2. Consciousness
• It is defined as a state of awareness of
one’s self and of one’s environment , as
well as a state of responsiveness to that
environment or adaptation to the external
milieu.
4. CLASSIFICATION OF ALTERED LEVELS OF
CONSCIOUSNESS
1. Confusional States
2. Delirium
3. Obtundation
4. Stupor
5. Coma
5. 1. CONFUSIONAL STATES
People who do not respond quickly with information about
their name, location, and the time are considered
"confused". A confused person may be bewildered,
disoriented, and have difficulty following instructions. The
person may have slow thinking and possible memory loss.
This could be caused by sleep deprivation, malnutrition,
allergies, environmental pollution, drugs (prescription and
nonprescription), and infection.
6. DELIRIUM: person may be restless or agitated and
exhibit a marked deficit in attention.
OBTUNDATION: a person has a decreased interest in
their surroundings, slowed responses, and sleepiness.
STUPOR: only respond by grimacing or drawing away
from painful stimuli.
7. COMA
• State in which a patient is totally unaware of both self and
external surroundings, and unable to respond
meaningfully to external stimuli touch, pain,light etc. Do
not have sleep-wake cycles.
• Coma usually lasts a few days to a few weeks. After this
time, some patients gradually come out of the coma,
some progress to a vegetative state, and some die
8. PERSISTENT VEGETATIVE STATE
• Can result from diffuse injury to the cerebral
hemispheres of the brain without damage to the
cerebellum and brainstem .
• Opens eyes spontaneously
• Does not follow commands
• No intentional movements
• Demonstrate sleep -wake cycle
9. LOCKED IN SYNDROME
Patient is listening to you
• Caused by damage to specific portions of the
lower brain and brainstem with no damage to the
upper brain. Eye opening is well sustained
• Basic cognitive abilities are evident on
examination
• Mode of communication is eye movements or
clinking of the upper eyelid
10. AKINETIC MUTISM
• Patients are immobile and usually lie with their
eyes closed.
• Sleep wake cycles exists.
• There is little or no vocalization.
• Motor response to noxious stimuli is absent or
minimal
• Command following or verbalization can be
elicited but occur infrequently
19. PATHOPHYSIOLOGY -UNCONSCIOUSNESS
Conscious state depends on intact cerebral
hemisphere and RAS
Exposure to etiological causes
diffusely affects the cerebral hemisphere and RAS
Impairment of consciousness
20. Probing consciousness with event-
related potentials in the vegetative
state.
• Faugeras F, Rohaut B, Weiss N, Bekinschtein
TA, Galanaud D, Puybasset L, Bolgert F, Sergent
C, Cohen L, Dehaene S, Naccache L.
• Source
• AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Department
of Neurophysiology, Paris, France.
21. .
Abstract
OBJECTIVE:
• Probing consciousness in noncommunicating patients is a
major medical and neuroscientific challenge. While
standardized and expert behavioral assessment
of patients constitutes a mandatory step, this clinical
evaluation stage is often difficult and doubtful, and calls
for complementary measures which may overcome its
inherent limitations. Several functional brain imaging
methods are currently being developed within this
perspective, including fMRI and cognitive event-
related potentials (ERPs). We recently designed an
original rule extraction ERP test that is positive only in
subjects who are conscious of the long-term regularity of
auditory stimuli.
22. METHODS:
• In the present work, we report the results of this test in a
population of 22 patients who met clinical criteria for
vegetative state.
RESULTS:
• We identified 2 patients showing this neural signature of
consciousness. Interestingly, these 2 patients showed
unequivocal clinical signs of consciousness within the 3 to
4 days following ERP recording.
CONCLUSIONS:
• Taken together, these results strengthen the relevance of
bedside neurophysiological tools to improve diagnosis of
consciousness in noncommunicating patients.
31. MOUTH
• Look for alcohol smell or poisons smell.
• Smell of ketones -Diabetic coma
• Uriniferous odour-Uremic coma
• Musty smell-Hepatic coma
• See for tooth's missing to prevent aspiration
33. CVS
• Rate and rhythm of pulse
• Rapid or slow rate may be associated with the
cerebral hypo perfusion
• Examination of the heart by auscultation
• Absent peripheral pulse-peripheral vascular
disease
37. ABDOMEN
• Assessment of abdominal girth is very
important -Since distended will impair
respiration.
• Tenderness and guarding – trauma or
rupture of abdominal viscera.
• Enlargement of liver- hepatitis
40. EXTREMITY
• Assess for tone ,muscle size in both side
• Assess for any contracture
• Asymmetric limb response ( hemi/ mono
paresis) – Focal brain damage,
e.g. Tumour ,trauma, hematoma,
• Symmetric limb response, suggest
metabolic encephalopathy and drug
toxicity.
46. SYMPTOMATIC TREATMENT
• Wernicke’s encephalopathy :thiamine100 mg IV
as an initial dose followed by 50 to 100 mg/day
IM or IV until the patient is on a regular, balanced,
diet.
• Opioid Drug overdose :Naloxone 0.4 to 2
mg/dose IV/IM/subcutaneously. May repeat every
2 to 3 minutes as needed.
48. SURGICAL MANAGEMENT
• Hematomas – Surgical evacuation
•Hemorrhage ,tumor, cerebral
abscess-Surgical decompression/
Partial or total resection
•Cerebral aneurysm - surgically
clipping or endovascular coiling
49.
50. • Risk for aspiration R/T unconscious
state
• Keep NPO until risk assessment is complete
• Do not feed if airway protection or swallowing is
compromised
• Position to facilitate oral drainage
• Follow precautions to prevent enteral feed aspiration
51. • Ineffective airway clearance R/T
unconsciousness
• Lateral or semi prone position
• Frequent position change
• Suctioning
• Elevating head end
• Chest auscultation
• Maintain patency of ET tube or TT
• Chest physiotherapy and postural drainage
• Ventilator settings
52. Risk for injury R/T unconsciousness
Check dressings and casts for constriction.
To protect the patient from self-injury and dislodging of
tubes, use padded side rails or wrap the patient’s hands
in mitts
Prevent injury from invasive lines and equipment
Careful suctioning
53. Ensure that oxygenation is adequate
Ensure that the bladder is not distended.
Enclosed or floor-level specialty beds may be indicated.
Protect the patient from hypothermia and hyperthermia.
Lubricate the skin with oil or emollient lotion to prevent
irritation due to rubbing against the sheet.
Minimize environmental stimuli
54. Risk for hyperthermia R/T brain damage
• Monitor the body temperature
• Environmental temperature control
• Prescribed antipyretic
• Cold sponge
• Hyperthermia blanket
• Prevent shivering
55. Risk for hypothermia R/T brain damage
Assess body temperature frequently
Provide a warm environment through use of heat shield,
space blanket, heat lights, or blankets.
Work quickly when any wounds exposed.
56. • Altered nutrition less than body requirement
R/T unconsciousness
Assess the Hydration status by examining tissue turgor
and mucous membranes, assessing intake and output
trends, and analysing laboratory data.
Meet the fluid needs initially by giving the required fluids
intravenously. However, intravenous solutions (and blood
transfusions) for patients with intracranial conditions must
be administered slowly
57. If the patient does not recover quickly and
sufficiently enough to take adequate fluids and
calories by mouth, a feeding tube will be inserted
for the administration of fluids and enteral
feedings
60. • Self care deficit R/T immobility and
unconsciousness
• Provide basic hygiene care
• Dress and groom patient
• Provide nutrition
• Provide for elimination needs of patient
61. • Impaired skin integrity R/T immobility and
nutritional deficit
• Assess the skin specially on bony
prominences for any color and temperature
change
• Position change
• Avoid dragging
• Correct body positioning
• Use comfort devices
• Trochanter role
• Air mattress
• Back care
62. • Sensory / perceptual alterations R/T
unconsciousness
• Communicate with patient
• Orienting patient
• Involve family members
63. • Altered family process related to
disease state
• Clarify doubts
• Involve in patient care
• Encourage ventilation of feelings
• Supporting in decision making
• Support groups
70. CONCLUSION
• An unconscious patient fully depends on us for his
recovery as such it is our responsibility to always think
critically before intervening.
• The more the knowledge we have the greater the
difference we can make to life of unconscious patients.
Consciousness describes the set of neural processes that allow an individual to perceive ,comprehend ,and act on internal and extrnal stimuli..consciouness can b only descriptively approached nt directly observed.
There are many different causes of unconsciousness.
The causes of unconsciousness may dictate the length of the coma and the prognosis .
Unconsciousness occurs when the RAS is damaged or inhibited, thus affecting the normal arousal mechanism (Pemberton 2000).
Intrinsic factors that affect the nervous system directly can be seen as primary causes. secondary causes most often involve other body systems compromising metabolic and endocrine homeostasis. Unconsciousness may be sudden, for example, following an acute head injury, or it may be gradual, for example, with the onset of poisoning or a deranged metabolism, as in hypoxia or hypoglycaemia.
It is also important to remember that unconsciousness may be induced, for example, the use of anaesthetics for surgical or medical intervention. Another example of this is in critical care units, such as intensive care, where an anaesthetist will intervene and induce unconsciousness pharmacologically to allow for emergency intervention to stop a decline in a patient’s condition.
Total paralysis below the level of nucleus of cranial nerve 3 with the ability to open eyes and follow commands with the eyes.No other motor movement is possible.this syndromre is often result of b/l ventral pontine lesions or b/l destruction of medulla oblongata.
Consciousness is a function of the reticular formation (RF), which has its origins in the brainstem .
The RF is a network of neurones that connect with the spinal cord, cerebellum, thalamus and hypothalamus.
All sensory pathways link into the RF .
The reticular activating system (RAS) is a feature of the RF and is responsible for arousal from sleep and maintaining consciousness .
The RAS has a large number of projections that are linked to the cerebral cortex (Pemberton 2000) and are concerned with the arousal of the brain during sleep and wakefulness .
Awareness is the result of the combined activity of the RF, RAS and higher cortical function. The two main identified parts of the RAS are the mesencephalon (upper pons and mid-brain) and the thalamus. Signals from specific parts of the thalamus initiate activity in specific parts of the cerebral cortex, as opposed to the diffuse flow of impulses from the mesencephalon that causes generalised cerebral activity (Pemberton 2000). This process of selection prevents the cerebral cortex from receiving too much information at once, thus possibly playing a part in directing an individual’s attention to specific mental activities.
Altered LOC is not a disorder itself; rather, it is a function and symptom of multiple pathophysiologic phenomena. The cause may be neurologic (head injury, stroke), toxicologic (drug overdose,alcohol intoxication), or metabolic (hepatic or renal failure, diabetic ketoacidosis)
A disruption in the basic functional units (neurons) or neurotransmitters
faulty impulse transmission, impeding communication within the brain or from the brain to other parts of the body
Clinical features, complications
Intact anatomic structures of the brain are needed for proper function. The two hemispheres of the cerebrum must communicate,via an intact corpus callosum, and the lobes of the brain (frontal, parietal, temporal, and occipital) must communicate and coordinate their specific functions
Impairments of consciousness indicates dysfunction of ARAS .Regardless of etiology ,the common pathophysiology for all impairments in arousability is either a reduction in the cerebral metabolism or a reduction in cerebral blood flow.
The GCS forms a quick, objective and easily interpreted mode of neurological assessment, avoiding subjective terminology, such as ‘stupor’ and ‘semi-coma’. As it is the internationally agreed common language in neurological assessment, it is essential that it is completed accurately, and that any uncertainties are reported immediately (Hickey 2003b). The GCS meas\ures the degree of consciousness under three distinct categories, and each category is further subdivided and given a scoreSource: redOrbit (http://s.tt/13Se7)
The oculocephalic test evaluates extraocular muscle movements (controlled by CNs III and VI). The examiner moves the patient’s head from side to side forcefully and quickly; in an abnormal response (an ominous sign), the eyes remain stationary. This exam is contraindicated in patients with suspected cervical spinal cord injury.The vestibulo-ocular reflex (VOR) is a reflex eye movement that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field. For example, when the head moves to the right, the eyes move to the left, and vice versa. Since slight head movement is present all the time, the VOR is very important for stabilizing vision: patients whose VOR is impaired find it difficult to read using print, because they cannot stabilize the eyes during small head tremors. The VOR does not depend on visual input and works even in total darkness or when the eyes are closed. However, in the presence of light, the fixation reflex is also added to the movement.
For instance, if the head is turned clockwise as seen from above, then excitatory impulses are sent from the semicircular canal on the right side via the vestibular nerve (cranial nerve VIII) through Scarpa's ganglion and end in the right vestibular nuclei in the brainstem. From this nuclei excitatory fibers cross to the left abducens nucleus. There they project and stimulate the lateral rectus of the left eye via the abducens nerve. In addition, by the medial longitudinal fasciculus andoculomotor nuclei, they activate the medial rectus muscles on the right eye. As a result, both eyes will turn counterclockwise.
Furthermore, some neurons from the right vestibular nucleus directly stimulate the right medial rectus motoneurons, and inhibits the right abducens nucleus.
In comatose patients, once it has been determined that the cervical spine is intact, a test of the vestibulo-ocular reflex can be performed by turning the head to one side. If the brainstem is intact, the eyes will move conjugately away from the direction of turning (as if still looking at the examiner rather than fixed straight ahead). This is how a doll's eyes would move. So having "doll's eyes" is a sign that a comatose patient's brainstem is still intact.
Pupil evaluation includes assessment of pupil size, shape, and equality before and after exposure to light. Normally, pupils are equal in size and about 2 to 6 mm in diameter, but they may be as large as 9 mm. Also, the pupils may be pinpoint, small, large, or dilated. Normal pupil shape is round; variations include irregular, keyhole, and ovoid. (See Visualizing a keyhole pupil.)
To assess the patient’s pupils, hold both eyelids open and shine a light into the eyes. The pupils should constrict immediately and equally bilaterally; after you remove the light, they should immediately dilate back to baseline. Document the response: Is it brisk, sluggish, nonreactive, or fixed? Immediately report any changes from baseline. In many cases, a change in pupillary response, such as unequal or dilated pupils, results from a progressive neurologic condition.
Fixed and dilated pupils are an ominous sign that warrant immediate physician notification (unless the patient’s pupils have just been dilated chemically). For true changes in pupillary response, expect the physician to order further diagnostic tests, such as a CT scan.
Assess the patient’s neurologic function frequently. Keep him in a supine position to decrease pressure on dural tears and to minimize CSF leakage. Avoid nasogastric intubation and nasopharyngeal suction, which may cause cerebral infection. Also, caution the patient against blowing his nose, which may worsen a dural tear.
The patient may need skull X-rays and a CT scan to help confirm a basilar skull fracture and to evaluate the severity of the head injury. Typically, a basilar skull fracture and associated dural tears heal spontaneously within several days to weeks. However, if the patient has a large dural tear, a craniotomy may be necessary to repair the tear with a graft patch. If the injury was due to abuse, notify the appropriate authority in the facility.
Patient teaching
Explain all procedures and tests. Inform the patient with a basilar skull fracture that he’ll require bed rest for several days to weeks. Explain the need to avoid placing pressure on the brain tissue, and advise him on proper positioning. Also tell him to refrain from blowing his nose.
If the injury was due to an accidental fall, advise the patient’s family to assess the household for safety hazards and remove precipitating factors such as throw rugs
As with any patient, give top priority to assessing the ABCs—airway, breathing, and circulation. Ask yourself: Is the airway patent? If so, is the patient able to maintain it?
Next, check vital signs: Are her respirations adequate? Are her vital signs stable? Is her blood pressure high enough to perfuse the brain and other vital organs? Be aware that current or progressive injury to the brain and brain stem may make vital signs unstable, but this situation can be complex: Although unstable vital signs can reduce neurologic response, brain injury itself may cause unstable vital signs.
To appropriately assess the patient’s peak neurologic status, be sure to evaluate oxygenation and circulation. Ideally, you should conduct the neuro exam when the patient’s blood pressure, temperature, heart rate, and heart rhythm are normal. Be aware that a temporary decline in neurologic status caused by insufficient oxygenation or circulation still represents a neurologic change—and leads to permanent neurologic loss unless the underlying problem is corrected.
People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause unconsciousness during sleep
Unconsciousness due to hypoglycemia can occur within 20 minutes to an hour after early symptoms and is not usually preceded by other illness or symptoms. Twitching or convulsions may occur. A person unconscious from hypoglycemia is usually pale, has a rapid heart beat, and is soaked in sweat: all signs of theadrenaline response to hypoglycemia. So there is no set limit below which the brain shall have a seizure but speaking in broader terms usually the brain does not tolerate blood sugar below 60mg/dl and below 40 mg/dl most patients shall be symptomatic (either have a convulsion or be confused and obtunded.
Microbial keratitis is a severe complication of corneal exposure in unconscious patients.
Without meticulous care, corneal exposure and its sequelae, sometimes with devastating consequences, is very likely. We emphasise the need for maintenance of lid closure in at risk patients. Early referral in suspicious circumstances is essential. Fluorescein aided examination may enhance the care of such patients by detecting an epithelial defect before the onset of superimposed corneal infection. In cases with an epithelial defect, particularly with exacerbating risk factors, early lid closure with a lower lid traction suture may be appropriate, as lid closure is maintained, but examination of the eye is still possible.
