Coma final

Ambo University
College of Medicine and Health
Sciences
Department of Medicine
C2 Pediatrics
Seminar presentation on:
The management of coma
By:
Hayelom Michael
Habtamu Mokonen
Hailemariam Bekele
Moderator: Dr. Kissu
Ambo,Ethiopia

Outline
• Objective
• Introduction
• Coma mimicking states
• Cause
• Pathophysiology
• clinical features
• Approach to comatose patient
• Management of coma

Objective
• To define coma and similar clinical
conditions.
• To describe the etiologies of coma
• To describe the pathophysiologic
mechanism of coma in terms of the
underlying anatomic and physiologic
alterations.
• To explain the approach to a comatose
patient.
• To explain the management of comatose
patient

Introduction
• Consciousness is arousal, in which one
is able to interact with the environment,
and awareness, with the ability to know
"what is going on.
• Is the product of two closely related
cerebral functions:
– Wakefulness i.e. arousal, alertness.
– Content i.e. awareness of self and the env’t.

Cont….
• Coma is a state of unrousable, unconsciousnes
without any psychologically understandable
response to external stimuli or inner need.
• It is among the most common and striking
problems in general medicine.
• There is a continuum of the states of
consciousness, coma being the most severe.

Level of consciousness
• Reflects awareness and response to the
environment:
• Alert - Appearance of wakefulness, awareness of
the self and environment
• Lethargy :mild reduction in alertness
-tends to drift of to sleep when not stimulated
-when aroused has appropriate response
• Obtundation - moderate reduction in alertness.
- It requires touch or voice to maintain arousal.
-When aroused is in confusional state.
-Usually constant stimulation is required

• Stupor: Deep sleep, patient can be
aroused only by vigorous and repetitive
stimulation.
-Returns to deep sleep when not continually
stimulated.
• Coma:
-Sleep like appearance and behaviorally
unresponsive to all external stimuli
(Unarousable unresponsiveness, eyes
closed)

Coma mimicking states
– Minimally conscious
state(MCS)
– Persistently vegetative
state(PVS)
– Locked in
syndrome(LIS)
– Psychogenic
unresponsiveness
– Brain death
• Differentiating coma
from related states:
1.purpose full response
to stimuli?
2.Brain stem reflex?
3.Sleep wake cycle?
4.EEG?

Minimally conscious state(MCS)
• The patient has rudimentary vocal or
motor behaviors, often spontaneous, but
some in response to touch, visual stimuli,
or command.
• Cardiac arrest with cerebral hypoperfusion
and head injuries are the most common
causes.

Persistently vegetative
state(PVS)
• Signifies an awake but nonresponsive state
in a patient who has emerged from coma.
• The vegetative state is characterized by
loss of all cognitive functions & the un
awareness self &surroundings.
• Reflex & vegetative function, including sleep
wake cycles.
• These individuals have spontaneous eye
opening with out concurrent awareness.

• Diagnosis criteria for Vegetative state
include:
-The absence of awareness self&environment
and inability to interact with others.
-The absence of sustained or reproducible
voluntary behavioral responses.
-lack of language comprehension
-Suffiently preserved hypothalamus & brain
stem function to maintain life.

-Bowel and bladder incontinence
-Variably preserved cranial nerves(e.g.
pupillary & gag) and spinal cord reflexes.
NB. The PVS requires that condition has
continued for at least 1 month.
Few, if any, meaningful responses to the
external and internal environment—in
essence, an "awake coma."
• Indicates extensive damage in both
cerebral hemispheres, usually 2° to
ischemic injury

Locked in syndrome
• An awake patient has no means of producing
speech or volitional movement but retains
voluntary vertical eye movements and lid
elevation, thus allowing the patient to signal
with a clear mind.
• The pupils are normally reactive.
• The usual cause is an infarction or
hemorrhage of the ventral pons that transects
all descending motor (corticospinal and
corticobulbar) pathways

Psychogenic unresponsiveness
• Also termed 'pseudocoma‘, this describes
a patients who appear to be unconscious
and in coma but who are not.
• Oculovestibular testing, will reveal the
presence of nystagmus and indicate that
the patient has an intact brainstem and
cortex.

Brain death
• This is a state of cessation of cerebral function with
preservation of cardiac activity and maintenance of
somatic function by artificial means.
• It is equivalent to death.
• Brain death Criteria:
(1) widespread cortical destruction that is reflected by
deep coma and unresponsiveness to all forms of
stimulation;
(2) global brainstem damage demonstrated by absent
pupillary light reaction and by the loss of
oculovestibular and corneal reflexes;
(3) destruction of the medulla, manifested by complete
apnea.

Cause
• A more practiced &clinically relevant
categorization of CNS insults sever
enough to cause coma involves the
categorization of as:
-Structural : supra tentorial
Infra tentorial
-Metabolic toxic: common etiologies
uncommon etiologies

Structural
Supratentorial
• Hemorrhage
-epidural
-subdural
-subarachnoid
-intraparenchymal
• Ischemic stroke (massive
cerebral infarct)
• Cerebral contusion
• Sagital sinus thrombosis
• Abscess
• Tumors
• Hydrocephalus
Infratentorial
• Hemorrhage -pontine
-cerebellar
• Ischemic stroke (basilar
artery and its branches)
• Central pontine mylinolysis

Toxic/metabolic
Common
• Drug intoxication (alcohol,
benzodiazepines,
opiates)
• Hyper-/hyponatremia
• Hyper-/hypoglycemia
• Hypercarpia
• Shock (due to any cause)
Uncommon (easily
identifiable)
• Hyper-/hypocalcaemia
• Hepatic encephalopathy
• Uremic encephalopathy
• Anoxic encephalopathy
• Meningitis/encephalitis
• Adrenal crisis
• Myxoedema coma
• Hyper-/hypothermia
• Hypertensive encephalopathy
• Post ictal state
• Any end stage
neurodegenerative condition
• Extreme acid-base disturbance

Cont….
Uncommon (not easily identifiable)
• Drug intoxication (TCAs, neuroleptics,
antihistamines, anticonvulsants, salisylates,
lithium)
• Poisoning (CO, methanol, ethylene glycol,
cyanide, heavy metals, organophosphates)
• Thiamin deficiency
• Serotonin syndrome
• Nonconvulsive status epilepticus
• Reversible posterior leukoencephalopathy
syndrome

Pathophysiology
• Almost all instances of diminished alertness
can be traced to:
widespread abnormalities of the cerebral
hemispheres
reduced activity of a special thalamocortical
alerting system termed the reticular
activating system (RAS).
• The proper functioning of this system, its
ascending projections to the cortex, and the
cortex itself are required to maintain alertness
and coherence of thought.

Cont…
• The ascending RAS,
from the lower border
of the pons to the
ventromedial
thalamus
• The cells of origin of
this system occupy a
paramedian area in
the brainstem

Cont…
• It follows that the principal causes of coma
are:
(1) lesions that damage the RAS in the
upper midbrain or its projections
(2) destruction of large portions of both
cerebral hemispheres
(3) suppression of reticulocerebral function
by drugs, toxins, or metabolic
derangements such as hypoglycemia,
anoxia, uremia, and hepatic failure

Coma Due to Cerebral Mass
Lesions
• Herniation is the
principal mechanism
A) Uncal (most common)
B) central
C) transfalcial
D) foraminal

Coma Due to Metabolic Disorders
 Interruption of the delivery of energy substrates
(e.g., hypoxia, ischemia, hypoglycemia)
 Alteration of neuronal excitability (drug and alcohol
intoxication, anesthesia, and epilepsy)
• Unlike hypoxia-ischemia, which causes neuronal
destruction, most metabolic disorders such as
hypoglycemia,hyponatremia,hyperosmolarity,
hypercapnia, hypercalcemia, and hepatic and renal
failure : - impaired energy supplies,
-changes in ion fluxes across neuronal
membranes, and
-neurotransmitter abnormalities.

Toxic (Including Drug–Induced)
Coma
• Many drugs and toxins are capable of:
depression of nervous system function.
producing coma by affecting both the
brainstem nuclei, including the RAS, and the
cerebral cortex.
• The combination of cortical and brainstem
signs, which occurs in certain drug overdoses,
may lead to an incorrect diagnosis of
structural brainstem disease.
• Overdose of medications that have atropinic
actions produces signs such as dilated pupils,
tachycardia, and dry skin; opiate overdose
produces pinpoint pupils <1 mm in diameter.

Coma Due to infection
• The most common causes include: Pyogenic
menigitis ,TB meninigitis, Cerebral malaria,HIV,
encephiltis,
• Widespread structural cerebral damage→ a
metabolic disorder of the cortex.
• Hypoxia-ischemia is perhaps the most known
→hypoperfusion and oxygen deprivation of the
brain.
• Similar bihemispheral damage is produced by
disorders that occlude small blood vessels
throughout the brain
• Diffuse white matter damage from inflammatory
demyelinating diseases causes a similar syndrome

Clinical features
• Sleeplike state from which the patient cannot
be aroused.
• Eyes are closed and remain closed in the face
of vigorous stimulation.
• Do not speak.
• Do not arouse to verbal,tactileor noxious stimuli
• Motor activity is absent or abnormal and
reflexive rather than purposeful or defensive.
• as opposed to state of transient
unconsciousness such as syncope&
concussioncoma must last ≥1 hr.

Approach to a patient in Coma
Comaisamedical emergency whoseevaluation requires
arapid, comprehensive, and systematic approach.
Early identification of theunderlying causeof comacan
becrucial for patient management and prognosis.
A. Immediatelifesupport
B. Identification of causes
C. Specific therapy

A. Immediate life support
Assessment and maintenance of vital function is the initial step
(ABC of life)
• Maintain the air ways patency and ensure adequate breathing
• Maintain circulation
B. Establishment of cause of coma:
is done by taking a careful history, doing rapid but through
physical examination and investigations.

Patient History
• It is often useful to obtain a history from witnesses, friends or
family members, and emergency medical technicians.
• The patient's personal effects: a Medical Alert bracelet or
necklace and/or a card in the wallet may contain a list of
illnesses and medications.
• Past medical history: looking for disease like diabetes,
hypertension, cirrhosis, chronic renal disease, malignancies
and other diseases.

• History of medications: legal or illicit drugs (sedatives, hypnotics,
narcotics ) and history of drug abuse.
• Details regarding the site where the patient was found
(e.g. the presence of empty drug vials or evidence of fall or trauma),
• If the cause is unknown, Hx assessment should focus on:-
-detail of social and family history including recent travel.
-hx of recent preceding illness e.g. fever, headache.

• Circumstancesand rapidity with which changein mental status
developed.
 sudden onset suggestsintracranial hemo rrhage, seizure,
cardiac arrhythmia, trauma, or into xicatio n.
gradual onset suggestsan infectio us process, metabo lic
abnormality, or slowly expanding intracranialmass lesion.
fluctuations suggest subdural hematoma.
A history of preceding headache, doublevision, or nausea
suggestsincreased ICP.

Physical examination
Vital signs: Extremesof BP, pulseor temperatureand abnormal pattern of
breathing.
Temperature
 Hyperthermia: suggestsinfectio n, but isalso seen with inflammato ry
diso rders, environmental or exertional heat stro ke, neuroleptic malignant
syndrome, status epilepticus, hyperthyro idism, and anticho linergic po iso ning.
 Hypothermia: can occur with infection in infantsbut ismoreoften dueto
drug intoxication, environmental exposure, or hypothyroidism.

34
Heart rate
• Tachycardiacan occur with fever, pain, hypovolemia, cardiomyopathy,
/tachyarrhythmia, and also in statusepilepticus.
• Bradycardiaoccurswith hypoxemia, hypoxic ischemic myocardial injury,
and with increased ICP
Blood pressure
 Hypertension– hypertensiveencephalopathy or hypertensiveintracerebral
hemorrhage, pain, intoxication, renal failure, or increased ICP
 Hypotensionsuggestsshock, intoxication, or adrenal insufficiency.

Respirations
 Tachypnea can beseen with pulmonary infections, pain,
hypoxia, metabolic acidosis, and pontineinjury.
 Slow, irregular, or periodic respirationsoccur with metabolic
alkalosis, sedativeintoxication, and injury to extrapontine
portionsof thebrainstem.
 Irregular breathing-increased ICP

• Headandneck:
Signsof head injury
lacerationsor bruising to thehead,
Sx of basal skull Fructure
Raccon Sx (around theeyes),
Battle’s sign (behind theear )
Rhenorrhea &otorrhea(CSF leak from thenoseor ears)

Fundoscopy
• Papilledema may suggestsincreased ICP.
• Retinal hemorrhages aremost commonly associated with
shaken baby syndrome.
Meningismus
• Meningeal irritation or inflammation suggesting meningitis
or subarachnoid hemorrhage.

• Skin:
 Lo o k fo r signs o f trauma o r injectio n.
 Co lo r- pallo r(hemo rrhage) , cyano sis(inadequate
o xyginatio n)
 Rash- menengoco ccemia, bacterialendo carditis
 Sweating- hypo glycemia, sho ck
 Dry & ho t skin- heat stro ke

General systemic examination: looking for evidences of systemic
illnesses like cirrhosis, chronic renal failure, meningococcemia etc.
 Jaundice could indicate liver disease.
 A cherry red color, especially of the lips and mucous membranes,
suggests carbon monoxide intoxication.
 Pallor, especially with a sallow appearance, may suggest uremia,
myxedema, or severe anemia.
 A tongue bitten on the lateral aspect suggests a recent convulsive
seizure.

Neurologic examination:
is to determining whether the pathology is structural or due to
metabolic dysfunction.
• The examiner assesses:
– Level of consciousness(GCS)
– Motor responses
– Brainstem reflexes

Level of consciousness
It can be assessed semi quantitatively using the Glasgow coma
Scale.
Glasgow coma scale:
- Provides easily reproducible and somewhat predictive basic
neurologic exam.
-It is useful as an index of the depth of impaired
consciousness and for prognosis, but does not aid in the
diagnosis of coma.

• Glasgow coma scale is used for adults and older children and
its modification is used in infants and young children (<2
yearsof age) (PGCS) .

07/23/15 43
ACTIVITY BESTRESPONSE
Adults/OlderChildren Infants (modifiedGCS) Score
EyeOpening
(E)
Spontaneous
Tospeech
Topain
None
• Spontaneous
• Tospeech
• Topain
• None
4
3
2
1
Verbal
(V)
Appropriatespeech
Confusedspeech
Inappropriatewords
Incomprehensibleornone
specific sounds
None
• Appropriat vocalization, smile,
or orientation to sound,
interacts (coos, babbles),
follows object
• Irritable, cries
• Cries topain
• Moans topain
• None
5
4
3
2
1
Obeys commands
Localizes pain
Withdraws totouch
Decorticatetopain
Decerebratetopain
• Normalspontaneous
movement
• Withdraws totouch
• Withdraws topain
• Decorticatetopain
6
5
4
3
Glasgow coma scale

• TheGlasgow comascale(GCS) isscored between 3 and 15, 3
being theworst, and 15 thebest.
• Individual elements as well as the sum of the score are
important.
• Hence, the score is expressed in the form "GCS 8 = E2 V3 M3
at 02:30 PM

Significance of GCS
1. To classify/grade altered consciousness
2. Follow up
3. Prediction of prognosis of comatose child
1.clssification
Generally, comas are classified as:
• Severe, with GCS ≤ 8
• Moderate, GCS 9 - 12
• Minor, GCS ≥ 13.

2. Follow up
Used in assessment of responseto therapy.
3. Prediction of prognosis
-GCS ≤ 5 on admission, theprobability of death is90%
- GCS ≥ 10, the probability of death is decreasing to 1%

Brain stem reflexes
• helpsto localizethecauseto specific regionsof thebrainstem
and/or impending transtentorial herniation, or aconsistent
asymmetry between right- and left-sided responses.
• Theseare
- pupillary light,
- extraocular movement,
- corneal and respiratory reflexes.

a) Pupillarylightresponse
• Pupillary reactionsareexamined with abright, diffuselight.
• Thepupillary reflex dependson intact transmission within the
afferent optic nerve(CNII), theEdinger Westphal nucleusin
themidbrain, and theefferent oculomotor nerve(CN III).
• Parasympathetic impulsesco nstrict the pupils, while
• sympathetic dischargeleadsto pupillary dilation.
• During examination size, shape, symmetry and reaction to
light should benoted on both eyes.

• Normally reactiveand round pupilsof midsize(2.5 to 5 mm)
essentially excludemidbrain damage.
• Enlarged (>6mm) and unreactive pupil on one side signifies a
compression or stretching of the third nerve from the effects
of a mass above.
• Bilaterally dilated and unreactive pupils, indicates severe
midbrain damage, usually from compression by a mass.

• Bilaterally small (1 to 2.5 mm) and reactive pupils (not pinpoint) are seen in
metabolic encephalopathies or in deep bilateral hemispheral lesions such as
hydrocephalus or thalamic hemorrhage.
• Very small but reactive pupils (< 1 mm)/pinpoint pupils, characterize
narcotic or barbiturate overdoses but also occur with extensive pontine
hemorrhage.

b) Ocular Movements
The po sitio n and spontaneousmovementsof theeyeballs.
controlled by thecranial nervesIII, IV, and VI).
Lidtoneistested by lifting the eyelids :
 Resistance to opening the eye lids may suggest hysteric conversion.
 Easy eyelid opening with slow closure indicates sever coma.
• Midline deviation suggests frontal/pontine damage.
• Dysconjugate gaze (abduction or adduction) suggests cranial nerve
abnormalities.
• Spontaneous eye movements roving, dipping, bobbing suggest damages
being at different sites.

Occulocephalic reflex
• Elicited by moving the head from side to side or vertically with eyes held
open.
In comatose patient:-
 If the eyeballs move to the opposite direction of the head movement =
intact brainstem function (“doll’s eyes” movement is positive.)
 If the eyeballs move to the same direction of the head movement=
Brainstem dysfunction

Caloric (occulovestibular) reflex
• This test is performed by irrigating the ear with ice (cold) to
stimulate the vestibular apparatus.
• In patients with intact brain stem the eyes move to the irrigated
ear.

c) Corneal reflex
Thecorneal reflex teststhesensory function of thetrigeminal
nerveand themotor function of thefacial nerve.
• This test assesses the integrity of dorsal midbrain and
pontine.
• It is lost if the reflex connections between the fifth and the
seventh cranial nerves within the pons are damaged.

d) Respiration:
less localizing value in comparison to other brainstem signs.
• Shallow, slow, but regular breathing suggests metabolic or drug
depression.
• Cheyne-Stokes respiration signifies bihemispherical damage or metabolic
suppression, and commonly accompanies light coma.
• Kussmaul breathing usually implies metabolic acidosis but may also occur
with pontomesenephalic lesions and severe pneumonia.
• Agonal gasps aretheresult of lo wer brainstem (medullary) damageand
arerecognized astheterminal respiratory pattern of severebrain damage.

3. Motor function /response
 Quadriparesis and flaccidity-suggest pontine or medullary damage.
 Decorticate posturing: flexion of the elbows and the wrists with supination
of the arms, and extension of the legs, suggests severe bilateral or
unilateral hemispheric or diencephalic lesion (damage above the
midbrain.)

 Decerebrate posturing (extension of elbows and the wrist with pronation of the
forearm and extension of the legs) indicates damage to the brainstem( midbrain or
pontine compromise )
 Abnormal body movements – seizure, myoclonus may suggest the cause of the
coma is status epelepticus, uremia etc.

DIAGNOSTIC STUDIES
• Studies can be guided by HX and PE,
but most patients presenting with coma
of unknown etiology require laboratory
testing and a neuroimaging study.

Laboratory Testing
• Patients presenting with altered
consciousness should undergo a rapid
bedside test for blood glucose and basic
laboratory testing including:
• Serum electrolytes, calcium, magnesium,
glucose
• Arterial blood gas
• Liver function tests, ammonia
• Complete blood count
• Blood urea nitrogen, creatinine
• Urine drug screen

• blood and urine tests
• Testing for fungi, rickettsia,
mycobacteria, and parasites
• thyroid function tests
• cortisol levels/ carboxyhemoglobin,
and coagulation studies

• Neuroimaging — CT is the best initial
neuroimaging test. CT quickly detects
hydrocephalus, herniation, and mass
lesions due to infection, neoplasia,
hemorrhage, and edema.

• When lumbar puncture is indicated, a
CT is required in the comatose patient
to rule out a mass lesion that might
precipitate transtentorial herniation as
a result of the procedure.

• MRI - provides greater structural detail
and is more sensitive for early
evidence of encephalitis, infarction,
diffuse axonal injury from head injury,
petechial hemorrhages, cerebral
venous thrombosis, and demyelination.
• Lumbar puncture

• Electroencephalogram : coma of
unknown etiology
• It is often the only means of recognizing
non convulsive status epilepticus
(NCSE), especially in patients who are
paralyzed.

Treatment and Prognosis of
Coma in Children
• TREATMENT — Early treatment of
coma is generally supportive
• An important goal of early treatment is
to limit brain injury.
• RX for dangerous etiologies (eg,
hypoglycemia, increased ICP, bacterial
meningitis) are often initiated
empirically

• The primacy of ABCs applies to coma as
to other medical emergencies.
Airway
• attained by repositioning the child to open
the airway
• Patients with GCS <8 are usually unable
to adequately protect their airway and
should be intubated.
• If trauma is suspected, the cervical spine
should be stabilized with a collar while
securing the airway.

• Breathing — O2 saturation should be
measured and supplemental O2 provided.
• Adequacy of ventilation should be assessed
by examination and arterial blood gases.
• Moderate hyperventilation (target PaCO2 30 to
35 mm Hg) should only be initiated for
patients with increased ICP.
• Extreme hyperventilation /aggressive
hyperventilation (PaCO2 <30 mmHg) are only
justified in patients with transtentorial
herniation.

Circulation
Depressed level of consciousness may
be an early indicator of poor end-organ
perfusion in a patient with shock
Hypotension
• IV administration (NS or LR) and
inotropes, if necessary, is essential to
deliver oxygen and metabolic substrates
to the brain and remove toxic metabolites.

Hypertensive encephalopathy
• The goal of therapy is to lower the DBP
to 100 to 110 mmHg (or by a maximum
of 25 percent) within two to six hours
• Hypertensive encephalopathy has an
excellent prognosis for recovery if
ischemia can be avoided

• Glucose — Glucose (2.5 mL/kg of 10
percent dextrose solution) should be
administered even before test results
are known. If hypoglycemia is revealed,
then ongoing monitoring and treatment
will be needed.

• Intracranial pressure — When increased
ICP is suspected, emergent RX is
recommended. Increased ICP is assumed
when there is coma after head injury.
• Early interventions to reduce ICP include
treating fever, elevating the head of the
bed to 30 degrees above horizontal,
moderate hyperventilation (target PaCO2
30 to 35 mmHg) and administering
mannitol(0.25 to 1 g/kg IV). Neurosurgery
should be consulted.

• Seizures — If seizures have occurred,
phenytoin or fosphenytoin(15 to 20
mg/kg phenytoin equivalent IV) should
be administered.

• Non convulsive status epilepticus should
be considered as a diagnosis even when
there are no obvious seizure movements.
• If non convulsive seizures are suspected
and an electroencephalogram (EEG) is not
available, a therapeutic trial of phenytoin
or lorazepam (1 to 2 mg IV) is reasonable.

• Infection — Empiric antibiotic and antiviral therapy are
recommended
• If bacterial meningitis (eg, ceftriaxone100 mg/kg per day
in one or two divided doses, maximum dose 4 g per day,
plus vancomycin 60 mg/kg per day in four divided doses)
• Viral encephalitis ( acyclovir 30 to 60 mg/kg per day, in
three divided doses) are among the suspected entities.
• Blood cultures should be obtained prior to starting
antibiotics but initiation of therapy should NOT await LP.
• Therapy should be continued until these conditions have
been excluded

• Temperature control — Hyperthermia
(>38.5 degrees C).
• Fever should be lowered with
antipyretics and/or cooling blankets
immediately. Shivering, which can
contribute to elevated ICP, should be
avoided.

• Hypothermia to 32 to 36 degrees has been
suggested as a therapy for refractory
increased ICP in children with traumatic
brain injury - currently not recommended
• May be appropriate for children with
o out-of-hospital arrest
o persistent coma
o ventricular fibrillation or
o pulseless ventricular tachycardia

• Acid-base and electrolyte imbalance —
resuscitation of patients with
cardiovascular compromise should use
isotonic solutions only (NS or RL).

• Antidotes — use is recommended only in
the setting of known or strongly
suspected drug overdose.
• Naloxone(0.1 mg/kg IV in patients up to 20
kg or ≤5 years; maximum 2 mg) - possible
opiate ingestion.
• Flumazenil - benzodiazepine overdose, but
will render benzodiazepines ineffective in
the event of a seizure, so it should also be
used with caution.

• Agitation — sedation - should be
administered only when the benefits of
relieving agitation outweigh the need
for close neurologic monitoring by
exam.

Management algorithm for infants (≥1
month) and children with suspected
bacterial meningitis
07/23/15 Aproch to comatous child 80

Tb meningitis
• Chemotherapy should be initiated with
RHZS in an initial phase for 2 months
and RH should be continued for 7 to 10
months in the continuation phase.
• Adjunctive corticosteroid therapy with
dexamethasone is recommended for all
patients. The recommended regimen is:

• Dexamethasone- a total dose of 8 mg/day
for children weighing less than 25 kg and
12 mg/day for children weighing 25 kg or
more.
• The initial dose is given for 3 weeks and
then decreased gradually during the
following 3 weeks.
• Prednisolone- a dose of 2-4mg/kg/day for
children for 3 weeks, then tapered of
gradually over the following three weeks.

Long term essentials
• Skin care
• Oral hygiene
• Eye care
• Fluids
• Calories
• Sphincters

PROGNOSIS
• The prognosis in coma is etiology specific.
• Mass lesions at the fully developed midbrain stage
do poorly even after surgical evacuation.
• Sedative drug induced coma has a good
prognosis with proper supportive care.
• Coma with purulent meningitis doubles
unfavorable outcome or death.
• In hepatic or other metabolic comas, the absence
of pupillary, oculovestibular, and corneal reflexes
on admission is a grave prognostic sign.

• Brisk, small-amplitude, mainly vertical eye
movements are predictive of a fatal outcome.
• In cardiac arrest patients without seizures,
return of pupillary reactivity and purposeful
motor movements within the first 72 hours is
highly correlated with a favorable outcome.
• Bilateral absence of somatosensory evoked
responses in the first week predicts death or
a persistent vegetative state.

PX Factors
• GCS
• Age
• Clinical features
• EEG
• MRI
• Serum biomarkers

• GCS - is associated with prognosis in a
number of conditions as TBI.
• In some cases, “Age” < 2 years is
associated with worse px.

• Clinical features — the presence and
severity of certain early complications
has been linked to worse outcome
• EEG -a predictor of outcome in coma of
certain etiologies.
• Sedative drugs cause EEG
abnormalities and make interpretation
difficult, particularly for prognosis.

• An isoelectric baseline or a burst
suppression pattern during the first
week after coma - 100 % specific for
poor outcome
• Other EEG patterns associated with
poor outcome(but have poor sensitivity
and specificity)
o periodic epileptiform discharges
o nonreactive rhythms

MRI
• Presence and extent of brain edema,
brainstem injury, and diffuse axonal injury
-associated with poorer prognosis in
patients with TBI.
• Serum biomarkers — Elevated neuron
specific enolase (NSE) levels have been
associated with poor outcome after HIE,
TBI and other conditions (e.g.,
encephalitis, Reye's syndrome).

Reference
92
1. Nelson text book of pediatrics 19th
ed.
2. Up to date 21.2
3. Harrison 19th
ed.
4. Kumar and clark med
5. ceil

Coma final

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