Coma and Related Disorders of

Consciousness
Dr. Enrique De La Mora Glasker
coma
 Reduced alertness and responsiveness
represents a continuum that in severest form
, a deep sleeplike state from which the
patient cannot be aroused.
Stupor
 Lesser degrees of unarousability in which
the patient can be awakened only by
vigorous stimuli, accompanied by motor
behavior that leads to avoidance of
uncomfortable or aggravating stimuli.
Drowsiness
 which is familiar to all persons, simulates
light sleep and is characterized by easy
arousal and the persistence of alertness for
brief periods.
Drowsiness and stupor

 are usually attended by some degree of

confusion.
vegetative state
 signifies an awake but unresponsive state.
Most of these patients were earlier
comatose and after a period of days or
weeks emerge to an unresponsive state in
which their eyelids are open, giving the
appearance of wakefulness.
vegetative state
 Yawning, grunting, swallowing, limb and
head movements persist, but there are few,
if any, meaningful responses to the external
and internal environment-in essence, an
"awake coma.“
 respiratory and autonomic functions are
retained
vegetative state
most common causes

 Cardiac arrest

 head injuries
Akinetic mutism
 Partially or fully awake patient who is able to
form impressions and think but remains immobile
and mute, particularly when unstimulated.
 Causes: damage in the regions of the medial
thalamic nuclei, the frontal lobes (particularly
situated deeply or on the orbitofrontal surfaces), or
from hydrocephalus.
Abulia
 Mental and physical slowness and lack of
impulse to activity that is in essence a mild
form of akinetic mutism.
 with the same anatomic origins.
Catatonia
 Hypomobile and mute syndrome associated with a
major psychosis.
 patients appear awake with eyes open but make no
voluntary or responsive movements, although they
blink spontaneously, swallow, and may not appear
distressed.
 Eyes are half-open as if the patient is in a fog or
light sleep.
 NO clinical evidence of brain damage.
Locked-in state
 describes a pseudocoma in which an awake
patient has no means of producing speech
or volitional limb, face, and pharyngeal
movements in order to indicate that he or
she is awake, but vertical eye movements
and lid elevation remain unimpaired, thus
allowing the patient to signal. Such
individuals have written entire treatises
using Morse code
Locked-in state
 Infarction or hemorrhage of the ventral
pons, which transects all descending
corticospinal and corticobulbar pathways, is
the usual cause
Anatomy and Physiology of
Unconsciousness
 Cerebral cortex

 neurons located in the upper brainstem

and medial thalamus

 RAS, maintains the cerebral cortex in a

state of wakeful consciousness.
Anatomy and Physiology of
Unconsciousness
 principal causes of coma

 (1) lesions of the RAS
 (2) destruction of large portions of both
cerebral hemispheres
 (3) suppression of thalamocerebral
function by drugs, toxins,
 metabolic causes: hypoglycemia,
anoxia, azotemia, or hepatic failure.
Anatomy and Physiology of
Unconsciousness
 Pupillary enlargement, loss of vertical and
adduction movements of the globes suggest upper
brainstem damage.
 lesions in one or both cerebral hemispheres do not
affect RAS, a large mass on one side of the brain
may cause coma by secondarily compressing the
upper brainstem and abnormalities of the pupils
and eye movements .
Anatomy and Physiology of
Unconsciousness
 Mass effect: most typical of
cerebral hemorrhages and of
rapidly expanding tumors within a
cerebral hemisphere. In all cases
the degree of diminished alertness
also relates to the rapidity of
evolution and the extent of
compression of the RAS.
 RAS and the thalamic and cortical areas
utilize a variety of neurotransmittors.
Acetylcholine,biogenic amines Cholinergic
fibers connect the midbrain to other areas
of the upper brainstem, thalamus, and
cortex.
 Serotonin and norepinephrine regulation of
the sleep-wake cycle.
 Alerting effects of amphetamines are likely
to be mediated by catecholamine release.
Herniation
 transfalcial (displacement of the
cingulate gyrus under the falx and
across the midline),
 transtentorial (displacement of the
medial temporal lobe into the tentorial
opening),
 foraminal (downward forcing of the
cerebellar tonsils into the foramen
magnum.
Epileptic Coma

 metabolic derangements in some way alter

neuronal electrophysiologic function,
epilepsy is the only primary excitatory
disturbance of brain electrical activity that
is encountered in clinical practice.
Pharmacologic Coma

 Can be reversible and leaves no residual

damage.
 Many drugs and toxins are capable of
depressing nervous system function.
Approach to the Patient

 The diagnosis and management of coma depend on

knowledge of its main causes.
 interpretation of clinical signs, brainstem
reflexes and motor function.
 Acute respiratory and cardiovascular
problems
 complete medical evaluation, vital signs,
funduscopy, and examination for nuchal
rigidity, (complete neurologic evaluation
for know the severity and nature of coma.
History

 trauma, cardiac arrest, or known drug

ingestion.
 (1) Circumstances and rapidity with which
neurologic symptoms developed
 (2) confusion, weakness, headache,
fever, seizures, dizziness, double vision,
or vomiting
 (3) use of medications, illicit drugs, or
alcohol
 (4) chronic liver, kidney, lung, heart,
History

 Direct interrogation or telephone

calls to family and observers on
the scene are an important part of
the initial evaluation. Ambulance
technicians often provide the most
useful information in an enigmatic
case.
General Physical
Examination
 temperature, pulse, respiratory rate and pattern,
Tachypnea may indicate acidosis or pneumonia
blood pressure.
 Fever suggests a systemic infection, bacterial
meningitis, or encephalitis; only rarely is it
attributable to a brain lesion that has disturbed
temperature-regulating centers.
General Physical
Examination

 High body temperature, 42 to 44°C,

associated with dry skin should arouse the
suspicion of heat stroke or anticholinergic
drug intoxication.
 Hypothermia itself causes coma only when
the temperature is <31°C.
General Physical
Examination
 Alcoholic, barbiturate, sedative, or
phenothiazine intoxication
 Hypoglycemia, peripheral circulatory
failure, or hypothyroidism,etc.

General Physical
Examination
 Funduscopic examination is
invaluable in detecting
subarachnoid hemorrhage
(subhyaloid hemorrhages),
hypertensive encephalopathy
(exudates, hemorrhages, vessel-
crossing changes, papilledema),
and increased intracranial pressure
(papilledema).
Neurologic Assessment

 Observation first without examiner

intervention.
 Patients who toss about, reach up toward
the face, cross their legs, yawn, swallow,
cough, or moan are close to being awake.
Lack of restless movements on one side or
an outturned leg at rest suggests a
hemiplegia.
 Neurologic Assessment
Multifocal myoclonus almost always
indicates a metabolic disorder
.
 In a drowsy and confused patient
bilateral asterixis is a certain sign
of metabolic encephalopathy or
drug ingestion.
Neurologic Assessment
 Decorticate rigidity and decerebrate
rigidity, or "posturing," describe
stereotyped arm and leg movements
occurring spontaneously or elicited by
sensory stimulation.
Brainstem Reflexes

 pupillary responses to light,spontaneous and

elicited eye movements, corneal responses,

 Respiratory pattern
A.- PUPILLARY LIGHT RESPONSES:
 
      Simmetrically reactive round pupils: Exclude
midbrain
damage.
(2 to 5 mm )

      Enlarged pupil (>5 mm),

unreactive or poorly reactive: Intrinsic
midbrain lesion
(ipsilateral) or
by mass
effect
(contralateral).
 Unilateral pupillary enlargement:
Ipsilaterall
mass.
  
 Oval and slightly eccentric pupils: Early midbrain
third nerve
compression.
  
 Bilaterally dilated and unreactive Severe midbrain
damage by
transtentorial

 pupils: herniation or
anticholinergic
drugs toxicity.
      Reactive bilaterally small but not pin-
point (1 to 2.5 mm): Metabolic
encephalopathy,
deep bilateral
hemispheral

lesions as
hydrocephalus or
thalamic
hemorrhage
 

      Very small but reactive pupil Narcotic or barbiturate

overdose or bilateral
(Less than 1 mm): pontin damage.
 

 
Ocular Movements

 Eye movements are the second sign of

importance in determining if the brainstem
has been damaged.
 EYE MOVEMENTS
  
       Adducted eye at rest: Lateral rectus paresis due to VI nerve
 lesion. If is bilateral is
due to intracraneal hypertension.

 Abducted eye at rest, plus ipsi Medial rectus paresis due to III nerve
 lateral pupilary enlargement : dysfunction.
  

 Vertical separation of the ocular Pontin or cerebellar lesion

Globes. (Skew deviation) :
  
 Coma and spontanous conjugate Midbrain and pons intact
horizontal roving movements :
  
 “Ocular bobbing”. Brisk downward
    and slow upward movement of the

globes with loss of horizontal eye

   movements : Bilateral pontine
damage
 
   “Ocular dipping”. Slower, arrhytmic
downward followed by a faster upward
movement with normal reflex horizontal
gaze : Anoxic
damage to the cerebral
cortex.

   Thalamic and upper midbrain lesions: Eyes turned down

and inward.
F.- RESPIRATION PATTERNS.

  
  
       Shallow, slow, well-timed regular Suggest metabolic or drug depression.
 Breathing:
  
       Rapid, deep (Kussmaul) breathing: Metabolic acidosis or
ponto- mesencephalic lesions.
  
       Cheyne-Stokes breathing, with light Mild bihemispherical damage
or
Coma: metabolic supression.
 

      Agonal gasps: Bilateral lower brainstem damage.

Terminal respiratory pattern.
Laboratory Studies and
Imaging

 chemical-toxicologic analysis of blood and

urine,

 cranial CT or MRI, EEG,

 Lumbar puncture and CSF examination
(cultures)
Laboratory Studies and
Imaging

 Arterial blood-gas analysis is helpful in

patients with lung disease and acid-base
disorders.

 Toxicologic analysis
 Brain Death

 Neurological examination
 EEG
 Radionuclide brain scanning, cerebral
angiography, or transcranial Doppler
measurements may also be used to
demonstrate the absence of cerebral blood
flow
TREATMENT FOR THE
PATIENT IN COMA.
 1.- The treatment must be instituted
inmediately even when there is no a certain
diagnosis.
 The inmediate goal is the prevention of
further nervous system damage.
 2.- Diagnostic procedures and general
treatment mus be performed simultaneously
and to install the specific treatment when the
etiology is known.
TREATMENT FOR THE
PATIENT IN COMA.
 A.- Permeable airway. Oxygen supply through
nasal fossae to endotraqueal intubation..
 B.- Politrauma patient’s evaluation. Stabilize the neck
and the rest of the vertebral colum.
 C.- Establish an intravenous access. Water
administration carefully monitored.
 D.- Maintain the body temperature the closest to the
normal values as possible.
TREATMENT FOR THE
PATIENT IN COMA.
 E.- I.V. administration of 50 ml of 50%
glucose.
 F.- Administrate thiamine in malnourished and
alcoholic patients. 10 mg I.V. and 100 mg
 I.M. /day /3 days.
 G.- Naloxone (0.4 to 0.8 mg) or flumazenil
(0.5 to 1 mg) I.V administration
 H.- Appropriate treatment of intracraneal
hypertension and seizures.
TREATMENT FOR THE
PATIENT IN COMA.
 I.- General measures for the unmovable patient.
       Appropriate nutrition and hydration.
       Posture changes every two hours.
       Mobilization of joints.
       Ocular metilcelulose drops, 1 every 4 hours.
       I.V. ranitidine 50 mg every 8 hours, or 300 mg in
250 ml of 5% dextrose in 24 hours; or sucralfate 1 g
per nasogatric tube every 6 hours.
       S.C. Heparin, 5000 U every 12 hours.
       Urinary tract care.
 J.- Etiologic treatment.