ALTERED SENSORIUM
Kristine Latorre-Mendoza, MD, FPPS, FPNSP, FPNA
Madeleine Grace M. Sosa, MD, FPPS, FPNSP, FPNA
October 28, 2014, 8:00 12:00 (A/B)
Pediatrics
OUTLINE
Define different stages of consciousness
Discuss the anatomic basis of consciousness
Pathophysiology of altered state of consciousness
Causes, signs and symptoms of increased ICP
Diagnostic approach and therapeutic modalities
for increased ICP
INCREASED INTRACRANIAL PRESSURE
Neurologic emergency that requires prompt
recognition and control to prevent serious
sequelae or death
Concepts of increased intracranial pressure in
adults may not be applicable in children
E.g. In children, increased ICP may manifest as
failure to reach developmental milestones or
increasing head circumference (As compared to
adults wherein what is usually seen is stroke. Epilepsy is
a common sequelae of stroke in pediatric patients.
What is usually seen in adults are demyelinating
diseases, brain and spinal diseases and/or tumors.)
What we mean by the example above is that it is not only acute
condition that will have to be seen as a neurologic emergency, but
increased intracranial pressure may actually start in an early onset
until the development of signs and symptoms of increased
intracranial pressure.
REMEMBER
ME!! DESCRIPTION OF STATES OF NORMAL &
IMPAIRED CONSCIOUSNESS
NORMAL CONSCIOUSNESS
A condition of the normal person when awake
State of the patients awareness of self and
environment and his responsiveness to
external stimulation and inner need
How do you say that a 1-month-old is conscious?
A 1-month-old patient is noted to be awake or conscious if he
responds to all forms of stimulation: Verbal, Auditory, and
Sensory or Tactile Stimulation. So if you touch a newborn and
he/she looks at you or stares, that newborn is awake. Kasi may
ibang newborn, kapag natutulog, bukas ang mata (half open), and
that doesnt mean that the baby is awake. The baby must respond
to you in all forms of stimulation. If you produce a sound and the
patient did not respond, one consideration is deafness. If you use
visual stimuli and the patient followed the object with his/her eyes
then the patient is awake. Or, if the patients diaper is wet, the
patient should cry.
Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,
Aubrey Medina
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona
CONFUSION
Patient does not take into account all elements
of his immediate environment
A state that implies a degree of
imperceptiveness and distractibility
Referred traditionally as clouding of
sensorium
Inability to think with customary speed and
clarity, marked by some degree of
inattentiveness and disorientation
It is easy to determine if the patient is confused if he/she is 2 or 3
years old or older. The parents might report change in behavior.
For example, in conversations, the patient is giving inappropriate
answers, but was previously well. In a 6-month old or in young
infants, confusion might manifest as irritability, which is why
confusion is difficult to identify in infants.
What you have to write in your report would be the description of
details of how the child reacted to the stimuli that the examiner
gave. Thats when we say that the patient has an altered state of
consciousness.
DROWSINESS
Denoted inability to sustain a wakeful state
without the application of external stimuli
Inattentiveness and mild confusion, which both
improves with arousal (either both verbally or
physical stimuli)
Lids droop without closing completely, limb
muscles are relaxed
The baby seems sleepy or is asleep, but when you touch him/her,
the baby opens his eyes and looks at you. It is difficult to determine
if the patient is just sleepy or if there is already an altered state of
consciousness. In your history, ask the primary care giver if the
patient is usually like that (sleepy). You can note in the history if
there is a change in behavior and level of consciousness. Usually, if
the patient is just sleepy, when you wake him up, he will already be
up and about, but if the patient is drowsy, the patients eyes will
open to stimulation for a few minutes then go back to sleep again.
Touch or voice lang, magrerespond na, then matutulog uli.
STUPOR
Patient can be roused only by vigorous and
repeated stimuli, at times patient opens eyes,
looks at the examiner and does not appear to be
unconscious
Respond to spoken commands is either absent
or slow and inadequate
Restless or stereotyped motor activity is
common in stuporous patients and do not shift
position as frequently as patients who are only
drowsy
Tendon and plantar reflexes and breathing
pattern may or may not be altered
If the patient is stuporous, the patient will only respond in a more
vigorous or painful stimulation.
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 COMA
Appears to be asleep at the same time
incapable of being aroused by external
stimuli or inner need
Brainstem reflexes are usually diminished
Respiration may be slow, rapid , periodic or
deranged (like in Kussmauls breathing) due to brainstem involvement
Deep sleep soil the bed, cannot respond to inner need
No response to any stimulation. If you have a patient who came
in a state of drowsiness or confusion, we dont want this to
progress into stupor, nor into coma, because after, coma, its death.
ANATOMIC SUBSTRATE OF ALERTNESS
The maintenance of consciousness depends on
interaction between the ascending reticular
activating system (ARAS) and the cerebral
hemispheres
Damage to the ARAS induces a state of coma in
which the patient becomes unresponsive
ARAS lies in the paramedian tegmental region
of the posterior portion of the pons and the
midbrain
Thalamus is the source of diffuse
thalamocortical projections that regulate and
coordinate activity
The state of consciousness lies particularly in the PONS and
MIDBRAIN inside the area of the brainstem.
If there is damage on the ARAS or the bilateral cerebral
hemispheres, there will be altered state of consciousness. Damage
to the ARAS can induce a patient to a state of coma, in which a
patient becomes unresponsive. If you have a patient who comes in,
in coma, then a damage to any of the two (ARAS or Bilateral
Cerebral Hemispheres) is considered.
The MLF (Median Longitudinal Fasciculus)
which connects the abducens ,oculomotor and
trochlear nuclei are situated amid the neurons
of the pontine and midbrain portions of the
ARAS
Unresponsiveness is caused by brainstem
damage, the lesion affects the mechanisms of
ocular motility, and its location can often be
determined by abnormal patterns of ocular
motility
From past transcriptions:
The Median Longitudinal Fasciculus (MLF) is the part of the
brainstem connecting the ARAS to the cerebral hemisphere
connecting them to the 3 main extraocular muscle cranial nerves.
These cranial nerves are the abducens (CN VI), oculomotor (CN
III), trochlear (CN IV) because they are situated within the neurons
of the pons and midbrain, where the ARAS is located. Any
abnormality, whether morphologic or metabolic causing edema or
compression in any of the surface of the midbrain or pons, can
affect the nuclei of these 3 cranial nerves thereby clinically
presenting as abnormalities in extraocular movements.
This is the reason why the pupils, eye movements (EOM) etc. are
evaluated clinically, because it tells a lot how the midbrain and/or
brainstem, in particular, are affected.
PATHOLOGIC CONDITIONS IN ALTERED
STATE OF CONSCIOUSNESS
TRAUMATIC
Shaken Baby Syndrome
Vehicular accidents (results in head trauma)
Birth injuries
NONTRAUMATIC
HIE (Hypoxic Ischemic Encephalopathy)
Cerebrovascular
CNS Infection
Metabolic
Toxins
Epilepsy
Endocrine
Structural lesions

MASS LESIONS
Tumor
Abscess
Meningitis (sometimes result to subdural effusions or
subdural Empyema)
Massive edematous infarct
Intracerebral hemorrhage
This is the cerebral hemisphere in median section, with the cerebral cortex
and the cerebellum. The ARAS usually lies on the medial portion of the METABOLIC
brainstem. So, the paramedial tegmental region of the posterior portion of Hypoxia/ Ischemia
the pons and the midbrain is actually the ARAS. Acidosis/ Alkalosis
If there is a lesion in the ARAS, other manifestations besides altered states Hypo and Hyperosmolar states
of consciousness would be cranial nerve deficits, specifically, in the area Hypercarbia
of the pons, there will be ocular signs. Hyperammonemia
Examples: Hypokalemia, Hypocalcemia
A. Abducens affectation (CN 6)
Lateral Rectus Palsy 1. HYPOXIC ISCHEMIC ENCEPHALOPATHY
B. Oculomotor affectation (CN 3) Near drowning
Ptosis Perinatal asphyxia
Medial Rectus Palsy (outward deviation)
Cardiovascular arrest
Unreactive pupils
C. Trochlear affectation (CN 4) Suffocation
Superior Oblique Palsy (upward outward)
Unresponsiveness is caused by brainstem damage and its location can be
Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,
determined by altered
Aubreypatterns
Medina of ocular motility. D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 2 of 9
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona
If drowning resulted in HIE, then thats the only time the patient
Transient changes (coughing, sneezing,
will have altered state of consciousness. If the hypoxia and acidosis
is severe, then it resulted to edema of the bilateral cerebral straining) may produce pressure of 30 to 55
hemisphere, then thats the only time the patient will have altered mmHg but returns rapidly to baseline values
state of consciousness. Lesions that can mimic masses and Conversion: 1mmHg = 13.6 mm of saline
produce increased intracranial pressure, like bleeding can also water
result to HIE. The location and the size of the bleed affects whether
the patient will have altered state of consciousness or not. You have the patient lying prone or seated, but most commonly
done in lateral decubitus. Insert the needle between L4 and L5 and
2. CEREBROVASCULAR LESIONS then connect it into a manometer and what goes up will be your
Subarachnoid bleed CSF. The manometer will be measuring in mmH2O. Whatever you
Subdural bleed get there, convert it to 1mmHg=13.6mmH2O so you can get your
mmHg.
Extradural bleed
Vasculitis
Venous sinus thrombosis COMPONENTS OF ICP
Sickle cell encephalopathy 1. Cerebrospinal Fluid (CSF) (10%) any changes in these 3 may result

AV malformation 2. Blood (10%) in ICP --> altered sensorium

3. Brain Parenchyma (80%)

3. CNS INFECTIONS Remember, the brain is inside a rigid skull already. Sometimes in
Encephalitis pediatric patients who are stuporous or comatose, somehow their
Meningitis brains do not herniate (even if they have increased ICP for 3 or 4
Brain Abscess days already), unlike in adults which usually herniate (just in a
Post infections encephalopathy matter of hours). The reason for which is because the anterior and
sometimes the posterior fontanels (of pedia patients) are not yet
4. EPILEPSY fully fused. Somehow, this is a good thing for these children
Status epilepticus (prolonged seizure more than 5 because they could tolerate the increase in ICP.
mins)
Post ictal state
You can have altered state of consciousness during the attack or
after the attack.

5. TOXINS/DRUGS
Barbiturates
Anti-epileptic drugs
Tricyclic antidepressants
Antihistamines (can cause drowsiness)
Phenothiazine
Alcohol
Amphetamines
Lead and heavy metals
Organophosphates
Salicylates
Barbiturates and anti-epileptic drugs when taken in high doses or
even in therapeutic doses can produce side effects of alteration in
state of consciousness. The CSF is produced from the choroid plexus and passes
through the lateral ventricles connected via the foramen
6. ENDOCRINE ABNORMALITIES rd
of Monroe to the midline of the 3 ventricle. Then
Diabetes Insipidus th
connected to the 4 ventricle via the aqueduct of Sylvius
Diabetes mellitus (cerebral aqueduct) and exits the 4th ventricle via the
Diabetic ketoacidosis foramen of Luschka (lateral) and Magendie (midline)
7. DEGENERATIVE CNS DISORDER and leads to a system interconnecting draining through the
Lysosomal disorders subarachnoid space surrounding the brain and spinal cord
(into the lumbar cisterns) and goes around the venous
Leukodystrophies
channels and drains through the arachnoid granulations
Neuronal Ceroid Lipofuscinosis
into the superior sagittal sinus which goes back into the
Peroxisomal disorders
ventricular system

NORMAL INTRACRANIAL PRESSURE The pathway is very important in the determination of the
obstruction. If a certain part is obstructed, there will be
NORMAL VALUES (MUST KNOW) enlargement of the part preceding it. The parts after the
1.5 to 6 mmHg Young infants obstruction will seem constricted or small. Any obstruction in the
3 to 7 mmHg Children flow of CSF will result in the accumulation of the CSF and this will
15 mmHg Older children and adults result in hydrocephalus, and that will cause increased intracranial
pressure.

Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,

Aubrey Medina D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 3 of 9
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona

In children, what is the condition wherein the CSF could be the
culprit for increased ICP? Its CONGENITAL HYDROCEPHALUS.
The main reason for this is the malformation of aqueduct of
Sylvius.
Headache is mediated by the pain fibers of trigeminal nerve (CN V)
within the dura and blood vessels.
Cushings triad (may not be appreciated in children)
Systemic hypertension
Bradycardia
Irregular respirations
Parinauds Syndrome, also known as dorsal midbrain syndrome is
a group of abnormalities of eye movement and pupil dysfunction. It is
caused by lesions of the upper brain stem. It is seen mostly in
patients with macrocephaly primarily because of congenital
hydrocephalus. They will present with sunset eyes or persistent
downward gaze. Whenever you ask them to look up, they wont be
able to perform the maneuver, because the long tract of the third
nerve is being pulled by the enlarging ventricle and it limits the
function/movement of the third nerve to pull-up the eye. Most of
them could have lateral rectus palsy (CN VI or Abducens nerve
affectation). Remember LR6 and SO4?
Behavioral changes - Not all patients with increased ICP would
have depressed sensorium, some of them would be so irritable or
combative at the start and then, later on becoming so quiet and
sleeping most of the time. In the initial stages of increased ICP,
sometimes they do present without any behavioral changes.

MONROE-KELLIE DOCTRINE COMMON TO OLDER

ICP depends on the constancy of volume. Any INFANTS
BOTH CHILDREN
changes in the volume of normal intracranial Irritable Lethargy Headache
contents will occur at the expense of the other Full fontanel Vomiting Double vision
States that for ICP to remain normal, Big head with VI and III nerve Hemiparesis
intracranial volume must remain constant distended scalp palsies CN palsies
because the skull, after closure of fontanel and veins Personality
sutures , forms a rigid container Setting Sun sign changes
MacEwen sign
V Intracranial (Constant) = V CSF + V Blood + V Brain (+V Others)
th
From Nelsons Textbook of Pediatrics 19 Ed.:
Any changes between the 3, the other 2 would compensate to In children with hydrocephalus, impairment of vertical gaze and
maintain normal ICP. pathologic lid retraction are referred to as the setting-sun sign.
Anterior fontanel will close at 18 months
MacEwens sign is a sign to detect hydrocephalus and brain
Posterior fontanel will close at 2 months abscess. Percussion on the skull at a particular spot (near the
All suture lines should close at 18 junction of the frontal, temporal and parietal bones) yields an
(V= volume unusually resonant sound in the presence of hydrocephalus or
brain abscess. The resonant sound is due to the separation of the
FACTORS AFFECTING ICP cranial sutures.

INCREASE ICP DECREASE ICP PAPILLEDEMA

Hypercarbia Hypocapnea This is the most reliable objective sign of
Hypoxia Hyperoxia increased ICP, however, it rarely occurs in
Nitrous Oxide Hypothermia
young infants with open sutures and fontanels
REM Barbiturates
Arterial Hypertension Neuroleptanalgesia
Intracranial Mass Arterial Hypotension
Hypertonic solutions
Corticosteroids

SIGNS AND SYMPTOMS

Headache
Diplopia Papilledema is characterized by blurring of the optic disc
Decreased sensorium margins, loss of physiologic cupping, hyperemia and fullness of
the veins.Due to the continuationof dural sheath covering the
Parinauds Syndrome
optic nerve.
Behavioral changes
Cushings triad HEADACHE FEATURES SUGGESTING
Herniation syndrome INCREASEP ICP
Nocturnal awakening (because of increased ICP when lying
down)
Worsening by cough, micturition, or defecation
Recurrent and localized
Progressive increase in frequency or severity
Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,
Aubrey Medina D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 4 of 9
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona
Note progression of symptoms. In a simple headache, the
BRAIN HERNIATION
headache is not progressive. It may be resolved and will have a 1. Uncal
relapse, but nevertheless, it is not progressive. In increased ICP, 2. Central
there is progression of symptoms (from confused, to drowsy, to 3. Cingulate/Subfalcine
worse). 4. Transcalvaria
5. Upward
CONVENTIONAL GLASGOW COMA SCALE 6. Tonsillar

EYE OPENING (E)

Spontaneously 4
To speech 3
To pain 2
None 1
BEST VERBAL RESPONSE (V)
Oriented 5
Confused conversation 4
Inappropriate words 3
Incomprehensible words 2
None 1
BEST MOTOR RESPONSE (M)
Obeys 6
Localizes pain 5
Withdraws to pain 4
Flexion (decorticate) 3
Extension (decerebrate) 2
None 1

Coma Score = E + M + V
Maximum score = 15 / Minimum score = 3
This scale is used for adults and teenagers, 10 years old and above.

PEDIATRIC GLASGOW COMA SCALE

INFANTS (<1year) CHILDREN (>1year)
EYE OPENING (E)
4 Spontaneously
3 To speech
2 To pain
1 None
BEST VERBAL RESPONSE (V)
5 Coos and babbles
4 Irritable cries
3 Cries in response to pain
2 Moans in response to pain
1 None
BEST MOTOR RESPONSE (M)
5 Spontaneous
4 Localizes to pain
3 Flexion to pain
2 Extension to pain
1 None
NORMAL AGGREGATE SCORE
Birth to 6 months
Less than 6 to 12 months
Less than 1-2 years
Less than 2-5 years
More than 5 years
Spontaneously
To speech
To pain Brain herniations are the most common sequelae of patients with
None increased ICP that doctors want to avoid because it is a neurologic
emergency. Uncal and central herniations are usually seen in
adults especially during massive bleeding but not so much during
Oriented infarction. Transcalvarial herniations usually occur during
Confused vehicular accidents. Upward herniations usually occur as a
Inappropriate words complication of post-surgical patients and Tonsillar herniations
Incomprehensible sounds usually occur in the presence of a tumor.
None
TRANSTENTORIAL/CENTRAL HERNIATION
Spontaneous Diencephalon is displaced through tentorium
Localizes to pain
cerebelli notch into posterior fossa
Flexion to pain
Presents with rostro-caudal progression
Extension to pain
None Results from cerebral edema, posttraumatic,
toxic or metabolic, hydrocephalus due to 3 rd
ventricular and aqueductal obstruction and
9 bilateral cerebral hemispheric lesions
11
12 STAGE 1 (DIENCEPHALIC STAGE)
13
Regular or Cheyne-Stokes respiration
14
Small reactive pupils
Reflex ocular movements present
Hypertonicity
Decorticate rigidity

STAGE 2 (MIDBRAIN STAGE)

Regular or increased respiration
MIDposition fixed pupils
Reflex ocular movements dysconjugate or
absent
Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,
Aubrey Medina D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 5 of 9
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona
 Hypertonicity
Decerebrate rigidity
STAGE 3 (MEDULLARY STAGE)
Slow, irregular and gasping respiration
MIDposition or dilated fixed pupils
Reflex ocular movements absent
Flaccidity
Transtentorial/Central Herniation
TONSILLAR HERNIATION
Cerebellar tonsils becomes impacted into the
foramen magnum thus compressing the
medulla oblongata and the upper cervical
spinal cord
Can occur in supratentorial or infratentorial
mass lesion
From past transcriptions:
SUPRATENTORIAL = tumor in the CEREBRUM (such as gliomas,
astrocytomas, ependymomas)
INFRATENTORIAL = tumor in the CEREBELLUM (such as
medullablastoma, most common tumor in children, in this area)
Characterized by
Abrupt loss of consciousness
Opisthotonic posturing
Stiff neck
Irregular respiration
Apnea
Cerebellar Tonsillar Herniation
INFRATENTORIAL HERNIATION
Brainstem herniation occurs as a
consequence of intracranial hypertension
localized to the posterior fossa
HALLMARK: Focal cranial nerve abnormalities
and asymmetric motor signs
Vegetative functions of respiration, cardiac
rhythm and blood pressure can be compromised
early and severely with preservation of pupillary
light reflex and vertical eye movement
Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,
Aubrey Medina
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona
UNCAL HERNIATION***
Occurs as a result of a mass lesion occupying in
the middle area of the parenchyma or either
side of the temporal lobe. There would be
displacement of the uncal or the
hippocampal gyrus encroaching the 3rd nerve
and later on, the midbrain
The earliest sign that we see clinically would be
anisocoria with pupillary dilatation same
side to the lesion
Uncal Herniation
SUBFALCINE/CINGULATE HERNIATION***
Because of the mass lesion, there would be
subfalcine herniation characterized by shifting
of the swollen cingulate gyrus underneath
the edge of the falx cerebri causing ipsilateral
or bilateral anterior cerebral artery and the
internal cerebral brain compression leading to
infarction
MANAGEMENT
GOAL OF TREATMENT
1. To maintain adequate cerebral perfusion
2. To prevent brain herniation
1ST COMPONENT: CSF
Treatment should be directed to the underlying
cause
Surgical
Excision of tumor
VENTRICULOSTOMY temporary
external drainage
VENTRICULOPERITONEAL SHUNT
permanent internal drainage
If for example, the underlying cause of the patients increased ICP
is hydrocephalus, then management should be geared towards
treating it. The difference between a TEMPORARY and
PERMANENT drain is that if the CSF is infected do a temporary
drain (Ventriculostomy). If the CSF is NOT infected use a
permanent internal drain (VP shunt).
METHODS TO MONITOR ICP
VENTRICULOSTOMY
Intraventricular catheter/ ventriculostomy drain
A soft tube placed through a burr hole into the
lateral ventricles of the brain
The most accurate way to receive and
monitor an ICP
Also for therapeutic drainage of CSF
D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 6 of 9
 Tissue fragments or blood clots can obstruct the
catheter, hence alter measurements/drainage
Complications:
Infection
Bleeding
CSF leakage
Air leakage
Over drainage of CSF
SUBARACHNOID SCREW/BOLT
Placed into the skull abutting the dura
A hollow screw which allows CSF to fill the bolt
allowing the pressures to become equal
Low risk of infection or bleeding
Errors from ICP underestimation, misplacement
of the screw and occlusion of debris
SUBDURAL/EPIDURAL CATHETER
Less invasive but less accurate
Cannot drain CSF
INTRAPARENCHYMAL OF A FIBEROPTIC
TRANSDUCER TIPPED CATHETER
Second most accurate
Cannot drain CSF but complication rates are low
GENERAL SUPPORTIVE MEASURES OF
INCREASED ICP
Maintain airway
Monitor vital signs: treat shock
For neck trauma, apply cervical collar
Elevated head to 15 to 30 degrees (done to
maintain good venous drainage and circulation)
Reduce fever (to decrease metabolism of the brain
that would contribute to an increased ICP)
Establish IV line
Empty stomach with NG tube
Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,
Aubrey Medina
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona
Place indwelling urinary catheter (to monitor urine
output during mannitol treatment)
Avoid excessive procedures worsening ICP (like
vigorous suctioning, coughing)
Remove airway secretion by gentle suction (to
decrease pooling of secretions)
Give enema or antitussive agents if necessary
Controlling shivering in intubated patients with
muscle relaxants
Administering prophylactic anticonvulsant drugs
MEDICAL MANAGEMENT
OSMOTIC AGENTS
Increase serum osmolality and creates an
osmotic gradient between the brain and serum
Draws free water from the brain into the
intravascular compartment along the osmotic
gradient.
Eg. Mannitol, urea and glycerol
MANNITOL
Most often used and considered as agent
of choice
Dose of 500 to 1000 mg/kg
Onset of action: 1 to 5 minutes
Duration of action: 2 to 4 hours
Complications:
Dehydration
Electrolyte imbalance
Extreme hyperosmolarity with renal
failure
LOOP DIURETICS
Furosemide works synergistically with mannitol
to remove free water
Dose: 1mg/kg IV
2ND COMPONENT: BLOOD
Blood is contained in the cerebral vasculature
PIAL BLOOD VESSELS: contains most of the of
the cerebral blood vasculature
PRECAPILLARY ARTERIOLES: controls
cerebral blood flow
HYPERVENTILATION
Causes respiratory alkalosis vasoconstriction
of pial vessels limit cerebral blood flow
Extreme hyperventilation can also cause
excessive vasoconstriction leading to cerebral
ischemia
Patient should be ventilated at PaCO2 of
30mmHg
Maintain PaCO2 levels at 20mmHg
When Hyperventilation is discontinued, it should
be tapered 24 to 48 hours.
Indications for intubation: GCS < 8 or
pupillary dilatation
Patients with increased ICP are usually vasodilated so
hyperventilation is induced through intubation to decrease ICP.
Do not overly hyperventilate the patient. Maintain a PCO2 level of
30mmHg. Do not go below 20mmHg. There should be an ABG to
monitor the PCO2.
D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 7 of 9
ELEVATION OF HEAD BY 30 DEGREES INTERSTITIAL EDEMA***
Decreases ICP by encouraging venous return Transependymal movement of fluid from
It does not alter cerebral perfusion pressure ventricles to brain
Occurs when the CSF absorption is blocked
CSF DRAINAGE and the ventricles enlarged
Uncontrolled intracranial hypertension
Chiefly in the periventricular white matter
Remove CSF and monitor ICP
Acetazolamide and furosemide may be helpful
Small changes in volume (eg. the removal of as
little as 1 mL of CSF) can significantly reduce ICP CORTICOSTEROIDS
Inhibit membrane lipid hydrolysis and decrease
3RD COMPONENT: BRAIN TISSUE free radical induced lipid peroxidation (principal
CEREBRAL EDEMA: defined as increased in molecular basis for posttraumatic neuronal
water content of the brain degeneration)
Methylprednisolone - has the highest lipid
TYPES OF EDEMA antioxidant capacity.
VASOGENIC EDEMA Methylprednisolone > Prednisolone >
Leakage of protein rich fluid across the Dexamethasone > Hydrocortisone (no
capillary membrane into the extracellular space antioxidant activity)
of the white matter
Caused by increased capillary permeability DEXAMETHASONE
Eg: neoplasms, infections, trauma Dose: 0.4 to 1mg/kg/day in divided doses)
CYTOTOXIC EDEMA Adult dose: 4mg every 6 hours
Particularly effective if tumor is the case
Caused by expansion of the Intracellular
Onset of action: 12 to 24 hours
fluid compartment due to cellular toxins or
injury.
Swelling of the neurons, glial and endothelial OTHER MEASURES
cells Avoid hypotension
Eg. Metabolic, toxic and Hypoxic ischemic Ensure patent airway
disorders Maintain normocarbia and avoid
hypercarbia and hypoxia
Monitor blood gas and electrolytes
Control seizures
Pentobarbital: LD 15mg/kg
Phenobarbital: LD: 20mg/kg
Barbiturates can reduce ICP especially
in head injury
Pentobarbital > Phenobarbital
If the patient presents with seizures, treat them well and treat
them HARD. If the dose indicated is 20mg then give the patient
20mg.
If there is hypotension, there would be decreased cerebral blood
flow. At the same time, we also do not want to overhydrate
because this will increase the fluid levels in the brain, leading to
more cerebral edema. Maintain an adequate blood pressure.

BARBITURATE COMA
From past transcriptions (Dr. Latorre-Mendozas lecture): MECHANISM: cerebral metabolic rate
VASOGENIC EDEMA = STEROIDS will be the best medical CBF ICP mortality rate
treatment. Osmotic agents have no effect on vasogenic edema, Treat intracranial hypertension that is refractory
but they can decrease the volume of normal brain tissue and in to other modalities
that way reduces total intracranial pressure. Pentobarbital is the barbiturate that is best
studied and most commonly used
CYTOTOXIC EDEMA = Corticosteroids do not decrease edema but
OSMOTIC AGENTS may relieve intracranial pressures by reducing Barbiturate produce cardiac suppression, which
brain volume may result in hypotension
A barbiturate coma is performed when you have exhausted all
From section B recording (Dr. Sosa):
other forms of treatment and the patient still has increased ICP.
STEROIDS are the drug of choice for these types of lesions
especially for vasogenic edema or cytotoxic edema.

Editors Note:
According to Medscape: both are unresponsive to steroids
According to Nelsons: Steroids should not be used unless adrenal
insufficiency is present.
kayo na ang bahala kung sino papaniwalaan niyo.
Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,
Aubrey Medina D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 8 of 9
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona
 REVIEW QUESTIONS:

1. Patient can be roused only by repeated and vigorous stimuli. stupor

2. Maintenance of consciousness depends on these two anatomic structures. ARAS + cerebral hemisphere
3. Unconsciousness is caused by damage to this structure. ARAS
4. A state that implies a degree of imperceptiveness and distractibility. confusion
5. Three cranial nerves connected to the medial longitudinal fasciculus. 3, 4, 6
6. States that for the ICP to remain normal, intracranial volume must remain constant. Monroe Kellie Doctrine
7. Patient is incapable of being aroused. coma
8. The most reliable objective sign of increased ICP. papilledema
9. Most often used and considered as the drug of choice for the medical management of increased intracranial pressure. mannitol

10. Denoted inability to sustain a wakeful state without the application of external stimuli drowsiness
11. Trace the CSF pathway.
lateral ventricle -> foramen of monroe -> 3rd vent -> aq of sylvius -> 4th vent -> foramen of magendie/luschka -> subarach -> villi

COMPUTE FOR THE GLASGOW COMA SCALE:

1. C.P., 5 years old, flexes elbows and wrist abnormally in response to pain, makes incomprehensible sounds, opens eyes in
response to speech. 3

2. A.C., 15 years old, unable to speak or open eyes and has no response to pain. 1 + 1 + 1
3. H.O., 12 months old, does not move when you put pressure on the nails or elsewhere, confused and opens eyes in
response to pain. 1 + 4 + 2
4. W.P., 13 years old, opens eyes when spoken to and can hold conversation, though apparently disoriented. Patient flexes
elbow and wrist when pressure is applied on the nail beds. 3 + 4 + 3
5. Y.D., 14 months old, smiles, oriented to sound and interacts normally, extends arm when pressure or pain is applied,
spontaneously opens eyes. 5 + 2 + 4

-END-

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Formatters note: Those with *** in the heading were not actually discussed nor was it included in the lecture and were
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REMARKS for the sake of completion. RAYOR!

Yey to all the winners of JFT 2014! #PowerfulBatch2016

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Go back?" he thought. "No good at all! Go sideways? Impossible! Go forward? Only thing to do! On we go!" So up he got, and trotted along
with his little sword held in front of him and one hand feeling the wall, and his heart all of a patter and a pitter. J.R.R. Tolkien, The Hobbit

Transcribers: Almon Constantino, Lenz Tan-Hoyumpa,

Aubrey Medina D L S H S I M e d i c i n e B a t c h 2 0 1 6 | 9 of 9
Formatting: Gladys Dianne Hulipas
Editing: John Neal Bastona