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Premium member Presentation Transcript Approach to A case of meningitis : Approach to A case of meningitis Presented by Lt Col K Mohan, Resident DNB(Fam Med) INTRODUCTION : INTRODUCTION Slide 3: MENINGES Slide 4: MENINGES Slide 5: Meningitis is an inflammatory response to infections of the meninges and CSF,caused by bacteria, viruses, fungi, and other organisms such as protozoa and rickettsia. MENINGITIS Types of Meningitis : Types of Meningitis Pyogenic Bacterial meningitis Aseptic (viral) meningitis Tubercular meningitis : Significant Morbidity/Mortality Prognosis determined by early diagnosis & treatment Usually secondary to a bacteraemic illness Primary may result due to spread from Ear, Skull #,Sinuses Age specific pathogens Neonates Pre-school children Older children and Adults CAUSES Bacterial meningitis BACTERIAL PATHOGENS : Neonates E. Coli Proteus Group B Streptococci Listeria monocytogenes Enterococcus, Enterobacter, Klebsiella, Salmonella, BACTERIAL PATHOGENS BACTERIAL PATHOGENS : Pre School Children Hemophilus influenzae Neisseria meningitidis Streptococcus pneumoniae Mycobacterium tuberculosis BACTERIAL PATHOGENS BACTERIAL PATHOGENS : Older Children and Adults Neisseria meningitidis (Meningococcus) Streptococcus pneumoniae Mycobacterium tuberculosis Listeria monocytogenes Hemophilus influenzae Staphylococcus aureus BACTERIAL PATHOGENS ASEPTIC MENINGITIS : ASEPTIC MENINGITIS All non-bacterial causes of meningitis Most common cause is viral Enterovirus (coxsackie, echovirus) Typically occurs during late summer and fall Spread via respiratory secretions and fecal-oral Affects all ages Generally self-limiting illness HSV Consider especially in infants presenting with seizure Usually HSV type II Treat with acyclovir ASEPTIC MENINGITIS : ASEPTIC MENINGITIS Other Viral HIV Lymphocytic choriomeningitis virus Arbovirus Mumps * CMV EBV VZV Adenovirus Measles Rubella Rotavirus Influenza and parainfluenza ASEPTIC MENINGITIS : ASEPTIC MENINGITIS Fungal Cryptococcus Coccidiodes Histoplasmosis Parasitic Toxoplamosis Autoimmune Sarcoidosis Behcet’s Disease SLE Slide 14: NORMAL COMMENSALS OF MOUTH AND THROAT INVADE THROUGH THE NASOPHARYNX MENINGITS SEPICAEMIA PATHOPHYSIOLOGY (MENINGOCOCCI) OTITIS MEDIA PNEUMONIA (PNEUMOCOCCI) (HAEMOPHILUS) CLINICAL PRESENTATION : CLINICAL PRESENTATION Bacterial meningitis usually presents in two patterns Acute - common with S. pneumoniae and N. meningitides Subacute - preceding URI like symptoms, more common with H. influenza and other pathogens Slide 16: Headache Fever Drowsiness Neck stiffness Nausea and vomiting Irritability Aversion to light Restlessness Altered mental status (Stupor,Coma) Seizure Menngococcal meningits - Purpural rashes(70%) Most common CLINICAL PRESENTATION Skin rashes : Skin rashes Is due to small skin bleed All parts of the body are affeced The rashes do not fade under pressure Pathogenesis: a. Septicemia b. wide spread endothelial damage c. activation of coagulation d. thrombosis and platelets aggregation e. reduction of platelets (cosumption ) PHYSICAL EXAM FINDINGS : PHYSICAL EXAM FINDINGS Bulging fontanel Focal neurological signs Neck rigidity Ptosis, papilloedema, Cushing’s triad (Bradycardia, Hypertension, Altered respirations) Positive Kernig’s and Brudzinski’s sign KERNIG’S SIGN : KERNIG’S SIGN Patient placed supine with hips flexed 90 degrees. Examiner attempts to extend the leg at the knee Positive test elicited when there is resistance to knee extension, or pain in the lower back or thigh with knee extension due to meningeal irritation BRUDZINSKI’S SIGN : BRUDZINSKI’S SIGN Patient placed in supine position and neck is passively flexed towards the chest Positive test is elicited when flexion of neck causes flexion at knees and/or hips of the patient VIRAL MENINGITIS : VIRAL MENINGITIS Benign and self limiting Headache and irritability with rapid onset of meningism High Pyrexia Focal neurological signs- Rare TUBERCULAR MENINGITIS : TUBERCULAR MENINGITIS Most serious of all forms of TB TBM : 5-8 % of clinical TB Common in Immuno compromised patients More frequent and virulent in children Local source of infection : Caseous focus adjacent to CSF pathway Slide 26: TUBERCULAR MENINGITIS Slide 27: TUBERCULAR MENINGITIS MENINGITIS-DIFFERENTIAL DIAGNOSIS : MENINGITIS-DIFFERENTIAL DIAGNOSIS Brain abscess Encephalitis Epidural abscess Bacterial endocarditis with septic embolism Subarachnoid hemorrhage Tumor MENINGITIS-DIAGNOSIS : MENINGITIS-DIAGNOSIS Slide 30: CSF Patterns in Meningitis Slide 31: APPROACH TO A CASE OF SUSPECTED MENINGITIS OTHER INVESTIGATIONS : OTHER INVESTIGATIONS CBC Normal WBC does not rule out meningitis Blood cultures Electrolytes Renal function Serum glucose - Useful to compare with CSF glucose Other relevant investigations TREATMENT : Quick initiation of antibiotics is a must Typical Meningococcal rash Benzyle Penicillin 2.4 G IV 6th hrly Adults without Typical Meningococcal rash Cefotaxime 2 G IV 6th hrly or Ceftriaxone 2 G IV 12th hrly Pinicillin Resistant pnuemococci Cefotaxime or Ceftriaxone + Vancomycin 1gm IV 12th hrly Alter antibiotic choices once CSF gram stain results are available . TREATMENT Bacterial Meningitis Slide 35: N . meningitidis Inj Benzyle Penicillin 2.4 G IV 6th hrly * 5-7 days Strep. pneumoniae / H. influenae Inj Cefotaxime 2 G IV 6th hrly or Inj Ceftriaxone 2 G IV 12th hrly * 10-14 days Pinicillin Resistant pnuemococci Inj Cefotaxime or Ceftriaxone + Inj Vancomycin 1gm IV 12th hrly Listeria monocytogenes Inj Ampicillin 2G iv 6 hrly + Inj Gentamycin 5g/kg iv * 8- 10 days Slide 36: Supportive Care Steroids Steroids thought to blunt effects of host inflammatory response Theoretical concern of steroids reducing permeability of blood brain barrier to antibiotics Consider repeat LP 24-36 hours after initiating treatment to assure sterilization of CSF if resistant organism or poor response to treatment Features of Septicaemia – ICU Care Why do we use steroids? : Why do we use steroids? Decreases inflammation which can lead to decreased intracranial pressure. May interrupt the cytokine mediated neurotoxic effects of bacteriolysis, which are at a maximum during the first few days of antibiotic therapy. Proven reduction in morbidity, such as severe hearing loss, in children with HiB meningitis and Strep. Pneumo meningitis. Proven reduction in mortality in adults and children with tuberculous meningitis(particularly due to a reduction in hepatitis secondary to treatment of TB.) When Do We Use Steroids? : When Do We Use Steroids? Therapy should be initiated shortly before or at the same time as the first dose of antibiotics, (likelihood of unfavorable outcome was much higher in patients in whom dexamethasone was given after antibiotics). Dexamethasone should not be given to adults who have already received antibiotics, because it has not been shown to improve patient outcomes. Slide 39: Benign and self limiting No specific treatment Symtomatic treatment in a quite room Recovery within few days Viral Meningitis Slide 40: ATT- 2 EHRZ/10 HR Steroid therapy Fewer deaths, decreased disability Dexamethasone / prednisolone – tapering doses over 3 – 6 wks Raised ICT Frusemide, Acetazolamide, steroids, repeated LP Fluid & electrolyte balance Tubercular Meningitis COMPLICATIONS : COMPLICATIONS Delayed or untreated cases - can be fatal Healing by fibrosis cause obliteration of subarachenoid space – Hydrocephalus Brain abscess Encephalitis Septic shock Renal Failure DIC Chronic Meningococcaemia -Rare PROGNOSIS : PROGNOSIS Even with appropriate antibiotics, mortality rate is significant 8% H.influenza, 15% Neisseria meningitidis, 25% Pneumococcal Up to 35% of survivors have sequelae including deafness, seizures, blindness, paresis, ataxia, hydrocephalus Slide 43: Poor prognosis associated with Young age Long duration of illness prior to antibiotics Late-onset seizures Coma at presentation Immuno compromised state Slide 44: THANK YOU You do not have the permission to view this presentation. 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