 65. Complication Measures • Hydrocephalus –Operative treatment • Adhesiolysis • By-pass operation of cerebrospinal fluid • Dilatation of aqueduct • SIADH (Cerebral hyponatremia) – Restriction of fluid – supplement of serum sodium – diuretic
- 66. Prognosis • Appropriate antibiotictherapy reduces the mortality rate for bacterial meningitis in children, but mortality remain high. • Overall mortality in the developed countries ranges between 5% and 30%. • 50 percent of the survivors have some sequelae of the disease.
- 67. Prognosis • Prognosis dependsupon many factors: – Age – Causative organism – Number of organisms and bacterial virulence – Duration of illness prior to effective antibiotic therapy – Presence of disorders that may compromise host response to infection
- 68. Aseptic Meningitis Definition: Asyndrome characterized by acute onset of meningeal symptoms, fever, and cerebrospinal fluid pleocytosis, with bacteriologically sterile cultures. Laboratory criteria for diagnosis: CSF showing ≥ 5 WBC/cu mm No evidence of bacterial or fungal meningitis. Case classification Confirmed: a clinically compatible illness diagnosed by a physician as aseptic meningitis, with no laboratory evidence of bacterial or fungal meningitis Comment Aseptic meningitis is a syndrome of multiple etiologies, but most cases are caused by a viral agent
- 69. Viral Meningitis Etiological Agents: Enteroviruses(Coxsackie's and echovirus): most common. -Adenovirus -Arbovirus -Measles virus -Herpes Simplex Virus -Varicella Reservoirs: -Humans for Enteroviruses, Adenovirus, Measles, Herpes Simplex, and Varicella -Natural reservoir for arbovirus birds, rodents etc. Modes of transmission: -Primarily person to person and arthopod vectors for Arboviruses Incubation Period: -Variable. For enteroviruses 3-6 days, for arboviruses 2-15 days Treatment: No specific treatment available. Most patients recover completely on their own.