Coma and related disorders of consciousness


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Coma and related disorders of consciousness

  1. 1. Coma and Related Disorders of Consciousness
  2. 2. coma <ul><li>Reduced alertness and responsiveness represents a continuum that in severest form , a deep sleeplike state from which the patient cannot be aroused. </li></ul>
  3. 3. Stupor <ul><li>L esser 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. </li></ul>
  4. 4. Drowsiness <ul><li>which is familiar to all persons, simulates light sleep and is characterized by easy arousal and the persistence of alertness for brief periods. </li></ul>
  5. 5. Drowsiness and stupor <ul><li>are usually attended by some degree of confusion. </li></ul>
  6. 6. vegetative state <ul><li>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. </li></ul>
  7. 7. vegetative state <ul><li>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 &quot;awake coma.“ </li></ul><ul><li>respiratory and autonomic functions are retained </li></ul>
  8. 8. vegetative state most common causes <ul><li>Cardiac arrest </li></ul><ul><li>head injuries </li></ul>
  9. 9. Akinetic mutism <ul><li>P artially or fully awake patient who is able to form impressions and think but remains immobile and mute, particularly when unstimulated. </li></ul><ul><li>Causes: damage in the regions of the medial thalamic nuclei, the frontal lobes (particularly situated deeply or on the orbitofrontal surfaces), or from hydrocephalus. </li></ul>
  10. 10. A bulia <ul><li>M ental and physical slowness and lack of impulse to activity that is in essence a mild form of akinetic mutism . </li></ul><ul><li>with the same anatomic origins. </li></ul>
  11. 11. Catatonia <ul><li>H ypomobile and mute syndrome associated with a major psychosis. </li></ul><ul><li>patients appear awake with eyes open but make no voluntary or responsive movements, although they blink spontaneously, swallow, and may not appear distressed. </li></ul><ul><li>E yes are half-open as if the patient is in a fog or light sleep. </li></ul><ul><li>NO clinical evidence of brain damage . </li></ul>
  12. 12. L ocked-in state <ul><li>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 </li></ul>
  13. 13. L ocked-in state <ul><li>Infarction or hemorrhage of the ventral pons, which transects all descending corticospinal and corticobulbar pathways, is the usual cause </li></ul>
  14. 14. Anatomy and Physiology of Unconsciousness <ul><li>C erebral cortex </li></ul><ul><li>neurons located in the upper brainstem and medial thalamus </li></ul><ul><li>RAS, maintains the cerebral cortex in a state of wakeful consciousness. </li></ul>
  15. 15. Anatomy and Physiology of Unconsciousness <ul><li>principal causes of coma </li></ul><ul><li>(1) lesions of the RAS </li></ul><ul><li>(2) destruction of large portions of both cerebral hemispheres </li></ul><ul><li>(3) suppression of thalamocerebral function by drugs, toxins, </li></ul><ul><li>metabolic causes: hypoglycemia, anoxia, azotemia, or hepatic failure. </li></ul>
  16. 16. Anatomy and Physiology of Unconsciousness <ul><li>Pupillary enlargement , loss of vertical and adduction movements of the globes suggest upper brainstem damage . </li></ul><ul><li>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 . </li></ul>
  17. 17. Anatomy and Physiology of Unconsciousness <ul><li>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. </li></ul>
  18. 18. <ul><li>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. </li></ul><ul><li>Serotonin and norepinephrine regulation of the sleep-wake cycle . </li></ul><ul><li>A lerting effects of amphetamines are likely to be mediated by catecholamine release. </li></ul>
  19. 19. Herniation <ul><li>transfalcial (displacement of the cingulate gyrus under the falx and across the midline), </li></ul><ul><li>transtentorial (displacement of the medial temporal lobe into the tentorial opening), </li></ul><ul><li>foraminal (downward forcing of the cerebellar tonsils into the foramen magnum. </li></ul>
  20. 20. Epileptic Coma <ul><li>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. </li></ul>
  21. 21. Pharmacologic Coma <ul><li>Can be reversible and leaves no residual damage . </li></ul><ul><li>Many drugs and toxins are capable of depressing nervous system function. </li></ul>
  22. 22. Approach to the Patient <ul><li>The diagnosis and management of coma depend on knowledge of its main causes . </li></ul><ul><li>interpretation of clinical signs, brainstem reflexes and motor function. </li></ul><ul><li>Acute respiratory and cardiovascular problems </li></ul><ul><li>complete medical evaluation, vital signs, funduscopy, and examination for nuchal rigidity, (complete neurologic evaluation for know the severity and nature of coma. </li></ul>
  23. 23. History <ul><li>trauma, cardiac arrest, or known drug ingestion. </li></ul><ul><li>(1) C ircumstances and rapidity with which neurologic symptoms developed </li></ul><ul><li>(2) confusion, weakness, headache, fever, seizures, dizziness, double vision, or vomiting </li></ul><ul><li>(3) use of medications, illicit drugs, or alcohol </li></ul><ul><li>(4) chronic liver, kidney, lung, heart, </li></ul>
  24. 24. History <ul><li>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. </li></ul>
  25. 25. General Physical Examination <ul><li>temperature, pulse, respiratory rate and pattern, Tachypnea may indicate acidosis or pneumonia blood pressure . </li></ul><ul><li>Fever suggests a systemic infection, bacterial meningitis, or encephalitis; only rarely is it attributable to a brain lesion that has disturbed temperature-regulating centers. </li></ul>
  26. 26. General Physical Examination <ul><li>High body temperature, 42 to 44°C, associated with dry skin should arouse the suspicion of heat stroke or anticholinergic drug intoxication. </li></ul><ul><li>Hypothermia itself causes coma only when the temperature is <31°C. </li></ul>
  27. 27. General Physical Examination <ul><li>A lcoholic, barbiturate, sedative, or phenothiazine intoxication </li></ul><ul><li>H ypoglycemia , peripheral circulatory failure , or hypothyroidism ,etc. </li></ul>
  28. 28. General Physical Examination <ul><li>F unduscopic examination is invaluable in detecting subarachnoid hemorrhage (subhyaloid hemorrhages), hypertensive encephalopathy (exudates, hemorrhages, vessel-crossing changes, papilledema), and increased intracranial pressure (papilledema). </li></ul>
  29. 29. Neurologic Assessment <ul><li>O bserv ation first without examiner intervention. </li></ul><ul><li>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. </li></ul>
  30. 30. Neurologic Assessment <ul><li>Multifocal myoclonus almost always indicates a metabolic disorder </li></ul><ul><li>In a drowsy and confused patient bilateral asterixis is a certain sign of metabolic encephalopathy or drug ingestion. </li></ul>.
  31. 31. Neurologic Assessment <ul><li>D ecorticate rigidity and decerebrate rigidity , or &quot;posturing,&quot; describe stereotyped arm and leg movements occurring spontaneously or elicited by sensory stimulation. </li></ul>
  32. 32. Brainstem Reflexes <ul><li>pupillary responses to light, s pontaneous and elicited eye movements, corneal responses, </li></ul><ul><li>R espiratory pattern </li></ul>
  33. 33. 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).
  34. 34. <ul><li>Unilateral pupillary enlargement: Ipsilaterall mass. </li></ul><ul><li>  </li></ul><ul><li>Oval and slightly eccentric pupils: Early m idbrain third nerve compression. </li></ul><ul><li>  </li></ul><ul><li>Bilaterally dilated and unreactive Severe midbrain damage by transtentorial </li></ul><ul><li>pupils: herniation or anticholinergic drugs toxicity. </li></ul>
  35. 35.        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.
  36. 36. Ocular Movements <ul><li>Eye movements are the second sign of importance in determining if the brainstem has been damaged. </li></ul>
  37. 37. EYE MOVEMENTS <ul><li>  </li></ul><ul><li>      Adducted eye at rest: Lateral rectus paresis due to VI nerve </li></ul><ul><li>lesion. If is bilateral is due to intracraneal hypertension. </li></ul><ul><li>Abducted eye at rest, plus ipsi Medial rectus paresis due to III nerve </li></ul><ul><li>lateral pupilary enlargement : dysfunction. </li></ul><ul><li>  </li></ul><ul><li>Vertical separation of the ocular Pontin or cerebellar lesion </li></ul><ul><li>Globes. (Skew deviation) : </li></ul><ul><li>  </li></ul><ul><li>Coma and spontanous conjugate Midbrain and pons intact </li></ul><ul><li>horizontal roving movements : </li></ul><ul><li>  </li></ul>
  38. 38. <ul><li>“ Ocular bobbing”. Brisk downward </li></ul><ul><li>   and slow upward movement of the </li></ul><ul><li>globes with loss of horizontal eye </li></ul><ul><li>  movements : B ilateral pontine damage </li></ul><ul><li>  </li></ul><ul><li>   “ Ocular dipping”. Slower, arrhytmic </li></ul><ul><li>downward followed by a faster upward </li></ul><ul><li>movement with normal reflex horizontal </li></ul><ul><li>gaze : Anoxic damage to the cerebral cortex. </li></ul><ul><li>    Thalamic and upper midbrain lesions: E yes turned down and inward. </li></ul>
  39. 39. F.- RESPIRATION PATTERNS. <ul><li>  </li></ul><ul><li>  </li></ul><ul><li>      Shallow, slow, well-timed regular Suggest metabolic or drug depression. </li></ul><ul><ul><li>Breathing: </li></ul></ul><ul><li>  </li></ul><ul><li>      Rapid, deep (Kussmaul) breathing: Metabolic acidosis or ponto- mesencephalic lesions. </li></ul><ul><li>  </li></ul><ul><li>      Cheyne-Stokes breathing, with light Mild bihemispherical damage or </li></ul><ul><li>Coma: metabolic supression. </li></ul><ul><li>  </li></ul><ul><li>     Agonal gasps: Bilateral lower brainstem damage. </li></ul><ul><ul><ul><ul><ul><li> Terminal respiratory pattern. </li></ul></ul></ul></ul></ul>
  40. 40. Laboratory Studies and Imaging <ul><li>chemical-toxicologic analysis of blood and urine, </li></ul><ul><li>cranial CT or MRI, EEG, </li></ul><ul><li>Lumbar puncture and CSF examination (cultures) </li></ul>
  41. 41. Laboratory Studies and Imaging <ul><li>Arterial blood-gas analysis is helpful in patients with lung disease and acid-base disorders. </li></ul><ul><li>Toxicologic analysis </li></ul>
  42. 42.   Brain Death <ul><li>Neurological examination </li></ul><ul><li>EEG </li></ul><ul><li>Radionuclide brain scanning, cerebral angiography, or transcranial Doppler measurements may also be used to demonstrate the absence of cerebral blood flow </li></ul>
  43. 43. TREATMENT FOR THE PATIENT IN COMA. <ul><li>1.- The treatment must be instituted inmediately even when there is no a certain diagnosis. </li></ul><ul><li>The inmediate goal is the prevention of further nervous system damage. </li></ul><ul><li>2.- Diagnostic procedures and general treatment mus be performed simultaneously and to install the specific treatment when the etiology is known. </li></ul>
  44. 44. TREATMENT FOR THE PATIENT IN COMA. <ul><li>A.- Permeable airway. Oxygen supply through nasal fossae to endotraqueal intubation.. </li></ul><ul><li>B.- Politrauma patient’s evaluation. Stabilize the neck and the rest of the vertebral colum. </li></ul><ul><li>C.- Establish an intravenous access. Water administration carefully monitored. </li></ul><ul><li>D.- Maintain the body temperature the closest to the normal values as possible. </li></ul>
  45. 45. TREATMENT FOR THE PATIENT IN COMA. <ul><li>E.- I.V. administration of 50 ml of 50% glucose. </li></ul><ul><li>F.- Administrate thiamine in malnourished and alcoholic patients. 10 mg I.V. and 100 mg </li></ul><ul><li>I.M. /day /3 days. </li></ul><ul><li>G.- Naloxone (0.4 to 0.8 mg) or flumazenil (0.5 to 1 mg) I.V administration </li></ul><ul><li>H.- Appropriate treatment of intracraneal hypertension and seizures. </li></ul>
  46. 46. TREATMENT FOR THE PATIENT IN COMA. <ul><li> I.- General measures for the unmovable patient. </li></ul><ul><li>      Appropriate nutrition and hydration. </li></ul><ul><li>       Posture changes every two hours. </li></ul><ul><li>       Mobilization of joints. </li></ul><ul><li>       Ocular metilcelulose drops, 1 every 4 hours. </li></ul><ul><li>       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. </li></ul><ul><li>       S.C. Heparin, 5000 U every 12 hours. </li></ul><ul><li>       Urinary tract care. </li></ul><ul><li>J.- Etiologic treatment. </li></ul>