Approach_ to_ a comatos patient........pptx

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1. Presenter: Belachew Dagne- C-I Moderator: Dr. Urji (MD) August , 2024 Yekatit 12 Hospital Medical College Dept. of Medicine APPROACH TO A COMATOSE PATIENT

2. Introduction Objective Pathophysiology of Coma Causes Approach to Diagnosis Management Prognosis Outlines

3. Objectives To understand the levels of consciousness To know how to diagnose coma pt How to manage comatose pt 3

4. Introduction Consciousness The ability to arouse & respond spontaneously and appropriately to stimuli. It is dependent upon the integrity & interaction b/n the cerebral cortecs & ascending reticular activating system (ARAS). 4

5. Has two domains: 1. Arousal reflecting the individual's wakefulness and responsiveness to stimuli. performed by deep brainstem and medial thalamic structures. 2. Cognition Encompassing awareness of self and surroundings, perception, and cognitive functions. Through integrity of the cerebral cortex and its subcortical structures

6. Structures involved in consciousness Brainstem Reticular Formation Thalamus Hypothalamus Ascending Projection Pathway Widespread Areas in the Cerebral Cortex 6

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9. The Reticular Activating System Initiation of Consciousness Modulation of Consciousness , sleep, and altered states. Integration of Information

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11. Coma Coma is a state of prolonged unconsciousness in which the patient cannot be aroused (awakened) even with painful stimuli. It is a serious life-threatening condition, which necessitates urgent diagnostic and therapeutic measures to preserve life.

12. Pathophysiology Altered consciousness due to Diffuse lesions of cerebral cortex Focal lesions of ARAS disruption of ascending reticular activating system projecting to the thalamus and cortex from midbrain and pons.

13. Causes of coma The causes of coma can be divided into three broad categories: Those without focal neurologic signs Those with prominent focal signs and Meningitis syndromes

14. 1. Those without focal neurologic signs Intoxication Metabolic disturbances Severe systemic infections Shock from any cause Status Epilepticus Hyper perfusion syndromes like hypertensive encephalopathy Sever hypothermia or hyperthermia

15. 2.Those with prominent focal signs Basal ganglia and thalamic hemorrhage Pontine hemorrhage Cerebellar hemorrhage Basilar artery thrombosis Subarachnoid hemorrhage Brain tumor with surrounding edema widespread traumatic brain injury Brain abscess

16. 3.Meningitis syndromes Bacterial meningitis & meningoencephalitis Subarachnoid hemorrhage Paraneoplastic or autoimmune encephalitis Carcinomatous & lymphomatous meningitis

17. Causes of coma Trauma: Head injury, shaken baby syndrome Infections: Meningitis Encephalitis Cerebral Abscess Cerebral malaria septic shock Tumor: Space-occupying lesions 17

18. Metabolic Disturbances: Hypo/Hyperglycemia, DKA Electrolyte imbalances (hypo/hypernatremia, hypocalcemia, hypomagnesemia) Thiamine (Vitamin B1) deficiency Pyridoxine (Vitamin B6) deficiency Toxins: Uremic/Hepatic Encephalopathy Porphyria Barbiturates Opioids 18

19. Vascular Issues: Stroke Hypertensive encephalopathy Polycythemia Vasculitis AV malformation Hypoxic-Ischemic Encephalopathy (HIE) 19

20. Approach to a pt in coma

21. Primary survey and rescucitation Initial stabilization includes assessment of: Airway (with C-spine precautions) The tongue is the most common cause of obstruction in the unconscious child. Intubation is needed for: Poor airway or approaching loss of patent airway Raised ICP Precaution during transport or CT scanning Breathing Must ensure adequate oxygenation and ventilation Asses respiratory rate and chest movement

22. 3. Circulation Check vital signs The patient may be in shock. Is Cushing response (↑BP, ↓HR, abnormal breathing pattern due to ↑ICP) present? 4. Disability Primary survey and rescucitation... (Cont’d)

23. Secondary Survey History Taking: Trauma (head injury) Drugs and chemicals Time course: onset and progression lucid interval Preceding symptoms:- Seizure, headache, depression, hemiplegia, fever, vertigo & vomiting Preceding event - Headache:- common in intracranial space occupying lesion of any cause - Seizure of recent onset:- strongly suggest cerebral lesion (encephalitis, abscess, or trauma)

24. What is around the patient:- drug containers and alcohol Previous illness - Previous attack:- HTN, DM, epilepsy, lung & heart disease, uremia, cirrhosis, Cancer, allergy, infectious disease, endocrine ds, Psychiatric ds

25. Details of any immediately preceding medical and neurological symptoms (confusion, fever, headache, seizures, double vision or vomiting Pallor, sweating, unsteady gait and slurred speech suggests hypoglycemia and DM History of trauma few days back with fluctuating drowsiness => subdural hematoma Rapid loss of consciousness after trauma => extradural hematoma 25

26. Physical Examination Heart Rate: Bradycardia: raised ICP Tachycardia: AF, Ventricular tachycardia, Ventricular fibrillation Blood Pressure: Hypertension: raised ICP, HT-Encephalopathy Hypotension: Decreased Cerebral Perfusion Pressure Temperature : >41c0: Hyperthermia <34c0: Hypothermia Vital Signs

27. Neurologic evaluation Level of consciousness – Use GCS or modified GCS GCS < 8 suggests coma, < 5 = Grave prognosis 5-8 = A better prognosis in children than in adult 31

28. Scoring systems

29. 2. AVPU (ALERT, VOICE, PAIN, UNRESPONSIVENESS) system used by first responders& emergency medical professionals A= Alert- can answer questions V=Voice- respond to verbal commands P=Pain- reponds to pain U=Unresponsiveness Advantages: Unlike GCS not developmentally dependent (a child does not have to understand spoken language or follow commands.)

30. 3. FULL OUTLINE OF UNRESPONSIVENESS (FOUR ) Sixteen point scale, with potential scores ranging from 0-16. Evaluates four variables Eye response Motor response Brainstem reflex- pupillary & corneal reflex Respiratory effort Has advantage for intubated patients

31. Decerebrate posturing Extension and internal rotation of the arms and legs. Implies brain stem involvement from a compressive or destructive process. B. Decorticate posturing Produces adduction and flexion at the elbow s, wrists and fingers with leg extension and rotation. o Implies hemispheric dysfunction with an intact brainstem 2.Posturing

32. 3) Focal neurologic deficit :- Muscle tone, Reflexes, weakness, and mov’ts Look for position of limbs 4) Meningeal signs :- Neck stiffness, Brudzinski and Kerning sign 37

33. Brainstem reflexes Oculocephalic reflex (doll's eye reflex)

34. Oculovestibular reflex (caloric reflex test)

35. Pupillary Response

36. Investigations Blood glucose measurement hypoglycemia CBC with differentials Leukocytosis or leukopenia in severe infections Serum Electrolytes and b lood ammonia Atrial blood gas and PH Organ function tests ( LFT and RFT ) 43

37. 44 Septic Screen: blood culture, urinalysis for microscopy, sensitivity and culture Peripheral smear and rapid diagnostic test for malarial parasite( if suspected of malaria ) Toxicology (serum and urine) i.e. salicylates, organophosphates, opiates plasma amino acids, urine organic acids and the appropriate metabolic workup Chest x ray

38. Lumbar puncture High pressure during intracranial infections and space-occupying lesions Cell count Glucose, protein, gram stain Viral PCR for HSV , GeneXpert 45

39. Contra-indications for Lumbar Puncture Elevated ICP and focal Neurologic deficit Severe cardio respiratory compromise Infection of the overlying skin Thrombocytopenia (Relative) Congenital abnormalities of the overlying skin Evidence of increased ICP (other than a bulging fontanel),

40. CT scan of the head The method of choice in traumatic brain injury since it can detect density changes between brain tissue and acute hemorrhages with high resolution First choice in emergency A normal CT doesn’t rule out elevated ICP. 47

41. MRI Advantages Superior imaging of soft tissue More precise demonstration of lesions of the posterior fossa Can identify severe lesions of the brain stem, which can’t be found using CT (superior prognostic value since these lesions are of great importance for prognosis) 48

42. EEG The “gold standard” for the detection of epileptic functional disturbances. Can verify the diagnosis quickly Determines the adequate therapy Monitors the effect and success of treatment 49

43. BRAIN DEATH Brain death is a state of irreversible cessation of all cerebral and brainstem function with preservation of cardiac activity and maintenance of respiratory and somatic function by artificial means. Established criteria contain two essential elements, after assuring that no confounding factors (e.g., hypothermia, drug intoxication) are present: Widespread cortical destruction that is reflected by deep coma and unresponsiveness to all forms of stimulation; and Global brainstem damage as demonstrated by absent pupillary light reaction, absent corneal reflexes, loss of oculovestibular reflexes, and destruction of the medulla, manifested by complete and irreversible apnea.

44. Apnea testing can be done by the use of preoxygenation with 100% oxygen prior to and following removal of the ventilator. CO2 tension increases ~0.3–0.4 kPa/min (2–3 mmHg/min) during apnea. Apnea is confirmed if no respiratory effort has been observed in the presence of a sufficiently elevated Pco2 . An isoelectric EEG Radionuclide brain scanning, cerebral angiography, or transcranial Doppler measurements

45. Management Stabilization ( ABC of life ) 52

46. The immediate goal in a comatose patient is prevention of further nervous system damage. Hypotension, hypoglycemia, hypercalcemia, hypoxia, hypercapnia, and hyperthermia should be corrected rapidly specific mgt depends on the cause identified

47. Administration of hypotonic IV solutions should be monitored carefully in any serious acute brain illness because of the potential for exacerbating brain swelling.

48. 55 Control of ICP S edation Hyperventilation Blood pressure control Corticosteroid proper positioning

49. Follow up Nutritional support Close monitoring with Neuro-Sign Chart Skin/Position: Turn patient every 2-3 hours to prevent decubitus ulcer Eye care: eye padding Nosocomial infections Important complications during hospitalization Must be prevented and treated promptly

50. Neuro-Sign Chart (components) Vital signs Oxygen saturation Random blood sugar Seizure occurrence, Glasgow Coma Scale (GCS) Muscle tone & power Deep tendon reflex Pupillary reaction, documented Vomiting, Fluid input & output, and Remarks.

51. Predictors of outcome in non-traumatic coma a) Cause of coma - Metabolic => good prognosis - CVA & hypoxic ischemic insult => poor prognosis b) Depth of coma - No eye opening after 6 hours of coma - only 10% have good or moderate recovery c) Duration of coma - The longer the coma persists, the less likely the chance for recovery d) Brainstem reflexes: Signs of poor prognosis 1) Corneal reflex:- absent 24 hours after onset of coma 2) Pupilary reflex:- absent 24 hours after onset of coma 3) Roving eye sign:- absent by the 7 th day of onset of coma 58

52. Reference s Harrison's principles of Medicine 21 st Edition Bates guide to physical examination and History taking 13 th Edition MSD Manual professional version 59

53. Thank you !