Acute meningoencephalitis Powerpoint presentation.
It comprises of acute meningitis and acute encephalitis, their clinical features, physical assesment, diagnosis and treatment.
Acute Meningoencephalitis meningoencephalitis is an acute inflammatory process involving the meninges and, to a variable degree, brain tissue. Acute Bacterial Meningitis Acute Viral Meningoencephalitis 2
Risk Factors Age Low socioeconomic status Head trauma Splenectomy Chronic diseases Children with facial cellulitis , periorbital cellulitis , sinusitis and septic arthritis Maternal infection and pyrexia at the time of delivery. 7
8
9
Clinical features Newborn & Infants: non-specific Fever Irritability Lethargy Vacant stare Poor tone Poor feeding High pitched cry Bulging anterior fontanelle Convulsions Opisthotonus 10
Older children 11
Seizures Alteration in mental status Hypotension, fever or Hypothermia, Tachycardia (Septic shock) Bleeding, Renal dysfunction (DIC) 12
TB meningitis Children 6 months – 5 years Local microscopic granulomas on meninges Meningitis may present weeks to months after primary pulmonary process CSF: Profoundly low glucose High protein Acid-fast bacteria (AFB stain) PCR Steroids + antitubercular agents (2HRZE+ 10 HR) WITH steroid for 4-6 weeks 15
Stages Stage 1: stage of invasion Low grade fever, loss of appetite, vomiting, headache, photophobia, irritable, restless Stage 2: Stage of meningitis Neck rigidity, focal neurological deficits, isolated cranial nerve palsies, loss of sphincter control Stage 3: Stage of coma Loss of consciousness, altered respiratory pattern, dilated pupils, ptosis , ophthalmoplegia , coma 16
Neisseria meningitis (Meningococcemia) Neisseria meningitidis : serotype Grp B commonest Endotoxin causes vascular damage vasodilatation, third spacing, severe shock Severe complication: Waterhouse- Friderichsen syndrome : massive haemorrhage of adrenal glands secondary to sepsis: adrenal crisis-low B.P, shock, DIC, purpura , adreno -cortical insufficiency 17
Morbiliform , non blanching petechiae to purpura involving mostly extensor surfaces Tumbler test 18
Investigations Complete blood count C- Reactive Protein Renal function test Serum glucose Blood culture and sensitivity If tubercular suspected PCR Chest X-ray Mantoux test Arterial blood gas Fundoscopy CT scan 19
CSF analysis 20
Management Medical emergency • Early diagnosis essential Immediate optimum treatment Intensive supportive therapy Rehabilitation Prophylaxis to family Notification to Public Health 21
Treatment Managed in Intensive Care Unit Manage airway, breathing and circulation first Management of raised ICP Fluid management Dexamethasone : only in Pneumococcal and H. Influenzae B, given 1-2 hours before antibiotics Antibiotics Inotropes : increasing aortic diastolic pressure and improving myocardial contractility 22
ICP treatment 3% NaCl , 5 cc/kg over ~20 minutes May utilize osmotherapy ( Mannitol ) - if serum osmolarity < 320 mOsm /L Mild hyperventilation PaCO 2 <28 may cause regional ischemia Typically keep PaCO 2 32-38 mm Hg Elevate head end of bed by 30 o
Fluid management Restore intravascular volume & perfusion Monitor serum Na + ( osmolality , urine Na + ): If serum Na + <135 mEq /L then fluid restrict (~2/3x), liberalize as Na + improves If severely hyponatremic , give 3% NaCl SIADH 4 - 88% in bacterial meningitis 9 - 64% in viral meningitis Diabetes insipidus Cerebral salt wasting 24
Antibiotics Best started within 60 min Empirical therapy Meningococcal meningitis Benzyl penicillin 400-500,000 units/kg/day q 4 hour Pneumococcus / H. influenza Ampicillin (if penicillin susceptible) 300 mg/kg/day IV q6 hour Ceftriaxone (if penicillin resistant) 100-150 mg/kg/day q12 hour Cefotaxime 150-200 mg/kg/day q8 hour Vancomycin 60 mg/kg/day 25
Meningitis - Treatment duration Gram negative organisms: 21 days Pneumococcal ( ampiclox / ceftriaxone ): 10-14 days H influenza: 7-10 days Meningococcal: 7 days No growth: 7-10 days The CSF should be sterile within 24–48 hr of initiation of appropriate antibiotic therapy. 26
Dexamethasone use in meningitis Consider if H. influenza & Streptococcus pneumoniae > 6 wks old Dose: 0.6 mg/kg/day in 4 divided doses for 2 days MOA: local synthesis of TNF- , IL-1, PAF & prostaglandins resulting in BBB permeability, meningeal irritation incidence of hearing loss May adversely affect the penetration of antibiotics into CSF May decrease fever, giving false impression of improvement 27
Prophylaxis Rifampicin : Children 5mg/kg bd x 2 days Adults : 600 mg bd x 2 days Pregnant contact: Cefuroxime IM x 1 dose 28
Meningitis – Early complications Encephalitis Septic shock DIC Abscess SIADH Subdural effusion or empyema ~30% Dural sinus thrombophlebitis Stroke
Intermediate Hydrocephalus Cranial nerve palsy Late Cerebral palsy Hearing loss Learning disability 30
Acute Encephalitis Encephalitis is an acute inflammatory process affecting the brain Viral infection is the most common and important cause, with over 100 viruses implicated worldwide Symptoms Fever Headache Behavioral changes Altered level of consciousness Focal neurologic deficits Seizures 31
Etiology Non- Arbo viral Herpes viruses (sporadic) HSV-1 , HSV-2 varicella zoster virus cytomegalovirus Epstein-Barr virus human herpes virus 6 Adenoviruses Influenza A Enteroviruses, poliovirus Mumps Rabies Arbo -Viral (epidemic) Flaviviridae Japanese encephalitis St. Louis encephalitis West Nile Togaviridae Eastern equine encephalitis Western equine encephalitis 32
Herpes simplex virus (HSV) the most common etiology of acute sporadic encephalitis Arboviruses – arthropod-borne virus outbreaks in summer time… mosquitos and ticks Varicella zoster virus (VZV ) immunosuppressed patients 33
Japanese encephalitis Most important cause of arboviral encephalitis worldwide Transmitted by culex mosquito, which breeds in rice fields Commonly involve Basal ganglia : Extra pyradimal symptoms Post-immunization: Measles, Mumps 34
Herpes Simplex Encephalitis Primary infection: On the mucosa of oropharynx , mostly asymptomatic Following primary infection, a latent infection in trigeminal ganglion Inflammation and necrotizing lesion s in Inferior and medial temporal lobe Orbito -frontal lobe Limbic structures 35
Evolve over several days or acutely Fever, headache, confusion, stupor, coma, seizures, status epilepticus Personality changes, irritability, delirium Temporal lobe seizures: Gustatory or olfactory hallucinations, anosmia 36
CSF Analysis Increases CSF pressure Cell count: 10-500 cells/mm 3 Lymphocyte predominance Erythrocytes (in 80% of the cases) Normal CSF findings in 10% Xanthochromia : Due to lysis of RBC Glucose (mg/dl): normal or low Protein (mg/dl): >50 mg/dl HSV PCR : For the first 24-48 hours, detecting HSV DNA by PCR in CSF: specific ( 100%) and sensitive (75-98%) 37
Neuroimaging Contrast Enhanced MRI Sensitive for early period HSV encephalitis Edema in orbitofrontal and temporal regions CT Scan Less sensitive than MRI EEG If seizures are the features 38
Treatment If shock/hypotension exists, crystalloid infusion If unconscious, provide airway/breathing Seizure, lorazepam 0.1 mg/kg, IV Acyclovir IV, 14 – 21 days Neonates and infant: 60 mg/kg/day in 3 divided doses Children: 30 mg/kg in 3 divided doses Reduce ICP: restrict fluid, hyperventilation Acute psychosis: Haloperidol 39
References Nelson Textbook of Pediatrics 20 th edition Essential Pediatrics, OP Ghai , 8 th Edition Harrisons textbook of Internal Medicine AAP Guidelines 2016 40