Case presentation on tuberculous
meningitis
Presented by :
METI.BHARATH KUMAR
16DK1T0014
Pharm-D(Intern)
Demographics
• Name :xyz
• Age :45
• Sex:female
• Admission No:69495
• Department : general medicine
unit :fm-7
• Date of admission :18-12-2021
• Consultant physician:Dr Maheswara Reddy
Subjective evidence
• A 45yrs old female patient admitted to female
medical ward with complaints of –
c/o fever with altered sensorium
c/o giddiness since 15 days
c/o generalized weakness associated with
body pains
Past history : CVA with left hemiparesis
Objective evidence
Assessment
• Based on subjective and objective the current
condition is diagnosed as bacterial
tuberculous meningitis
planning
vitals
• On examination patient is
conscious and incoherent
• Temp : afebrile
• BP: 110/70mmhg
• PR: 110/min
• RR: 20/min
• Saturation of oxygen : 98%
• RS : BAE +
• CVS: s1 s2 +
• CNS : terminal neck stiffness
plantar b/l extension
Treatment
• Inj ceftriaxone 2g iv bd
• Inj decadron 2cc iv tid
• Inj artesunate 120mg iv od
• Inj pct infusion 100ml iv tid
• Inj pantop 40mg iv od
• RTF with 200 ml milk
• Tab ecospirin 150mg po od
• Tab atorvastatin 40mg po
od
planning
vitals
• On examination patient is
conscious and incoherent
• Temp : afebrile
• BP:120/90mmhg
• PR: 80/min
• RR: 20/min
• Saturation of oxygen : 97%
• RS : BAE +
• CVS: s1 s2 +
• CNS : neck stiffness ++
plantar left extension
right flexor
Treatment
• Inj ceftriaxone 2g iv bd
• Inj decadron 2cc iv tid
• Inj pct infusion 100ml iv tid
• Inj pantop 40mg iv od
• RTF with 200 ml milk
• Tab ecospirin 150mg po od
• Tab atorvastatin 40mg po
od
• Tab benadon 40 mg od
Vitals
• Pt is conscious and
incoherent
• PR: 82/min
• BP:100/60mmhg
Treatment
• Continue ATT
• Tab benadon 40mg od
• Inj ceftriaxone 2g iv bd
• Inj rantac 200 iv bd
• Inj decadron 2cc iv bd
• Tab pct 500mg tid
• Tab ecospirin 150 mg bd
• Tab atorvastatin 40mg od
• RTF with 100ml milk
Drug chart
S.N
O
GENERI
C NAME
BRAND
NAME
INDICATION DO
SE
RO
A
FREQUE
NCY
1 Pyridoxi
ne HCL
benadon Vitamin B6 supplement for numbness 40
mg
po od
2 Ceftriax
one
To reduce infection 2g iv Bd
3 dexamet
hasone
decadron To reduce inflammatory condition 2cc iv Bd
4 acetami
nophen
To reduce fever 500
mg
po Tid
5 ranitidin
e
rantac To reduce gi irritation 2cc iv Bd
6 aspirin ecospirin To remove infarcts 150
mg
po Bd
7 atorvast
stin
atorvas To reduce cholesterol synthesis 40
mg
po Od
Pharmaceutical care issues
Drug interactions:
• Atorvastatin+dexamethasone :atorvastatin
increases the level or effect of dexamethasone
by P-Gp (MDR) efflux transporter
• Aspirin+dexamethasone : either increase
toxicity of the other by pharmacodynamic
synergism( increase risk of GI ulceration)
discussion
• Meningitis is an inflammation (swelling) of the
protective membranes covering the brain and
spinal cord. A bacterial or viral infection of the
fluid surrounding the brain and spinal cord
usually causes the swelling.
• Pathophysiology. The brain is protected by the
skull and the pia, arachnoid, and dural meninges
as well as the blood–brain barrier. When any of
these defenses are breached by a microbial
pathogen an infl ammatory response within the
CSF occurs
• Classification and Risk Factors. Most commonly classified
based on the infecting pathogen and location at the onset
of illness.
• 1. Community-acquired meningitis. Patients have not been
recently hospitalized and/or undergone any recent
procedures (e.g., CSF shunt). Predisposing factors include
preexisting diabetes mellitus, otitis media, sinusitis,
pneumonia, and alcohol abuse. Pathogens can include
bacterial, viral, fungal, or parasitic agents.
• 2. Nosocomial meningitis and ventriculitis. Most commonly
related to infections associated with CSF shunts, CSF drains,
intrathecal drug therapy, deep brain stimulation hardware,
neurosurgery procedures, and head trauma. Also usually
associated with a typical nosocomial bacterial pathogen
(e.g., methicillin-resistant Staphylococcus aureus [MRSA] or
vancomycin-resistant Enterococcus spp)
CAUSES OF MENINGITIS
• A. Bacterial.
Predisposing factors depend on age, comorbid status, immune state,
and/or alcoholism.
• 1. Streptococcus pneumoniae. Most common cause of both
community and nosocomial infections despite the patient age or
immune status.
• 2. Haemophilus influenzae type B. Vaccination efforts have declined
rates in children.
• 3. Neisseria meningitidis (serogroups A, B, C, W135, and Y). Most
common pathogen in healthy young adults.Serogroup Y is
predominant in the United States and the second most common in
parts of Europe. Serogroup B is the most common strain across
Europe. Serogroup A has been responsible for large outbreaks in
the meningitis belt of Africa.
• 4. Listeria monocytogenes. Most commonly occurs in
infants and patients over the age of 50 years with cell-
mediated immune deficits and/or alcoholism.
• 5. Streptococcus pyogenes (group A beta-hemolytic
streptococci). Usually secondary to otitis media.
• 6. Streptococcus agalactiae (group B beta-hemolytic
streptococci). Most often occurs in poorly controlled
diabetic patients with an associated infection who are
greater than 65 years of age.
• 7. Staphylococcus (S. aureus or coagulase-negative
staphylococcus). Most frequently occur in the setting of
neurosurgical procedures or placement of CSF shunts.
• 8. Gram-negative bacilli (Pseudomonas or enteric
pathogens). Have been associated with
nosocomial meningitis in patients over the age of
50.
• 9. Mycobacterium tuberculosis (MTB). Usually
occurs in the setting of extrapulmonary
disseminated disease (see Chapter 14,
Tuberculosis, for more information).
• 10. Spirochetes. Treponema pallidum (secondary
syphilis) and Borrelia burgdorferi (Lyme disease)
• B. Viral.
Most commonly affect children but can occur at any age.
• 1. Enteroviruses (e.g., Coxsackie A and B, echovirus, poliovirus, and
enterovirus 71). Account for the majority of viral meningitis cases
with a fecal–oral transmission during late summer and autumn in
temperate climates (occurs year-round in the tropics).
• 2. Herpes simplex virus (HSV-1, HSV-2). HSV-2 accounts for the
majority of cases in association with primary genital herpes. In
immunocompetent patients, pure HSV meningitis is a self-limiting
condition, whereas HSV meningitis in immunocompromised hosts
or HSV encephalitis is a life-threatening medical emergency
requiring treatment.
• 3. Varicella-zoster virus (VZV). Almost always associated with
reactivation (e.g., shingles) rather than primary infection (e.g.,
chickenpox).
• 4. HIV. Most often occurs in the setting of acute infection (e.g.,
acute retroviral syndrome—lymphadenopathy, dermatitis,
pharyngitis, and oral candidiasis).
• 5. Measles–mumps–rubella (MMR) viruses. Rates have
declined with vaccination efforts, but the most
common cause in unvaccinated patients would involve
mumps (more common in males with or without
parotid gland swelling).
• 6. Arthropod-borne viruses and West Nile virus. Most
commonly associated with meningoencephalitis (see
Chapter 33, Infectious Encephalitis).
• 7. Lymphocytic choriomeningitis virus and Hantavirus.
These are rare causes associated with contact by
infected rodents.
C. Fungal. Pathogens most commonly occur in nosocomial
infections or immunocompromised patients such as
transplantation of stem cells or solid organs and with
HIV/AIDS (i.e., CD4 cell count below 200 cells/mmÂł).
While Candida and Aspergillus species are common,
other pathogens include:
1. Cryptococcus neoformans
2. Histoplasma capsulatum
3. Coccidioides immitis
D. Parasitic. Rare cause of community-acquired meningitis,
but the freshwater amoeba Naegleria fowleri can cause
primary amebic meningoencephalitis. Amoeba gain
access to the meninges and brain through disruption of
the cribriform plate and olfactory nerve and are nearly
always fatal.
CLINICAL PRESENTATION OF
MENINGITIS.
While the clinical presentation of meningitis may vary in children and
older adults, the classic triad is: acute onset fever, neck stiffness,
and altered mental status.
• A. Fever. Present in the majority of patients but may be absent in
older adults or immunocompromised.
• B. Neck Stiffness. Occurs in the majority of patients and most
commonly associated with headache.
• C. Altered Mental Status. Is typically defi ned as a Glasgow coma
score of less than 12 or a change in the patient’s baseline mental
status (e.g., dementia)
• D. Headache. Occurs in response to meningeal infl ammation. E.
Photophobia. Reduced tolerance to bright light presumed to be due
to meningeal infl ammation of the trigeminal nerve (ophthalmic
branch of cranial nerve 5). More commonly occurs with viral
meningitis. F. Nausea and Vomiting
CSF analysis
• Normal CSF values are: glucose 45 to 80
mg/dL with a bloodto-CSF glucose ratio
greater than or equal to 0.6; protein 15 to 45
mg/dL; and white blood cell (WBC) count less
than 5/mcL. CSF values should be obtained as
soon as possible following LP, as delays can
alter the cell count and glucose (falsely low
values).
Typical CSF Findings for Meningitis
Pathogen WBC Count Differential CSF/Serum
Glucose
Protein
Viral 50–1,000 Lymphocytic
*
≥0.6 Minimally
elevated
Bacterial** 500–5,000 Neutrophilic ≤0.4 Elevated
Tuberculosis 50–300 Monocytic ≤0.3 Elevated
Cryptococcu
s
20–500 Monocytic ≤0.5 Elevated
Treatment
As it is diffi cult to differentiate bacterial from viral or fungal meningitis on
clinical grounds alone, patients often are placed on empirical antimicrobial
therapy based on the most likely pathogen that should be initiated as soon as
the diagnosis is considered.
Viral Meningitis
1. HSV a. Immunocompetent host. Usually due to
HSV-2 with primary genital herpes. Thus, the
treatment is directed to genital herpes. b.
Immunocompromised host. Usually treatment is
with acyclovir 10 mg/kg IV q8 (adjusted for renal
failure) for 14 to 21 days.
2. 2. VZV. Usual treatment is the same as for
shingles with acyclovir 10 mg/kg IV q8 for 7 to
10 days or valacyclovir 1 g PO q8 for 7 to 10
days.
A Case Presentation on Tuberculous meningitis

A Case Presentation on Tuberculous meningitis

  • 1.
    Case presentation ontuberculous meningitis Presented by : METI.BHARATH KUMAR 16DK1T0014 Pharm-D(Intern)
  • 2.
    Demographics • Name :xyz •Age :45 • Sex:female • Admission No:69495 • Department : general medicine unit :fm-7 • Date of admission :18-12-2021 • Consultant physician:Dr Maheswara Reddy
  • 3.
    Subjective evidence • A45yrs old female patient admitted to female medical ward with complaints of – c/o fever with altered sensorium c/o giddiness since 15 days c/o generalized weakness associated with body pains Past history : CVA with left hemiparesis
  • 4.
  • 6.
    Assessment • Based onsubjective and objective the current condition is diagnosed as bacterial tuberculous meningitis
  • 7.
    planning vitals • On examinationpatient is conscious and incoherent • Temp : afebrile • BP: 110/70mmhg • PR: 110/min • RR: 20/min • Saturation of oxygen : 98% • RS : BAE + • CVS: s1 s2 + • CNS : terminal neck stiffness plantar b/l extension Treatment • Inj ceftriaxone 2g iv bd • Inj decadron 2cc iv tid • Inj artesunate 120mg iv od • Inj pct infusion 100ml iv tid • Inj pantop 40mg iv od • RTF with 200 ml milk • Tab ecospirin 150mg po od • Tab atorvastatin 40mg po od
  • 8.
    planning vitals • On examinationpatient is conscious and incoherent • Temp : afebrile • BP:120/90mmhg • PR: 80/min • RR: 20/min • Saturation of oxygen : 97% • RS : BAE + • CVS: s1 s2 + • CNS : neck stiffness ++ plantar left extension right flexor Treatment • Inj ceftriaxone 2g iv bd • Inj decadron 2cc iv tid • Inj pct infusion 100ml iv tid • Inj pantop 40mg iv od • RTF with 200 ml milk • Tab ecospirin 150mg po od • Tab atorvastatin 40mg po od • Tab benadon 40 mg od
  • 9.
    Vitals • Pt isconscious and incoherent • PR: 82/min • BP:100/60mmhg Treatment • Continue ATT • Tab benadon 40mg od • Inj ceftriaxone 2g iv bd • Inj rantac 200 iv bd • Inj decadron 2cc iv bd • Tab pct 500mg tid • Tab ecospirin 150 mg bd • Tab atorvastatin 40mg od • RTF with 100ml milk
  • 10.
    Drug chart S.N O GENERI C NAME BRAND NAME INDICATIONDO SE RO A FREQUE NCY 1 Pyridoxi ne HCL benadon Vitamin B6 supplement for numbness 40 mg po od 2 Ceftriax one To reduce infection 2g iv Bd 3 dexamet hasone decadron To reduce inflammatory condition 2cc iv Bd 4 acetami nophen To reduce fever 500 mg po Tid 5 ranitidin e rantac To reduce gi irritation 2cc iv Bd 6 aspirin ecospirin To remove infarcts 150 mg po Bd 7 atorvast stin atorvas To reduce cholesterol synthesis 40 mg po Od
  • 11.
    Pharmaceutical care issues Druginteractions: • Atorvastatin+dexamethasone :atorvastatin increases the level or effect of dexamethasone by P-Gp (MDR) efflux transporter • Aspirin+dexamethasone : either increase toxicity of the other by pharmacodynamic synergism( increase risk of GI ulceration)
  • 12.
    discussion • Meningitis isan inflammation (swelling) of the protective membranes covering the brain and spinal cord. A bacterial or viral infection of the fluid surrounding the brain and spinal cord usually causes the swelling. • Pathophysiology. The brain is protected by the skull and the pia, arachnoid, and dural meninges as well as the blood–brain barrier. When any of these defenses are breached by a microbial pathogen an infl ammatory response within the CSF occurs
  • 13.
    • Classification andRisk Factors. Most commonly classified based on the infecting pathogen and location at the onset of illness. • 1. Community-acquired meningitis. Patients have not been recently hospitalized and/or undergone any recent procedures (e.g., CSF shunt). Predisposing factors include preexisting diabetes mellitus, otitis media, sinusitis, pneumonia, and alcohol abuse. Pathogens can include bacterial, viral, fungal, or parasitic agents. • 2. Nosocomial meningitis and ventriculitis. Most commonly related to infections associated with CSF shunts, CSF drains, intrathecal drug therapy, deep brain stimulation hardware, neurosurgery procedures, and head trauma. Also usually associated with a typical nosocomial bacterial pathogen (e.g., methicillin-resistant Staphylococcus aureus [MRSA] or vancomycin-resistant Enterococcus spp)
  • 14.
    CAUSES OF MENINGITIS •A. Bacterial. Predisposing factors depend on age, comorbid status, immune state, and/or alcoholism. • 1. Streptococcus pneumoniae. Most common cause of both community and nosocomial infections despite the patient age or immune status. • 2. Haemophilus influenzae type B. Vaccination efforts have declined rates in children. • 3. Neisseria meningitidis (serogroups A, B, C, W135, and Y). Most common pathogen in healthy young adults.Serogroup Y is predominant in the United States and the second most common in parts of Europe. Serogroup B is the most common strain across Europe. Serogroup A has been responsible for large outbreaks in the meningitis belt of Africa.
  • 15.
    • 4. Listeriamonocytogenes. Most commonly occurs in infants and patients over the age of 50 years with cell- mediated immune deficits and/or alcoholism. • 5. Streptococcus pyogenes (group A beta-hemolytic streptococci). Usually secondary to otitis media. • 6. Streptococcus agalactiae (group B beta-hemolytic streptococci). Most often occurs in poorly controlled diabetic patients with an associated infection who are greater than 65 years of age. • 7. Staphylococcus (S. aureus or coagulase-negative staphylococcus). Most frequently occur in the setting of neurosurgical procedures or placement of CSF shunts.
  • 16.
    • 8. Gram-negativebacilli (Pseudomonas or enteric pathogens). Have been associated with nosocomial meningitis in patients over the age of 50. • 9. Mycobacterium tuberculosis (MTB). Usually occurs in the setting of extrapulmonary disseminated disease (see Chapter 14, Tuberculosis, for more information). • 10. Spirochetes. Treponema pallidum (secondary syphilis) and Borrelia burgdorferi (Lyme disease)
  • 17.
    • B. Viral. Mostcommonly affect children but can occur at any age. • 1. Enteroviruses (e.g., Coxsackie A and B, echovirus, poliovirus, and enterovirus 71). Account for the majority of viral meningitis cases with a fecal–oral transmission during late summer and autumn in temperate climates (occurs year-round in the tropics). • 2. Herpes simplex virus (HSV-1, HSV-2). HSV-2 accounts for the majority of cases in association with primary genital herpes. In immunocompetent patients, pure HSV meningitis is a self-limiting condition, whereas HSV meningitis in immunocompromised hosts or HSV encephalitis is a life-threatening medical emergency requiring treatment. • 3. Varicella-zoster virus (VZV). Almost always associated with reactivation (e.g., shingles) rather than primary infection (e.g., chickenpox). • 4. HIV. Most often occurs in the setting of acute infection (e.g., acute retroviral syndrome—lymphadenopathy, dermatitis, pharyngitis, and oral candidiasis).
  • 18.
    • 5. Measles–mumps–rubella(MMR) viruses. Rates have declined with vaccination efforts, but the most common cause in unvaccinated patients would involve mumps (more common in males with or without parotid gland swelling). • 6. Arthropod-borne viruses and West Nile virus. Most commonly associated with meningoencephalitis (see Chapter 33, Infectious Encephalitis). • 7. Lymphocytic choriomeningitis virus and Hantavirus. These are rare causes associated with contact by infected rodents.
  • 19.
    C. Fungal. Pathogensmost commonly occur in nosocomial infections or immunocompromised patients such as transplantation of stem cells or solid organs and with HIV/AIDS (i.e., CD4 cell count below 200 cells/mmÂł). While Candida and Aspergillus species are common, other pathogens include: 1. Cryptococcus neoformans 2. Histoplasma capsulatum 3. Coccidioides immitis D. Parasitic. Rare cause of community-acquired meningitis, but the freshwater amoeba Naegleria fowleri can cause primary amebic meningoencephalitis. Amoeba gain access to the meninges and brain through disruption of the cribriform plate and olfactory nerve and are nearly always fatal.
  • 20.
    CLINICAL PRESENTATION OF MENINGITIS. Whilethe clinical presentation of meningitis may vary in children and older adults, the classic triad is: acute onset fever, neck stiffness, and altered mental status. • A. Fever. Present in the majority of patients but may be absent in older adults or immunocompromised. • B. Neck Stiffness. Occurs in the majority of patients and most commonly associated with headache. • C. Altered Mental Status. Is typically defi ned as a Glasgow coma score of less than 12 or a change in the patient’s baseline mental status (e.g., dementia) • D. Headache. Occurs in response to meningeal infl ammation. E. Photophobia. Reduced tolerance to bright light presumed to be due to meningeal infl ammation of the trigeminal nerve (ophthalmic branch of cranial nerve 5). More commonly occurs with viral meningitis. F. Nausea and Vomiting
  • 21.
    CSF analysis • NormalCSF values are: glucose 45 to 80 mg/dL with a bloodto-CSF glucose ratio greater than or equal to 0.6; protein 15 to 45 mg/dL; and white blood cell (WBC) count less than 5/mcL. CSF values should be obtained as soon as possible following LP, as delays can alter the cell count and glucose (falsely low values).
  • 22.
    Typical CSF Findingsfor Meningitis Pathogen WBC Count Differential CSF/Serum Glucose Protein Viral 50–1,000 Lymphocytic * ≥0.6 Minimally elevated Bacterial** 500–5,000 Neutrophilic ≤0.4 Elevated Tuberculosis 50–300 Monocytic ≤0.3 Elevated Cryptococcu s 20–500 Monocytic ≤0.5 Elevated
  • 23.
    Treatment As it isdiffi cult to differentiate bacterial from viral or fungal meningitis on clinical grounds alone, patients often are placed on empirical antimicrobial therapy based on the most likely pathogen that should be initiated as soon as the diagnosis is considered.
  • 25.
    Viral Meningitis 1. HSVa. Immunocompetent host. Usually due to HSV-2 with primary genital herpes. Thus, the treatment is directed to genital herpes. b. Immunocompromised host. Usually treatment is with acyclovir 10 mg/kg IV q8 (adjusted for renal failure) for 14 to 21 days. 2. 2. VZV. Usual treatment is the same as for shingles with acyclovir 10 mg/kg IV q8 for 7 to 10 days or valacyclovir 1 g PO q8 for 7 to 10 days.