Approach to unconsciousness

Consciousness consists of awareness of one’s surrounding and responsiveness to external stimulation and inner need.
A normal level of consciousness (wakefulness) depends upon activation of the cerebral hemispheres and by neurons located in the brainstem reticular activating system (RAS).
Both components and the connections between them must be preserved for consciousness to be maintained

1. Approach to Unconsciousness Dr. Aminur Rahman FCPS (Med), MD ( Neuro ) ,FINR (Switzerland), FACP (USA) Fellow Interventional Neuroradiology (Thailand) Assistant Professor Department of Neurology Sir Salimullah Medical College

2. Consciousness Consciousness consists of awareness of one’s surrounding and responsiveness to external stimulation and inner need. A normal level of consciousness (wakefulness) depends upon activation of the cerebral hemispheres and by neurons located in the brainstem reticular activating system (RAS ). Both components and the connections between them must be preserved for consciousness to be maintained

3. Level of consciousness Obtundation: Responds-to verbal stimuli although slow and inappropriate Stupor : The subject can be aroused only by vigorous and repeated noxious stimuli. Coma: Unarousable and unresponsive.

4. Unconsciousness/Coma Coma is a state of unconsciousness in which a person cannot be awakened; fails to respond normally to painful stimuli, light, or sound; lacks a normal wake-sleep cycle and does not initiate voluntary actions.

5. Unconsciousness/Coma Clinically, a coma can be defined as the inability to consistently follow a one-step command.  It can also be defined as a score of ≤ 8 on the Glasgow Coma Scale lasting ≥ 6 hours. A person in a state of coma is described as being  comatose. 

6. Pathophysiology To maintain consciousness, two important neurological components must function. The first is the cerebral cortex and reticular activating system (RAS). Ischemia, trauma etc to either or both of these components is sufficient to cause a patient to experience a coma. The cerebral cortex is a group of tight, dense; "gray matter" composed of the nuclei of the neurons whose axons then form the "white matter," and is responsible for perception, relay of the sensory input via the thalamic pathway and many other neurological functions, including complex thinking.

7. Causes of Coma Vascular: Stroke (20%) : Intracerebral hemorrhage, Subarachnoid hemorrhage or large hemispheric ischaemic stroke Anoxic brain injury : Cardiac arrest (25%) Infections: encephalitis and Meningoencephalitis and severe systemic infections e.g. pneumonia, peritonitis, typhoid fever, malaria, septicemia, Waterhouse-Frederickson syndrome. Traumatic brain injuries:  Traumatic brain injuries, often caused by traffic collisions or acts of violence, are common causes of comas .

8. Causes of Coma Metabolic disturbances (15%): diabetic ketoacidosis, uremia, hepatic failure, nonketotic hyperosmolar hyperglycemia, hypo- and hypernatremia, hypoglycemia, Addisonian crisis, Hashimoto encephalopathy etc. Neoplastic / herniation of brain.  Tumors in the brain or brainstem. Drugs and toxin (40%):  Overdosing on Alcohol, Barbiturates and Other Sedative Drugs, Opiates, etc. and exposure to toxins, such as carbon monoxide or lead. Degenerative diseases- Late stages of certain degenerative diseases and Creutzfeldt-Jakob disease.

9. Clinical features Common features include: Unable to voluntarily open the eyes, Mild agitation and confusion, but progress to obtundation, stupor and finally complete unconsciousness Irregular breathing Depressed brainstem reflexes, such as pupils not responding to light No responses of limbs, except for reflex movements No response to painful stimuli, except for reflex movements.

10. Management Emergency management of the comatose patient. After initial management , then perform The history General physical and Neurologic examinations

11. Table Emergency Management of the Comatose Patient. Immediately Next Later Ensure adequacy of airway, ventilation, and circulation If signs of meningeal irritation are present (Figure 2–3) perform LP to rule out meningitis ECG Obtain a history if possible Draw blood for serum glucose, electrolytes, liver and renal function tests, PT, PTT, and CBC Perform detailed general physical and neurologic examination Correct hyper- or hypothermia Start IV and administer 25 g of dextrose, 100 mg of thiamine, and 0.4–1.2 mg of naloxone IV Order CT scan of head if history or findings suggest structural lesion or subarachnoid hemorrhage Correct severe acid-base and electrolyte abnormalities Draw blood for arterial blood gas determinations   Chest x-ray Treat seizures   Blood and urine toxicology studies; EEG

12. History

13. History History is obtained by family, friends or EMS. Proper history of: Onset of coma (abrupt, gradual) Recent complaints (headache, depression, focal weakness, vertigo) Previous medical illness (diabetes, uraemia, heart disease etc.) Access to drugs (sedatives, psychotropic drugs) Situation and timing of altered state of consciousness. History of recent trauma.

14. General Physical Examination

15. General Appearance: Torn or disheveled clothing may indicate prior assault. Urinary or fecal incontinence indicates an epileptic seizure or may result from a generalized autonomic discharge resulting from the same cause as for the coma. Vomiting may be a sign of increased ICP, drug overdose or metabolic or other toxic cause. Body habitus may reveal cushingoid patients at risk for an acute addisonian crisis with abrupt withdrawal of their medications or additional stress from intercurrent illness. Cachexia suggests cancer, chronic inflammatory disorders, Addison's disease, hypothyroid coma or hyperthyroid crisis. Gynecomastia , spider nevi, testicular atrophy and decreased axillary and pubic hair are common in the alcoholic with cirrhosis .

16. Pulse Tachycardia: Hypovolemia/haemorrhage Hyperthermia Intoxication Uremia Bradycardia: Raised intracranial pressure Heart blocks Opiates and Myxedema

17. Blood pressure Increased Hypertensive encephalopathy Cerebral haemorrhage Raised intracranial pressure Decreased Hypovolemia / hgr Myocardial infarction Intoxication/poisoning Profound hypothyroidism and Addisonian crisis

18. Temperature Increased Sepsis Meningitis ,encephalitis Malaria ,Pontine haemorrhage Decreased Hypoglycemia Hypothermia (less than 31 C) Myxedema Alcohol, Barbiturate , Sedative or Phenothiazine intoxication.

19. Respiratory rate Increased (tachypnae): Pneumonia Acidosis (DKA, renal failure) Pulmonary embolism Respiratory failure Decreased: Intoxication/poisoning

20. Pattern of respiration: a ) Hyperventilation - midbrain and upper pons lesion Metabolic diseases e.g. hepatic coma, diabetes and generalised raised intracranial pressure in its early stages. (b) Hypoventilation - medullary, upper cervical spinal lesion Drug overdose and later stages of cerebral herniation. (c) Cheyne -Stoke respiration – usually diencephalic lesion Central transtentorial herniation and obstructive hydrocephalus. (d) Ataxic respiration (completely irregular breathing) Brain-stem dysfunction of a diffuse nature.

21. Figure: Pattern of respiration

22. Odor of breath: Smell of alcohol, Musty fetor→ hepatic coma, Uriniferous smell of uremia, Spoiled fruit smell of DKA Burnt almond→ cyanide poisoning

23. Skin petechial rash Meningococcal meningitis Endocarditis Sepsis,thrombotic thrombocytopenic purpura Rickettsial infection- RMS (rocky mountain spotted fever)

24. Multiple injection marks: Drug addiction Acute endocarditis Hepatitis B /C with encephalopathy HIV

25. Examination of Lymph Nodes: Generalized lymphadenopathy is nonspecific, because it may be seen with Neoplasm, infection (including AIDS), Collagen vascular disease, Sarcoid, Hyperthyroidism, Addison's disease and Drug reaction (especially that due to phenytoin). Local lymph node enlargement or inflammation, however, may provide clues to a primary tumor site or source of infection.

26. Neurological Examination

27. Neurological Examination The neurologic examination is the key to etiologic diagnosis in the comatose patient. General posture, Level of consciousness, Pupillary size and reactivity, Ocular motility, Corneal reflex, Brain stem reflexes ( oculocephalic and vestibulo-ocular reflexes) and The motor system Fundoscopy Head and Neck Examination Meningismus

28. A. General posture : Lack of restless movements on one side or an outturned leg - hemiplegia. Intermittent twitching movements of a foot, finger or facial muscle - sign of seizures. Multifocal myoclonus - metabolic disorder, particularly uremia, anoxia or drug intoxication (lithium and haloperidol) or prion disease(rare0 or “ hashimoto encephalopathy.” In a drowsy and confused patient bilateral asterixis is a certain sign of metabolic encephalopathy or drug intoxication. Decorticate rigidity and decerebrate rigidity, or “posturing,”

29. Decorticate posturing indicates that there may be damage to areas including the cerebral hemispheres, the internal capsule, and the thalamus. Decerebrate posturing indicates brain stem damage, specifically damage below the level of the red nucleus (e.g. mid-collicular lesions).

30. B. Level of consciousness The  AVPU scale  is a system by which a health care professional can measure and record a patient's level of consciousness. The AVPU scale is a quick and easy method to assess level of consciousness (primary survey) .

31. CONTD. AVPU: A –Alert V – Verbal : Respond to voice stimulus P –Pain : Respond to pain U – Unresponsive Interpretations: AVPU is incorporated into many early-warning score systems for critically ill patients, as it is simpler tool than GCS, but is not suitable for long-term observation. During the initial rapid assessment of the critically ill patient, it is helpful to use the AVPU scale, but is not suitable for long-term observation. The GCS should be used in the full assessment recommends using GCS to assess all patients with head injuries.

32. Glasgow Coma Scale (GCS) GCS is a neurological scale which aims to give a reliable and objective way of recording the conscious state of a person for initial as well as subsequent assessment.

33. Table: Glasgow  Coma Scale (GCS) Eye-opening (E) Spontaneous 4 To speech 3 To pain 2 Nil 1 Best motor response (M) Obeys 6 Localizes 5 Withdraws 4 Abnormal flexion 3 Extensor response 2 Nil 1 Verbal response (V) Orientated 5 Confused conversation 4 Inappropriate words 3 Incomprehensible sounds 2 Nil 1 Coma score = E + M + V Minimum 3 Maximum 15

34. Interpretations of GCS It is now almost universal use for assessing people with traumatic brain injury or an altered level of consciousness. Brain injury is classified according to GCS as follows: Severe: GCS 3-8 Moderate: GCS 9-12 Mild: GCS 13-15

35. C. Pupils Normal Pupils: Normal pupils are 3–4 mm in diameter and equal bilaterally; they constrict briskly and symmetrically in response to light. Normal pupils, however, are larger in children and smaller in the old.

36. Pupillary changes Pupils Causes 1 B/L Pin-point pupils ( less than 1mm)but responsive Opiates poisoning , extensive pontine hgr . 2 B/L small pupils but responsive B/L diencephalon involvement or destructive pontine leison 3 B/L slightly small pupils (1 to 2.5 mm) but responsive Metabolic encephalopathies , deep B/L hemisphere lesion or thalamic hgr . 4 B/L dilated and fixed Severe midbrain damage, Overdose of atropine, scopolamine, glutethemide .

37. Pupillary changes Cont d. Sr. no. Pupil Causes 6 U/L small pupil Horner syndrome 5 Ipsilateral dilated pupil with no direct or consensual reflexes Compression of 3 rd cranial nerve e.g , uncal herniation 7 U/L small and irregular pupil unresponsive Leison in pretectal area of midbrain

38. Figure: Schematic presentations of common abnormalities of pupils

39. D. Ocular motility Asymmetric ocular motility accompanies structural more than metabolic coma. Roving eye movement →light coma of metabolic origin. Lateral & slight downward deviatioin→3 rd nerve palsy Failure to move right eye downward when right eye is adducted→4 th nerve palsy Medial deviation→ 6 th nerve palsy

40. D. Ocular motility contd … Figure: Right 3rd nerve palsy- position of eyeball is abducted, downwards and outwards & ptosis . Figure : Right 4th nerve palsy – unable to move right eye downward when right eye is adducted. Figure: Left 6th nerve palsy – Failure to abduct of left eye and medially when right eye is adducted.

41. Conjugate deviation Cerebral hemispherical lesion – “looks at the lesion” With unilateral pontine lesion → “looks away from lesion ” pontine lesion Cerebral hemispherical lesion

42. E . Corneal reflex It is retained until coma is very deep. Bilateral loss of corneal reflex with light coma considers drug effect or local anesthetics in both eyes. Unilateral loss indicates focal neurological disease. Corneal reflexes are absent in brain death Corneal reflexes - tested by using a cotton-tipped swab . Figure: There is no blink response to direct corneal stimulation.

43. F. Brain stem reflexes 1 . Oculo -cephalic Reflex(OCR): OCR is a reflex eye movement that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field. Figure: 14.6 Positive oculo -cephalic reflex (when the head moves to the right, the eyes move to the left, and vice versa)

44. 2. Vestibulo-ocular reflexes Douching of one ear with cold water produces ipsilateral deviation of both eyes with a contralateral quick phase nystagmus lasting for 1—2 minutes. Use of hot water produces the opposite effect i.e. contralateral deviation with ipsilateral quick phase nystagmus . Bilateral douching with cold water gives rise to downward deviation with upward nystagmus and with hot water the opposite response. Figure: Vestibulo-ocular reflexes Absence or abnormal response indicates brain-stem dysfunction Metabolic diseases affecting the brain-stem often give rise to loss of vestibulo ocular and oculo -cephalic responses in their early stages whereas structural diseases of brain-stem often give rise to abnormal responses e.g. skew deviation or asymmetrical responses.

45. G. The motor system The motor system is assessed by testing deep tendon reflexes , feeling the resistance of the patient's limbs to passive movements, and testing the strength of posturing and local withdrawal movements. Local withdrawal movements may be elicited by pressing a pen hard on the patient's fingernail, pinching of limbs, rubbing the sternum to elicit pain and observing if the patient withdrawals the respective limb from the noxious stimulus.

46. G. The motor system contd … Posture and spontaneous movements: Appropriate response – brushing away the source of stimulus. Inappropriate response – decerebrate or decorticate rigidity. Motor response is also of localizing value Paralyzed limb will show no response and presence of hemiplegia can therefore be evident. Decerebrate rigidity indicates brain-stem damage and if bilateral - a very poor prognosis. Complete flaccidity with no response to noxious stimuli is often indicative of severe CNS depression due to drug overdose.

47. G. The motor system contd … Motor response: Asymmetric response indicates structural lesion, cerebral hemisphere or brainstem. Symmetric lesion indicates more diffuse lesion (metabolic encephalopathy).

48. G. The motor system contd … Movement of limbs: Unilateral spontaneous limb movement indicates cerebral hemisphere or brain stem lesion. Passive movement of suspected paralyzed limb fall like “dead weight” indicates mono or hemiplegia. The rest of the neurological examination is also important in the diagnosis e.g. presence or absence of other cranial nerve involvement; states of intracranial pressure as revealed by fundal examination i.e. papilledema

49. H . Fundoscopy Fundoscopy examination can detect : Papilloedema Hypertensive changes Subarachnoid haemorrhage Diabetic retinopathy

50. I .Head and Neck Examination The head and neck must be carefully examined for signs of trauma. Signs of Trauma: Inspection of the head may reveal signs of basilar skull fracture , including the following: Raccoon Eyes Periorbital ecchymoses . Battle Sign Hematoma and discoloration overlying the mastoid bone behind the ear Hemotympanum Blood behind the tympanic membrane . Cerebrospinal Fluid (CSF) Rhinorrhea or Otorrhea

51. I . Head and Neck Examination contd.. Palpation of the head may demonstrate a depressed skull fracture or swelling of soft tissues at the site of trauma. Laceration or edema of the scalp is indicative of head trauma. Scars on the neck may be from endarterectomy, implying vascular disease or from thyroidectomy or parathyroidectomy , suggesting concomitant hypothyroidism, hypoparathyroidism or both. Goiter may be found with hypothyroidism or hyperthyroidism

52. J . Meningismus Neck stiffness may be a sign of infectious or carcinomatous meningitis , subarachnoid hemorrhage, or central or tonsillar herniation. Neck stiffness may be absent, however, in coma from any cause but is likely to be present in less severe alterations in arousal.

53. Investigations Bearing in mind the clinico -pathological causes of coma the following investigatory scheme can be adopted. Focal neuronal lesions Skull radiograph CT/ MRI of brain Ventriculography EEG, ECG, cardiac monitoring Carotid angiography Vertebral angiography

54. Investigations Diffuse neuronal lesions - Examination of CSF (cerebral spine fluid) Serum glucose, calcium, Na+, K, magnesium Blood gases and PH Liver and renal functions Drug levels Blood for MP Blood culture Complete blood count and PBF

55. Management

56. General management In general, management of the comatose patient depends on the cause. However, while the patient is undergoing evaluation, it is essential to : A (airway), B (breathing), C (circulation ) Take blood test as putting in lines Nursing attention to pressure areas and eyes Bronchial toilet

57. General management Contd.. Nutrition-needs NG tube also for decompression Bladder care-catheter Bowel care Monitoring - vital signs/neurology Infection control Definitive management of unconsciousness

58. Table: Emergency Management of the unconscoiusness Patient. Immediately Next Later Ensure adequacy of airway, ventilation, and circulation If signs of meningeal irritation are present (Figure 2–3) perform LP to rule out meningitis ECG Obtain a history if possible Draw blood for serum glucose, electrolytes, liver and renal function tests, PT, PTT, and CBC Perform detailed general physical and neurologic examination Correct hyper- or hypothermia Start IV and administer 25 g of dextrose, 100 mg of thiamine, and 0.4–1.2 mg of naloxone IV Order CT scan of head if history or findings suggest structural lesion or subarachnoid hemorrhage Correct severe acid-base and electrolyte abnormalities Draw blood for arterial blood gas determinations   Chest x-ray Treat seizures   Blood and urine toxicology studies; EEG

59. Summary of Management ABC of life support Oxygen and I.V access Stabilize cervical spine

60. Summary of management Contd.. . Blood glucose Control seizures Consider I.V glucose, thiamine, naloxone , flumazenil

61. Summary of management Contd.. . Brief examination and obtain history Investigate Reassess the situation and plan further

62. Prognosis of Coma: Regarding all forms of coma, but particularly after cardiac arrest, if there are no pupillary, corneal, or oculovestibular responses within several hours of the onset of coma, the chances of regaining independent function are practically nil . As a rule, recovery from coma of metabolic and toxic causes is far better than from anoxic coma, with head injury occupying an intermediate prognostic position. Most patients who are comatose because of a stroke will die; subarachnoid hemorrhage in which coma is due to hydrocephalus is an exception.

63. Thank you