ACUTE BACTERIAL MENINGITIS Acute bacterial meningitis is an acute infection of the subarachnoid space and meninges characterizes by polymorphonuclear cells in the cerebrospinal fluid (CSF). Bacteria may invade the subarachnoid space directly by spread from contiguous structure, e.g. sinuses, or more commonly indirectly from the bloodstream.
Causative organisms In neonates – gram -ve bacilli, e.g. E. coli, Klebsiella. In children – Haemophiles influenzae. Pneumococcus, meningococcus In adults – Pneumococcus, Meningococcus Host factors – congenital or acquired immune deficiency, predispose to infection, overcrowding and poverty. May occur following head injury, mastoiditis or after lumbar puncture.
Nasopharyngeal colonisation Replication & growth Blood Subarachnoid Space invasion Replication of subarachnoid space Infection & inflammation of sub arachnoid space Pathology
Clinical features c/f are present on the basis of 3 main causes: Infection Increased ICP Meningeal inflammation & irritation Meningitis symptoms Severe frontal/occipital headache Stiff neck Fever, vomiting Photophobia
C/F ACCORDING TO STAGE OF MENINGITIS : STAGE-1 STAGE OF INVASION: Sudden onset Severe head ache Vomiting Fever Neck and back pain Convulsion Insomnia Severe confusion
STAGE-2 MENINGEAL STAGE : More severe head ache Lumbar pain Muscular stiffness & neck stiffness Kernig's & Brudzinski's signs +ve Muscular twitching & tenderness Temperature variable Exaggerated DTR Sensory loss Sensory neural deafness Pulse : slow & irregular
PROGNOSIS Over all prognosis- good Depends upon different factors E.g. Infective organism Response to antibiotics Stages of illness when pt comes Presence of complications Over all mortality- 15-25%
TREATMENT
PT EVALUATION OF THE PATIENT WITH MENINGITIS Observation of current functional status of the patient Assessment of standard vital signs Assessment of cognitive status Assessment of sensory integrity Assessment of movement abilities Assessment of functional abilities
AIMS OF THE PT INTERVENTIONS Optimization of postural control Optimization of functional activities with selective voluntary movement pattern control Improvement of performance of functional activities Enhancement of integration of sensory information Optimization of cognitive status and psychosocial responses
ENCEPHALITIS
INTRODUCTION Encephalitis is a non-suppurative inflammation of the parenchyma of the brain which contain neuronal and glial cell damage with associated inflammation and oedema. The inflammatory process can also involve the spinal cord i.e. encephalomyelitis. Viral encephalitis is a worldwide disorder with the highest incidence.
Virus causing encephalitis : Enterovirus Herpes simplex (usually type 1) Mumps virus Influenza virus Varicella zoster Japanese encephalitis virus
The most common virus responsible for large-scale epidemic in India is Japanese B encephalitis virus. It is spread by mosquito that extensively in rice ecosystem. In adults, >90% of cases of herpes simplex encephalitis result from infection with HSV-1. In children, influenza virus is an important cause of encephalitis.
CLINICAL FEATURES GENERAL : pyrexia, myalgia Specific to causative virus, Meningeal involvement (slight) – neck stiffness, cellular response in CSF. Sign and symptoms of parenchymal involvement – focal / diffuse.
INVESTIGATION CT SCAN : In temporal lobes with surrounding oedema. CSF : Increased pressure Protein levels are mildly elevated Cell count is increased EEG : periodic high voltage slow wave complexes over the involved temporal lobe.
DIFFERNTIAL DIAGNOSIS Post infectious encephalomyelitis Bacterial or tubercular infections of the brain
PROGNOSIS It is highly variable, in chronic cases high mortality is seen. Many may be left with residual deficit like dementia, focal deficits and epilepsy. Complications remain such as flexion deformities of arms, hyperextension of the legs, language impairment, learning difficulties and behavioral problems. Many recover completely if the illness is mild.
TREATMENT General measures to care for the unconscious patient should be started. Anticonvulsants are often necessary. Dexamethasone 4 mg 6 hourly for brain oedema. HSE responds well to acyclovir (10 mg/kg IV 8 hourly for 14-21 days)
The goals of therapeutic intervention program for patients with inflammatory CNS disorders :