HOW TO CARE FOR THE UNCONSCIOUS PATIENT.pptx

How to approach an unconscious patient

1. THE UNCONSCIOUS PATIENT A Presentation by Shakira, Ishaque and Moses

2. OUTLINE OF PRESENTATION Consciousness Pathophysiology Levels Assessment Unconscious Causes Clinical features Management

3. Consciousness Consciousness is defined as the awareness of oneself, the surroundings and the ability to respond to external stimulation and inner need.

4. PATHOPHYSIOLOGY A normal level of consciousness depends upon activation of the cerebral Cortex and brainstem reticular activating system (RAS). Both components and the connections between them must be preserved for consciousness to be maintained

5. Pathophysiology The cerebral cortex is a group of neuronal cell bodies called gray matter and their myelinated axons called white matter and is responsible for perception, relay of the sensory input via the thalamic pathway and many other neurological functions, including complex thinking . The reticular activating system(RAS) is a network of neurons in the brainstem that plays a crucial role in regulating arousal, consciousness and sleep-wake cycles

6. Level of consciousness T here are various levels of Consciousness comprising a continuum from full alertness to deep coma. Drowsiness or lethargy_it is characterized by easy arousability with light stimuli 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.

7. Assessment The Glasgow Coma Scale (GCS) is the main tool used to assess the level of consciousness or unconsciousness in a patient. It was originally designed to assess head injury but is well validated in non traumatic patients. It is based on three parameters; Eye opening(E), motor response(M) and verbal response(V)

8. E Action Confirm Score Spontaneous Eyes open and fixed on objects 4 Speech Eyes open to a specific reques or shouting 3 Pain Eyes open to pain 2 Nil No opening to pain 1

9. M Action Confirm Score Obeys commands Patient does simple thtings you ask 6 Localizes pain Patient does purposeful movements in response to pressure on the nail bed, supraorbital ridges and sternum 5 Withdraws to pain Patient pulling limb away from a painful stimulus 4 Abnormal flexion (decorticate response) to pain flexion of limb to pain 3 Abnormal extension ( decerebrate response) to pain Adduction of shoulder and pronation of arm to pain 2 Nil Total silence 1

10. V Action Confirm Score Oriented Pt knows name, place, why, year, season, month. 5 Confused conversation Pt talks in sentences but disoriented 4 Inappropriate words random words but no sentences 3 Incompehensble sounds Moaning but no words 2 nil total silence 1

11. GCS GCS Score Interpretation 15 No brain damage 13-15 minor 9-12 moderate 3-8 severe 3 very severe Less than 15 Altered consciousness 8 or less Coma

12. Unconsciousness/Coma A patient is considered unconscious when they are not able to respond to external stimuli such as sounds or touch. The unconscious patient and coma patient are often used interchangeably though coma is more specific. All coma patients are unconscious but not all unconscious patients are in 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

13. Causes of Coma Vascular: Stroke : Intracerebral hemorrhage, Subarachnoid hemorrhage or large hemispheric ischaemic stroke Anoxic brain injury : Cardiac arrest. 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 .

14. Causes of Coma Metabolic disturbances ; 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  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.

15. 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.

16. Management In general, management of the comatose patient depends on the cause. However, while the patient is undergoing evaluation, it is essential to : Take blood test while putting in lines Nutrition-needs NG tube also for decompression Bladder care-catheter

17. Management 1.Immediate management of the comatose patient. 2.After initial management , then The history General physical and Neurologic examinations

18. Management IMMEDIATE MANAGEMENT ABC OF LIFE SUPPORT A Airway with cervical spine control B Breathing C Circulation Note : it is always safe to start with the alphabet ABC

19. Airway Assess patency of airway and imminent threats e.g. Mucosal damage, anaphylaxis Assess by talking to patient. Appropriate response suggests clear airway Open the airway with a chin lift or jaw thrust Check for upper airway obstruction – foreign bodies, dislodged teeth, dentures, macroglossia etc. Look for facial fractures and injuries to the neck (trachea and larynx). Listen for abnormal breathing sounds, stridor or hoarseness. Feel for the movement of air Appreciate the potential for cervical spine injury

20. Airway MANAGEMENT Protect c-spine in any suspected trauma associated cases, before attempting any interventions Remove foreign body by direct vision and suction secretion Administer high concentrations of inspired oxygen using the appropriate face mask for patient and monitor oxygen saturation Intubate immediately: patients with inhalation burn Severe anaphylaxis reactions Trauma (GCS <8 or any spinal injuries )

21. Breathing Determine centrality of the trachea and apex beat Look for symmetrical expansion and respiratory rate. Look for obvious contusion, laceration or flail segments. Listen for movements of air: normal, absent or decreased Listen for heart sounds: normal or muffled Recognise specific life-threatening conditions eg : Tension pneumothorax Flail chest with pulmonary contusion Life-threatening bronchospasm Pulmonary oedema

22. Breathing R ate: Normal rate in adults 12-20 . A ir entry: Look and feel for bilateral chest rise; listen for bilateral air entry. C olour: Assess for cyanosis. Also assess for pallor. E ffort: Increased respiratory efforts means the patient is in distress. S ATS Action: Supplement oxygen Definitive air-way and assisted ventilation if necessary

23. Circulation Identify pulses and asses rate, rhythm and character and check BP Assess peripheral perfusion using capillary refill time Assess BP, JVP, the apex beat and listen to the heart for extra sounds Look for obvious source of bleeding in trauma Identify specific shock state and treat all shocked patients promptly. IV access with administration iv crystalloid solution Draw blood for base line lab investigations, cross-match and icon Blood transfusion if indicated Prevent hypothermia Start ECG monitoring

24. M anagement 2.After initial management , then The history General physical and Neurologic examinations

25. History History is obtained by family, friends or EMS pesonnel . 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.

26. General Physical Examination

27. 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. 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 .

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

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

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

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

32. 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.

33. Figure: Pattern of respiration

34. Odor of breath: Smell of alcohol, fetor hepaticus (rotten eggs smell) in hepatic coma Uremic fetor (urine or ammonia-like smell) of uremia fruity-like smell in DKA

35. Skin petechial rash Meningococcal meningitis Endocarditis Sepsis,thrombotic thrombocytopenic purpura

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

37. Neurological Examination

38. 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

39. A. General posture : Intermittent twitching movements of a foot, finger or facial muscle - sign of seizures. Multifocal myoclonus - metabolic disorder, particularly uremia, anoxia or drug intoxication 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,”

40. 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).

41. B. Level of consciousness The  AVPU scale GCS

42. CONTD. AVPU: A –Alert V – Verbal : Respond to voice stimulus P –Pain : Respond to pain U – Unresponsive it is simpler tool than GCS, but is not suitable for long-term observation.

43. 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.

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

45. 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 7 U/L small and irregular pupil unresponsive Lesion in pretectal area of midbrain

46. Figure: Schematic presentations of common abnormalities of pupils

47. 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

48. 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.

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

50. 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.

51. 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)

52. 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.

53. 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.

54. 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.

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

56. G. The motor system contd … Movement of limbs: Unilateral spontaneous limb movement indicates cerebral hemisphere or brain stem lesion

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

58. 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

59. 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 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

60. J. Meningismus Neck stiffness may be a sign of infectious or carcinomatous meningitis, subarachnoid hemorrhage, or central or tonsillar herniation. .

61. 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

62. 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

63. 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

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

65. Summary of management Contd.. . Blood glucose Control seizures Consider I.V glucose

66. Summary of management Contd.. . O btain history and perform examination Investigate Reassess the situation and plan further

67. 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.

68. Thank you