The document discusses meningitis, including: 1. It defines meningitis as inflammation of the meninges covering the brain and spinal cord. Meningitis can be caused by viruses, bacteria, fungi or other microorganisms. 2. It classifies meningitis based on etiology, including bacterial, viral, fungal and parasitic meningitis. The most common bacterial causes are S. pneumoniae, N. meningitidis and H. influenzae. 3. It notes that while viral meningitis is more common, bacterial meningitis requires urgent treatment due to high mortality and morbidity. Prompt diagnosis and treatment are critical for improving prognosis.

1. Meningitis
Shobith 170614007
Priyanka 170614015
Sharanam 170614019
Vignesh 170614040

2. Definition
• WHO :- Meningitis is inflammation of the meninges, the
membranes covering the brain and spinal cord
• It is an inflammation of the meninges and subarachnoid space
that can also involve the brain cortex and parenchyma
• Proximity of the inflammation to the brain makes it a medical
emergency
• The inflammation may be caused by infection with Viruses
(Aseptic meningitis), Bacteria or other Microorganism
• Certain drugs and toxins can also cause meningitis
• Symptoms and Prognosis is dependent on Etiology and Host
factors

3. Classification
• Bacterial – S. pneumoniae, Neisseria meningitidis, Haemophilus
influenzae, Listeria monocytogenes
• Viral - Enteroviruses, Herpes Simplex Virus ect
• Fungal – Cryptococcus neoformans
• Parasitic – Nematodes and other parasites
• Non Infectious – Neoplasm, Drugs ( NSAIDs, IV
immunoglobulins), Auto-immune disorders ect.

4. Bacterial Meningitis
While viral meningitis accounts for more than 60% of cases,
bacterial meningitis is considered an medical emergency
because of its poor prognosis
H. influenzae, S. pneumoniae and N. meningitidis Bacterial
meningitis is associated with high mortality and morbidity
worldwide, with an estimated 16 million cases in 2013,
causing 1.6 million years lived with disability each year.
Although the incidence of bacterial meningitis has declined
significantly since the advent of routine childhood vaccination

5. Causative Organisms
61%19%
8%
12%
BACTERIAL MENINGITIS
S. pneumoniae N. meningitidis H. influenzae Others
Type of Microbe depends on
1. Location
2. Vaccination Pattern
3. Age
4. Immune System of Patient
Other microbes
- Listeria monocytogenes
- Mycobacterium tuberculosis
- Group B Streptococcus

7. Meningitis Outbreak In Africa

8. Tuberculous meningitis
• Tuberculosis remains a global health problem, with an
estimated 10.4 million cases and 1.8 million deaths
resulting from the disease in 2015.
• The most lethal and disabling form of tuberculosis is
tuberculous meningitis (TBM), for which more than
100,000 new cases are estimated to occur per year
• Drug-resistant TBM in people co-infected with HIV-1
has a particularly poor prognosis, approaching 100%
mortality

9. Epidemiology of tuberculosis
https://reports.nikshay.in/Reports/TBNotification

10. Pathophysiology of Meningitis
• The development of bacterial
meningitis depends on the following
steps of bacterial-host interaction:
1. Mucosal colonization (usually upper
respiratory or gastrointestinal tract)
2. Systemic invasion
3. Meningeal invasion
4. Bacterial survival and replication in
the subarachnoid space
5. Induction of an inflammatory
response
6. Neuronal injury
An incomplete understanding of the pathophysiology of bacterial meningitis contributes to the
devastating impact of this disease.

11. Bacilli could reach brain blood capillaries
within cells or as extracellular bacilli; the
precise mechanism is unknown.
The endothelium itself can be infected, or infected cells can adhere and
undergo diapedesis. Both processes result in breakdown of tight endothelial
junctions and the basement membrane.
Microglial cells can become infected, and these cells,
together with infiltrating cells, produce inflammatory chemo
attractants that result in further breakdown of the blood–
brain barrier and influx of uninfected cells, including innate
and specific T and B lymphocytes.
The nascent granuloma might rupture via
necrosis, leading to meningeal and
intracerebral dissemination of infection
Entry of Mycobacterium tuberculosis through BBB

12. Entry of microbe into CNS followed by Host immune response leads to CNS inflammation
causing
• Increased intracranial pressure due to increased BBB
permeability.
• Leukocyte and bacterial toxins induce cellular swelling as
well as obstruction of CSF flow, which can lead to
hydrocephalus.
• Cerebral blood flow may be decreased because of vasculitis
and may lead to thrombosis and ischemia.
• Free radicals produced by granulocytes, endothelial cells,
and bacteria contribute to direct neuronal injury.

13. Signs and symptoms
• More severe and acute than Viral
meningitis.
At least Two of the following 4
symptoms will be present
• Headache - 85%
• Fever – 80%
• Neck stiffness
• Altered Mental status (GCS < 14)
Other common Symptoms seen
• Neurological deficits
• Seizures
• Papilledema
• Cranial nerve palsies
• Photophobia and Phonophobia
• Nausea and Vomiting
• Rash ( N meningitidis –
common)
Lateral rectus palsy – 6th nerve palsy

14. • Kernig sign - painful knee extension
after flexing the thigh with the hip
and knee at 90° angles
• Brudzinski sign - reactive hip and
knee flexure when the neck is flexed,
pulling both legs up toward the chest
Even though these signs have high
specificity towards meningitis, the
sensitivity of these signs are low ( 15-
30%)
Therefore physicians conduct many
tests to diagnose meningitis
• Purpuric lesions are seen on the
trunk and extremities of a young
child with meningococcemia

15. Risk factors
• Age: < 5 years and >60 years
• Trauma and Neuro-surgery
• IV drug abusers
• Immuno-compromised state
• Immuno-suppression
• Crowding – easy spread
• Travel – to endemic areas
• Low Socio-economic status
• Congenital deformities of CNS
• Comorbidities- Diabetes mellitus, chronic kidney failure, adrenal
insufficiency, hypoparathyroidism, or cystic fibrosis, alcoholism
and cirrhosis.

16. Diagnosis
• Rapid diagnosis and treatment of bacterial meningitis are critical and
reduce patient morbidity
• Travel history, symptoms of otitis media / sinusitis, contact with
another person with meningitis, sepsis or tuberculosis are other useful
diagnosis.
Diagnostic Tests
• Lumbar puncture is considered gold standard in diagnosing Meningitis
- CSF collected is used for various tests
• Neuroimaging - CT and MRI, reveal raised ICP, lesions and
hydrocephalus
• Blood tests - Culture and Antigen tests
• Swabs - Nasopharyngeal samples for culture

17. Lumbar Puncture
• Lumbar puncture (LP), also known as a spinal
tap, is a medical procedure in which a needle is
inserted into the spinal canal, most commonly
to collect cerebrospinal fluid (CSF) for
diagnostic tests.
• Allows rapid diagnosis of meningitis
• Usually performed before administration of
antibiotics
Collected CSF are used in following tests
• Cerebrospinal fluid cell count - Pleocytosis
indicates meningeal inflammation, of which
infection is the most common cause
More than >90% of adults with bacterial
meningitis had a CSF > leukocyte count >100
cells/µL.
Lumbar puncture

18. Cerebrospinal fluid leukocyte differential - Helps determine type of Meningitis
• Lymphocytes – Viral . Neutrophils – Bacterial
Cerebrospinal fluid parameters - Appearance, opening pressure and biochemistry.
• Cerebrospinal fluid protein is normally <0.4 g/L. Elevated protein suggests
inflammation. A CSF protein < 0.6 g/L largely rules out bacterial infection.
A CSF:blood glucose ratio <0.36 is an accurate (93%) marker for distinguishing
bacterial from viral meningitis. Glucose ratio depends on plasma conc of glucose,
Normal 1/3rd of plasma conc

19. Pathogen detection
Cerebrospinal fluid microscopy with Gram stain
• Cerebrospinal fluid microscopy with Gram stain (or an acid fast stain for M tuberculosis ) can rapidly
detect bacteria. It has a sensitivity between 50% and 99%
Cerebrospinal fluid culture
• It is diagnostic in 70–85% of cases prior to antibiotic exposure. Sensitivity decreases by 20% following
antibiotic pretreatment. Delay in culture results – affects prognosis
Bacterial antigen testing
• bacterial specific antigen tests can be performed.
Cerebrospinal fluid polymerase chain reaction
• Cerebrospinal fluid polymerase chain reaction (PCR), using pathogen specific nucleic acid sequences,
can detect both bacteria and viruses with high sensitivity.
• Polymerase chain reaction is the ‘gold standard’ for diagnosis of viral meningitis.
Lactate, procalcitonin and C-reactive protein levels
• Procalcitonin (PCT) is a precursor of the hormone calcitonin. Rises in response to proinflammatory
stimuli, particularly bacteria.
Blood Cultures. Blood cultures should be done routinely in cases of suspected bacterial meningitis.
Overall, blood cultures are able to identify the causative pathogen in 50% to 80% of case

20. Neuroimaging - CT
• Computed tomography before lumbar puncture is not usually required.
• Performing a lumbar puncture (LP) and starting empirical treatment are unnecessarily
delayed while waiting for computed tomography (CT) of the head
• Delay in empirical therapy – delay in treatment
• If antibiotics are given prior to CT and LP, the sensitivity of few tests decrease, leading to
further delay
• Also the yield of CT is low in patients who do not have clinical features of raised
intracranial pressure (ICP), with 97% having a normal result.
• However CT us preferred prior to LP in certain conditions

21. Investigation Algorithm

22. Prognosis
• Failure to diagnose and treat promptly has devastating consequences, including
death or significant morbidity
• Untreated, bacterial meningitis is uniformly fatal
• 30% of mortality from bacterial meningitis is secondary to cerebral herniation
• Mortality rates for adults range from below 5% (Haemophilus influenzae type b
meningitis) to approximately 25% (pneumococcal meningitis)
• Fatality rates for children with meningitis caused by Hemophilus influenzae,
Streptococcus pneumoniae, and Neisseria meningitidis are 0.0%, 9.2%, and
7.5%, respectively
• Overall mortality rate for neonates with meningitis is 13% but reaches 25% in
preterm or small-for-gestational-age infants

23. Complications
• Acute complications
• Seizures
• Septic shock
• Respiratory failure
• Disseminated intravascular coagulopathy
• Syndrome of inappropriate antidiuretic hormone secretion
• Long-term neurologic sequelae
• Nerve deafness
• Cortical blindness
• Hemiparesis
• Muscular hypertonia
• Ataxia

24. Case Analysis - SOAP
Tuberculous Meningitis

25. Problem
• TB Meningoencephalitis ( Gene X PERT mild positive,
rifampicin sensitive)
• B/L Lateral Rectus Palsy
• Leptospirosis IgM positive
• ATT Induced hepatitis
Subjective evidence
• fever since 8 days
• vomiting since 1 day
• seizures - 2 episodes – Early morning GTCS
• decreased responsiveness

26. Objective evidence
• Age – 18 y
• Gender: Female
Medical History present illness: c/o fever in the last 8 days, initially high grade, associated
with chills and rigors- did not subside.
• c/o vomiting 2-3 episodes - non- projectile, non-bilious, not blood
• diffuse headache+
• decreased responsiveness - gradually progressive, progressed to decreased verbal
response in one day.
• 2 episodes of GTCS - early morning, Inter/post ictal confusion+
• a/w bladder incontinence not associated with tongue bite.
MEDICATION HISTORY:
• Paracetamol i.v.
• Esomeprazole i.v.
• Faropenem i.v.
• Clopidogrel Tab
• Levetiracetam i.v.
• Mannitol i.v.

27. Physical Examination
• mildly febrile
• RR-26 /min
• PR-115/min
CNS -
• neck stiffness+, Kernig's sign+, Brudzinski's sign+, No FND
• Spontaneous movement of all limbs to pain+, hypotonia+ of all 4 limbs, no facial
deviation, all limbs reflexes 3+
• ROUTINE BIOCHEMICAL INVESTIGATIONS
• S.Cr : 0.37mg/dL
• Na:135mmol/l
• AST:36 IU/L

28. • Platelet count:529x103/mcL (150 400x103/microliter)
• RDW:19%(11.6-14%)
• PCT: 0.114%
• Absolute eosinophil count :<0.04 x 10³/μL
• Absolute neutrophil count:10.78 x 10³/μL
• Patient APTT – 21.0 sec
Urinalysis
• RBC: 328.80 /hpf
• WBC: 12.10 /hpf
• Blood: 3+ (0.75mg/dl)
Hematology
• RBC : 3.59x106/microliter
• (3.8-4.8x106/microliter)
• Normocytic normochromic: +; Anisocytosis: +
;Microcytes:+ ;Polychromasia:+
• WBC: 12.2x103/mcL (4-10x103/mcL)
•
• N:88.4%(42-74%)
• L: 6.0%(18-44%)
• E:0.0%(1-8%)
• B:0.1%(1-2%)
• Hb: 11.5 g/dL (12-15g/dL)
• MPV:7.2 fL

29. Other Tests
• Chest X ray done on 23/08 - normal
• EEG done – suggestive of mild encephalopathy (24/08)
• ECG – 90 BPM
• 24/08 –Blood culture – sterile after 5 days
• MRI – revealed multiple tuberculomas ( no rich focus)
• 24/08- CSF culture
• CSF analysis was done on 24/08/19
- PCR – Gene XPert – MTB/RIF sensitive
• CT BRAIN done on 28-08-2019
- No significant abnormality detected
• 6/09 – Automated perimetry
Blood antigen - antibody Tests
• Hep C- negative and Hep B – negative
• Antibodies to Leptospira IgM – positive
• Scrub typhus - negative

30. CSF analysis
• CSF glucose – 17mg/dL
• CSF protein > 200 mg/dL
• CSF chloride – 113 mmol/L (118 -132 mmol)
• Total WBC count 200 cells/cu.mm ( 0-5 )
Gram stain - no bacteria seen
Staining for Acid Fast bacilli – No AFB bacteria
seen
GeneXpert test for Mycobacterium tuberculosis -
MTB detected very low, RIF sensitive (PCR test)

31. Assessment
Diagnosis
• TB Meningoencephalitis (rifampicin sensitive)
• B/L Lateral Rectus Palsy
• Leptospirosis IgM positive
Etiology and risk factors
• College student
• Low socio-economic status
• Assessment if therapy is indicated –
Yes, To decrease the Morbity and Mortality of the disease and to improve
QOL

32. Standard Therapy of Bacterial Meningitis
Goals of therapy
1. Treating Infection
2. Manage respiratory and circulatory distress if present
3. Supportive therapy
4. Monitoring -To prevent complications and ADRs
5. To prevent complications in treated patients
Considerations.
• If the patient presents with sepsis, they should be managed according to the
sepsis guidelines.
• If the infective focus of sepsis is meningitis, then the antibiotic treatment should
follow the guidelines for meningitis.
• Drug must penetrate CSF and must achieve therapeutic concentration
• Drugs must be selected based on susceptibility, resistance patterns and patient
factors

33. Treatment Algorithms
Initial investigations and
management

34. Bacterial Meningitis
management

35. Tuberculous Meningitis
• Tuberculous meningitis results from the hematogenous
dissemination of Mycobacterium tuberculosis to the brain
• Followed by granuloma rupture and bacterial inoculation
into the subarachnoid space and inflammation
• Management as recommended by WHO
• Standard HRZES [DOTS] therapy – for minimum of 12
months.
• Children must be treated for 12 months with combination
antibiotic therapy and adjunctive corticosteroids.

36. • Screening for HIV must be done
• The principles of CNS tuberculosis
diagnosis and treatment are the same for
HIV infected and uninfected individuals
• Although HIV infection broadens the
differential diagnosis and anti-retroviral
treatment complicates management.
• Toxicity of drugs must be monitored
frequently
- Hepatotoxic drugs

37. Patient’s Total score - 9/15
GCS was recorded
Presence of a rash and use of preadmission antibiotics was also investigated
during admission
Severity classification

38. Drugs used in Tuberculous meningitis.

39. WHO recommended Standard therpay

41. Supportive therapy
• Adjunctive therapies that may be used as needed for bacterial
meningitis include : IV fluids
• Use of corticosteroids lies in reduce the harmful effects of
inflammation.
• If intracranial pressure is elevated, raise head to approximately
30°
ICU monitoring
• Patients who cannot protect their airways or who have respiratory
failure may require invasive hemodynamic monitoring or mechanical
ventilation
• Vitals, Blood sugar level ect
• Patients with bacterial meningitis and signs of elevated intracranial
pressure might need an intracranial pressure monitoring device

42. Supportive care - TB meningitis

43. Drug induced Hepatitis management

44. Immunization
Vaccines have significantly reduced the occurrence of the
disease
• Haemophilus influenzae type b vaccine
• 13-valent pneumococcal conjugate vaccine and 23-valent
pneumococcal polysaccharide vaccine. (Recommended to
adults aged 65 years or older)
• Neisseria meningitidis (meningococcal) vaccine against
serogroups A, C, W, and Y, available in both polysaccharide
and conjugate forms
• BCG vaccine against Tuberculosis

45. Assessment of Current therapy
Course of therapy
• Patient was started on Antibiotics empirically and also anti seizure
meds were started. IV fluids were supplemented.
• ATT was initiated after diagnosis, DOTS started on 29th . Patient
developed ATT induced hepatitis, drug were discontinued and
introduced one by one as the LFT was coming back to normal.
• Pain management was done appropriately
Therapeutic complications
• ATT induced hepatitis

46. Ativan 1mg iv
• Name - Lorazepam
• Class – Benzodiazepines
• Indication – Chemical restraint
• Justification -Alford EL et al -J Pediatr Pharmacol Ther. 20(4):260-89,
2015 – Sedation might be required if patient’s mental
status is altered, use of benzodiazepines is safe.
• Dose – 1mg , Refer PPF
• CI - Hypersensitivity, coadministration with other CNS
depressant
• ADR - agitation, hypersensitivity, blurred vision
• Monitoring parameters – Not necessary

47. Inj Seranace 2.5mg iv D2
• Name – Haloperidol
• Class - antipsychotics
• Indication- chemical restraint, agitation, seizures
• Justification - David MD et al -Emergency Medicine Clinics of North America,
2015-11-01, Volume 33, Issue 4, Pages 753-764, 2015 – In pediatric patients
haloperidol can be used to sedate the patients.
• Dose - 2.5mg iv
• CI –CNS depression
• ADR – blurred vision , agitation, anemia
• Monitoring parameters – CBC , eye exam, s}Serum
prolactin, urinalysis

48. Inj Monocef 2g iv
• Name - Ceftriaxone
• Class – 3rd generation cephalosporins
• Indication- leptospirosis
• Justification - Shah I: Leptospirosis. Pediatric Infectious Disease. 4(1):4-8,
2012 – in moderate to severe disease, treating with
cephalosporins are additional second line options
• Dose -2g iv refer PPF
• MOA – Cell wall synthesis inhibitor
• CI - resistance, hypersensitivity, liver disease
• ADR – anemia, abdominal pain
• Monitoring parameters - LFT

49. Inj Pan 40mg
• Name – pantoprazole
• Class – proton pump inhibitor
• Dose- 40mg iv, later switched to tabled
• Justification – polypharmacy? Or to decrease
increased gastric perforation risk associated with
corticosteroids
• Dose - 40mg iv

50. Inj Finamac 1g iv
• Name - Paracetamol
• Class – analgesic, antipyretic
• Justification – Fever being one of the common symptoms of
Meningitis, can be alleviated using antipyretics/analgesics
• Dose – 1000mcg infusion
• MOA - The exact mechanism of action is unknown, but acetaminophen
is thought to mediate its actions centrally through activation of the
descending serotonergic pathways
• CI – hepatotoxicity, hepatitis, G6PD deficiency
• ADR – agitation , anemia, liver enzyme elevation
• Monitoring parameters – LFT, Serum creatinine, blood urea
nitrogen

51. Inj Emeset 4mg iv
• Name - ondansetron
• Class – anti emetic
• Indication – Nausea, vomiting
• Dose – 4mg iv
• MOA - Ondansetron is a highly specific and selective serotonin 5-HT3
receptor antagonist. The 5-HT3 receptors are present both peripherally
on vagal nerve terminals and centrally in the chemoreceptor trigger
zone.
• CI – hepatic disease, children, cardiac arrythmia
• ADR – blurred vision, constipation
• Monitoring parameters – ECG, LFT, Serum electrolytes

52. Inj Levera 500 mg
• Name - Levetiracetam
• Class – Anti seizure
• Indication- seizure prophylaxis
• Dose – 500mg
• MOA - The precise mechanism of action of levetiracetam is
not known
• CI – renal impairment, pregnancy
• ADR – anemia, arthralgia, anaphylaxis
• Monitoring parameters – Serum creatinine, BUN
• Brands used - Epilive

53. IVF DNS
• Name – iv fluid dextrose normal saline
• Indication- Fluid supplement, glucose supplement
• Justification - Careful fluid and electrolyte management
must be taken into consideration along with treating the
infection
• CI - Diabetes
• ADR – edema, inflammation
• Monitoring parameters – Glucose levels, Na+ levels
– very important

54. Inj Dexa 4mg
• Name - Dexamethasone
• Class – corticosteroids
• Indication – anti inflammatory
• Justification –BRITISH INFECTION SOCIETY GUIDELINES - G. Thwaites et al. -
Patients with TBM are recommended to receive adjunctive corticosteroids
regardless of disease severity at presentation Adults (>14 years) should be
treated with dexamethasone 0.4 mg/kg/ 24 h with a reducing course over 6-8
weeks.
• Dose - 4mg iv, then switched to 4mg tablets
• MOA – Decrease the inflammatory response
• CI – cushing syndrome, hypersensitivity, hepatic disease
• ADR – anemia , arrythmia, angioedema, dizziness,
xeropthalmia
• Monitoring parameters – BP, Blood sugar, Ophthalmic exams

55. Inj Univir 1 g D2-3
• Name - Acyclovir
• Class – antiviral
• Indication- empiric therapy for viral meningitis
• Justification -Aseptic meningitis or meningoencephalitis
resulting from herpes simplex virus (HSV) can have serious
neurologic sequelae, empiric therapy with acyclovir
• Dose – 1g iv
• MOA - Acyclovir is a synthetic purine nucleoside analogue.
Acyclovir inhibits viral DNA synthesis and must be phosphorylated
intracellularly to be active.
• CI – hypersensitivity, hepatic disease, immunosuppression
• ADR – angioedema, anemia , crystalluria
• Monitoring parameters – Serum creatinine, BUN

56. T. R-cinex 300/450 mg
• Name – INH 300mg + Rifampicin 450
• Class – anti tuberculoid drugs
• Justification – WHO recommends INH and Rifampicin for 12 months to
treat meningitis
• Dose - 300/450mg OD, refer PPF
• MOA – Rifampicin - inhibits bacterial RNA synthesis by binding strongly
to the beta subunit of DNA-dependent RNA polymerase
INH -inhibition of mycolic acid synthesis and disruption of the cell wall in
susceptible organisms
• CI – hypersensitivity, liver disease, along with some antiviral drugs
• ADR - Hepatitis, Jaundice, reddish-orange urine, , Peripheral neuropathy,
loss of appetite, Nausea, Vomiting
• Monitoring parameters -LFT, CBC, RFT, ECG
• Brands – Rcin, Solonex dt

57. T. Pyzina 1000 mg
• Name - Pyrazinamide
• Class -Antitubercular Agents
• Justification – WHO recommends pyrazinamide for 2
months to treat meningitis
• Dose – 1000mg OD refer ppf
• MOA - Pyrazinamide is bacteriostatic or bactericidal
• CI - Severe hepatic damage, acute gout, hypersensitivity
• ADR - Malaise, Nausea, Vomiting, Anorexia, Arthralgia
• Monitoring parameters –uric acid level, LFT, platelet,
CBC

58. T. Combutol 800 mg
• Name - Ethambutol
• Class –Anti TB
• Justification – WHO recommends ethambutol for 2
months to treat meningitis
• Dose – 800mg 0D refer ppf
• MOA - targets Mycobacteria tuberculosis and inhibits
the synthesis of metabolites
• CI - Hypersensitivity, Visual impairment, Optic neuritis.
• ADR - Hepatotoxicity, Optic neuritis, hypersensitivity
reactions
• Monitoring parameters -

59. Tab Benadon 40 mg
• Name - Pyridoxine
• Class – vitamin B6
• Indication- prophylaxis to INH induced peripheral
neuropathy
• Dose – 40mg * half tablet
• ADR – nausea, ataxia, metabolic acidosis,
paresthesia
• CI- renal impairment, pregnancy , breast feeding

60. Inj Ambistrin
• Name - Streptomycin
• Class – Antibacterial, ATT
• Indication- alternate to pyrazinamide
• Justification – Streptomycin is a recommended ATT for
susceptible strains of Mtb and it also penetrates BBB
• Dose – 750mg iv, later reduced to 500mg
• MOA – protein synthesis inhibitor
• CI – hypersensitivity, resistance, impaired kidney function
• ADR – angioedema, anaphylaxis, hemolytic anaemia,
nephrotoxicity, hearing impairement
• Monitoring parameters – audiometry, BUN

61. Eyemist eyedrops 1-1-1-1 both eyes
• Name – Hydroxypropyl methyl cellulose
• Indication- dry eyes

62. Tramazac 50mg iv
• Name - Tramadol
• Class - analgesic
• Indication- pain
• Dose – 50mg iv
• MOA – tramadol is an opioid analgesic

63. T. Ultracet 37.5mg/325mg
• Name –Tramadol + paracetamol
• Class - Analgesic
• Indication – patient had pain score of 2 –3

64. T. Levoflox 500mg
• Name - Levofloxacin
• Class – flouroquinolones
• Indication- 2nd line agent in ATT with drug induced hepatitis
• Justification – BRITISH INFECTION SOCIETY GUIDELINES - G. Thwaites et al- If the
transaminases continue to rise, isoniazid and rifampicin should be
withdrawn . Streptomycin and ethambutol should be given, and
the addition of moxifloxacin or levofloxacin should be considered
• Dose – 500 mg
• MOA – Inhibits bacterial DNA synthesis
• CI – diarrhea, C. defficle infection, cardiac disease
• ADR – headache, nausea, vomiting, blurred vision
• Monitoring parameters – Serum Cr, BUN

65. Complications
Major complications
• cognitive or motor deficit
• Seizures
• visual or bilateral hearing
impairment
• hydrocephalus
Minor complications
• learning or behavioral
problems
• unilateral hearing
impairment
• Diplopia
• hypotonia

66. Planning
• Discharge date : 12/09/18 ( 21 days of hospital stay)
• Condition on discharge: Stable

67. Monitoring
Meningitis
• Fluid intake and output, - BP, pulse, respiratory
rate, temperature
• Blood tests, LFT, Electrolytes, routine biochemistry
• Leptospirosis- Continuous cardiac monitoring
Monitoring for ATT
• Hepatic function- LFT
• Blood tests – Hematology, routine biochemistry
• Ethambutol – Visual toxicity

68. 0
500
1000
1500
2000
2500
3000
25.08.2019 26.08.2019 31.08.2019 01.09.2019 02.09.2019 03.09.2019 04.09.2019 05.09.2019 06.09.2019 07.09.2019 08.09.2019
INTAKE AND OUTPUT
Input (ml) Output (ml)

69. 0
20
40
60
80
100
120
140
8/29/201922:00
30-Aug
9:20AM
3:35PM
10:00PM
8/31/20195:00
8:45AM
3:15PM
10:00PM
9/1/20195:30
9/2/20196:00
8:00AM
4:00PM
10:00PM
9/3/20195:30
8:00AM
5:00PM
10:00PM
9/4/201917:30
8:00AM
3:30PM
10:00PM
9/5/20195:30
11:00AM
4:00PM
10:00PM
9/6/20195:00
11:00AM
4:30PM
10:00PM
9/7/20195:00
8:45AM
5:30PM
10:00PM
9/8/20199:30
3:30PM
10:00PM
9/9/20195:00
8:00AM
BP CHART
Systolic Diastolic

70. Points to physician
• Elevation of Transaminases (AST, ALT) on 31/08/19 and was interpreted by physician as
Paradoxical reaction to ATT
• Paradoxical reactions are worsening signs and symptoms of tuberculosis despite effective
anti-tuberculosis chemotherapy. These reactions are commonly considered an excessive
inflammatory response to dead or dying bacteria.
• This is less likely, because of adjuvant corticosteroid therapy.
• We believe that drug induced hepatitis is more likely due to misinterpretation of
prescription by the nurse.
• Patient was initiated with DOTS regimen by a physician on 29th Aug, with standard
doses
• INH 225mg, Rifampicin 450mg, Pyz -1200mg, Ethambutol - 800mg was prescribed in 4
fixed dose combination. Fixed dose combination being 1/3rd of actual normal dose of
each drug, to compensate this doctor had prescribed 3 tablets in the morning.
• But the in the nurse records, it was stated that the nurse had given 3 tablets each of the
4 ATT drugs (Standard dose i.e. did not give fixed dose combination).
• We believe that patient had received thrice the normal dose which might have caused
the Drug induced hepatitis and elevation of Transaminases

71. Patient counselling
Disease
• Inform patient about meningitis, tuberculous meningitis,
complications associated and also inform patient party about
risks of spreading ect.
About treatment
• Drugs – dosing, regimen Adverse effects, Self monitoring, follow
up.
• Inform about side effects of Anti-tuberculosis therapy
• Lifestyle modifications required ( include hygiene practices ect)
• Recommended diet – As advised by the dietician

73. Recent advancements

75. References
1. Donovan, Joseph, et al. “The Neurocritical Care of Tuberculous Meningitis.” The Lancet Neurology,
vol. 18, no. 8, Aug. 2019, pp. 771–783, 10.1016/s1474-4422(19)30154-1. Accessed 19 Oct. 2019.
2. Griffiths, Michael J, et al. “Management of Acute Meningitis.” Clinical Medicine, vol. 18, no. 2, Apr.
2018, pp. 164–169, 10.7861/clinmedicine.18-2-164.
3. Thwaites, Guy, et al. “British Infection Society Guidelines for the Diagnosis and Treatment of
Tuberculosis of the Central Nervous System in Adults and Children.” Journal of Infection, vol. 59, no.
3, Sept. 2009, pp. 167–187, 10.1016/j.jinf.2009.06.011. Accessed 19 Oct. 2019.
4. van de Beek, Diederik, et al. “Community-Acquired Bacterial Meningitis.” Nature Reviews Disease
Primers, vol. 2, 3 Nov. 2016, p. 16074, 10.1038/nrdp.2016.74. Accessed 7 Apr. 2019.
5. Wilkinson, Robert J., et al. “Tuberculous Meningitis.” Nature Reviews Neurology, vol. 13, no. 10, 8
Sept. 2017, pp. 581–598, 10.1038/nrneurol.2017.120. Accessed 19 Oct. 2019.
6. Putz, Katherine, et al. “Meningitis.” Primary Care: Clinics in Office Practice, vol. 40, no. 3, Sept. 2013,
pp. 707–726, 10.1016/j.pop.2013.06.001. Accessed 19 Oct. 2019.
7. Youmans and Winn Neurological Surgery Textbook- Meningitis and Encephalitis
8. WHO TB reports 2018
SITES USED
1. https://www.cdc.gov/meningitis
2. https://sci-hub.tw/ - SCI-HUB -To remove all barriers in the way of science