The document discusses the medical emergency of fever with altered sensorium, emphasizing the importance of early recognition and treatment. It outlines various causes including infectious (e.g., encephalitis, meningitis) and non-infectious (e.g., neuroleptic malignant syndrome, heat stroke) origins, along with diagnostic approaches and treatment strategies. Key points include careful patient history, thorough physical examination, and tailored investigations to differentiate between potential etiologies.

1. Fever with altered sensorium
Shilanjan Roy
Dept Of Medicine
Burdwan Medical College

2. Introduction
A patient with fever and altered sensorium constitutes
a medical emergency.
Early recognition, efficient decision making and rapid
institution of therapy can be life saving.

3. Levels of consciousness:
Alert: Fully conscious
Lethargic: Appear somnolent, but may be able to
maintain arousal.
Obtunded: Requires touch or voice to maintain arousal.
Stuporous: Unresponsiveness from which the individual
can be aroused only by painful stimulus.
Comatose: State in which patient is unable to arouse or
respond to noxious stimuli and is completely unaware
of self and surroundings.

4. Fever with altered sensorium-- causes
A. INFECTIONS
•
•
•
•
Encephalitis
Meningitis
Cerebral malaria
Brain abscess, subdural or
epidural empyema
• Sepsis associated
encephalopathy(SAE)
• Sepsis with DIC/TTP

5. Causes contd..
B. NON INFECTIOUS CAUSES OF FEVER
a. OVERPRODUCTION OF HEAT :
1. Neuroleptic malignant syndrome
2. Malignant Hyperthermia.
3.Serotonin Syndrome
4.Cocaine, Amphetamine, ecstasy toxicity
5.Salicylate poisoning.
6.Thyrotoxic encephalopathy.
7.Convulsive status epilepticus.
8.Catatonic schizophrenia

6. b. IMPAIRED HEAT DISSIPATION
1.Anticholinergic toxicity e.g amitriptyline
2.Heat Stroke.
c. STRUCTURAL LESIONS( IMPAIRED
THERMOREGULATORY MECHANISM)
1.Hypothalamic lesion.
2.Brainstem lesion( stroke)
3.Intraventricular and subarachnoid haemorrhage
ICH with Intraventricular extension
d. MISCL.
1. ADEM(infectious or post infectious)
2.cerebral fat embolism
3.Altered sensorium with secondary cause of fever eg. Aspiration
pneumonia in a stroke patient.

7. Important points:
Presence of fever alone is not sufficient to make a diagnosis of
an infectious etiology( e.g Meningitis or encephalitis)
Encephalopathy may be precipitated by systemic infections or
sepsis without cerebral inflammation (septic encephalopathy)
Sepsis can lead to altered sensorium secondary to metabolic
alterations like hypoglycaemia
, hyperpyrexia, hypovolemia, hepatic or renal failure.
Even in absence of infection there can be high rise of temp due
to mechanisms such as overproduction or impaired dissipation
of heat, non infectious CNS diseases, hypothalamic lesion.

8. Patients of NMS may have fever, neck stiffness, delirium,
generalised rigidity, even after the offending drug has been
withdrawn.
WORLDWIDE , infection of the CNS is the
commonest cause of Fever with altered sensorium.
In a study from India among children < 18 yrs of age,
commonest cause of acute febrile encephalopathy was
VIRAL MENINGITIS, accounting for 40% of the cases.
Among non viral, bacterial ( 34%), tubercular meningitis
(7.9%) and cerebral malaria (5.2%) were most common.

9. Causes of infectious meningoencephalitis:
A. VIRAL:
a. DNA virus:
1. Herpes viruses: herpes simplex (HSV1,HSV2)
other herpes viruses (HHV6, EBV, VZV, CMV)
2. Adenovirus.
b. RNA viruses:
Influenza, Polio, Entero,
Measles, Rubella, Mumps,
Rabies, Arbo, Reo, & Retrovirus

10. B. BACTERIAL:
1. Pyogenic meningitis
2. Mycobacterium tuberculosis
3. Mycoplasma pneumoniae
4. Listeria monocytogenes
5. Borrelia burgdorferri.
6. Tropheryma whippeli
7. Leptospira,
8. Brucella,
9. Legionella
10. Salmonella typhi.

11. C. RICKETTSIAL:
Rickettsia rickettsii, R. typhi,
R. prowazekii
Coxiella burnetti
D. FUNGAL:
Cryptococcosis, coccidiomycosis, histoplasmosis, blastom
ycosis, candidiasis
E. PARASITIC:
Plasmodium, trypanosoma, Toxoplasma, Naegleria, schist
osoma

12. APPROACH TO THE PATIENT
HISTORY:
 Most important
 Sometimes only clue to correct
diagnosis.
 Careful and systematic clinical
assessment is key to management of
a patient of febrile encephalopathy.
 Imp to differentiate infective vs non
infective causes.
 Temporal course is also imp –
whether fever preceded or followed
altered sensorium or simultaneous.
 Classical triad of CNS inf – fever,
neck rigidity, altered mental status.
(present in majority of patients)

13. HISTORY: imp points:
 Onset of altered sensorium
 Headache
 Fever – grade/type
 Joint pain /rashes
 Nausea/vomitting
 Contact with animals/dog bite
 Seizures – imp in children
 Focal deficits
 Geographical area
 Recent travel
 Drug addiction/use of antipsychotics
 Treatment with immunosuppressants/chemotherapy
 Trauma
 Recent illness/surgery
 Comorbidity such as diabetes

14. Physical examination:
Thorough physical examination & neurological examination can
provide imp clues to underlying aetiology.
 Skin rashes are common in meningococcal infn, rickettsial fever, VZV,
colorado tick fever
 Parotitis in mumps
 Erythema nodosum may be a/w TB
& histoplasmosis
 mucous membrane lesions common in Herpes virus infn,
 Upper resp tract infn favour Influenzae or Mycoplasma
 Look for lymphadenopathy, hepatosplenomegaly.

15. Detailed neurological examination including
Pupillary size(anisocoria) & reaction(loss)
Forced eye deviation,
Cranial nerve involvement,
Decerebrate rigidity,
Papilloedema
Focal neuro deficit,
Fundus examination for papilloedema help in diagnosis &
planning investigations.
Common focal abnormalities are
Hemiparesis, Aphasia, Ataxia,
Pyramidal Signs, Cranial Nerve Deficits,
Involuntary Movements (Myoclonus & Tremors),
Partial Seizures & Papilloedema.
warrant neuroimaging prior to LP
Babinski sign

16. Signs of suspected meningitis:
 Kernig sign: flexing hip & extending knee – elicit
pain in back n legs.
 Brudzinski sign: passive flexion of neck elicits
flexion of hip
 Nuchal rigidity: severe neck stiffness.
 Jolt accentuation: exacerbation of existing headache
with rapid head rotation

17. After getting clues from History and
examination,
investigations are tailored as per
provisional diagnosis.

18. Investigations:
BLOOD INVESTIGATIONS:
 TC, DC - CBC
 Coagulation profile
 Blood culture: +ve in 30-80% cases of
bacterial meningitis.
 Serum CRP & Procalcitonin
 Blood biochemistry
 Arterial blood gases
 PBS:
 Relative lymphocytosis in viral meningitis.
 Leucopenia & thrombocytopenia – in
rickettsial infn & viral haemorrhagic fevers.
 For definitive diagnosis of malarial infn
P. falciparum gamet

19. CXR:
May reveal changes suggestive of infn such as
Mycoplasma, Legionella, Tuberculosis
LP:
Always indicated when meningitis or meningoencephalitis is
suspected.
Includes:
CSF pressure
Gross examination for turbidity, cob web coagulum
Colour
Chemical examination: sugar, protein
Cell count & cell types
Microbiological examination: gram stain, india ink
preparation, cultures
PCR for tuberculosis, viral infn
Latex agglutination
Limulus lysate assay

20. CSF
findings
Normal
Viral
Bacterial
tubercular
Fungal
Opening
pressure
60-180 mm
of H2O
Normal
elevated
Elevated/
variable
Elevated/
variable
Colour
Clear
Usually
clear
Turbid/xant
hochromic
Xanthochro Clear/
mic/variable variable
TC
<5cells/cmm
<100/cmm
>1000/cmm
Variable(100 Variable
-500/cmm)
DC
lymphocytes lymphocytes PMNs
lymphocytes lymphocytes
protein
20-40mg/dl
N/ ed
elevated
elevated
elevated
Glucose
40-80mg/dl
Usually
normal
decreased
decreased
decreased
Usually
normal
Gm stain
+ve/variable
AFB +ve
India ink
prepn
Microscopy

21. Neuroimaging:
MRI
CT scan
Characteristic neuroimaging changes:
 Fronto temporal changes in HSV
 Thalamic & midbrain changes in Japanese encephalitis
 Basal exudates after contrast adm in TB Meningitis.
 Basal ganglia ring enhancing lesion in Toxoplasmosis.
 Multiple ring enhancing lesions in tuberculoma.
TB meningitis
HSV encephalitis

22. EEG:
 imp to rule out non convulsive status.
 d/d of focal encephalitis vs generalised encephalopathy
Characteristic EEG changes:
 Diffuse bihemispheric slowing in gen.
encephalopathy
Triphasic slow waves in hep encephalopathy.
 2-3 Hz, periodic lateralised epileptiform
discharges from temporal lobe in HSV.

23. Others:
Thyroid function test
Drug levels
Urine toxicology screen

24. Patient with Fever and altered sensorium
Precipitant known – drugs/toxins/heat
Yes
Treat acc to cause
No
C/F
1
2
Sudden onset altered
sensorium followed by fever
Seizure, psychiatric features/
minimal MIS/ FD +/-
CT head
Abnormal
Fever f/b altered sesorium
(ac/subac./chr)
3
Fever f/b altered sesorium
(course unclear)
MIS+++;FD +/-
Normal
MRI brain/ CSF
examintion/ PBS
Brain stem stroke,
hypothalamic lesion &
IVH/SAH
Encephalitis/
cerebral malaria
CSF examintion/
CT/MRI brain
Meningitis

25. 3
Fever f/b altered sesorium (course unclear)
MIS/FD/Imaging/ CSF
MIS +++; FD+/-;
Imaging +/- ;
CSF+++
Meningoencephalitis
MIS +/-; FD ++;
Imaging +++;
CSF+/-
Structural lesion of brain
MIS - ; FD - ;
Imaging +/- ;
CSF -
Metabolic/ psychiatric /
toxic

26. Management
algorithm for
suspected
bacterial
meningitis
Suspicion of bacterial meningitis
Immunocompromised
state, papilloedema, focal nero
deficits, delay in LP
No
Blood culture &
lumberpuncture stat
Dexamethasone + emperical
antimicrobial therapy stat
Yes
Blood culture stat
Dexamethasone + emperical
antimicrobial therapy stat
Negative CT
CSF suggesting of
bacterial meningitis
Continue / modify therapy
Perform LP

27. Evaluation of patient of febrile encephalopathy: Summary
A. History:
Fever, headache, vomitting, altered sensorium
Geographical & seasonal factors
Immune status, drug intake
Contact with animals, insect bite, dog bite
Foreign travel
Occupation
B. Clinical signs:
Fever, neck stiffness, altered sensorium
Kernig sign, Brudzinski sign, Jolt accentuation
Skin & mucous membrane changes
Lymph node, liver, spleen
Other sites of concomitant infn.
Neurological examn

28. C. Investigations:
Blood:
Urine: including myoglobinuria
CXR:
LP:
Neuroimaging:
EEG:
In selected cases
TFT
Drug levels
Urine toxicology screen
D. management:
Acc to cause