Febrile coma

Febrile comaFebrile comaBY:

Dr, WALAA SALAH MANAA SPECIALEST OF PEDIATRIC & FEVER

مـستشفى حمـيات كـفر الشـيخ

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.

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

=sound=moan to pain

Words=irritable cry (ped.)=Cry to pain

=decorticated =Decerebrated

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).

*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).

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.

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.

Don't diagnose hysterical coma in a febrile pt.

Don‘t lose the hope or the prognosis in prolonged coma.

Golden roles

Causes of febrile coma:

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-Rechetsiald-Fungal e-Parasitic e.g. malaria,

trypanosomaiasis, cystocercosis,,,,,,,,,,,.

2- Cerebro-vascular stroke

1- Pontine hemorrhage2- Subarachnoid hemorrhage.3- Cerebral hemorrhage.4-infarction (massive-multiple).

Subarachnoid hemorrhage

Pontine hemorrhage

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

So what will we do?

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 ???

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)

C on s id er C N Sin fec tion (L P )or C V s trok eif th ere is n o im p rvem en t

a fte r corre c t ion (2)

Treatm entaccordingly

+ve for toxicand

m etabolic com a

Treatm entaccording

to CSFfindings (3)

L.P .Lumber Puncture

-ve for toxicand m etabolic

com a

B loodchem is try(1)

N o Foca l s igns

C on su lt n eu ro su rg ery& con s id er L .P .

in cas e o f

in fa rc tion (6)

Em pericaltreatm ent

(5)

B lood C ulture

Focal lesion(4)

Treatm entaccording toCSF findings

(7)

L.P .Lum ber Puncture

NoFocal lesion

C T

Foca l s igns **

Treatmentaccordinbg toC T and CSFfindings (9)

L.P . w ith caution(8)

CT

W ithfoca l s igns

Treatmentaccording toCSF findings

(10)


W ithoutfoca l s igns

+ve m eningeal s igns**

Figure (2).

N euro log ica l Exam ination**

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

1- Stabilize the patient: ABC-is very important step to save the

life of the pt.

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

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????.

Past history :-Similar attack (DM-renal-hepatic comas).-History of co-morbidity.

family history :• Neurological diseases

(epilepsy).

Examination.

*Should be rapid-from scalp hair to his toes.

*Special stress on:

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

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

Extremities. Arms: sites of IV injection. Edema LL.

• Murmurs -pneumonias-br.asthma .

• Masses-organomegally –ascites- signs of trauma-.

Heart-Chest-Abdomen

Skin Rashes-signs of trauma.

L.Ns. • Enlargement-masses,,,,,brain

secondries or (HIV).

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




+ve for toxicand

m etabolic com a

Treatm entaccording

to CSFfindings (3)



com a


N o Foca l s igns


in cas e o f

in fa rc tion (6)


(5)

B lood C ulture

Focal lesion(4)


(7)


NoFocal lesion

C T

Foca l s igns **



CT

W ithfoca l s igns


(10)




Figure (2).


Neurological examination. Need special (experiences & precaution).1-Depth of coma…..GCS2-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.

5-Cranial nerve O/E

5-Cranial nerve O/E : is difficult in coma BUT ALSO important to detect 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.

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

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

compression.

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.




+ve for toxicand

m etabolic com a

Treatm entaccording

to CSFfindings (3)



com a


N o Foca l s igns


in cas e o f

in fa rc tion (6)


(5)

B lood C ulture

Focal lesion(4)


(7)


NoFocal lesion

C T

Foca l s igns **



CT

W ithfoca l s igns


(10)




Figure (2).


Focal signs =hemi plegia-hemiparisis,paraplegia-paraparisis-monoplegia,monoparesis,,,,,, and or cr nerves lesions.

Meningeal signs can not be detected if GCS<6

(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.

Probable case=Suspected case +LP

Clear Hazy turbid

Sptiicmeningitis T.BPt

consciousPtUn-

conscious

Bloody

Asepticmeningitis

meningism

encephalitis

EarySeptic

meningT.B. Traumatic

Subarachnoid

hge

TraumaticIn septic

meningitis

Probable cases +Probable cases +biochemical& biochemical& BacteriologicalBacteriological

analysis of CSF.analysis of CSF.

Chemical normalChemical normalBacteriologicalBacteriological

freefreeSterile CSF

Protein++++

WBCS(PNL++)Isolated

organismPr+++Gl---

WBCS++SUGER—

Gr-ve diplococci

WBCS>>300cell/ccWithout

isolated organism

Viral meningioencephalitis

1-viral meningioencephalitis2-T.B.3-Encephalitis

Septic meningiioencephalitis

Meningococcal mening

Septic meningioenceph

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 the state of coma

I-Atypical presentation.

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,.

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

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.

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.

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

So, empirical treatment must be given when 3 of the following:

Temp > 39هC Duration > 6 days Protein > 100 CSF glucose <50 CSF leucocytes > 1000 CSF lymphocytes > 50%

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.

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.

9-Prion diseases (previously known as slow virus diseases– spongiform encephalopathes of humans-):

*Creutzfeldt-Jacob disease (CJD). *Variant CJD (-CJD). *Kuru. *Fatal familial insomnia. *Gerstmann-Starausler- Scheinker

syndrome.

II- Association of Lesions

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.

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.

III- Complications

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.:

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

2-Diabetic coma may be complicated by

subarachnoid hemorrhage,cerebral hemorrhage or cerebral infarction due to the diabetic angiopathy.

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.

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

coma).

Health & Medicine

Febrile coma