INFECTION OF THE CENTRAL NERVOUS SYSTEM

1. INFECTION OF THE CENTRAL NERVOUS SYSTEM

2. INFECTIONS OF THE CENTRAL NERVOUS SYSTEM • Meningitis • Pyogenic bacterial meningitis • Viral meningitis • Tubercular meningitis • Fungal ( in immune-deficient) meningitis • Aseptic meningitis • Encephalitis • Rabies • Cerebral abscess • Poliomyelitis Dr. Alka Stoelinga

3. Definition Meningitis • An infection or inflammation of meninges (Connective tissue covering the central nervous system) Dr. Alka Stoelinga

4. Dr. Alka Stoelinga

5. ACUTE PYOGENIC BACTERIAL MENINGITIS Dr. Alka Stoelinga

6. Causative organisms • Neonate (E.coli) • Children (Hemophilus influenzae, Nesierria meningitidis, Streptococcus pneumoniae) • Adults (Nesierria meningitidis, Streptococcus pneumoniae) • Routes of infection • Hematogenous • From adjacent structures (Sinusitis, CSOM, Head injuries) • Iatrogenic ( Post LP, After neurosurgical procedures) NOTE • At all age groups- Strep. Pneumoniae • Adolescents- N. meningitidis • Very young and very old- Listeria monocytogens • After any neurosurgery- Staph • HIV- Cryptococcus Dr. Alka Stoelinga

7. Pathology • In acute bacterial meningitis: The pia-arachnoid is congested with polymorphs. • A layer of pus forms. This may organize to form adhesions, causing cranial nerve palsies and hydrocephalus. • In chronic infection (e.g. TB): The brain is covered in a viscous grey-green exudates with numerous meningeal tubercles. Adhesions are invariable. Cerebral oedema occurs in any bacterial meningitis. • In viral meningitis : There is a predominantly lymphocytic inflammatory CSF without pus formation, polymorphs or adhesions; there is little or no cerebral edema unless encephalitis develops Dr. Alka Stoelinga

8. Clinical features: • The classic clinical triad of meningitis is • Nuchal rigidity ("stiff neck"). • Sudden High Fever • Altered mental status • Other signs associated with meningitis are • Headache • Photophobia (intolerance to bright light) • Phonophobia (intolerance to loud noises) • Nausea, vomiting • Alteration in mental status (confusion, delirium, lethargy, coma) • Progressive drowsiness, cranial nerve palsy and focal neurological deficits indicate complications such as severe cerebral edema or hydrocephalus or think of alternative diagnosis such as cerebral abscess or encephalitis when these symptoms/ signs are seen • Kernig'sand Brudzinski's signsare classic signs of meningeal irritation. • Seizures • Rashes(meningococcemia) • Signs of increased ICP • ↓ level of consciousness, sluggish pupils, bradycardia, hypertension, irregular respiration Dr. Alka Stoelinga

9. Meningococcal meningitis • Meningitis caused by the bacterium Neisseria meningitidis (known as "meningococcal meningitis“) • It can be differentiated from meningitis with other causes by a rapidly spreading petechial rash which may precede other symptoms. • The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjunctiva, and (occasionally) the palms of the hands or soles of the feet. • The rash is typically non-blanching: the redness does not disappear when pressed with a finger or a glass tumbler. Dr. Alka Stoelinga

10. Features of Meningococcal Septicemia: • Meningitis • Rash • Shock • DIC • Renal failure • Peripheral gangrene • Arthritis(Septic/Reactive) • Pericarditis(Septic/Reactive) Dr. Alka Stoelinga

11. Examination: • Altered consciousness • Hypotension/Hypertension • Bradycardia • Rash • Neurological: • Neck stiffness • Jolt accentuation maneuver +ve • Kernig’s sign +ve • Brudzinski's sign +ve • Hypertonia • Increased DTR Dr. Alka Stoelinga

12. Dr. Alka Stoelinga

13. Specific Examinations • Kernig's sign • It is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. • In a patient with a positive Kernig's sign, pain limits passive extension of the knee. • Brudzinski's sign • It is said to be positive when flexion of the neck causes involuntary flexion of the knee and hip. • Jolt accentuation maneuver • Helps determine whether meningitis is present in patients reporting with fever and headache. • The patient is told to rapidly rotate his or her head horizontally; if this does not make the headache worse, meningitis is unlikely Dr. Alka Stoelinga

14. Kernig’s sign Dr. Alka Stoelinga

15. Brudzinski’s sign Dr. Alka Stoelinga

16. Investigations : • Single most important investigation is • Examination of CSF. • Always examine optic fundi before LP • Typical CSF picture • Increased Cells (Poly-morpho-nuclear leukocytosis >100) • Decreased Sugar (CSF: Blood ratio <0.4) • Increased protein (Above 0.5 gm/l) • Increased pressure (>18cm of CSF) • Positive cultures or Gram’s stain Other investigations: • CT scan/ MRI head to r/o any mass lesions/ raised ICP in brain • Blood: TC,DC, Culture and sensitivity, CRP Dr. Alka Stoelinga

17. Typical CSF changes in meningitis Dr. Alka Stoelinga

18. Management: • Recognition and immediate treatment of acute bacterial meningitis is vital. • Minutes save lives. • Bacterial meningitis is lethal. Even with optimal care, mortality is around 15%. 1. Supportive measures: • Airway, Breathing, Circulation • Electrolyte balance 2. Antimicrobial therapy • High dose parenteral antibiotics 3. Management of complications Dr. Alka Stoelinga

19. Empirical Treatment • Empirical treatment with 3rd generation cephalosporin • Ceftriaxone 2gm 12 hourly /Cefotaxime 2gm 6 hourly for 10-14 days • Alternative: Benzyl Penicillin 3 lakh unit/Kg/Day in 6 divided doses • Organisms are isolated: • N. meningitidis : • Benzyl penicillin 2.4 gm IV 4 hourly for 5-7 days orCeftriaxone/Cefotaximeor Chloramphenicol for 5-7 days • For contacts: • Ciprofloxacin 500mg single dose or • Rifampicin 600mg bid for 2 days or • Ceftriaxone 250 mg IM single dose Dr. Alka Stoelinga

20. Strep. Pneumoniae : • Cefotaxime 2 gm IV 6 hourly or Ceftriaxone 2gm 12 hourly for10-14 days • Strep pneumomiae resistant to cephalosporin : • Add vancomycinorrifampicin • H.influenzae : • cefotaximeorceftriaxoneor chloramphenicol • Listeria monocytogenous : • Ampicillin +Gentamicin Dr. Alka Stoelinga

21. Antibiotics and acute bacterial meningitis Dr. Alka Stoelinga

22. Steroid (Dexamethasone) • Steroid are used in initial few days of the treatment in cases of S.pneumoniae and H. influenzae meningitis. • It should be started before antibiotics and should be tapered 2 days there after. • It lowers the rate of meningeal adhesion and thus decreasing the long term complications • Control of seizures • Control of raised intracranial pressure • Management of Raised intracranial pressure: • Head end elevation to 15-30 ̊ • Hyperventilation • Osmotic agent: 20%Mannitol 125ml every 8hourly • Dexamethasone 4mg IV 6 hourly • Furesomide IV • Glycerol Dr. Alka Stoelinga

23. Prognosis: • Mortality is : • 3 to 7% in meningitis caused by H. influenzae and N. Meningitides • 15% in that due to L. monocytogenes and • 20% in S. pneumoniae • Residual neurological deficit occurs in about 25 % of the patients Dr. Alka Stoelinga

24. Poor prognostic factors • Decreased level of consciousness on admission • Onset of seizures within 24h of admission • Signs of raised intra cranial pressure. • Young age (infancy) and age >50 Dr. Alka Stoelinga

25. Complications: ACUTE: • Shock • Status epilepticus • Brainstem herniation • Multisystem failure-Septicemia, DIC, Shock CHRONIC: • Hydrocephalus • Neurological deficit: Hemiplegia/Quadriplegia/Cranial nerve palsy, Deafness, Blindness • Decreased cognitive function Dr. Alka Stoelinga

26. Differential Diagnosis: • Viral meningitis • Tuberculous meningitis • Encephalitis • Brain abscess • Subarachnoid hemorrhage • Cerebral malaria • Brain tumor • Meningism Dr. Alka Stoelinga

27. Viral meningitis • Most common of all meningitis • This is almost always a benign, self-limiting condition lasting 4-10 days. • Causes: • Mumps, influenza, herpes, polio, Epstein-Barr, HIV are the usual pathogens. • Clinical course is less severe compared to bacterial meningitis. • Headache may follow for some months. There are no serious sequel • In viral meningitis there is a predominantly lymphocytic inflammatory CSF reaction without pus formation, polymorphs or adhesions, with normal glucose and protein. • There is little or no cerebral edema unless encephalitis develops • Complete recovery occurs without any specific treatment. Dr. Alka Stoelinga

28. Case • A 45 year old man is brought to ER (Emergency Department) with one day of fever, headache, nausea and vomiting. On physical examination he is found to have neck stiffness and photophobia. How will you diagnose and manage the case? Dr. Alka Stoelinga

29. CHRONIC MENINGITIS Dr. Alka Stoelinga

30. Tubercular meningitis • Fungal meningitis • Tuberculous meningitis (TBM) and cryptococcal meningitis commence typically with vague headache, lassitude, anorexia and vomiting. Acute meningitis can occur but is unusual. • Meningitic signs usually take some weeks to develop. • Drowsiness, focal signs (e.g. Diplopia, Papilloedema, Hemiparesis) and seizures are common. • Syphilis, Sarcoidosis and Behcet's syndrome [Triad of recurring crops of mouth ulcers (aphthous ulcers), genital ulcers, and inflammation of a specialized area around the pupil of the eye (the uvea)] also cause chronic meningitis. • In some chronic meningitis organisms are never identified. Dr. Alka Stoelinga

31. Tuberculous meningitis • Severe form of tuberculosis • More in immunocompromised patients,AIDS patients • Hematogenous spread secondary to primary or post primary tuberculosis • Occurs soon after a primary infection or as a part of milliary tuberculosis Dr. Alka Stoelinga

32. Clinical features: • Early stage: Nonspecific symptoms: • Headache, low grade fever, vomiting, loss of appetite, lassitude , irritability, depression and confusion are the presenting symptoms • Over 1-2 weeks: • Neck stiffness • Occulomotor palsy • Papilloedema • Decreased conscious level • Seizure • Sometimes Focal neurological deficits • Coma Dr. Alka Stoelinga

33. Signs: • Occulomotor palsies • Papilloedema • Depression of conscious level • Absence of Meningism during the onset of disease Dr. Alka Stoelinga

34. Investigations: 1. CSF analysis: • Examination of CSF shows elevated cells,100-500 (predominant lymphocytes) • Markedly increased protein (spider web formation) and • Reduced sugar • AFB stain positive 2. Imaging: • CT scan head CT may show basal meningeal enhancement due to exudates • CXR Imaging of lungs may show the primary site 3. Sputum for AFB 4. Mantoux test Dr. Alka Stoelinga

35. TREATMENT: • Treatment should be initiated when CSF report is available with : 1. ATT : 2HRZE/S +7HR (9-12 months) 2. Steroid • Should be given for 4-8 weeks • Decrease neurological deficit 3. Sometimes surgical intervention is necessary. 4. Treatment of cerebral edema 5. Control of seizure 6. Treatment of Hydrocephalus if present 7. Physiotherapy • Despite effective treatment some patients are left with permanent neurological deficit. Dr. Alka Stoelinga

36. Complications: ACUTE: • Status epilepticus • Cerebral edema • Coma LATE: • Focal neurological deficit • Cognitive defects • Hydrocephalus • Seizure • Cranial nerve palsies Dr. Alka Stoelinga