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Dr. M.A. Sofi MD;FRCP (London)FRCPEdin; FRCSEdin Al Maarefa College of Science & Technology.

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Presentation on theme: "Dr. M.A. Sofi MD;FRCP (London)FRCPEdin; FRCSEdin Al Maarefa College of Science & Technology."— Presentation transcript:

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2 Dr. M.A. Sofi MD;FRCP (London)FRCPEdin; FRCSEdin Al Maarefa College of Science & Technology

3 Coma: A state of unconsciousness lasting more than six hours, in which a person:  cannot be awakened  fails to respond normally to painful stimuli, light, or sound  lacks a normal sleep-wake cycle  does not initiate voluntary actions. Consciousness requires:  An intact pontine reticular activating system  An intact cerebral hemisphere, or at least part of a hemisphere Coma requires: dysfunction of either the:  Pontine reticular activating system, or  Bihemispheric cerebral dysfunction COMA: DIAGNOSIS & MANAGEMENT

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

5 Sites and causes of coma.

6 ARAS  Diffuse mass of neurons & nerve fibers that make the core of the brain stem.  Fibers run through medulla oblongata, pons & midbrain.  Receives fibers from the sensory pathways via long ascending spinal tracts. Ascending ReticularActivating System

7  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.

8  Identify causes(s) of a deteriorating conscious level.  Stabilize, evaluate, and treat the comatose patient in the emergency setting.  Use an organized, sequential, prioritized approach.  Use the Glasgow coma scale for assessment of altered conscious level.

9  Altered level of consciousness: Measure of arousal other than normal.  Level of consciousness (LOC): Measurement of a person's arousability and responsiveness to stimuli from the environment.  Lethargy: A mildly depressed level of consciousness or alertness, can be aroused with little difficulty.  Obtundation: refers to less than full alertness, typically as a result of a medical condition or trauma.  Stupor: Decreased response to environmental stimuli and absence of spontaneous movement.  Coma: State of unconsciousness lasting more than six hours, in which a person:  Cannot be awakened.  Fails to respond normally to painful stimuli.  Lacks a normal sleep-wake cycle.  No voluntary actions. Altered levels of consciousness

10 I.Head Trauma Coma may result from significant traumatic injury to the head, such as from a car accident or fall. II.Bleeding (Hemorrhage) into the brain or skull Types of brain/skull hemorrhage include: a.Intracerebral hemorrhage: bleeding within the brain tissue b.Epidural hemorrhage: bleeding inside the skull, but outside the dura, (the covering of the brain) c.Subdural hemorrhage: bleeding inside the skull, and inside the dura, but not in the brain tissue itself d.Subarachnoid hemorrhage: bleeding in the space immediately adjacent to the brain tissue Coma: Causes

11 III.Causes of brain/skull hemorrhage include: a.High blood pressure (hypertension) b.Cerebral aneurysm: a weak spot in a blood vessel of the brain c.Arteriovenous malformation (AVM): an abnormal cluster of blood vessels d.Tumors IV.Swelling of the brain (cerebral edema) Causes of swelling of the brain: a.Infections b.Metabolic imbalances c.Traumatic injuries d.Problems with the flow of cerebrospinal fluid (CSF)

12 V.Lack of oxygen to the brain The most common causes for lack of oxygen to the brain include: a.Heart arrhythmias b.Lung disease, including pneumonia, emphysema, or asthma. c.Anemia (low red blood cell count) d.Toxins VI.Poisons External poisons are those that are ingested or inhaled. Internal poisons are by-products of the body's normal metabolism that for some reason cannot be excreted properly. VII.Endocrine disorders a.Myxedema coma (hypothyroidism) b.Diabetes Mellitus: Hypoglycemia or Hyperglycemia Coma: Causes

13 CLINICAL ASSESSMENT OF COMA Coma is an acute, life threatening situation and evaluation must be swift, comprehensive and include: Resuscitation of CVS and respiratory system.  Correction of blood glucose and thiamine  Control of seizures  Temperature If Indicated  Specific treatments— naloxone. Assessment now should comprise: 1.History—through friend, family or emergency medical personnel 2.General physical examination 3.Neurological assessment—to define the nature of coma

14 CLINICAL ASSESSMENT OF COMA The approach to clinical evaluation is used to categories coma into: A.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. B. Coma without focal signs with meningism. This results from subarachnoid hemorrhage, meningitis, and meningoencephalitis. C.Coma with focal signs. This results from intracranial haemorrhage, infarction, tumor or abscess.

15 THE ABCD 2 E APPROCH TO COMA A AIRWAYS B BREATHING C CIRCULATION D DRUGS/DISABILITY E EXPOSURE

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

17 CLINICAL ASSESSMENT OF COMA Brain stem functionRespiratory pattern Pupillary responsesCheyne Stokes: hemisphere Spontaneous eye movementsCentral neurogenic hyperventillation: Oculocephalic responsesrapid/midbrain Caloric responsesApneustic: Rapid with pauses/lower Corneal responses pontine

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

19 Abnormalities of respiration: Ataxic (Biot) breathing is a random pattern of shallow and deep breaths interspersed with irregular pauses – pontine lesions Apneustic breathing involves repetitive gasps, with pauses at full inspiration lasting a few seconds - pontine disease. Cheyne-Stokes respiration is cyclic, with a crescendo-decrescendo pattern interrupted by apneas – brainstem lesions.

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21  Systematic assessment of brainstem function via reflexes  Cranial Nerve Exam ◦ Pupillary light response (CN 2-3) ◦ Occulocephalic/calorics (CN 3,4,6,8) ◦ Caloric reflex test ◦ Corneal reflex (CN 5,7) ◦ Gag refelx (CN 9,10)

22 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/myosis). lower intensity of light causes the pupil to dilate (mydriasis, expansion) (allowing more light in).

23  Pons-pinpoint pupils ◦ Symp. Dysfinction plus parasymp.irritation  Midbrain-Large fixed pupils unresponsive to light, hippus  Horner’s- symp.dysfunction  Unilateral dilation- parasymp. Dysfunction usually due to 3 rd nerve lesion

24 Pupils: Localizing Value Bilateral pupillary constriction- Opiod toxicity Dilated Rt. Pupil & eye deviated to right Normal size Lft.pupil & eye mid- primary position

25 Pupils: Localizing Value Horner’s syndrome Midriasis-sympathetic stimulation

26 Pupils: Localizing Value

27 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)

28  Definition: The gag reflex evaluates the integrity of Cranial nerves IX and X  Test procedure: Using a long handle swab stick (orange swab) 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

29  Brisk rotation of head with eyes held open  Watch for contraversive movements  Next: ◦ Flexion: eyes deviate up and eyelids open (doll’s head phenomenon) ◦ Extension:eyes deviate downward

30  Brisk rotation of head with eyes held open  Watch for contraversive movements  Flexion: eyes deviate up and eyelids open (doll’s head phenomenon)  Extension: eyes deviate downward Doll’s Eye reflex movement Abnormalities are caused by lesions of the inner ear or brainstem, especially the pons and midbrain.

31 Caloric reflex test 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 mnemonic used to remember the FAST direction of nystagmus is COWS. COWS: Cold Opposite, Warm Same.

32  Before maneuvers attempted note resting position ◦ Midline  Deviation suggests frontal/pontine damage ◦ Conjugate  Dysconjugance suggests CN abn. ◦ Moving  Roving, dipping, bobbing

33 Left 6 th Nerve Palsy Left 3 rd Nerve Palsy

34  Akinetic mutism  ‘Locked-in’ syndrome  Catatonia  Conversion reactions

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

36  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 “Locked-In’ Syndrome Bilateral Pontine Infarction

37  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

38  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


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