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Meningitis
- 1. DR. DHRUVI MISTRY (MPTIN NEUROLOGICAL SCIENCES)
- 2. Include: • Introduction • Definition •Cause • Pathophysiology • Types • Investigations • Treatment
- 3. • The brainand spinal cord are enclosed in three protective membranes called ‘meninges’. • From outward to inward: dura mater arachnoid mater pia mater • Arachnoid mater and pia mater together are termed leptomeninges.
- 4. • Subarachnoid space: space exist between arachnoid mater and pia mater that contain cerebro-spinal fluid.
- 6. Definition • Meningitis isthe inflammation of the meninges caused by infectious agents . • The inflammation is usually caused by infection of the fluid surrounding the brain and spinal cord. • Meningitis can be life-threatening because of the inflammation’s proximity to the brain and spinal cord, therefore it is classified as a medical emergency.
- 8. • Meningitis mayalso be non-infectious in origin. E.g. in malignancy & toxic drugs • Micro organism can reach meninges by: -- blood stream -- skull fracture --midle ear infection --sinus
- 9. Causes: infectious Non infectious BacterialMalignant Viral Vasculitis Protozoal Sarcoidosis Mycobacterial SLE Fungal RA Spirochaetal ricketssial
- 10. PATHOPHYSIOLOGY Causative organism entersthe blood stream cross blood barriers inflammation in meninges inflammation of subarachnoid space CSF cloudiness ↑ ICP ↑ CSF cell count
- 11. Types Bacterial viral parasiticfungal non infectious
- 12. Bacterial meningitis • Itis potentially life threatening form of disease that can cause a serious complications such as brain damage, hearing loss and ultimately death. • Inflammation of leptomeninges and fluid in subarachnoid space occur. • Most commonly transmitted by blood stream.
- 13. • It isalways cerebrospinal as the subarachnoid space is continuous around brain and spinal cord. • Causes: N. meningitidis H. influenza S. pneumoniae E .coli Group B Strepto.
- 14. Clinical features • Infection: fever, rigors • ↑ ICP : headache, nausea, vomiting, hypertension, bradycardia • Meningeal irritation : neck stiffness photophobia seizures
- 15. Clinical menifestation : •Kernig’s sign : severe stiffness of hamstrings causes an inability to straighten the leg when hip is flexed 90˚. • Brudzinski’s sign: passive flexion of the neck causes involuntary flexion of the knee and hip. • Carnial nerve palsies : 3rd , 4th, 6th & 7th • Nystagmus, aphasia, ataxia, peripheral nerve palsy.
- 17. Investigations: • CSF :↑ WBC ↑ protein ↓ glucose • Blood culture : positive for H. influenzae, meningococci or pneumococci. • Blood urea ↑ • X-ray : chest : pneumonia skull : # mastoid : mastoiditis
- 18. • CT scan: cerebritis, vascular occlusion, encephalomalacia, hydrocephalus, brain abscess.
- 19. Medical treatment • Neonates: ampicillin (100-150 mg/d) + cefotaxime (50mg /kg) • Older infant : ceftriaxone + vancomycin • Elderly : ampicillin + ceftriaxone • Older adult : vancomycin ( 1gm q8h)+ ceftriaxone (100mg/kg/day)
- 20. VIRAL (ASEPTIC )MENINGITIS • It does not typically cause notable paranchymal involvement of brain and spinal cord. • It has a more benign clinical course. • Cause : herpes simplex virus - E-B virus - cytomegalovirus
- 21. - mumps virus -varicella zoster virus - rabies virus • Transmitted by droplet infection, close personal contact or faeco-oral contact. • Viral meningitis is sually self limited.
- 22. • Clinical features: fever headache vomiting meningealirrritation arthralgia myalgia sore throat weakness lethargy
- 23. Tuberculous meningitis • Itis caused by mycobacterium tuburculum. • Blood- borne spread certainly occurs. • Aetiology : age : 6months to 3 years sex : equal incidence primary infection : lung or mediastinal gland
- 24. pathophysiology • Tuberculus bacillicarried in the blood stream produce caseous foci called “RICH’s focus “ in the brain, spinal cord , meninges. • It is only when these rupture into CSF that meningitis results.
- 25. Clinical features • 1)prodromal stage of sensory irritability: high fever drowsiness anorexia headache restlessness constipation
- 26. • 2)Stage ofmeningeal irritation : convulsion kernig’s sign brudzinski sign neck stiffness exaggeration of deep reflexes muscular twitching grinding teeth squint, ptosis altered consciousness
- 27. • 3) terminalstage of coma : - irritability replaced by coma - rapid loss of weight -tachycardia, irregular pulse - irregular respiration ,chyne stoke breathing - tremors of limb , choreic movement
- 28. Investigation • CT scan •X-ray • Blood culture • Assess ICP
- 29. Treatment • Antituberculin drugsRNTCP regimes drugs Daily mg /kg Int15ermitten t thrice weekly mg/kg Adverse effect Isoniazid 5 12-17 hepatotoxicity polyneuritis Rifampicin 10 15 hepatotoxicity Red coloured body Pyrazinamide 25 35 hepatotoxicity Streptomycin 15 15 Vestibular damage ethambutol 15 30 Retrobulbar neuritis
- 30. Fungal meningitis • Cause: cryptococcus candida blastomyces aspergillus • It is not spread from person to person. • It can develop after a fungus spread through blood stream from somewhere else in the body to the brain or spinal cord. • It may also get after taking medications that weaken immune system.
- 31. Parasitic meningitis • Causeis often assumed when there is a predominance of eosinophils in tne CSF. • Common parasites : schistosoma amoeba plasmodium toxoplasma
- 32. Non -infectious meningitis •Spread of cancer to the meninges and certain drugs like NSAIDS , antibiotics • Several inflammatory conditions like sarcoidosis, SLE
- 33. CSF comparison cause appearancePolymorpho nuclear cells lymphocyte protein Glucose Bacterial meningitis Yellowish, turbid Markedly increased Slightly increased or normal Markedly increased Decreased Viral meningitis Clear fluid Slightly increased or normal Markedly increased Slightly increased or normal Normal Tuberculous meningitis Yellowish and viscous Slightly increased or normal Markedly increased increased Decreased Fungal meningitis Yellowish and viscous Slightly increased or normal Markedly increased Slightly increased or normal Normal or decreased
- 34. Physiotherapy treatment Aims • Chestcare • Normalization of tone • Facilitation of ambulation • Improve ROM • Prevent DVT • Improve functional activities • Prevent bed sores
- 35. • Chest care: breathing exercise chest expansion exercise coughing ,huffing positioning chest clearance technique • Normalization of tone: icing slow passive movt
- 36. - electrical stimulationto antagonist - PNF technique like slow reversal - sustained stretching • Facilitation of ambulation : - orthosis - wheelchair - training in parallel bar
- 37. • Atxia :frenkel’s exercise balance exercise • Cranial nerve palsy : electrical stimulation eye exercise facial muscles exercise • To prevent DVT : ankle pump exercise • To prevent bed sores : move patient every 2 hours and positioning. • Sensory integration
- 38. Reference • 1. Golwalla’sMEDICINE for students; A.golwalla, S.golwalla; 25th edition • 2.MEDICINE prep manual for undergraduates; K.Mathew , P,Aggarwal; 5th edition • 3. Textbook of CLINICAL NEUROANATOMY; Vishram Singh; 2nd edition • 4. Umphred’s neurological rehabilitation; U.darcy; 6th edition