Neurologic Critical Care

Based on Eelco WJ Widjdicks

General Principles of Recognition of Critically Ill

Neurologic Patients in the Emergency Department
• Acute neurologic manifestations are a consequence of:
- major trauma
- acute stroke
- emerging infection
- Intoxication
Patients may also come to the hospital as an urgent referral or
even as a walk-in.
In these circumstances, acutely unfolding neurologic signs are
obvious, yet difficult to interpret, and physicians feeling
“uncomfortable” with such a progressive neurologic picture
have a low threshold for sending patients to the ED.

Notes: Acute neurologic disease is bound to get worse. In some it is

critical and unquestionably life- threatening.
Acute neurologic conditions can be seen everywhere in the hospital,
this lecture will tru to introduce the emergency department (ED) and
NICU with all its complexities, as seen from a neurologist’s
perspective.
A major reason for the ED admission of patients with a critical
neurologic manifestation lies in the fact that the ED may provide
immediate advanced care and triage. But in other situations, patients
with a not yet known neurologic emergency may present with
nonspecific symptoms, such as weak- ness, twitching, agitation,
dizziness, or headaches, or they may be simply not reacting and
staring into space. All these symptoms carry a broad dif- ferential
diagnosis and therefore are a serious test to any physician in any
field.
THE NEUROLOGIC EMERGENCY AND ITS
ASSESSMENT
• Neurologic emergency is defined by certain clinical
manifestations, abnormality on neuroimaging, and, most
important, by a progression of symptoms.
• Neurologic symptoms often fluctuate, and an improvement
in symptoms may not necessarily mean that the patient is
improving
Notes: A neurologic consultation is often triggered by the presence of
any obvious localizing sign or abnormal responsiveness. In most
instances, the presentation is dramatic, attracts attention, and requires
specialty care. The condition of some patients worsens rap- idly, and
in these cases an acute neurosurgical intervention is necessary.
Notes: There are plenty of potential errors to consider (Table 1.3), and
emergency physicians are often subject to blame and critique.
Some have cat- egorically and unfairly characterized the ED as a “natural
laboratory for the study of error.”
The best-case scenario is that of a specialist in the
neurosciences seeing any acute neurologic or neurosurgical
emergency and handling it competently together with the
attending ED physician.
Criteria of Triage
• Ideally, the main priority for physicians with a patient with
acute neurologic disease is to quickly triage to the
neurosciences intensive care unit (NICU).
• In many medical institutions without a specialized ICU,
patients are admitted to a general ICU or, depending on the
cause of injury and neurosurgical involvement, to a trauma
or surgical ICU.
• Criteria for NICU admission should be flexible.
• Criteria can be developed to assist in the initial assessment
of NICU eligibility.
• These criteria can involve signs and symptoms or
specifically refer to major neurologic or neurosurgical
disorders.
Neurologic critical care focuses on
1. preservation of neurologic tissue
2. prevention of secondary brain injury caused by ischemia,
hemorrhage, edema, herniation, and elevated intracranial
pressure (ICP)

Four neurologic tests

1. computed tomography (CT) scanning
2. magnetic resonance imaging (MRI)
3. cerebrospinal fluid (CSF) examination
4. Electroencephalography (EEG)
-should be immediately available and may narrow the
diagnostic evaluation substantially.
None of these studies can replace a neurologic examination
Neurologic Critical Care
Based on Eelco WJ Widjdicks
COMATOSE
The assessment of comatose patients permeates the practice of all physicians.
Finding the cause of coma requires a specific neurologic assessment and
considerable deductive effort.
The priorities in the evaluation of comatose patients have changed
considerably with the arrival of neuroimaging, possibly leading to the
misconception that the cause of coma usually is easily established with
computed tomography (CT) scan or magnetic resonance imaging (MRI).
Relying solely on these tests can be counterproductive and, in some instances,
potentially dangerous.
Failure to recognize diabetic coma, thyroid storm, acute hypopituitarism,
fulminant hepatic necrosis, or any type of poisoning while spending valuable
time performing neuroimaging tests may poten- tially result in a rapidly
developing medical fiasco.
The evaluation of comatose patients is best approached
systematically
• five major categories
(1) unilateral hemispheric mass lesions that compress or
displace the diencephalon and brainstem
(2) bilateral hemispheric lesions that damage or compress the
reticular formation in the thalamus, interrupting the
projecting fibers of the thalamocortical circuitry
(3) lesions in the posterior fossa that damage or compress the
reticular formation in the brainstem
(4) diffuse brain lesions affecting the physiologic processes of
the brain
(5) less commonly, psychiatric unresponsiveness, mimicking
coma
EXAMINATION OF A COMATOSE PATIENT
• Physical examination that sorts out specific and localizing
neurologic findings remains of great importance and is
necessary in trying to get to the nature of coma.
• Equally important is a reliable history.
• One needs to know the onset of coma.
• Acute onset in a previously healthy person points to
aneurysmal subarachnoid hemorrhage (SAH), a
generalized tonic-clonic seizure, traumatic brain injury,
self-induced drug poisoning, or an environmental injury.
• Gradual worsening in responsiveness to stupor may
indicate an evolving intracranial mass, a diffuse infiltrative
neoplasm, or inflammatory neurologic disorder.
Notes: Relatives, bystanders, and police may all provide important
information, but personal belongings, medical alert cards, and bracelets can
provide invaluable clues.
However, the patient’s history, particularly of those “wheeled in,” is always
unclear and fragmentary, and there is often little or no documentary evidence,
leaving physi- cians to work with snippets culled from existing medical
records.
General appearance:
• Extremely poor hygiene or anorexia may indicate alcohol
or drug abuse.
• A foul breath in most instances means poor dental and
periodontal hygiene or alcohol consumption.
• classic types of foul breath should be known, but not many
physicians are alerted by it
- “dirty rest- room” (uremia)
- “fruity sweat” (ketoacidosis)
- “musty or fishy” (acute hepatic failure
- “onion” (paraldehyde)
- “garlic” (organophosphates, insecticides, thallium)
Vital Signs
• Fever and particularly hyperthermia (> 40°C) in
comatose patients may indicate a fulminant infection,
endocarditis with multiple emboli, or a central nervous
system (CNS) infection,
• High fever may be part of a hyperthermia syndrome such
as serotonin syndrome or neuroleptic malignant
 Neurologic Critical Care
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syndrome, but both are suggested by the additional

presence of rigidity or severe myoclonus
• Hypothermia (≤ 35°C) indicates exposure to a cold
environmental temperature, marked hypothyroidism,
Addison’s disease, hypoglycemia, or intoxication.
• In patients with a devastating traumatic brain and spine
injury, it may be a systemic sign of brain death or acute
spinal cord transection.

Notes: but can occur in massive pontine hemorrhage, aneurysmal SAH, and
traumatic brain injury. It may originate from direct compression, ischemia, or
contu- sion of the hypothalamus.

• Hypertension is a common clinical feature in coma

associated with acute structural CNS lesions and therefore
has little predictive value.
• Hypotension may indicate that coma is a result of severe
sepsis or a sign of a rapidly developing meningococcal
meningitis.
• Hypotension may also be due to loss of vascular tone, when
all brain function is lost or as a consequence of acute spinal
cord injury

The skin should be touched at different areas to assess its

texture; both dry skin and skin drenched in sweat may point to
certain intoxications (Table 12.2). Dry skin in a comatose
patient (particularly in typically moist areas such as the

NEUROLOGIC FEATURES OF CLINICAL

Skin:
• Bullous skin lesions (“coma blisters”)
- can be seen at pressure points
- very uncommon at other sites
- suggesting skin necrosis from ischemia rather than a
specific cutaneous toxicity.
- expected in patients found down after someone was
checking up.
• Acute appearance of blisters may indicate:
- Barbiturate
- Amitriptyline
- theophylline intoxication
• In a patient with a long-bone fracture:
- rapidly developing pulmonary edema, acute
unresponsiveness, and petechiae in the axilla strongly
indicate fat emboli.
• Skin rash in a comatose patient may indicate a
rapidly evolving encephalitis or fulminant
meningococcal meningitis
• Intravenous illicit drug use should be considered
when appropriate, and the skin should be carefully
inspected for needle marks in multiple sites outside
the cubital fossa.
• Significant periorbital ecchymosis (“raccoon eyes”)
and retroauricular ecchymosis (Battle sign) indicate
midface or skull base fractures
EXAMINATION
• The depth of the coma should be documented
• The depth of coma should be documented.
• It should reflect the astuteness of a clinical neurologist to first evaluate
whether the patient truly is comatose, in a locked-in syndrome, or even
malin- gering.
• Every physician should appreciate that a major lesion in the brainstem
may not necessarily cause coma but rather a so-called locked-in syn-
drome. In locked-in syndrome, an acute struc- tural lesion in the pons
(which spares pathways to oculomotor nuclei of the mesencephalon and
reticular formation) causes a nearly uncommuni- cative state. Patients
often have eyes partly open but cannot move their limbs or grimace.
Before pain stimuli are applied, the patient should be asked to blink and
look up and down. (Grim accounts have been published of failure to
appre- ciate this entity.4) Psychogenic unresponsiveness is often
considered but is rare and requires a skill not only to think about it in
the first place but also before ordering a battery of tests.
OBTUNDATION
- Mild to moderate reduction in alertness
- Slower psychologic responses to stimulation
- Increased number of hours to sleep
- Obtundation, from the Latin ‘‘to beat against or blunt,’’ literally means
mental blunting or torpidity. In a medical setting, such patientshave
a mild to moderate reduction in alertness, accompanied by a lesser
interest in the environment. Such patients have slower psychologic
responses to stimulation. They may have an ncreased number of hours
of sleep and may bedrowsy between sleep bou
STUPOR
- condition of deep sleep or similar behavioral
unresponsiveness
- the subject can be aroused only with vigorous and
continuous stimulation
 Neurologic Critical Care
Based on Eelco WJ Widjdicks

- Stupor, from the Latin ‘‘to be stunned,’’ is a condition of deep sleep or - GCS 8– 12 stupor
similar behavioral unresponsiveness from which the subject can
- GCS 13–15 drowsiness
be aroused only with vigorous and continuous stimulation. Even when
maximally aroused, the level of cognitive function may be impaired.
Such patients can be differentiated from those with psychiatric impairment, FOUR Score
such as catatonia or severe depression, because they can be -Full Outline of
aroused by vigorous stimulation to respond to simple stimuli
Unresponsiveness (FOUR)
COMA score
- - a state of unresponsiveness in which the patient lies with - four components are :
eyes closed and cannot be aroused to respond appropriately 1. eye responses (eye
to stimuli even with vigorous stimulation opening and eye
- movements)
Coma, from the Greek ‘‘deep sleep or trance,’’ is a state of
unresponsiveness in which the patient lies with eyes closed and cannot be 2. motor responses
aroused to respond appropriately to stimuli even with vigorous stimulation. (following complex
The patient may grimace in response to painful stimuli and limbs commands and
may demonstrate stereotyped withdrawal responses, but the patient does not
make localizing responses or discrete defensivemovements.
response to pain
As coma deepens, the responsiveness of the patient, even to painful stimuli, stimuli)
may diminish or disappear. However, it is difficult to equate the 3. brainstem reflexes
lack of motor responses tothe depth ofthe coma,as the neural structures that (pupil, corneal, and
regulate motor responses differ from those that regulate consciousness, and
they may be differentially impaired by specific brain disorders
cough reflexes)
4. respiration
(spontaneous
respiratory rhythm or
presence of respiratory drive after intubation)

We have devised and extensively tested the Full Outline of

Unresponsiveness (FOUR) score,
The FOUR score has four testable compo- nents.
The FOUR score can be obtained in a few minutes.
The FOUR score not only measures eye opening but also
makes an assessment of voluntary horizontal and vertical eye
movements.
It therefore detects a locked-in syndrome in a patient with a
o A neurologic examination often initially starts with an
GCS score of 3.
assessment of the patient’s response to voice, a prod, or a
It may detect the presence of a vegetative state, in which the
squeeze.
eyes can be spontaneously open but do not track the
o An ideal noxious stimulus in the assessment of comatose
examiner’s finger.
patients must respect the patient and not be associated with
significant bruising. Proper stimuli are :
-sternal rubbing
-rubbing the knuckles against the ribs in the axilla,
-pressure on the supraorbital nerve.
o Deep pressure with a blunt object against the nail bed has
become standard
o deep pressure on both condyles at the level of the
temporomandibular joint can be

Deep pressure with a blunt object against the nail bed has
become standard but may cause subungual hematoma in
anticoagulated patients or those with an underlying
coagulopathy.

Coma scales are used to

grade the depth of coma.
• Glassgow Coma
Scale
-The individual
components of the GCS • motor category includes the presence of myoclonus
have been graded, most status epilepticus, a known poor prognostic sign after
often summed to a score cardiac resuscitation
between 3 and 15 • The motor component combines decorticate (abnormal
-the summed scores flexor response) and withdrawal responses, because this
represent only a crude difference is often difficult to appreciate
estimate of the depth of • Abnormal extensor response (decerebrate posturing)
coma involves adduction and internal rotation of the shoulder
- GCS 3–8 and pronation of the hand
represents coma
For localization of a pain response, one arm should cross the midline toward
the stimulated arm or reach above the shoulder toward the stim- ulus applied
 Neurologic Critical Care
Based on Eelco WJ Widjdicks
to the supraorbital nerve. The hand position tests (thumbs-up, fist, and peace
sign) can further assess alertness. To ask the patient to squeeze a hand may be
less valuable because reflex grasping may exis
• Three brainstem reflexes to test mesencephalon, pons,
and medulla oblongata functions are used in different
combinations.
• The three important pupil assessments in the FOUR
score remain unaffected by any degree of sedation.
Breathing Patterns are graded
• The FOUR score, unlike the GCS, does not include a
verbal response
• It is more valuable in ED or intensive care unit (ICU)
practices that typically have a large number of intubated
patients, and it may be useful in young children.
• Using the FOUR score when confronted with a patient who
has impaired consciousness, the examiner is forced to
describe essential, clinical features.
• Changes in the FOUR score are meaningful and imply a
deterioration or substantial improvement, unlike the GCS.
• When all categories are graded 0, the examiner is alerted to
consider a brain death examination.
• Neck stiffness can be assessed but becomes less apparent in
patients with deeper stages of coma (e.g., no eye opening to
pain and abnormal motor responses.).
• Muscle tone can be:
- flaccid (normal in coma but may indicate intoxication with
benzodiazepine or tricyclic antidepressant poisoning)
- rigid (e.g., neuroleptic agents, etomidate, strychnine,
malignant catatonia, or malignant hyperthermia
• Abnormal movements such as twitching in the eyelids (may
indicate seizures), myoclonus (anoxic–ischemic
encephalopathy, lithium intoxication, penicillin intoxication,
pesticides) asterixis (acute renal, liver, or pulmonary failure),
and shivering (sepsis, hypothermia) should be noted and
integrated into the interpretation of the examination.
Cranial Nerves
• The size of the pupils and whether they are equal, round,
oval, or irregular should be noted.
• It is important to understand the meaning of a :
1. unilateral dilated, fixed pupil (traction of the third nerve by
brainstem displacement)
2. bilateral fixed, mid-position pupils (may indicate
intoxication with scopolamine, atropine, or methyl alcohol,
or a mesencephalic lesion)
3. pinpoint pupils (frequently designate narcotic overdose or an
acute pontine lesion)
4. Anisocoria (mid position and pinpoint pupil) often indicates
a new brain- stem lesion affecting both mesencephalon and
pons.
Pupillary Reactions
• Identify if abnormal pupillary response in coma is
due to structural, pharma or metabolic.
• Metabolic encephalopathy= cause small , Reactive
pupils
• Pupillary light response = one of the most resistant
brain responses during metabolic encephalopathy,
impaired reflex = usually due to structural
• Hence if a coma patient presents with oculomotor
paralysis/midbrain depression but intact light reflex,
then the cause of coma is still likely a concurrent
metabolic disturbance
• Seizures = one/both may transiently (15-20min-
hour), react poorly , large
• Hypoxia /global ischemia = pupils large and fixed
(combination of systemic catecholamine release from
hypoxia and lack of response from the metabolically
depleted brain)
• Opiates = pinpoint pupils
Ppillary llight reflex: very resistant to metabolic except
applied drugs, sedation, usually structural causes
o Unilateral dilated pupil: third-nerve palsy from acute
intracranial mass, brainstem contusion, or, rarely,
pituitary apoplex
o Oval pupil (often transitory appearance of pupils
signaling increased intracranial pressure).
o Mydriasis (anxiety, delirium, pain, seizures, botulism,
atropine, aerosolized albuterol, amyl nitrite, magnesium
excess, norepinephrine, dopamine, aminoglycoside, and
tetracycline overdose).
o Pupils fixed in mid position (typical in end-stage
brainstem displacement syndromes and brain death).
 Neurologic Critical Care
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o Horner’s syndrome (traumatic carotid dis- section,
brachial plexopathy, trauma from internal jugular vein
catheter placement, major thoracic surgery).
o Miosis (acute pontine lesion, opioids, organophosphate
toxicity).
• Funduscopy
- may reveal new diagnostic findings in comatose patients
but rarely so.
- Subhyaloid hemorrhage is seldom seen in coma, but when
present implies aneurysmal SAH or shaken- baby
syndrome.
- Papilledema indicates acutely increased intracranial
pressure but also is present in some patients with acute
asphyxia and in patients with extreme hypertension (mean
arterial pressures over 150 mm Hg).
-
• Absence of spontaneous eye movement should be
documented
• lateral deviation to either side or dysconjugate gaze at rest.
• Forced gaze deviation indicates a large hemi- spheric lesion
at targeted gaze site.
• Spontaneous eye movements—periodic alternating gaze,
ocular dipping, and retractory nystagmus—may be seen in
coma but have no localization value other than indicating
diffuse brain injury.
• The oculocephalic responses are evaluated with brisk
horizontal head turning, and, if appropriate, the response to
vertical head movements can be tested.
• Oculovestibular responses are tested by irrigating each
external auditory canal with 50 mL of ice water, with the
head 30 degrees above the horizontal plane (an intact
tympanum needs to be confirmed).
• Bilateral testing can be done by rapidly squirting 50 mL of
ice water in each ear, resulting in a forced downward eye
movement. Abduction of only the eye on the side being
irrigated, with adduction paralysis of the opposite eye,
implies a brainstem lesion (internuclear ophthalmoplegia) as
a cause of coma.
(In patients with any suspicion of head or spine injury, the oculocephalic
responses should obviously not be tested because movement may luxate the
cervical spine if fractured and immedi- ately cause spinal cord trauma.)
Comatose patients exhibit tonic responses with conjugate deviation toward the
ear irrigated with cold water.
• corneal responses are tested by drawing a cotton wisp fully
across the cornea or by squirting saline.
• Spontaneous coughing or coughing after tracheal
suctioning is recorded (to-and- fro movement of the
endotracheal tube is not an adequate stimulus).
• Absence of coughing may indicate either that the
neurologic catastrophe has evolved into brain death or that
sedative or anesthetic drugs or neuromuscular blocking
agents for emergency intubation have markedly muted the
cough reflex.
Neurologic Critical Care
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• Coma or impaired consciousness in localized medulla

oblongata lesions therefore is only an indirect
consequence of hypercapnia or hypotension-induced
global hemispheric injury.
• These lesions do not involve the ARAS structures
and thus, by themselves, do not produce coma or
hypersomnia.

• These medullary structural lesions may involve

hemorrhages (often arteriovenous malformation or
cavernous hemangioma), metas- tasis, lateral or medially
located medullary infarct, or an inflammatory lesion such
as a bacterial or fungal abscess.

MAJOR CAUSES AND CATEGORIES OF COMA • Mesencephalic damage is seldom seen in isolation and
more commonly occurs from the extension of a lesion in
To develop the skills necessary to diagnose the cause of coma, the thalamus (e.g., destructive intracranial hematoma) or
some basic understanding of the anatomical changes that may as a result of occlusion of the tip of the basilar artery,
accompany coma and their consequences is required. producing simultaneous infarcts in both thalami and in
the mesencephalic tegmentum.
• ASCENDNG RETICULAR ACTIVATING •
SYSTEM (ARAS)
- boundary in the vertical axis is the lower pons
- Destructive lesions below this level may lead to acute
dysfunction of autonomic nuclei, resulting in failure
to drive respiration or vascular tone.
- Structural lesions are often acute (hemorrhage,
infarct, abscess) or may be a critical extension of an
infiltrating tumor, abscess, or giant mass.
- Structural injury to the brain results in coma if it
closely follows or directly affects the relay nuclei and
connecting fibers that make up the ascending
reticular activating system (ARAS).
- Its connections with the thalamus and both cortices
make for a complex network
-

PIHEMISPHERIC INJURY
 Neurologic Critical Care
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• may involve the white matter or cortex or both, and a

diversity of disorders may produce damage severe enough
to reduce arousal.
• The most notable disorders are anoxic–ischemic
encephalopathy from cardiac standstill that destroys most
of the cortical lamIna
False localizing signs occur in two contexts:
MAJOR CAUSES OF COMA- STRUCTURAL
As a consequence of raised ICP, which is symptomatic of
(BILATERAL)
intracranial pathology (tumor, hematoma, abscess)
or idiopathic (idiopathic intracranial hypertension
• Penetrating traumatic brain injury
[IIH]) and with spinal cord lesions. Associated lesions
• Multiple traumatic brain contusions
may be intra- or extraparenchymal. The course of the
• Anoxic-ischemic encephalopathy
associated disease may be acute (cerebral hemorrhage)
• Aneurysmal subarachnoid hemorrhage
or chronic (IIH, tumor)
• Multiple cerebral infarcts
Herniation sites7: 1. Subfalcine/Cingulate; 2. Central
• Bilateral thalamic infarcts
transtentorial; 3. Lateral transtentorial (Uncal); 4. Tonsillar; 5.
• Cerebral venous thrombosis
Transcalvarial
• Lymphoma
• Encephalitis
MAJOR CAUSES OF COMA- STRUCTURAL
• Gliomatosis
(UNILATERAL, BRAINSTEM)
• Acute disseminated encephalomyelitis
• Cerebral edema
Hemisphere Unilateral (with displacement)
• Multiple brain metastases
• Intraparenchymal hematoma
• Acute hydrocephalus
• Middle cerebral artery occlusion
• Acute leukoencephalopathy
• Hemorrhagic contusion
• Cerebral abscess
ACUTE UNILATERAL OR CEREBELLAS MASS
• Brain tumor
• Two major clinical manifestations may be observed
Brainstem
in patients with an acute hemispheric mass:
• Pontine hemorrhage
1. direct destruction of brain tissue, leading to clinical
• Basilar artery occlusion
features related to the involved lobe
• Central pontine myelinolysis
2. remote effects from the displacement of essentially
• Brainstem hemorrhagic contusion
normal tissue.
• The quintessential neuropathologic findings
Cerebellum (with displacement of brainstem)
associated with brain displacement are
• Cerebellar infarct
(1) displacement of the falx,
• Cerebellar hematoma
(2) central brainstem displacement (displacement of the
• Cerebellar abscess
diencephalon structures, such as the thalamus) lateral
• Cerebellar glioma
brain- stem displacement
(3) up- or downward dis- placement of brain tissue of the
POISONING OR DRUG ABUSE
posterior fossa.
• distribution of different causes may reflect the
Herniation Sites
geographic location of the hospital.
• The most common substances used for self-inflicted
death by poisoning are tricyclic anti- depressants,
salicylates (particularly children), and street drugs.
• In the elderly, suicide attempts and unintentional
intoxication through misjudgment of dose remain the
leading causes.

ALCOHOL INTOXICATION and RELATED DISORDERS

• Symptoms of alcohol intoxication are the result of

depressant action of alcohol on the cerebral and spinal
neurons
• Narrow margin in causing respiratory depression
• PATHOLOGIC INTOXICATION
- Rare occasions: alcohol has exclusively excitatory rather
than sedative effect
- Outburst of blind fury with assaultive and destructive
behavior
- Attack terminates with deep sleep occurs spontaneously or
in response to parenteral sedation
- On awakening the patient has no memory of the episode
- Differentiate from: temporal lobe seziures

Tx: use of restraints

Diazepam 5 to 10 mg
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Haloperidol 2 to 5 mg
Repeated once after 30 to 40 mins

• ALCOHOLIC BLACKOUTS
-interval of time during a period of severe intoxication for
which the patient later has no memory- even though the
state of consciousness as observed by others was not
grossly altered during that interval
-short retentive memory rather than immediate or long
term memory is impaired (transient global amnesia
-there is degree of intoxication that interferes with the
registration of events and formation of memories during
the period of intoxication

TREATMENT of SEVERE ALCOHOL INTOXICATION

- Coma caused by alcohol intoxication is a medical
emdergency
- Prevent aspiration and respiratory depression
- Use of HD if patient is comatose with extremely high
BAC > 500 mg/dl + acidosis and in those who
ingested methanol or ethylene glycol
ACUTE METABOLIC OR ENDOCRINE COMA
• Acute metabolic derangements may produce reduced
arousal and, when unrecognized, coma.
• Typical examples are :
Hypoglycemia
hyponatremia
acute uremia
acute liver failure
• Overt hemiparesis, pupil abnormalities, and gaze
preference are conspicuously absent on neurologic
examination
• asterixis, tremor, and myoclonus predominate before
deep coma sets in.
• Hyperglycemic non-ketotic hyperosmolar coma is a
notable exception.
• Focal signs may occur in this condition because of
previous strokes in these patients with severe
cerebrovascular risk factors.
2. CSF STUDIES
• Normal findings on neuroimaging, with no clinical
evidence of an acute cerebellar infarction or acute
basilar artery occlusion, should prompt immediate
examination of the CSF to search for possible CNS
infection.
• Failure to exclude a potentially treatable CNS
infection may have devastating consequences.
3. ECG
-can be useful, and results are nearly always abnormal if
intoxication is due to pheno- thiazines, quinidine,
procainamide, or tricyclic antidepressants
4. Abdominal radiographs
-can be helpful in establishing whether the patient has
ingested any tablets or foreign objects.
-Examples of radiopaque pills are chloral hydrate,
trifluoperazine, amitriptyline, and enteric-coated tablets;
however, many tablets may have dissolved before the
patient is admitted to the ED.
• When poisoning is strongly considered as a cause of
coma, laboratory tests are essential before time-
consuming toxicologic screening is performed.
• most poisons and illicit drugs do not cause significant
laboratory derangements.

NEUROIMAGING AND LABORATORY TEST

1. NEUROIMAING – CT SCAN/ MRI

Computed tomography scanning of the brain is particularly
useful when the neurologic examination reveals localizing
symptoms.
Acute lesions in the brainstem and cerebellum may not be
visualized on CT. CLINCHING THE CAUSE OF COMA
Neurologic Critical Care
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• With this armamentarium of knowledge, labo ratory
availability, and timely neuroimaging, a plan of
action can be constructed.
• The followIng steps might be useful:
(1) Categorize clinical findings (bihemispheric injury,
lateral brainstem displacement, central brainstem
displacement, and intrinsic brainstem injury);
(2) study the interpretation of neuroimaging and,
depending on findings of neuroimaging (diffuse
injury, mass, hydrocephalus, or even normal
findings), a more specific differential diagnosis
follows.
MANAGEMENT
First hour:
1. improve oxygenation (face mask with 10-liter oxygen
flow aiming at a pulse oximeter of more than 95%).
2. intubate if patient cannot protect airway (increased
work of breathing, pooling secretions, gurgling
sounds).
-Intubate any comatose patient with irregular ineffective
breathing drive and poor oxygenation, or consider emergency
tracheostomy in any comatose patient with major facial injury.
3. correct hypotension by placing patient in Trendelenburg
add crystalloids (rapid infusion of 500 cc normal saline
followed by 100 cc/ hour)
if no response, start vasopressors (use phenylephrine boluses
of 100 microgram until central catheter is placed).
Correct extreme hypertension (systolic above 250 mm Hg or
MAP above 130 mm Hg) with intravenous labetalol 20 mg IV,
hydralazine 20 mg IV, or nicardipine 5 mg IV.
4. correct hypothermia with warming blankets.
- consider induced hypothermia (33–34°C) treatment
in patients who have been successfully resuscitated
for cardiac arrest (patients who had ventricular
fibrillation or other shockable rhythms).5
- Correct hyperthermia with cooling blankets,
icepacks, and ice water lavage.
5. Correct major metabolic derangements.
No harm is done if a patient with a high likelihood of
hypoglycemia is given 50 mL/50% glucose solution even
before the blood sugar is known and is co-administered 100
mg thiamine IV. T
Treatment of severe hyponatremia involves hypertonic saline
(3% hypertonic saline, 0.5 mg per kilogram hourly) or a
vaptan.
Treatment of hypercalcemia is by saline rehydration infusion,
followed by par- enteral bisphosphonate pamidronate.
6. consider administering naloxone (0.4 to 2 mg every 3
minutes IV) if opioid intoxication is suspected, and consider
administering flumazenil (slow IV administration at 0.2 mg
per minute up to 1 mg) to reverse any benzodiazepine toxicity.
7. Seventh, consider elimination of the toxin by hemodialysis
or hemoperfusion.
• The next phase of management will be disease
specific.
• The first priorities when faced with a patient
presenting with an acute structural cause of coma can
be summarized in three steps
1. an attempt should be made to reduce presumed
increased intracranial pressure (ICP).
- Mass effect and clinical signs of brain- stem injury
(abnormal corneal, pupil, or oculocephalic reflexes)
should prompt immediate administration of osmotic
agents.
- Mannitol is best suited to the ED.
- Hypertonic saline is likely a better osmotic drug, but
it requires placement of a central venous catheter
first, and valuable time may be lost by placing this
catheter first.
- Hyperventilation is a useful simple additional
measure in intubated comatose patients, and through
this method PaCO2 can be lowered quickly to target
levels (PaCO2 of 25– 30 mm Hg)
2. consider evacuation of the mass.
-The early evacuation of a mass (e.g., traumatic subdural,
epidural, or lobar hematoma or contusion) is a definite early
option and requires immediate assessment by a neurosurgeon.
When performed within 6–12 hours of onset, the clinical
improvement following evacuation of such a mass is often
impressive.
3. consider decompressive craniectomy.
Diffusely swollen brain may compress the deeper diencephalic
structures or may move these tructures downward.
Pressure relief can rarely be accomplished with osmotic
agents, and removal of a large bone flap (or flaps) is the only
remaining option to salvage the patient with diffuse cerebral
edema.
Neurologic Critical Care
Based on Eelco WJ Widjdicks

• HYPOGLYCEMIA
-50 mL of a 50% glucose solution in a suspected
hypoglycemic
- immediate awakening during infusion is highly
indicative of severe hypoglycemia.
- Failure to awaken after hypoglycemia, however, may
indicate that hypoglycemia has been lengthy and has
caused significant brain damage, leading to
prolonged or no recovery.
• HYPONATREMIA
-hypertonic saline and furosemide (3% hyper- tonic saline, 0.5
mL/kg hourly) with frequent serum sodium surveillance.
-Overcorrection (> 150 mmol/L) and rapid correction (within
12 hours) have been linked to the development of central
pontine myelinolysis.

• Hypercalcemia
- saline rehydration infusion (3–4 L), followed by the
parenteral bisphosphonate pamidronate (infused at 60 mg over
24 hours).
• Inducing emesis in a patient who is stuporous from
poisoning may be a mistake because of the significant
danger of aspiration.
• Gastric lavage, which is possible if a comatose
patient is protected by endotracheal intubation,
should be done if the suspicion of a massive overdose
is great.
• Specific antidotes if indicated
• Elimination of the toxin can also be enhanced by
hemodialysis and hemoperfusion, and many drugs
and toxins can be cleared (the most common are
acetaminophen, amitriptyline, lithium, and
salicylates) using these methods.

Summary

• Neurologic examination followed by categorization

in bihemispheric, brainstem displacement or intrinsic
brainstem injury may be helpful in the focused
assessment and evaluation of coma.
• Early stabilizing of the comatose patient may include
intubation for airway protection, correction of
hypotension and hypovolemia, and correction of
acute metabolic derangements.
• Early recognition of increased ICP from mass effect
or acute hydrocephalus is essential, and early medical
and surgical intervention may reduce morbidity.
• Intoxications are common causes of coma in the ED,
and drug screens are mandatory, followed by specific
antidotes if indicated.

• The clinical history may have provided important

clues for a CNS infection.
• When CSF is suspicious for an infection, full
antibiotic coverage with cefotaxime (2 g every 6
hours), vancomycin (20 mg/kg IV every 12 hours
[goal trough level at 15–20 mcg/mL]), and ampicillin
(2 g IV every 4 hours), in combination with antiviral
coverage (acyclovir 10 mg/kg every 8 hours) is
needed until final results become available.
• A screening CT scan is preferable when a patient
with a suspicion of bacterial meningitis presents in
coma and, in particular, when CT can be obtained in
a matter of minutes.

MANAGEMENT OF ACUTE METABOLIC

DERANGEMENTS and INTOXICATION