1. Dr. M. Sofi MD; FRCP (London); FRCPEdin; FRCSEdin
UNCONSCIOUS PATIENT
Dr. M. Sofi MD; FRCP (London); FRCPEdin; FRCSEdin

2. NEUROLOGICAL ASSESSMENT
Coma is caused by disordered arousal rather than impairment of the content of consciousness.
Arousal depends on an intact:
ascending reticular activating system
connections with diencephalic structures
Coma is caused by:
Diffuse bilateral hemisphere damage.
Failure of the ascending reticular activating system, or both.
Consciousness is a state of awareness of self and the environment. This state is determined by two separate functions:
Awareness (content of consciousness).
Arousal (level of consciousness)

3. Sites and causes of coma.

4. ASCENDING RETICULAR ACTIVATION SYSTEM - ARAS
It’s believed to be the center of arousal and motivation in mammals.
Alertness, maintenance of attention and wakefulness.
Emotional reactions, important in learning processes.

5. Deep stupor; requires strong pain to evoke movement
Grady Coma Scale
Responds appropriately to:
Grade
State of awareness
Calling name
Light pain
Deep pain I
Confused, drowsy, lethargic, indifferent and/or uncooperative; does not lapse into sleep when left undisturbed
Yes II
Stupor; may be disoriented to time, place, and person; will lapse into sleep when not disturbed; or belligerent and uncooperative No
III
Deep stupor; requires strong pain to evoke movement IV
Exhibits decorticate or decerbrate posturing to a deep pain stimulus V
Does not respond to any stimuli; flaccid

6. Coma: Causes Hemorrhage Brain edema Hypoxemia Poisons Endocrine
Intracerebral
High BP
Epidural
Aneurysm
Hemorrhage
Subdural
AVM
Subarachnoid
Tumors
Infections
Trauma
Brain edema
Metabolic
CSF flow abno
Anemia
Arrhythmias
Hypoxemia
Toxins
Lung disease
Poisons
External
Myxoedema
Internal
Endocrine
Diabetes

7. THE ABCDE APPROCH TO COMA
AIRWAYS B
BREATHING C
CIRCULATION D
DRUGS/DISABILITY E
EXPOSURE

8. CLINICAL ASSESSMENT OF COMA
Coma is life threatening situation and evaluation must be swift, and include:
Resuscitation of CVS and respiratory system.
Correction of blood glucose and thiamine
Control of seizure
Temperature
Specific treatments— naloxone.
Assessment now should comprise:
History—through friend, family or emergency medical personnel
General physical examination
Neurological assessment—to define the nature of coma

9. Coma: Initial assessment and evaluation
Assess level of consciousness: response to vocal and painful stimuli; this is known as the AVPU (alert, vocal stimuli, painful stimuli, unresponsive) scale.
Make sure the patient is in an actual comatose state and or is not in locked-in state (patient is either able to voluntarily move their eyes or blink) or psychogenic unresponsiveness
Assess the severity of the coma with the Glasgow coma scale
Take blood for drug screen
Check for levels of “serum glucose, calcium, sodium, potassium, magnesium, phosphate, urea, and creatinine”
Perform CT or MRI scans
Continue to monitor brain waves and identify seizures of patient using EEGs

10. CLINICAL ASSESSMENT OF COMA
General examination
Neurological (general)
Skin: rash, anemia, jaundice
Head, neck and eardrum (trauma)
Temperature: (fever infection hypothermia-drugs/circulatory failure
Meningism (SAH/meningitis)
Blood pressure (for example, septicemia/Addison's disease)
Fundoscopy (Papilledema/ subhyaloid hemorrhage)
Breath (fetor hepaticus/alcohol)
Motor response
Cardiovascular (for example, arrhythmia)
Deep tendon reflexes: Biceps, Triceps, Brachioradialis, Patellar, Achilis
Abdomen (organomegaly)
Muscle tone/Planters

11. CLINICAL ASSESSMENT OF COMA
Clinical evaluation is used to categories coma into:
Coma without focal signs or meningism.
This is the most common form of coma and results from anoxic-ischaemic, metabolic, toxic, and drug induced insults, infections, and post-ictal states.
Coma without focal signs with meningism.
This results from subarachnoid hemorrhage, meningitis, and meningoencephalitis.
Coma with focal signs.
This results from intracranial haemorrhage, infarction, tumor or abscess.

13. Pupils: Localizing Value

14. Pupil sizes (left eye vs. right eye) Possible interpretation
Pupils: Localizing Value
Pupil sizes (left eye vs. right eye)
Possible interpretation
Normal eye with two pupils equal in size and reactive to light.
"Pinpoint" pupils indicate:
Heroin or opiate overdose/pontine ICH
The pinpoint pupils are still reactive to light, bilaterally (in both eyes, not just one).
The right eye is dilated, while the left eye is normal in size). This could mean uncal herniation/ PCOM aneurysm.
Pupils are dilated and unreactive to light.
This could be due to certain medications, hypothermia or severe anoxia (lack of oxygen).

15. CLINICAL ASSESSMENT OF COMA
Brainstem Reflexes
Reflex
Technique
Localization
Pupillary light reaction
Shine light on pupil and observe constriction
Midbrain and pontine tegmentum
Corneal response
Open lid if necessary; lightly stroke cornea with cotton wisp; observe for blink
Pons
Oculocephalic response (doll's eyes)
Hold lids open with one hand while turning head side to side with the other hand; observe rotation of eyes side to side
Pons—vestibular
Oculovestibular; cold-water calorics
With head at 30 degrees, irrigate external auditory canal and tympanic membrane slowly with up to 100 ml ice water; observe for conjugate rotation of the eyes toward the side irrigated

16. Puppilary light reflex
Pupillary light reflex (PLR) is a reflex that controls the diameter of the pupil, in response to the intensity (luminance) of light.
Controls adaptation to various levels of lightness/darkness.
A greater intensity of light causes the pupil to constrict (miosis).
lower intensity of light causes the pupil to dilate (mydriasis, expansion) (allowing more light in).

17. Corneal Reflex Afferent: Trigeminal Nerve Efferent: Third
Nerve (Bell’s
Phenomenon
and Facial Nerve
(Eye closure)
Tests dorsal
midbrain (Bell’s)
and pontine
integrity (Eye
closure)

18. Definition: The gag reflex evaluates the integrity of cranial nerves IX and X
Test procedure: Using a long handle swab stick gently and briskly touch the pharyngeal wall behind the pillars of the fauces.
Test findings:
A positive gag reflex will produce a non symmetrical elevation of the uvula or the fauces.
If there is no movement of the uvula with the gag reflex and with saying 'ahh' this may signify bilateral palatal muscle paralysis.
In a normal gag reflex there will be a symmetrical elevation of the uvula or the fauces /tonsilar arches.
Gag reflex

19. "The OCR/doll's eye reflex is movement of the eyes in the direction opposite that in which the head is moved. For example, the reflex is present if the eyes move to the right when the head is rotated to the left, and vice versa.
Caloric reflex test is a test of the vestibulo-ocular reflex that involves irrigating cold or warm water or air into the external auditory canal.
The eyes should move conjugately in the direction opposite to the cold irrigation and same side to warm irrigation. An abnormal response (absent or asymmetric) implies brain stem disease.
One mneumonic used to remember the FAST direction of nystagmus is COWS. COWS: Cold Opposite, Warm Same.

20. Abnormal breathing patterns
Ataxic (Biot) breathing Sequences of shallow and deep breaths interspersed with irregular pauses
Apneustic breathing
A prolonged inspiratory "cramp"; a prolonged gasp
Cheyne-Stokes breathing is cyclic, crescendo-decrescendo pattern interrupted by apneas –
pontine disease
pontine disease
Cerebral hemisphers; diancephalon
Central neurogenic hyperventilation
Central neurogenic hyperventilation: Deep, rapid respirations at a rate of 24 or more/min --
Midbrain; diencephalons

21. Assesses patient’s neurological condition
Value range 3 -15
3 totally comatose
patient
9-12 Moderate
altered conscious
level
15 fully alert

23. Coma Mimics Akinetic mutism Locked –in syndrome Catatonia
Conversion reaction

24. Silent, immobile but alert appearing
Akinetic Mutism
Silent, immobile but alert appearing
Usually due to lesion in bilateral mesial frontal lobes, bilateral thalamic lesions or lesions in peri-aqueductal grey (brainstem)
Many cases of akinetic mutism have occurred after a thalamic stroke

25. May spare eye-movements Often spares eye-opening
“Locked-In’ Syndrome
Infarction of basis pontis (all descending motor fibers to body and face)
May spare eye-movements
Often spares eye-opening
EEG is normal or shows alpha activity
Bilateral Pontine Infarction

26. Catatonia
Symptom complex associated with severe psychiatric disease with:
stupor, excitement, mutism, posturing
can also be seen in organic brain disease: encephalitis, toxic and drug-induced psychosis

27. Conversion reactions Fairly rare
Occulocephalics may or may not be present
The presence of nystagmus with cold water calorics indicates the patient is physiologically awake
EEG used to confirm normal activity

28. THANK
YOU
FOR
YOUR
ATTENTION