Patient coma (33)


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Patient coma (33)

  2. 2. Introduction Certain terms… Normal consciousness Sleep Akinetic Mutism Confusion Catatonia Delerium Persistent Vegetative State Drowsiness Locked-in Syndrome Stupor Coma 2
  4. 4.  Coma is always a symptomatic expression of an underlying disease A methodical approach that leaves none of the common and treatable causes of coma unexplored History taking , examination , and management go hand in hand…. Best thing is one person should take history and other person examine simultaneously along with taking care of immediate management 4
  5. 5. When a comatose patient is 1st seen…. ABC  Maintain airway….oropharyngeal… endotracheal….  Breathing… shallow….?........ Aspiration…?  If trauma… check for bleeding  If hypotension… iv fluids, pressors, volume expanders or blood preferably monitoring central venous pressure  O2 inhalationCervical Fracture …?Injection Thiamine followed by glucose (After taking blood for basic investigations) 5
  6. 6. History…OnsetFeverHeadacheVomiting….types..TraumaRecent altered behaviour..?h/o diabetes…?Hypertension? controlled…?Poison..? Prior suicidal attempts…? 6
  7. 7. History…Drugs…?  Insulin, OHA  Antipsychotics  Sedatives  Steroids  Anti coagulants  DiureticsAcute or Chronic alcohol intakeSeizure disorder…Prior episode of comaElderly… nothing predictable… 7
  8. 8. General Examination..Odor Alcohol Fruity DKA Uriniferous Uremia Musty fetor of Hepatic coma Burnt almond odor of Cyanide Organophospherous 8
  9. 9. SkinColour  Pallor  Severe internal hemorrhage, Hypothyroidism , Hypopituitarism , CKD  Cyanosis of lips and nails  Cherry red CO  Facial plethora  alcoholism  Maculo hemorrhagic rash  Meningococcemia , Typhus, RMSF, Staph endocarditis 9
  10. 10. General Examination..Diffuse petechiae  TTP, DIC, Fat embolismEchymotic patches..  Drug induced  CLD  DIC  TraumaNasal bleed, CSF leakAural bleed 10
  11. 11. Large blisters  Ifthe patient has been motionless for a time  Acute barbiturate, alcohol, or opiate intoxicationFacial puffiness  CKD  Myxedema, HypopituitarismCentral obesity, striaeNail  Splinterhemorrhage  White nail  Half and half nail  Clubbing 11
  12. 12.  Jaundice Features of chronic liver disease Fever  Pneumonia, sepsis, meningitis, sepsis Hyperthermia  Drugs with anticholinergic activity  Heat stroke Hypothermia  Alcoholic or barbiturate intoxication  Drowning  Exposure to cold  Peripheral circulatory failure  Myxedema 12
  13. 13. Bradycardia Hypotension  Heart block due to drugs  DKA  Myxedema  Alcohol, Barbiturate  Raised ICT  Internal hemorrhage  Myocardial infarctionMarked hypertension  Dissecting aortic  IC bleed aneurysm  Raised ICT  Septicemia  Hypertensive  Addison disease encephalopathy  Massive brain trauma 13
  14. 14. RespirationSlow  Opiate or barbiturate  hypothyroidismKussmaul  Pneumonia, DKA, Uremia, Pulmonary edema, or Intracranial diseaseCheyne-Stokes Raised ICT 14
  15. 15. Neurologic Examination 15
  16. 16. Most important even though limittedSimple observing of the patient may give valuable cluesAbnormal posturing of bodyAbnormal movement of one sideThe state of responsivenessVocalizationGrimacing and deft avoidance movements of the stimulated parts are preserved in light comaThe Glasgow Coma Scale 16
  17. 17. The Glasgow Coma Scale Motor Response  6 - Obeys commands fully Total – 15  5 - Localizes to noxious stimuli Poor - 3 or 4  4 - Withdraws from noxious stimuli  3 - Abnormal flexion, i.e. decorticate posturing  2 - Extensor response, i.e. decerebrate posturing  1 - No response Verbal Response  5 - Alert and Oriented  4 - Confused, yet coherent, speech  3 - Inappropriate words, and jarbled phrases consisting of words  2 - Incomprehensible sounds  1 - No sounds Eye Opening  4 - Spontaneous eye opening  3 - Eyes open to speech  2 - Eyes open to pain 17  1 - No eye opening
  18. 18. Signs of meningeal irritation  Meningitis  Subarachnoid hemorrhage (after 12-24 hrs in some)  In the infant, bulging of the anterior fontanel better signConfused with meningeal irritation  Phenothiazinepoisoning  Temporal lobe or cerebellar herniation  Decerebrate rigidity  Cervical spondylosis 18
  19. 19. Hemiplegia  Lack of movement on noxious stimuli  Hemiplegic leg lies in a position of external rotation ( // fracture femur)  Thigh may appear wider and flatter than the nonhemiplegic one  Inexpiration, the cheek and lips puff out on the paralyzed side 19
  20. 20. Hemispherical lesions 20
  21. 21.  Eyes are often turned away from the paralyzed side Opposite may occur with brainstem lesions Hemiplegia and an accompanying Babinski sign are indicative of a contralateral hemispheral lesion ( beware of Kernohan-Woltman sign ) A moan or grimace may be provoked by painful stimuli on one side but not on the other, reflecting the presence of a hemianesthesia During grimacing, facial weakness may be noted 21
  22. 22. Brain stem lesions 22
  23. 23. Of the various indicators of brainstem function, the most useful are pupillary size and reactivity, ocular movements, oculovestibular reflexes, and, to a lesser extent, the pattern of breathing.These functions, like consciousness itself, are to a large extent dependent on the integrity of structures in the midbrain and rostral pons 23
  24. 24. 24
  25. 25.  Unilaterally enlarged pupil (>5.5 mm diameter) ipsilateral 3rd nerve compression With continued compressioncorectopia (oval or pear ) The light-unreactive pupil continues to enlarge to a size of 6 to 9 mm diameter, associated with slight outward deviation of the globe In unusual instances, the pupil contralateral to the mass may enlarge first 25
  26. 26.  As midbrain displacement continues, both pupils dilate and become unreactive to light The last step in the evolution of brainstem compression tends to be a slight reduction in pupillary size, to 5 to 7 mm Normal pupillary size, shape, and light reflexes indicate integrity of midbrain structures and a cause of coma other than a mass lesion 26
  27. 27.  Pontine tegmental lesions cause extremely miotic pupils (<1 mm in diameter) with only a slight reaction to strong light Ciliospinal reflex lost A Horner syndrome homolateral to a lesion of the brainstem or hypothalamus or as a sign of dissection of the internal carotid artery 27
  28. 28.  Pupil is spared in metaboic conditions and intoxications Exceptions  Morphine  extremely pin point  Barbiturate  pin point 1cm or more  Atropine Dilated, non reacting even to physostigmine  Tricyclics  Hippus metabolic encephalopathy 28
  31. 31. Movements of Eyes and Eyelids and Corneal Responses In light coma of metabolic origin, the eyes rove conjugately from side to side in random fashion, sometimes resting briefly in an eccentric position These movements disappear as coma deepens and the eyes then remain motionless in slightly exotropic positions 31
  32. 32.  A lateral and slight downward deviation of one eye suggests the presence of a third nerve palsy Medial deviation sixth nerve palsy Away from the side of the paralysis  large cerebral lesion Toward the side of the paralysis with a unilateral pontine lesion “Wrong-way” conjugate deviation  thalamic and upper brainstem lesions 32
  33. 33.  During a one-sided seizure, the eyes turn or jerk toward the convulsing side The eyes may be turned down and inward (looking at the nose) with hematomas or ischemic lesions of the thalamus and upper midbrain Retraction and convergence nystagmus lesions in the tegmentum of the midbrain Ocular bobbing  Pons Ocular dipping Anoxia and Drug intoxications (horizontal eye movements are preserved ) 33
  34. 34. The coma-producing structural lesions of thebrainstem abolish most conjugate ocular movements,whereas metabolic disorders generally do not.(except for rare instances of hepatic coma andanticonvulsant drug overdose) 34
  35. 35. Oculocephalic reflex 35
  36. 36. Elicitation of these reflexes in a comatose patient provides two pieces of information Evidence of unimpeded function of the oculomotor nerves and of the midbrain and pontine tegmental structures that integrate ocular movements Loss of the cortical inhibition that normally holds these movements in check 36
  37. 37.  Sedative or anticonvulsant intoxication serious enough to cause coma may obliterate the brainstem mechanisms for oculocephalic reactions Asymmetry in elicited eye movements remains a dependable sign of focal brainstem disease 37
  38. 38. Caloric response 38
  39. 39.  10 mL of cold water In comatose patients, the fast “corrective” phase of nystagmus is lost and the eyes are tonically deflected to the side irrigated with cold water or away from the side irrigated with warm water; this position may be held for 2 to 3 min With brainstem lesions, these vestibulo-ocular reflexes are lost or disrupted 39
  40. 40. Corneal reflex Progressive deterioration in response to corneal touch are among the most dependable signs of deepening coma. A marked asymmetry in corneal responses indicates either an acute lesion of the opposite hemisphere or, less often, an ipsilateral lesion in the brainstem. 40
  41. 41.  Restless movements of both arms and both legs and grasping and picking movements  intact corticospinal tracts The occurrence of focal motor epilepsy usually indicates that the corresponding corticospinal pathway is intact Massive destruction of a cerebral hemisphere focal seizures are seldom seen on the paralyzed side Definite choreic, athetotic, or hemiballistic movements indicate a disorder of the basal ganglionic and subthalamic structures, just as they do in the alert patient 41
  42. 42. Abnormal postures 42
  43. 43. The decerebrate ‘State’Brainstem at the intercollicular levelIn a variety of conditions  Midbrain compression due to a hemispheral mass  with cerebellar or other posterior fossa lesions  Anoxia and hypoglycemia;  Rarely with hepatic coma and profound intoxicationIpsilateral to a one-sided lesion, hence not due to involvement of the corticospinal tracts 43
  44. 44. Decorticate rigidity Lesions at a higher level—in the cerebral white matter or internal capsule and thalamus Bilateral decorticate rigidity is essentially a bilateral spastic hemiplegia 44
  45. 45.  Diagonal postures, e.g., flexion of one arm and extension of the opposite arm and leg, usually indicate a supratentorial lesion Forceful extensor postures of the arms and weak flexor responses of the legs are probably due to lesions at about the level of the vestibular nuclei Lesions below this level lead to flaccidity and abolition of all postures and movements. The coma is then usually profound and often progresses to brain death 45
  46. 46.  Only in the most advanced forms of intoxication and metabolic coma, as might occur with anoxic necrosis of neurons throughout the entire brain, are coughing, swallowing, hiccoughing, and spontaneous respiration all abolished Tendon reflexes are usually preserved until the late stages of coma due to metabolic disturbances and intoxications Plantar flexor responses, succeeding extensor responses, signify ether a return to normalcy or, in the context of deepening coma, a transition to brain death 46
  47. 47. Motor response 47
  48. 48. Motor response 48
  49. 49. Breathing patterns Cheyne-Stokes  Massive supratentorial lesion  Bilateral deep-seated cerebral lesions  Metabolic disturbances Presence of CSR signifies bilateral dysfunction of cerebral structures, usually those deep in the hemispheres or diencephalon, and is seen with states of drowsiness or stupor Coma with CSR is usually due to intoxication or a severe metabolic derangement and occasionally to bilateral lesions, such as subdural hematomas 49
  50. 50. Central neurogenic hyperventilation  Lesions of the lower midbrain–upper pontine tegmentum, either primary or secondary to a tentorial herniation  Tumors of the medulla, lower pons, and midbrain  Primarybrain lymphoma without brainstem involvement 50
  51. 51.  Apneustic breathing  Low pontine lesions, usually due to basilar artery occlusion Biot breathing (chaotic)  lesions of the dorsomedial part of the medulla 51
  52. 52. Signs of Increased Intracranial Pressure Headache before the onset of coma Recurrent vomiting Severe hypertension beyond the patients static level Subhyaloid retinal hemorrhages Papilledema develops within 12 to 24 h in cases of brain trauma and hemorrhage, but if it is pronounced, it usually signifies brain tumor or abscess—i.e., a lesion of longer duration 52
  53. 53. 53
  54. 54. Case 1 15 yr old girl, recent weight loss and polydipsia presenting with a comatose state. She is dehydrated and in shock. Examination showed tachypnea and sweet odour 54
  55. 55. Case 2 A middle aged man brought in a comatose state by some passengers who got him from the pavement. There was smell of alcohol in his breath, and had dilated right pupil and left extensor plantar. 55
  56. 56. Case 3 A 10 yr old boy with h/o Fallot’s tetrology was brought by his parents with h/o headache and fever for 2 weeks, severe vomiting and progression into coma. He had left hemiplegia and lateral rectus palsy and b/l papilledema 56
  57. 57. Case 4 35 yr old lady who was on insulin for diabetic ketotic coma. Her sugar values and blood acetone improved, but she persisted in the comatose state. She had 3 episodes of GTCS. On examination she had b/l extensor plantar response and b/l papilledema. 57
  58. 58. Case 5 60 yr old lady presented with comatose state to the casualty. She had developed sudden onset of left sided weakness along with headache and vomiting. She had left hemiplegia, and bilateral papilledema. Her BP was normal. She had mild numbness in the left upper and lower limbs for last 1 month. 58
  59. 59. Case 6 21 yr old primi in 9th month of gestation presented with severe vomiting, headache and GTCS. She had mild fever also.She didn’t have any hypertension or edema during pregnancy. Examination showed normal BP and bilteral papilledema. There was no meningeal signs. 59
  60. 60. Case 7 56 yr old chronic alcoholic presented in comatose state to the gastroenterology department. He had mild abdominal pain for last 5 days. Examination showed b/ l extensor plantar response. 60
  61. 61. Case 8 65 yr old lady was admitted in a comatose state. She had received an injection for chest pain from a local hospital. Her skin was dry, she had low temperature. She had excessive day time somnolence for last 1 month 61
  62. 62. Thank you. 62