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COMA evaluation and treatment
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INTRODUCTION
An alteration in arousal represents an acute, life threatening emergency, requiring prompt

intervention for preservation of life and brain function
Stupor and coma are clinical states in which patients have impaired responsiveness (or are
unresponsive) to external stimulation and are either difficult to arouse or are unarousable.
Coma is defined as "unarousable unresponsiveness"
The terms stupor, lethargy, and obtundation refer to states between alertness and coma.
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ETIOLOGIES AND PATHOPHYSIOLOGY
Alterations in alertness can be produced by focal lesions within the upper brainstem by directly
damaging the ARAS
Injury to the cerebral hemispheres can also produce coma, but in this case, the involvement is
necessarily bilateral and diffuse, or if unilateral, large enough to exert remote effects on the
contralateral hemisphere or brainstem.
Coma in toxic, metabolic, and infectious etiologies and hypothermia: impair oxygen or substrate
delivery, which in turn alters cerebral metabolism or interferes with neuronal excitability and/or
synaptic function.
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ETIOLOGIES AND
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Hypoxic-ischemic brain injury
Hypoxic-ischemic brain injury most often results from insults such as cardiac arrest, vascular
catastrophe, poisoning (such as carbon monoxide intoxication or drug overdose), or head trauma
The induction of mild to moderate hypothermia (chill therapy) to a target temperature 32 to 34C in
the initial hours after cardiac arrest improves the neurologic outcome of resuscitated patients
Induced-hypothermia therapy impacts the prognostic utility of clinical examination findings and ancillary
testing
Validated protocols for assessing prognosis in the setting of therapeutic hypothermia are needed
Therapeutic hypothermia in traumatic brain injury need to be validated
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Pathophysiology
of increased ICP
Intracranial mass lesions (eg, tumor, hematoma)

Cerebral edema (such as in acute hypoxic ischemic encephalopathy, large cerebral infarction,
severe traumatic brain injury)
Increased cerebrospinal fluid (CSF) production, eg, choroid plexus papilloma
Decreased CSF absorption, eg, arachnoid granulation adhesions after bacterial meningitis
Obstructive hydrocephalus
Obstruction of venous outflow, eg, venous sinus thrombosis, jugular vein compression, neck
surgery
Idiopathic intracranial hypertension (pseudotumor cerebri)
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Intracranial pressure (ICP)
Intracranial pressure is normally 15 mmHg in adults, and pathologic intracranial hypertension (ICH) is present
at pressures 20 mmHg
Homeostatic mechanisms stabilize ICP, with occasional transient elevations associated with physiologic events,
including sneezing, coughing, or Valsalva maneuvers
Intracranial compartment (fixed internal volume of 1400 to 1700 mL):
ICP is normally lower in children than adults, and may be subatmospheric in newborns
Brain parenchyma 80 percent, Cerebrospinal fluid 10 percent, Blood 10 percent
CSF is produced by the choroid plexus and elsewhere in the central nervous system (CNS) at a rate of
approximately 20mL/h(500mL/day)
Problems with CSF regulation generally result from impaired outflow caused by ventricular obstruction or
venous congestion
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increased CBV
and hyperemia
CBF = (CAP - JVP) CVR

CAP=carotid artery pressure
JVP=jugular venous pressure
CVR=cerebral vascular resistance
CPP = MAP ICP

CPP=cerebral perfusion pressure
MAP= mean arterial pressure
ICP=intracranial pressure
The recommended CPP target is 60 mmHg, avoiding

levels below 50 mmHg and above 70 mmHg
In children these thresholds may be lower, 40 to 65
mmHg
hypoperfusion
and ischemia
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CLINICAL MANIFESTATIONS of elevated ICP
Bradycardia, respiratory depression, and hypertension (Cushing's triad)
Focal symptoms of elevated ICP
local effects in patients with mass lesions or by herniation syndromes
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Indications for ICP monitoring
Closed head injury is one of the most frequent and best-studied indications for ICP monitoring
Indications for ICP monitoring in TBI (Traumatic brain injury) are a GCS score 8 and an abnormal
CT scan showing evidence of mass effect from lesions such as hematomas, contusions, or swelling
ICP monitoring in severe TBI patients with a normal CT scan may be indicated if two of the following
features are present: age >40 years; motor posturing; systolic BP <90 mmHg
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HISTORY
What was the time course of the loss of consciousness?

Was it abrupt (eg, subarachnoid hemorrhage, seizure), gradual (eg, brain tumor), or fluctuating (eg,
recurring seizures, subdural hematoma, metabolic encephalopathy)?
Did focal signs or symptoms precede the loss of consciousness?
As an example, an initial hemiparesis suggests a structural lesion, likely with mass effect.
Transient visual symptoms, eg, diplopia or vertigo, suggest ischemia in the posterior circulation.
Did the patient have previous neurologic episodes that suggest transient ischemic attacks or
seizures?
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HISTORY
What recent illness has the patient had?
Has there been altered behavior or function recently?
A fever suggests infection;

An increasing headache suggests an expanding intracranial lesion, infection, or venous sinus thrombosis;
Recent falls raise the possibility of a subdural hematoma;
Recent confusion or delirium might indicate a metabolic or toxic cause.
What prescription or nonprescription drugs are used?
Are there medical or psychiatric conditions?
Is there history of alcohol or drug abuse?
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GENERAL EXAMINATION
Extreme hypertension may suggest
hypertensive encephalopathy,
hypertensive intracerebral/cerebellar/brainstem hemorrhage
reversible posterior leukoencephalopathy syndrome,

Hypotension may reflect
circulatory failure from sepsis,
hypovolemia,
cardiac failure,
certain drugs
Addison's disease.
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GENERAL EXAMINATION
Hyperthermia usually signifies
infection;
heat stroke,
anticholinergic intoxication
Hypothermia could be
accidental (cold exposure),
primary (due to hypothalamic dysfunction as in Wernicke's encephalopathy or tumor),
secondary (eg, adrenal failure, hypothyroidism, sepsis, drug or alcohol intoxication).
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Ventilatory pattern
Cheyne-Stokes respirations (a pattern of periodic waxing then waning hyperpnea, followed by brief
apnea) may occur with either impaired cardiac output or bicerebral dysfunction, and also in elderly
patients during sleep.
The shorter-cycle Cheyne-Stokes respiration linked to brainstem tegmental dysfunction may evolve
into irregular respirations with progression of downward herniation
Apneustic breathing (in which there is a prolonged inspiratory phase or end-inspiratory pause) is
rare and usually attributed to pontine tegmental lesions.
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NEUROLOGIC EXAMINATION
Level of consciousness
Motor responses
Brainstem reflexes: pupillary light, extraocular, and corneal reflexes
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Level of consciousness
Arousability is assessed by noise (eg, shouting in the ear) and somatosensory stimulation.
Pressing on the supraorbital nerve (medial aspect of the supraorbital ridge) or the angle of the jaw, or
squeezing the trapezius
Important responses include vocalization, eye opening, and limb movement
The GCS is useful as an index of the depth of impaired consciousness and for prognosis, but does
not aid in the diagnosis of coma.
The more recent FOUR score system has some advantages for intubated patients
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Motor examination
Decreased spontaneous or purposeful movement,
Acute structural disease usually produces decreased muscle tone or flaccidity
Flexion and extension movements usually represent reflex responses arising from subcortical
structures
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Decorticate posturing
upper-extremity adduction and flexion at the elbows, wrists, and fingers, together with
lower-extremity extension, which includes extension and adduction at the hip, extension at the knee, and
plantar flexion and inversion at the ankle
This occurs with dysfunction at the cerebral cortical level or below and may reflect a "release" of other
spinal pathways
Decerebrate posturing
Motor examination
upper-extremity extension, adduction, and pronation together with lower-extremity extension and
traditionally implies dysfunction below the red nucleus, allowing the vestibulospinal tract to predominate.
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Cranial nerve reflexes
Disruption of the pupillary light reflex in comatose patients usually occurs because of:
Downward herniation of mesial temporal structures from an expanding supratentorial mass and/or
a lateral shift in the supratentorial compartment with stretching of the oculomotor nerve against
the clivus or
Primary brainstem lesions
In transtentorial herniation, after initial dilation and loss of light reactivity, pupils become somewhat
reduced in size (4 to 5 mm) and remain unreactive; they are called midposition and fixed
In severe sedative drug overdose or in hypothermia, the pupils are midposition and fixed; this
syndrome can mimic brain death.
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Eye movements
Large cerebral lesions produce a persistent conjugate deviation of the eyes toward the side of the
lesion (contralateral to limb paralysis if present)
Lateral and downward eye deviation (usually with pupillary involvement) suggests oculomotor
involvement of the nerve or midbrain nuclei, while medial deviation suggests sixth nerve palsy
In the comatose patient, bilateral conjugate roving eye movements that appear full indicate an intact
brainstem and further reflex testing is not required. This is also a relatively favorable prognostic sign
when seen early after hypoxic ischemic insult
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Vestibuloocular reflexes
In the oculocephalic maneuver (or doll's eyes), the head is abruptly rotated from one side to the other in the
horizontal plane
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When the oculocephalic reflex is present (positive doll's eyes), the eyes do not turn with the head, but in
the opposite direction, as if the patient is maintaining visual fixation on a single point in space
Caloric testing of the oculovestibular reflex
At least 50 mL of ice water is injected into the ear canal using a syringe with a small catheter attached. This stimulus has
the same effect on the horizontal semicircular canal as sustained turning of the head in the opposite direction, and
results in sustained deviation of both eyes toward the ear being stimulated
Five minutes should elapse before testing the other side
With brainstem lesions, both VORs are often absent or abnormal
Profound toxic or metabolic pathology can also disrupt the VORs

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Corneal reflex
The corneal reflex's afferent limb arises from small unmyelinated pain fibers in the cornea, the fifth
or trigeminal nerve and nucleus, and activates the dorsal parts of both facial nuclei in the pons
The reflex can be suppressed acutely contralateral to a large, acute cerebral lesion, and also with
intrinsic brainstem lesions
Loss of the corneal reflex is also an index of the depth of metabolic or toxic coma
Absent corneal reflexes 24 hours after cardiac arrest is usually, but not invariably, an indication of
poor prognosis
Corneal reflexes may also be reduced or absent at baseline in elderly or diabetic patients
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Herniation syndromes
Transtentorial herniation can occur with expanding mass lesions (eg, intracerebral, subdural, or
epidural hemorrhage, large ischemic stroke, abscess, tumor, obstructive hydrocephalus)
Horizontal shifts of midline structures greater than 8 mm are associated with some impairment of
consciousness; patients with shifts of >11 mm are usually comatose
Two variants are recognized: a central herniation and an uncal herniation syndrome
Other signs of increased intracranial pressure (ICP), papilledema, and Cushing's triad
(hypertension, bradycardia, irregular respiration) may be observed in this setting.
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Brainstem lesions
Infarction or hemorrhage of the upper pons and/or midbrain

Osmotic demyelination syndrome (formerly called central pontine myelinolysis) and
brainstem encephalitis are other causes
May manifest with flaccid quadriparesis or decerebrate posturing
Eye movements may be notably asymmetric or absent and pupils are classically
small
hyperthermia
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Metabolic coma
Symmetrical nature of the neurologic deficits

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Exceptions occur; in particular, hypo- and hyperglycemia are frequently associated with lateralized motor
findings
Fluctuations in the examination are common.
Tremor, asterixis, and multifocal myoclonus, strongly suggest metabolic coma.

Muscle tone is usually decreased; decerebrate posturing is less common in metabolic coma, but
may occur.
Pupils may appear abnormal but almost always are symmetric and constrict with light.
Suppression of VORs and corneal reflex occur with very deep metabolic coma
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CONDITIONS MISTAKEN FOR COMA
Persistent vegetative state
Brain death
Locked-in syndrome
The locked-in syndrome is a consequence of a focal injury to the base of the pons, usually by embolic occlusion of the
basilar artery
Consciousness is preserved; however, the patient cannot move muscles in the limbs, trunk, or face, except that
voluntary blinking and vertical eye movements remain intact
May sometimes be mimicked by a severe upper spinal cord lesion, a motor neuropathy, myopathy, neuromuscular
junction disease, or extreme muscular rigidity
Akinetic mutism, psychogenic unresponsiveness, dementia
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Represent a subgroup of patients who suffer severe anoxic brain injury and progress to a state of wakefulness
without awareness
A vegetative state may represent a transition between coma and recovery or between coma and death
No evidence of awareness of self or environment and an inability to interact with others

No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory,
tactile, or noxious stimuli
No evidence of language comprehension or expression
Intermittent wakefulness manifested by the presence of sleep-wake cycles
Sufficiently preserved hypothalamic and brainstem autonomic function to permit survival with medical and
nursing care
Bowel and bladder incontinence
Variably preserved cranial nerve reflexes and spinal reflexes
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If a patient remains comatose, the usual outcome is to recovery, PVS, or death within two weeks
On the basis of available clinical data, PVS is judged to be permanent after three months if induced
nontraumatically
For traumatic brain injury, a year in this state is generally required to be considered permanent
The distinction between PVS and the minimally conscious state can be difficult
In patients who continue in PVS, life expectancy is approximately two to five years, and most patients die from
infection of the lungs or urinary tract, multiorgan system failure, sudden death of unknown cause, respiratory
failure, or underlying disease.
It is estimated that there are 10,000 to 25,000 adult patients in PVS in the United States, generating an
estimated annual cost of care of up to seven billion dollars.
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DIAGNOSIS
The goal of diagnostic testing in a patient in coma is to identify treatable conditions (infection,
metabolic abnormalities, seizures, intoxications/overdose, surgical lesions)
Early treatment in concert with the clinical evaluation
The presence of papilledema or focal neurologic deficits suggesting a structural etiology mandate
an urgent head computed tomography (CT) scan, particularly if the clinical presentation suggests
an acute stroke, expanding mass lesion, and/or herniation syndrome.
Fever suggesting bacterial meningitis or viral encephalitis mandates an urgent lumbar puncture.
Neuroimaging prior to lumbar puncture in a comatose patient is recommended
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DIAGNOSIS - Laboratory tests
Complete blood count

Serum electrolytes, calcium, magnesium, phosphate, glucose, urea, creatinine,
liver function tests, lactate, and osmolarity
Arterial blood gas
Prothrombin and partial thromboplastin time
Drug screen (usually done on urine and serum), including ethyl alcohol,
acetaminophen, opiates, benzodiazepines, barbiturates, salicylates, cocaine,
amphetamines, ethylene glycol, and methanol
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DIAGNOSIS supplementary laboratory tests
Adrenal and thyroid function tests

Blood cultures
Blood smear: screen for thrombotic thrombocytopenic purpura (fragmented erythrocytes, elevated
serum lactate dehydrogenase) or disseminated intravascular coagulation (DIC) (D-dimer and
fibrinogen determination); consider antiphospholipid determination if a coagulation problem is
suspected
Carboxyhemoglobin if carbon monoxide poisoning is suggested (patient found in a burning building
or in a stationary automobile)
Serum drug concentrations for specific drugs
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DIAGNOSIS - Neuroimaging
CT is the test of choice for initial evaluation
subarachnoid hemorrhage (95 percent in early presentation), other intracranial hemorrhage (essentially
100 percent), acute hydrocephalus, tumors, marked cerebral edema, and large ischemic strokes
CT angiography particularly when brainstem stroke is suspected
MRI
herpes simplex encephalitis, early ischemic strokes (especially involving the brainstem), multiple small
hemorrhages or white matter tract disruption associated with traumatic diffuse axonal injury, anoxicischemic damage from cardiac arrest, and most disorders affecting the white matter
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DIAGNOSIS - Lumbar puncture
Urgent evaluation of a patient with suspected infection of the CNS
Neuroimaging to exclude an intracranial mass lesion is required prior to lumbar puncture (LP) in
order to avoid precipitating transtentorial herniation
Coagulation test are needed
Empiric antimicrobial treatment may impair the diagnostic sensitivity of CSF

cultures but should not affect other tests (WBC, gram stain, PCR).
Blood cultures should be obtained prior to antibiotic intervention
CSF is also useful to exclude subarachnoid hemorrhage or carcinomatosis

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DIAGNOSIS - Electroencephalography
In the comatose patient, EEG is used primarily to detect seizures or if the cause of coma remains
obscure after other testing
Diffusely disorganized, slowed background rhythms confirm an impression of toxic metabolic
encephalopathy, while strongly lateralized findings suggest structural disease
In some patients with coma, 8 to 12 Hz activity is seen; this resembles normal alpha rhythm, but
extends beyond the posterior cerebral regions and does not react to stimuli
This so-called "alpha coma" is associated with pontine lesions, and has also been described with hypoxic
ischemic encephalopathy following cardiac arrest, traumatic brain injury, and drug overdose
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ANCILLARY TESTING
Somatosensory evoked potentials
SSEPs are the averaged electrical responses in the central nervous system to somatosensory
stimulation
SSEPs are the best validated and most reliable of the ancillary tests currently available for clinical
use.
Other evoked potentials (brainstem, auditory, visual, middle latency, and event-related) have not
been adequately evaluated
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ADVANCED NEUROMONITORING
Jugular venous oximetry:
Retrograde cannulation of the internal jugular vein that allows measurement of oxygen
saturation in the blood exiting the brain.
Normal jugular venous oxygen saturation (SjVO2) is about 60 percent.
SjVO2 <50 percent for 10 minutes is considered an "ischemic desaturation" and is associated
with impaired CPP and worsened outcome
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Brain tissue oxygen tension (PbtO2) monitoring:
Intraparenchymal oxygen electrode placed in a manner similar to a fiberoptic ICP probe that
measures PbtO2 in the white matter.
Normal PbtO2 is >20 mmHg;
Duration and depth of PbtO2 below 15 mmHg is associated with worsened outcome
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Cerebral microdialysis:
Intraparenchymal probe placed in a manner similar to a PbtO2 probe that allows measurement
of extracellular glucose, lactate, pyruvate, glutamate.
A lactate:pyruvate ratio >40 is suggestive of anaerobic metabolism, which is believed to
exacerbate secondary brain injury
Thermal diffusion flowmetry: intraparenchymal probe placed in a manner similar to a PbtO2

probe that allows continuous measurement of CBF, usually in the white matter
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Prognosis after a cardiac arrest
44 percent of patients receiving CPR survived initially,

30 percent were alive at 24 hours, 13 percent at one month, and only 6 percent were alive after six
months.
The duration of CPR significantly correlated with outcome; no patient who required more than 15
minutes of CPR survived more than six weeks
Age >70, stroke or renal failure prior to admission, fever within the first 48 hours, and recent
congestive heart failure were associated with a poor prognosis
Witnessed arrest and an initial rhythm of ventricular fibrillation (VF) or tachycardia have correlated
with a better prognosis
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ABCs (airway, breathing, and circulation)
Prevention of hypoxia (PaO2 <60 mmHg) and hypotension (systolic BP <90 mmHg) are
priorities in the management of patients with severe TBI
Normal saline to maintain euvolemia (Grade 1B)
Glasgow Coma Scale score
INITIAL MANAGEMENT
Patients with a GCS of 8 or less usually require endotracheal intubation to protect the airway
A set of arterial blood gases, along with the other blood and urine tests
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INITIAL MANAGEMENT
Treat hypotension (mean arterial BP of <70 mmHg) with volume expanders or vasopressors or
both.
With severe hypertension (mean arterial BP of >130 mmHg) repeated doses of intravenous
labetalol (5 to 20 mg boluses as needed) are often adequate for initial stabilization.
A 12-lead electrocardiogram should be done
It is recommended to give 25 g of dextrose (as 50 mL of a 50 percent dextrose solution) while
waiting for the blood tests, if the cause of coma is unknown
Thiamine, 100 mg, should be given with or preceding the glucose in any patient who may be
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Naloxone (0.4 to 2.0 mg IV) and flumazenil treatment should be used only in the setting of known or
strongly suspected drug overdose
Gastric lavage and activated charcoal are also often recommended for suspected toxic or drug
ingestions
If a herniation syndrome is evident clinically or appears imminent based on computed tomography
(CT) findings, urgent treatment is recommended.
INITIAL MANAGEMENT
Mannitol (1 g/kg IV) and hyperventilation
If the patient has had a seizure, treatment with phenytoin (15-20 mg/kg phenytoin equivalent IV)
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MANAGEMENT
antipyretics and/or cooling blankets should be administered immediately
Empiric antibiotic and antiviral therapy are recommended if bacterial meningitis (eg, ceftriaxone 2 g
IV every 12 hours and vancomycin 2 g/day IV in four divided doses) or viral encephalitis (acyclovir
10 mg/kg IV every eight hours) are among the suspected entities
2007-2013
Hyperthermia (T>38.5 degrees C) can contribute to brain damage in cases of ischemia

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These should be continued until these conditions have been excluded
Since hypothermia has neuroprotective effects in patients with cardiac arrest, only extreme
hypothermia (<33C) should be treated
Therapeutic hypothermia treatment should be limited to patients with elevated ICP refractory to
other therapies
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Initial ICP treatment
Head of bed elevation to 30 degrees

Optimization of venous drainage: keeping the neck in neutral position, loosening neck braces if too
tight
Monitoring central venous pressure and avoiding excessive hypervolemia
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ICP treatment
Most guidelines and clinical protocols recommend that treatment for elevated ICP should be
initiated when ICP rises above 20 mmHg
Ventricular drainage is generally attempted first. CSF should be removed at a rate of approximately
1 to 2mL/minute,for two to three minutes at a time, with intervals of two to three minutes in
between until a satisfactory ICP has been achieved (ICP <20 mmHg) or until CSF is no longer
easily obtained
Slow removal can also be accomplished by passive gravitational drainage through the
ventriculostomy
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Other targeted interventions in elevated ICP
Osmotic therapy
Hyperventilation
Sedation: barbiturates,propofol,fentanyl, benzodiazepines, andmorphine
In refractory cases:
barbiturate coma,
induced hypothermia,
decompressive craniectomy
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Osmotic therapy
Mannitol is administered in boluses of 0.25 to 1g/kgevery four to six hours as needed
Hypertonic saline is being used increasingly in this setting, (3 to 23.4%) and either as a bolus or infusion
Hyperventilation
control of ventilation helps prevent increases in intrathoracic pressure that may elevate central venous
pressures and impair cerebral venous drainage
hyperventilation-induced vasoconstriction may cause
secondary ischemia and may thereby worsen outcomes
increase extracellular lactate and glutamate levels that may contribute to secondary brain injury
guidelines recommend avoiding hyperventilation, especially in the acute phase (the first 24 to 48 hours)
following TBI
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MANAGEMENT
Adequate nutritional support,
Reducing the potential for nosocomial infection,
Providing adequate prophylaxis against venous thromboembolism and gastric

stress ulceration
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RECOMMENDATIONS for patients with severe traumatic brain injury (TBI)
Normal saline to maintain euvolemia (Grade 1B)
Glycemic control: a broad target range of up to 140mg/dLor possibly even 180mg/dL
Thromboprophylaxis for the prevention of venous thromboembolism (Grade 1A)
using intermittent pneumatic compression stockings in TBI
Coagulopathy should be corrected to maintain an INR < 1.4 and a platelet count >75,000/mm3
NOT using glucocorticoids for the management of patients with severe TBI (Grade 1A)
Short-term (one week) use of antiepileptic drugs (phenytoin,valproate) for the prevention of early
seizures (Grade 1B)
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Epidural hematoma
SURGICAL TREATMENTin TBI patients
larger than 30 mL
urgent surgical evacuation is recommended for patients with acute EDH and coma (GCS score 8) who
have pupillary abnormalities (anisocoria)
Subdural hematoma
Acute subdural hematomas (SDH) >10 mm in thickness or associated with midline shift >5 mm on CT
If the GCS score is 8 or if the GCS score has decreased by 2 points from the time of injury
The patient presents with asymmetric or fixed and dilated pupils,and/orintracranial pressure
measurements are consistently >20 mmHg
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Intracerebral hemorrhage
when there is evidence of significant mass effect
if the hemorrhage exceeds 50 cm3in volume, or
if the GCS score is 6 to 8 in a patient with a frontal or temporal hemorrhage greater than 20
cm3with midline shift of at least 5 mmand/orcisternal compression on CT scan
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Penetrating injury
Depressed skull fracture
Decompressive craniectomy
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REFERENCES
1.
2.
3.
4.
G Bryan Young. Stupor and coma in adults. UpToDate May 2015

J Claude Hemphill, III, Nicholas Phan. Management of acute severe traumatic brain injury. UpToDate sep
2015
Edward R Smith, Sepideh Amin-Hanjan. Evaluation and management of elevated intracranial pressure in
adults. UpToDate Jul 2013
Gerald L Weinhouse, G Bryan Young. Hypoxic-ischemic brain injury: Evaluation and prognosis. UpToDate
Aug 2013
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COMA evaluation and treatment

DEZVOLTAREA COMPETENELOR N TRANSPLANT

ACADEMIA DE TIINE MEDICALE

Bucureti, b-dul IC Brtianu nr.1, sector 3

Fondul Social European

An alteration in arousal represents an acute, life threatening emergency, requiring prompt

Coma is defined as "unarousable unresponsiveness"

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Bucureti, b-dul IC Brtianu nr.1, sector 3

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ETIOLOGIES AND PATHOPHYSIOLOGY

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Bucureti, b-dul IC Brtianu nr.1, sector 3

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Hypoxic-ischemic brain injury

Therapeutic hypothermia in traumatic brain injury need to be validated

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ACADEMIA DE TIINE MEDICALE

Bucureti, b-dul IC Brtianu nr.1, sector 3

Fondul Social European

Intracranial mass lesions (eg, tumor, hematoma)

ACADEMIA DE TIINE MEDICALE

Bucureti, b-dul IC Brtianu nr.1, sector 3

Fondul Social European

Beneficiar: Academia de Stiinte Medicale

Intracranial pressure (ICP)

Intracranial compartment (fixed internal volume of 1400 to 1700 mL):

Brain parenchyma 80 percent, Cerebrospinal fluid 10 percent, Blood 10 percent

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CBF = (CAP - JVP) CVR

CPP = MAP ICP

The recommended CPP target is 60 mmHg, avoiding

Fondul Social European

CLINICAL MANIFESTATIONS of elevated ICP

Bradycardia, respiratory depression, and hypertension (Cushing's triad)

Focal symptoms of elevated ICP

local effects in patients with mass lesions or by herniation syndromes

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Indications for ICP monitoring

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What was the time course of the loss of consciousness?

Did focal signs or symptoms precede the loss of consciousness?

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What recent illness has the patient had?

Has there been altered behavior or function recently?

A fever suggests infection;

What prescription or nonprescription drugs are used?

Are there medical or psychiatric conditions?

Is there history of alcohol or drug abuse?

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