This document discusses febrile coma, its causes, diagnosis, and management. It begins by defining coma and differentiating it from similar states like hysterical coma and syncope. The main causes of febrile coma are then outlined as CNS infections, cerebrovascular events, and infections/lesions elsewhere that can damage the CNS. The document emphasizes the importance of rapidly stabilizing patients and obtaining a thorough history and neurological exam. Key diagnostic tests are bloodwork, lumbar puncture if no contraindications, and CT scan if focal signs are present. Management involves treating any identified cause as well as empiric treatment of common infections if the cause is unknown. Proper diagnosis and management of fe

1. Febrile comaFebrile coma
BY:
Dr, WALAA SALAH MANAA
SPECIALEST OF PEDIATRIC & FEVER
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2. Coma is a state in which the pt is
unresponsive to environmental stimuli &
unable to communicate in any manner.
It is graded as (obtundation-confusion-
stupor-coma-deep coma).
0r scored by GCS from 15:3.
< 8 are typically regarded as coma.

3.  Proper diagnosis of coma is not difficult
with scientific systemic steps of diagnosis
after exclusion of the following condition:
1- Hysterical coma
2- Syncope and shock
3-Heavy sedation

4. =sound=moan to pain
Words=irritable cry (ped.)
=Cry to pain
=decorticated
=Decerebrated

5.  coma is associated with
structural or physiologic
damage.
 Coma is a critical condition
for both the patient and the
doctor (Dangerous for the
patient and difficult for the
physician).

6. *Hysterical coma :
 Profound response to very painful stimuli,
 Absence of incontinence or tongue bite,
 normal pupil response,
 pt does not harm him self.
*Syncope and shock:
Transient loss of consciousness for moment,
low BP ,pallor.
*Heavy sedation: (history).

7. Other difficulties :
 All types of coma can be presented to
the fever hospital because of the
possibility of the association of fever
with any type of coma.
 Prolonged coma is usually associated by
infection and other complications.

8. D.D.
 Shock is a serious condition
(BP low-COP low).
 It should be differentiated from coma.
 Coma is most serious if associated with
shock.

10.  Don't diagnose hysterical coma in a
febrile pt.
 Don‘t lose the hope or the prognosis in
prolonged coma.
Golden roles

11. Causes of
febrile coma:

12. 1- C.N.S. infections
(Encephalitis and meningoencephalitis)
a- Viral arbovirus encephalitis- Herpes
simplex -Rabis – mumps- measles,,,,
b-BacterialNeis.meningitidis
M.tuberculosis,streprococcal pneumonia, H.
influanza,,,,,,,,,,,,
c-Rechetsial
d-Fungal
e-Parasitic e.g. malaria, trypanosomaiasis,
cystocercosis,,,,,,,,,,,.

13. 2- Cerebro-vascular stroke
1- Pontine hemorrhage
2- Subarachnoid hemorrhage.
3- Cerebral hemorrhage.
4-infarction (massive-multiple).

14. Subarachnoid hemorrhage
Pontine hemorrhage

15. 3- Infection or Tissue Destruction
Associated with the Following
Conditions Causing Coma:
- Trauma of the C.N.S.
- Tumor (space occupying lesions).
- Cerebrovascular stroke (hemorrhagic, thrombotic or
embolic).
- Toxic coma due to
* External toxins (poison ingestion)
* Internal toxins e.g. Diabetic coma, uremia ,
hepatic coma and others,,,,,,,
4t

17. So what will we do?

18. 1- Stabilize the patient:
a- (A,B,C)*.
b-IV cannula
2- History
3- Clinical Examination:
- Assessment of coma (Glasgow scoring).
- Assessment of fever (pattern and relation to coma).
- Neurological examination.
- Assessment of all body systems
1- Blood sample for sugar, urea,
prothrombin and other chemistries
according to history and clinical
suspicion.
2- Drugs: -50 cc 25% dextrose)
-Thiamine ???
-Naloxone ???

19.  O2 if there is cyanosis.
 Thiamine 100 mg ,,,rarely needed now(rarity
of thiamine deficiency).
 Naloxone 2mg repeated every 2 hrs if there
is response to 1st
dose(very effective in opiate
poisoning)

20. C o n s id e r C N S
in fe c tio n (L P )o r C V s tro k e
if th e re is n o im p rv e m e n t
a fte r c o rre c tio n ( 2 )
T re a tm e n t
a c c o rd in g ly
+ v e fo r to x ic
a n d
m e ta b o lic c o m a
T re a tm e n t
a c c o rd in g
to C S F
fin d in g s (3 )
L .P .
L u m b e r P u n c tu re
-v e fo r to x ic
a n d m e ta b o lic
c o m a
B lo o d
c h e m is tr y (1 )
N o F o c a l s ig n s
C o n s u lt n e u ro s u rg e ry
& c o n s id e r L .P .
in c a s e o f
in fa rc tio n ( 6 )
E m p e ric a l
tre a tm e n t
(5 )
B lo o d C u ltu re
F o c a l le s io n
(4 )
T re a tm e n t
a c c o rd in g to
C S F fin d in g s
(7 )
L .P .
L u m b e r P u n c tu re
N o
F o c a l le s io n
C T
F o c a l s ig n s * *
T re a tm e n t
a c c o rd in b g to
C T a n d C S F
fin d in g s (9 )
L .P . w ith c a u tio n
(8 )
C T
W ith
fo c a l s ig n s
T re a tm e n t
a c c o rd in g to
C S F fin d in g s
(1 0 )
L .P .
L u m b e r P u n c tu re
W ith o u t
fo c a l s ig n s
+ v e m e n in g e a l s ig n s * *
F ig u re (2 ).
N e u ro lo g ic a l E x a m in a tio n * *

21.  All the steps of management of comatosed
pt. must be done rapidly & at the same time
with ttt.

22. 1- Stabilize the patient:
 ABC-is very important step to save the life
of the pt.

23. History
From the family or
relatives or any
person living with pt
or contacting him.

24. Present history :
• Onset….acute (CVS-CNS infection).
gradual (degenerative diseases –
CNS infection).
• Bed side bottles or drugs.
• Trauma-vigorous movement.
• Symptom preceding the onset of coma.
• Drug history????.

25. Past history :
-Similar attack (DM-renal-hepatic comas).
-History of co-morbidity.
family history :
• Neurological diseases (epilepsy).

26. Examination.
*Should be rapid-from scalp hair to his toes.
*Special stress on:

27. 1-Bite of the tongue. exclude hyst.
2-Smell of the mouth.(aceton-ammonia-fetor)
3-Cyanosis.(cariopulmonary-brain stem lesion.)
4-Head injury.
5-Signs of electrolyte imbalance.
6-Sclera.(jaundice-hge).
7-neck stiffness-neck veins-
8-nose or ear discharge.(blood or CSF)
Head & Neck

29. 9-pupils---unequal pupil in encephalitis.
---ppp in pontine he- organophos.pois.

30. Extremities.
 Arms: sites of IV injection.
 Edema LL.
• Murmurs -pneumonias-br.asthma .
• Masses-organomegally –ascites- signs
of trauma-.
Heart-Chest-Abdomen

31. Skin
 Rashes-signs of trauma.
L.Ns.
• Enlargement-masses,,,,,brain
secondries or (HIV).

32. 1- Stabilize the patient:
a- (A,B,C)*.
b-IV cannula---------
2- History
3- Clinical Examination:
- Assessment of coma (Glasgow scoring).
- Assessment of fever (pattern and relation to coma).
- Neurological examination.
- Assessment of all body systems
1- Blood sample for sugar, urea,
prothrombin and other chemistries
according to history and clinical suspicion.
2- Drugs: -50 cc 25% dextrose)
-Thiamine
-Naloxone

33. C o n s id e r C N S
in fe c tio n (L P )o r C V s tro k e
if th e re is n o im p rv e m e n t
a fte r c o rre c tio n ( 2 )
T re a tm e n t
a c c o rd in g ly
+ v e fo r to x ic
a n d
m e ta b o lic c o m a
T re a tm e n t
a c c o rd in g
to C S F
fin d in g s (3 )
L .P .
L u m b e r P u n c tu re
-v e fo r to x ic
a n d m e ta b o lic
c o m a
B lo o d
c h e m is tr y (1 )
N o F o c a l s ig n s
C o n s u lt n e u ro s u rg e ry
& c o n s id e r L .P .
in c a s e o f
in fa rc tio n ( 6 )
E m p e ric a l
tre a tm e n t
(5 )
B lo o d C u ltu re
F o c a l le s io n
(4 )
T re a tm e n t
a c c o rd in g to
C S F fin d in g s
(7 )
L .P .
L u m b e r P u n c tu re
N o
F o c a l le s io n
C T
F o c a l s ig n s * *
T re a tm e n t
a c c o rd in b g to
C T a n d C S F
fin d in g s (9 )
L .P . w ith c a u tio n
(8 )
C T
W ith
fo c a l s ig n s
T re a tm e n t
a c c o rd in g to
C S F fin d in g s
(1 0 )
L .P .
L u m b e r P u n c tu re
W ith o u t
fo c a l s ig n s
+ v e m e n in g e a l s ig n s * *
F ig u re (2 ).
N e u ro lo g ic a l E x a m in a tio n * *

34. Neurological examination.
Need special (experiences & precaution).
1-Depth of coma…..GCS
2-Tone & sensation.
3-Focal lesions :asymmetry in response to
painful stimuli (its detection is decreased
by increases depth of coma).
4-Signs of meningeal irritation & signs f
lateralization are disappear in GCS<7.

35. 5-Cranial nerve O/E

37. 5-Cranial nerve O/E :
is difficult in coma BUT ALSO important to de
depth of coma
1st nerve :face expression to very irritable odour smell.
Optic nerve: pupillary light reflex + fundoscop.
3rd
, 4th
, 6th
-------*pupillary light reflex..3rd
*spontaneous or induced
movement of the eye in various
direction.
*Doll's eye sign.

38.  Doll's eye sign.=oculocephalic reflex.
With the eyelids hold opened ,brisk lateral
rotation of the head normally opposite
rotation of eyeball as if to fix the gaze on
an object. It is lost in brain stem death

39.  5th cranial nerve :
corneal reflex.
jaw jerk.
jaw movement with supraorbital compression.

40.  7th
nerve :
supra orbital pressure
asymmetry of the nasolibial
fold.
 8th nerve: Doll's eye sign.
 9th-10th nerves
gag +cough reflexes.
 11th nerve:
spontaneous or induced elevation of shoulder.
 12th nerve:
spontaneous or induced elevation of tongue.

41. C o n s id e r C N S
in fe c tio n (L P )o r C V s tro k e
if th e re is n o im p rv e m e n t
a fte r c o rre c tio n ( 2 )
T re a tm e n t
a c c o rd in g ly
+ v e fo r to x ic
a n d
m e ta b o lic c o m a
T re a tm e n t
a c c o rd in g
to C S F
fin d in g s (3 )
L .P .
L u m b e r P u n c tu re
-v e fo r to x ic
a n d m e ta b o lic
c o m a
B lo o d
c h e m is tr y (1 )
N o F o c a l s ig n s
C o n s u lt n e u ro s u rg e ry
& c o n s id e r L .P .
in c a s e o f
in fa rc tio n ( 6 )
E m p e ric a l
tre a tm e n t
(5 )
B lo o d C u ltu re
F o c a l le s io n
(4 )
T re a tm e n t
a c c o rd in g to
C S F fin d in g s
(7 )
L .P .
L u m b e r P u n c tu re
N o
F o c a l le s io n
C T
F o c a l s ig n s * *
T re a tm e n t
a c c o rd in b g to
C T a n d C S F
fin d in g s (9 )
L .P . w ith c a u tio n
(8 )
C T
W ith
fo c a l s ig n s
T re a tm e n t
a c c o rd in g to
C S F fin d in g s
(1 0 )
L .P .
L u m b e r P u n c tu re
W ith o u t
fo c a l s ig n s
+ v e m e n in g e a l s ig n s * *
F ig u re (2 ).
N e u ro lo g ic a l E x a m in a tio n * *

42. Focal signs =
hemi plegia-hemiparisis,
paraplegia-paraparisis-
monoplegia,monoparesis,,,,,,
and or cr nerves lesions.
Meningeal signs
can not be detected if GCS<6

43. (1) blood chemistry RBS-BUL-Proth.time-
any suspected toxins or poisons.
(2) If the pt not recovered after
correction of metabolic causes…..
CNS infection or CVS is
considered ---so—LP & CT Br.

44. Probable case=Suspected case +LP
Clear Hazy turbid
Sptiic
meningitis
T.B
Pt
conscious
Pt
Un-
conscious
Bloody
Aseptic
meningitis
meningism
encephalitis
Eary
Septic
mening
T.B. Traumatic
Sub
arachnoid
hge
Traumatic
In septic
meningitis

45. Probable cases +Probable cases +
biochemical&biochemical&
BacteriologicalBacteriological
analysis of CSF.analysis of CSF.
Chemical normalChemical normal
BacteriologicalBacteriological
freefree
Sterile CSF
Protein++++
WBCS(PNL++(
Isolated
organism
Pr+++
Gl---
WBCS++
SUGER—
Gr-ve diplococci
WBCS>>300cell/cc
Without
isolated
organism
Viral
meningioe
ncephalitis
1-viral
meningioence
phalitis
2-T.B.
3-
Encephalitis
Septic
meningi
ioencep
halitis
Mening
ococcal
mening
Septic
meningio
enceph

46. In spite of this approach, Misdiagnosis of
coma may occur in the following
uncommon conditions:
1-Atypical presentation
of some types of coma.
2-Presence of associated pathology
which may cause or end in coma e.g. septic
meningitis in patients with cirrhotic liver.
3-Occurrence of complications:
that delay or prevent the recovery from

47. I-
Atypical presentation.

48. 1-Septic meningitis :modified by
antibiotics ttt may present by vague symptom
before stage of coma.
2-Measles encephalitis or Mumps
encephalitis
rarely presented by coma before the appearance
of the measles rash or the parotid swelling,.

49. 3-Uncommon cases of C.N.S.
infection: may be presented by
lateralization or any focal neurological
lesion and coma without meningeal signs
with sudden onset typically like cerebro-
vascular stroke. due to vasculitis
Diagnosis is easily achieved by CT scanning
and C.S.F. examination

50. 4-T.B. meningitis
Is very difficult to
diagnose because it is vague and
can mimic any infective or non
infective CNS disease clinically
and even in imaging findings.

51. High index of clinical
suspicion is mandatory
concerning the following
- Past history of T.B.
- Family History of TB.
- Presence of any primary T.B. lesion.
-Meningitis of prolonged course or resistant
to treatment.
-C.S.F. findings: very high protein and
reduced glucose, increase leucocytes with
predominant lymphocytes,.
-CT findings e.g. hydrocephalus, infarcts or
tuberculoma.

52. PCR and/or TB bacilli
isolation in CSF are
confirmatory for the
diagnosis

53.  So, empirical treatment must be given when
3 of the following:
Temp > 39C
Duration > 6 days
Protein > 100
CSF glucose <50
CSF leucocytes > 1000
CSF lymphocytes > 50%

54. 5-High fever in old age or in patient with
old brain lesion may cause coma.
6-Fulminant hepatic coma in rare
conditions can occur before the
appearance of jaundice.
Diagnosis is made by prothrombin time
and liver enzymes.

55. 7-Hepatic encephalopathy in cirrhotic
patients may present rarely initially by mild
seizures or abnormal involuntary
movements prior to, coma, these may
obscure the diagnosis of hepatic coma with
neurological disease,prolonged prothrombin
time is diagnostic.
8-Electrolyte imbalance or blood gas
disturbance regardless its cause can be
presented by coma.

56. 9-Prion diseases (previously known as
slow virus diseases– spongiform
encephalopathes of humans-):
*Creutzfeldt-Jacob disease (CJD).
*Variant CJD (υ-CJD).
*Kuru.
*Fatal familial insomnia.
*Gerstmann-Starausler- Scheinker syndrome.

57. II-
Association of Lesions

58. 1-Septic meningitis when occurred in
patients with advanced liver cirrhosis, may be
misdiagnosed as hepatic encephalopathy precipitated
by fever
Diagnosis by:
- Good clinical evaluation of the case.
- Prothrombin time.
- Unexpected unresponsiveness to anti-hepatic coma
measures.
- C.S.F. analysis.

59. 2-In diabetic coma when the
expected recovery is not achieved after
controlling the blood sugar and balancing the
electrolytes, we must search well for any
associated pathology that render the recovery
such as cerebro-vascular stroke, C.N.S. infection,
or toxic coma.
Diagnosis: can be achieved by
- Good clinical examination.
- CT brain.
- C.S.F. analysis.

60. III-
Complications

61. When coma is properly diagnosed
and proper treatment was given but
the expected response is not
gained, we must search well for
complications e.g.:

62. 1-Septic meningitis may be
complicated by brain abscess,
subdural effusion, or brain
infarction.

63. 2-Diabetic coma
may be complicated by
subarachnoid hemorrhage,cerebral
hemorrhage or cerebral infarction
due to the diabetic angiopathy.

64. 3-Encephalitis may be complicated by cerebral
infarction.
4-T.B. meningitis may be complicated by internal
hydrocephalus or brain infarction.
5-Electrolyte imbalance or blood gas disturbance
due to the original etiology of coma; or due to
improper management can prevent the recovery
of coma and cause death.

65. Take home message.
 Good observation,
 high experience ,
 high grade of clinical suspicion,
( are very essential in the diagnosis of
coma).