4. History of Present Illness
• Fever
– 100-101o
F
– Intermittent
– No chills & rigors
– Evening rise of fever present
– Defervescence with antipyretics
5. History of Present Illness
• Altered sensorium
– Insidious onset, gradually progressive
– Irritability with aggressive behavior
– Confusion with inability to recognize relatives
followed by increased sleepiness with poor
response to verbal commands
6. History of Present Illness
• Headache
– Global
– Associated with 1 episode of non bilious, non
projectile vomiting
• Weight loss
– Unintentional
– 4 Kgs in 01 month
7. Define fever, PUO
• Fever is an elevation of body temperature
that exceeds the normal daily variation and
occurs in conjunction with an increase in the
hypothalamic set point.
• an A.M. temperature of >37.2o
C (>98.9o
F) or a
P.M. temperature of >37.7o
C (>99. 90
F) would
define a fever.
8. PUO
• Fever >38.30
C ( 101 0
F) on at least two
occasions
• Illness duration of >3 weeks
• No known immuno-compromised state
• Diagnosis that remains uncertain after a
thorough history-taking, physical examination
and
9. PUO
• obligatory investigations: determination of erythrocyte
sedimentation rate (ESR) and C-reactive protein (CRP) level;
platelet count; leukocyte count and differential; hemoglobin
electrolytes, creatinine, total protein, alkaline phosphatase ,
alanine aminotransferase, aspartate aminotransferase ,
lactate dehydrogenase creatine kinase, ferritin, antinuclear
antibodies, and rheumatoid factor; protein electrophoresis;
urinalysis; blood cultures (n = 3); urine culture; chest x-ray;
abdominal ultrasonography; and tuberculin skin test (TST) .
10. Pain sensitive structures in head
• Scalp ,
• Middle meningeal artery ,
• Dural sinuses, falx cerebri
• proximal segments of the large pial arteries.
• The ventricular ependyma, choroid plexus ,
pial veins, and brain parenchyma are not pain-
producing
11. “Red Flags”
• New headache especially in over 50 y.o.
• Abrupt onset, unusually severe
• Change in usual headache pattern
• Associated with focal neurologic findings
• Change in LOC, personality, lethargy
• Fever, neck stiffness
• Systemic signs/symptoms
• Temporal artery tenderness
12. Tumor pain
• The head pain is usually nondescript
• intermittent deep, dull aching of moderate intensity
• worsen with exertion or change in position
• may be associated with nausea and vomiting
• headache of brain tumor disturbs sleep in about 10%
of patients.
• Vomiting that precedes the appearance of headache
by weeks is highly characteristic of posterior fossa
brain tumor.
13. History of Present Illness
No h/o
Seizures, hallucinations, focal weakness of any
limb
Jaundice, abdominal distension
Rash, joint pain, photosensitivity
Cough, hemoptysis
14. History of Present Illness
No h/o
Dysuria, hematuria, increased frequency of
micturition
Substance abuse
Palpitations, dyspnea, ankle edema
15. Past History
• H/o Hansen’s disease (BL) completed 02 years of
MDT, 02 years back
• No past history of TB
16. Personal History
• Mixed diet
• Normal sleep rhythm
• No alcohol/ tobacco consumption
• Denies history of high risk behavior
18. Summary
• 30 yrs old serving soldier, Old case of Hansen’s
disease, presented with fever of one month duration
along with progressively worsening sensorium with
headache of 8 days duration along with weight loss
19. Causes of Fever with Altered
Sensorium
• Infectious causes
– Encephalitis, Meningitis, cerebral malaria, brain
abscess, sepsis related encephalopathy, sepsis with
DIC/TTP
• Non infectious causes
– Overproduction of heat
– Impaired heat dissipation
– Structural lesions (impaired thermoregulatory
mechanism)
– Misc Causes
21. Non infectious causes of fever with
altered sensorium
• Overproduction of heat
– Malignant hyperthermia (NMS, serotonin synd),
Salicylate poisoning, Thyrotoxic encephalopathy,
convulsive status , catatonic schizophrenia
• Impaired heat dissipation
– Heat stroke, anticholinergic toxicity
• Structural lesions
– Hypothalamic lesion, brainstem stroke, SAH
• Misc
– ADEM, cerebral fat embolism, Altered sensorium with
secondary causes of fever
22.
23. Physical signs in suspected meningitis
Kernig’s sign Flexing the hip and extending the knee to elicit
pain in the back
and legs
Brudzinski’s sign Passive flexion of the neck elicits flexion of the
hip
Nuchal rigidity Severe neck stiffness
Jolt
accentuation
Exacerbation of existing headache with rapid
head rotation
27. General Examination
• Patient drowsy
• T -101O
F
• Pulse: 58/ min, regular
• BP: 116/70 mm Hg RAS
• RR: 20/ min, regular
• No Pallor, icterus, cyanosis, Clubbing, edema,
lymphadenopathy or Rash
28. General Examination
• Pupils- Normal size, sluggishly reacting to light
• Neck stiffness +
• Fundus examination normal with no evidence of
papilledema
• No cutaneous stigmata of HIV
29. Systemic Examination
• CVS
• S1 S2 heard
• No S3, S4,murmurs heard
• Resp
• Chest movement b/l equal
• No fullness/rib crowding
• No pleural rub, TVF normal
• Absent Breath sounds -left infra scapular region
51. Pleural fluid Analysis
Cytology WBC-210 (lymphocytes 95 %), RBC-Plenty
Pleural fluid for malignant cytology Negative
Gram stain/ZN stain- No organism seen/ -ve for AFB
Pleural fluid C/S- No growth
Protein 5.5 g/dl
Glucose 65 mg/dl
ADA 109 U/L (0-40)
52. Tubercular CSF picture
• Protein -100-500mg/dl, <100-25%, >500-10%
• Glu- <45mg/dl (80%)
• Cells- 100-500/mm3
, <100-15%,500-1500-20%
• Incidence of smear positive 1st
sample-37%,
four serial samples-87%
53. Improving AFB detection
• CSF leucocytes- treated with triton prior to
Ziehl–Neelsen staining
• The loop-mediated isothermal amplification
assay (LAMP)
54. How to increase sensitivity of smear?
• Prepare smear from clot
• Use 10ml of last removed CSF sample
• Add 2ml 95% alcohol to CSF if no clot, use
0.02ml for 1cm dia smear
• 200-500 hpf examined by more than one obs
55. Pathogenesis and factors leading to
TBM
• Extremes of age
• Alcoholism
• Drug induced immune suppression
• Malignancy
• AIDS
• Physical trauma
56. CT scan prognostication?
• Normal CECT head- 30% in stage 1
8% in stage 2
• Abnormal CT head in 100% pts stage 3
• Normal CECT in drowsy pt- unlikely to be TBM
57. Phases of tubercular meningitis?
Prodromal
phase
lasting two to three weeks, is characterized by the
insidious onset of malaise, lassitude, headache, low-grade
fever, and personality change.
Meningitic
phase
more pronounced neurologic features, such as
meningismus, protracted headache, vomiting, lethargy,
confusion, and varying degrees of cranial nerve and long-
tract signs.
Paralytic phase illness accelerates rapidly; confusion gives way to stupor
and coma, seizures, and often hemiparesis. For the
majority of untreated patients, death ensues within five to
eight weeks of the onset of illness
58. Stages of tubercular meningitis?
Stage 1 Patients are lucid with no focal neurologic
signs or evidence of hydrocephalus
Stage 2 Patients exhibit lethargy, confusion; they
may have mild focal signs, such as cranial
nerve palsy or hemiparesis
Stage 3 represents advanced illness with delirium,
stupor, coma, seizures, multiple cranial
nerve palsies, and/or dense hemiplegia
59. Pathological processes accounting for
clinical manifestations?
• Proliferative basilar arachnoiditis
• Vasculitis of arteries and veins traversing the
exudates
• Disturbed CSF circulation
63. Course in hospital
He was continued on ATT with iv steroids
Prophylactic anticonvulsants
Anti cerebral edema measures
He showed gradual improvement in sensorium
On 14th Feb 2017 he developed sudden loss of vision
in both eyes
70. Management
• VP shunt – 14 Feb 17
• Dexamethasone dose modification
• Mannitol
• Iv antibiotics
71. Present Status
• Four score 14
• Well oriented
• Able to walk with support
• Improving vision
72. Aim of Presentation
• To discuss approach to fever with altered sensorium
• Complications of Tubercular meningitis
• Management of Tubercular meningitis