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Dr. M.A. Sofi MD;FRCP (London)FRCPEdin; FRCSEdin DIAGNOSIS & MANAGEMENT Coma definition: 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 NEUROLOGICAL ASSESSMENT 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. Sites and causes of coma. 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 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. 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. Altered levels of consciousness Altered level of Drowsiness - this is similar to obtundation and probably represents a lesser loss of consciousness Obtundation: refers to less than full alertness, typically as a result of a medical condition or trauma. Stupor: Similar to coma in that responsiveness is greatly diminished. However, the person can still be partially roused by some stimuli, such as pain 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. Causes 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 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) Coma: Causes 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 INVESTIGATIONS Capillary blood glucose. Arterial blood gas. Bloods - FBC, renal function, LFTs, CK, TFTs, cardiac enzymes. Urine dipstick and pregnancy test (especially if seizures have occurred in a woman of childbearing age). Urine drug screen. Paracetamol and salicylate levels. Blood cultures. Thick and thin films for malaria. Ethanol levels. 12-lead ECG. CXR. CT scan of the brain/MRI scan (especially with focal signs). EEG and other electroneurophysiological tests. These can be useful for determining prognosis - eg, functional MRI. Functional neuro-imaging is likely to become very important in making decisions regarding outcome. Other investigations: these will in part depend on the suspected cause - eg, lumbar puncture, autoantibody screen 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 Specific treatments— naloxone. If Indicated 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 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 anoxicischaemic, 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. THE ABCD2E APPROCH TO COMA A AIRWAYS B BREATHING C CIRCULATION D DRUGS/DISABILITY E EXPOSURE 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 Breath (fetor hepaticus/alcohol) Motor response Cardiovascular (for example, arrhythmia) Deep tendon reflexes: Biceps, Triceps, Brachioradialis, Patellar, Achilis Abdomen (organomegaly) Muscle tone/Planters CLINICAL ASSESSMENT OF COMA Brain stem function Respiratory pattern Pupillary responses Cheyne Stokes: hemisphere Spontaneous eye movements Central neurogenic hyperventillation: Oculocephalic responses rapid/midbrain Caloric responses Apneustic: Rapid with pauses/lower Corneal responses pontine Assesses patient’s neurological condition Value range 3 -15 3 totally comatose patient 9-12 Moderate altered conscious level 15 fully alert patient 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. 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) • • • • 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). Pupils: Localizing Value Unilateral pupillary dilatation with lack of response to light - suggests uncal herniation of the temporal lobe over the tentorium entrapping the third nerve. Pupil fixed in the midposition with loss of light reflex - typical of midbrain lesions. Small pupils with response to light - lesions in the pons. Fixed dilatation - suggests significant damage to the brainstem. Horner's syndrome occurs in lesions of the hypothalamus or brainstem and in diseases affecting the wall of the carotid artery. Small pupils reacting briskly to light - metabolic cause (eg, hepatic or renal failure). Corneal reflexes: these are normally intact until there is a very deep coma. In drug intoxication, they may be absent in a patient otherwise in a light coma. Otherwise, loss of corneal reflex is indicative of a poor prognosis. Pupils: Localizing Value Bilateral pupillary constriction- Opiod toxicity Dilated Rt. Pupil & eye deviated to right Normal size Lft.pupil & eye midprimary position Pupils: Localizing Value Horner’s syndrome Midriasis-sympathetic stimulation Pupils: Localizing Value 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) Gag Reflex 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. Oculocephalic response in which the patient's head is rotated from side to side and the position of the eyes is observed. The eyes will move together in the opposite direction to the head movement - this is the normal oculocephalic response (also called doll's eye movement). Flexion: eyes deviate up and eyelids open (doll’s head phenomenon) Extension: eyes deviate downward Where a brainstem lesion is present this eye movement is absent or asymmetric. This procedure should only be done provided there is no neck instability Doll’s Eye reflex movement 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 Abnormalities are caused by lesions of downward the inner ear or brainstem, especially the pons and midbrain. Vestibulo-occular reflex Caloric reflex test caloric reflex test is a test of the vestibuloocular 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. Eye movements: Spontaneous eye movements Conjugate deviation of the eyes - possible focal hemispheric or brainstem lesion. Depression of the eyes lesion in the midbrain at the level of the tectum. Skew deviation of the eyes - lesion at the pontomedullary junction. Unco-ordinated eye movements - a small amount of eye divergence is normal in unconsciousness but more significant inco-ordination suggests damage to the 3rd or 6th nerves in the brainstem or pathways. Normal roving eye movement - similar to those of sleep - often occurs in light coma, and cannot be faked, so excludes the possibility of psychogenic unresponsiveness (jerky eye movement). Akinetic mutism ‘Locked-in’ syndrome Catatonia Conversion reactions Akinetic Mutism Silent, immobile but alert appearing Usually due to lesion in bilateral mesial frontal lobes, bilateral thalamic lesions or lesions in periaqueductal grey (brainstem) Many cases of akinetic mutism have occurred after a thalamic stroke “Locked-In’ Syndrome Infarction of basis pontis (all descending motor fibers to body and face) May spare eyemovements Often spares eyeopening EEG is normal or shows alpha activity Bilateral Pontine Infarction Symptom complex associated with severe psychiatric disease with: ◦ stupor, excitement, mutism, posturing ◦ can also be seen in organic brain disease: encephalitis, toxic and druginduced psychosis 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 Management Resuscitation - with intubation and ventilation if needed and rehydration. Give intravenous thiamine and glucose to all in whom diagnosis is unclear. Trial of naloxone or flumazenil is easily done and response is rapid. Treat any underlying cause (eg, antibiotics if meningitis is suspected, surgery to remove SD hematoma, anticonvulsants, etc). Raised intracranial pressure may require mannitol infusion. If there is a risk that the patient may have aspirated then they should be covered with antibiotics. Fluid rehydration, prevention of pressure sores and adequate nutrition should also be focused on.[ Prognosis Head injury then prognosis is directly proportional to the GCS score The lack of brainstem and lateralising signs suggests the cause is most likely metabolic and potentially reversible. Drug overdose - good prognosis with appropriate treatment. Coma not due to head injury or drug overdose, lasting longer than six hours - only 10% chance of recovery. Subarachnoid haemorrhage or stroke - <5% chance of recovery. Hypoxia or ischaemia (eg, after cardiac arrest) - ~10% chance of recovery. Coma >24 hours - 10% chance of recovery. After one week - 3% chance of recovery. After seven days - high incidence of death/persistent vegetative state (PVS). Absence of brainstem reflexes for 24 hours (without sedative drugs) very little chance of recovery.