Hydrocephalus, meningitis and encephalitis - Pathology

This presentation covers in brief the CNS pathology for nurses according to sem 4 syllabus. This covers disorders such as meningitis, encephalitis and also includes hydrocephalus.

1. CNS PATHOLOGY BY : MS. SAILI GAUDE PRINCIPAL SHIVAM COLLEGE OF NURSING, AMIRGADH

2. 1)HYDROCEPHALUS

3. Definition Increased volume of Cerebrospinal fluid within the skull along with dilatation of the ventricles

4. INTERNAL HYDROCEPHALUS Hydrocephalus involving ventricular dilatation EXTERNAL HYDROCEPHALUS Hydrocephalus without ventricular dilatation Localised collection of CSF in subarachnoid space

5. SOURCE AND CIRCULATION OF CSF Choroid plexus epithelium and ependymal cells of the ventricles produces CSF- 120 to 150ml CSF is secreted by choroid plexus in each lateral ventricles CSF flows through interventricular foramina into 3 rd ventricles Choroid plexus in third ventricles adds more CSF CSF flows down cerebral aqueduct to 4 th ventricles Choroid plexus in 4 th ventricles adds more CSF CSF flows out 2 lateral apertures and one median aperture CSF fills subarachnoid spaces and bathes external surfaces of brain and spinal cord At arachnoid villi, CSF is reabsorbed into venous blood of dural venous sinuses PRODUCTION OF CSF CIRCULATION OF CSF REABSORBTION OF CSF

6. FLOW DIAGRAM OF CSF CIRCULATION LATERAL VENTRICLES FORAMEN OF MONRO THIRD VENTRICLES AQUEDUCT OF SLYVIUS FOURTH VENTRICLES FORAMEN OF MAGENDIE AND LUSHKA SUBARACHNOID SPACE OF BRAIN AND SPINAL CORD

7. TYPES AND ETIOPATHOGENESIS

8. PRIMARY HYDROCEPHALUS Actual increase in the volume of CSF within skull along with elevated intracranial pressure Possible mechanisms of primary hydrocephalus 1) Obstruction of CSF flow 2) Overproduction of CSF 3) Deficient resorption of CSF

9. OBSTRUCTIVE HYDROCEPHALUS Most commonest type of primary hydrocephalus Depending on the site of obstruction, further classified as: 1) Non communicating hydrocephalus 2) Communicating hydrocephalus

10. 1) NON COMMUNICATING HYDROCEPHALUS When the site of obstruction of CSF pathway is in the third ventricles or at fourth ventricles Ventricular system enlarges CSF cannot pass into subarachnoid space Accumulation of CSF Causes : 1) Congenital – stenosis of aqueduct, Arnold chiari malformation, gliosis of aqueduct, intrauterine meningitis 2) Acquired- Expanding lesions inside skull eg tumors , inflammatory lesions, hemorrhage

11. 2) COMMUNICATING HYDROCEPHALUS When obstruction to the CSF flow is in the subarachnoid spaces at the base of the brain, it results in enlargement of the ventricular system but CSF flows freely between dilated ventricles and spinal cord. Causes are non obstructive in nature : 1) Overproduction of CSF- Choroid plexus pappiloma 2) Deficient reabsorbtion of CSF – after meningitis , subarachnoid hemorrhage

12. SECONDARY HYDROCEPHALUS Less common Compensatory increase of CSF due to loss of neural tissue without associated rise in intracranial pressure Eg . Cerebral atrophy and infarction

13. MORPHOLOGY GROSS MORPHOLOGY Dilatation of ventricles Thinning and stretching of brain Engorgement of scalp vein Fontanelle remains open HISTOLOGICALLY Damage to ependymal lining of ventricles Periventricular interstitial edema

14. MENINGITIS

15. DEFINITION Inflammation of all layers of meninges and CSF within the subarachnoid space Pachymeningitis- inflammation of dura matter Leptomeningitis - inflammation of pia and arachnoid matter Chemical meningitis- when non bacterial irritants causes meningitis Meningeal carcinomatosis – cancer cells infiltrate the meninges

16. ETIOPATHOGENESIS

17. 1) ACUTE PYOGENIC MENINGITIS Acute infection of the pia and arachnoid mater Neonates – E.Coli , Proteus, Group B streptococci Infants and Children – H. Influenza Adolescents and young adults- Nesseiria meningitidis Blood stream Adjacent foci of infection Iatrogenic- during lumbar puncture or during surgery ETIOLOGY ROUTES OF TRANSMISSION

18. CSF becomes purulent Accumulation of purulent CSF in subarachnoid space esp at the base of brain Meningeal artery becomes engorged and prominent In severe cases ventricles may get inflamed called as the ventriculitis GROSS APPEARANCE

19. Subarachnoid space is filled with plenty of neutrophils Meninges also contains neutrophils Gram staining may show different causative bacteria Arachnoid fibrosis can be seen Adhesive arachnoiditis in which the arachnoid mater starts to stick to the adjacent mater can be seen MICROSCOPICALLY

20. Fever Headache Vomitting Drowsiness Convulsion Coma Purpuric rash Neck rigidity CLINICAL FEATURES

21. Lumbar puncture may show : 1) Cloudy or purulent CSF 2) Increased CSF pressure 3) Increased protein levels in CSF 4) Decreased sugar in CSF 5) Increased Neutrophils in CSF Gram staining of culture of CSF 1) Shows the causative organisms Polymerase chain reaction may also be used DIAGNOSTIC FINDINGS

22. 2) ACUTE VIRAL MENINGITIS Also called acute lymphocytic meningitis or Aseptic meningitis Most common cause- Viral Benign self limiting disorder Entero virus ECHO virus Coxsackie virus Epstein Barr virus Mumps Herpes simplex CAUSATIVE ORGANISMS

23. Brain edema Inflammation of meninges Mild to moderate amount of lymphocytes are seen in CSF Inflammatory infiltrate in pia and arachnoid mater GROSS APPEARANCE MICROSCOPICALLY

24. Headache Meningeal irritability Hyperpyrexia Meningeal rigidity Weakness Complete recovery without specific therapy CLINICAL FEATURES

25. Clear or cloudy CSF Increased pressure more than 250mmHg Increased protein levels in CSF Normal CSF glucose levels Increased lymphocytes in CSF CSF bacteriologically sterile DIAGNOSTIC TEST

26. 3) CHRONIC MENINGITIS 2 disorders under this are : 1) TUBERCULOUS MENINGITIS 2) CRYPTOCOCCAL MENINGITIS

27. Most common in children May occur as a part of miliary tuberculosis Immunosupression may cause it Commonly seen in multidrug resistance TB Causative organism – M. tuberculosis TUBERCULOUS MENINGITIS

28. Occurs in immunocompromised patients as secondary infection Usually starts from a pulmonary lesion Important cause of meningitis in AIDS patient CRYPTOCOCCAL MENINGITIS

29. Thick greenish gelatinous pus Common at bases Many tubercles are present on the meninges- 1 to2 mm in diameter Brain edema In cryptococcal meningitis the exudate is less and gelatinous GROSS APPEARANCE

30. Exudate comprises of mixture of cells of both acute and chronic inflammatory cells Granulation and giant cells Zeil – neilson staining – AFB + ve Cryptococci seen on Indian ink preparation MICROSCOPICALLY

31. Low grade fever Headache Vomiting Malaise CLINICAL FEATURES

32. CSF is clear When allowed to settle, CSF may show a small clot formation Increased pressure- above 300 mmHg Increased protein in CSF Decreased glucose content Increased leucocyte count in CSF Special stains demonstrates the micro-organisms responsible for meningitis DIAGNOSTIC FINDINGS

33. ENCEPHALITIS

34. Infection of brain parenchyma Causative organism- any organism Normally occurs as a secondary infection after meningitis Tuberculosis and neurosyphilis are only 2 causes of primary infection which causes a brain lesion called as brain abscess The cerebral cortex is the place where this micro-organisms are found the most and thus it may causes cerebritis DEFINITION

35. TRANSMISSION : A) Direct implantation- during fracture of skull or surgery of the skull B) Local extension of the infection- sinusitis, otitis media, mastoiditis etc C) Blood spread- Especially infection from heart such as endocarditis, may spread through blood to brain PATHOLOGICAL CHANGES Cerebral abscesses are destructive lesions Walled off by pyogenic membrane 1. BACTERIAL ENCEPHALITIS

36. GROSS APPEARANCE: Abscess with central necrosis surrounded by fibrous capsule and edema Multiple abscesses Can occur in any lobe – frontal, parietal and cerebellum MICROSCOPICALLY Central liquefactive necrosis Acute and chronic inflammatory cells Neovascular blood vessels Edema Fibrous capsule Gliosis

37. Range of viruses can cause this disorder Preceding infection in other tissues Virus replication occurs outside brain Than affects nervous system ENTRY OF MICRO-ORGANISM Via gastrointestinal tract Skin and mucus membrane Transplacental Body fluids Animal bite 2) VIRAL ENCEPHALITIS

38. Inflammation of cortex, basal ganglia and brain stem Herpes simplex- temporal lobe Diffuse parenchymal infiltrate of lymphocytes, plasma cells and macrophages Clusters of glial cells Presence of specific inclusion bodies PATHOLOGICAL CHANGES

39. Necrotizing area Hemorrhage Eosinophillic Inflammatory infiltrate Edema Vascular congestion Pyramidal cells are seen in case of rabies MORPHOLOGY

40. Infection of ependymal cells and glial cells Owl eye like big inclusions seen inside nucleus or cytoplasm in cytomegalovirus infection Negri bodies- a small bullet shaped intra cytoplasmic inclusion seen in rabies Microglial nodules MICROSCOPICALLY

41. Usually develop by blood stream Systemic deep mycoses somewhere else in the body causes it Common in immunosuppressed individuals Common causative organisms- candida, mucormycosis , histoplasma, aspergillus, cryptococci Protozoal causes- malaria, toxoplasmosis, amoebiasis etc 3) FUNGAL ENCEPHALITIS

42. T HE END