ALTERED SENSORIUM AND COMA Consciousness
- 1. ALTERED SENSORIUM AND COMA Dr RAJESH M CONSULTANT EMERGENCYMEDICINE CARE HOSP BANJARA HILLS
- 2. DEFINITIONS
- 3. • Consciousness- It’s a state of being awake and aware of both self and ones surroundings, or its human awareness of both internal and external stimuli. • Spectrum of state of altered consciousness covers 1. Lethargy 2. Stupor 3. Coma
- 4. • Lethargy- mild depression in level of consciousness and can be aroused with little difficulty. • Stupor- can not be aroused from sleep like state ( only respond by grimacing or drawing away from painful stimuli). • Coma – more depressed level of consciousness and unable to make any purposeful response.
- 6. • Reticular formation system plays a major role in alertness, wakefulness and arousal. • Ascending reticular activating system is a group of neural connection that receive sensory input and projects to cerebral cortex through the midbrain and thalamus from the reticular formation.
- 8. • A 70years male k/c/o HTN,DM,CKD, HYPOTHYROIDISM, chronic alcoholic, presented to ED with complaints of fever, headache, associated with vomitings and altered mental status since 3days. H/O fall 4days back. • DD?
- 10. 1)TRAUMA • Epidural hematoma-due to rupture of artery (MMA). In about 85 % their would be associated skull fracture. • Subdural hematoma-due to tearing of bridging veins through dura and arachnoid. Skull factures present in 30% of cases. Retinal hemorrhage in 75% of cases. • Intra cerebral hematoma (ICH).
- 14. 2) STROKE
- 15. 1. Hemorrhagic stroke – due to aneurysm rupture, can cause headache then leading to altered sensorium. – AV malformation or cavernous hemangioma rupture can lead to altered sensorium. – Hemorrhagic stroke involving brainstem can lead to coma.
- 16. 2. Thrombosis or Embolic stroke – Occlusion of anterior ,middle or posterior cerebral artery rarely cause coma. – Infarcts eventually lead to increased ICP were than can lead to coma. – Cerebellar infarcts causes gait disturbance and rarely coma. – Basilar artery infarcts cause rapid coma due to brainstem involvement.
- 17. 3. Brain infections • MENINGITIS Bacterial meningitis is the most common cause of infections and can lead to profound ALOC. Non bacterial have slow onset of symptoms and delayed coma. • BRAIN ABSCESS Secondary to chronic sinusitis , ear infection, Dental infections , endocarditis or uncorrected cyanotic heart diseases increase the risk. • ENCEPHALITIS Inflammation of brain parenchyma usually due to viral infection. HSV – most common and devastating cause, leading to death or permanent neurological damage in 70% of cases. It affects temporal lobe causing seziures, parenchymal swelling and uncal herniation.
- 19. 1) Metabolic causes. • Glucose metabolism abnormality. – Hypoglycemia – Most common cause for ALOC. – Risk factors – insulin pumps, elderly, type 1 diabetics, insulin tumors. • Hyperglycemia (DKA , HHS ) – Were they present with tachypnea, nausea,vomiting, abdominal pain , dehydration .
- 20. 2) Endocrine causes. a) Adernal crisis They present with weakness , weight loss, hyoptension , hyperpigmentation . b) Thyrotoxic crisis- Present with fever , tachycardia , hypertension , Sweating , diarrhea. c) Myxedema coma Present with weight gain , edema , constipation , Hypotension , altered response.
- 21. 3. Electrolyte imbalance. A)Hyponatremia- present with progessive confusion ,headache, anorexia, seizures, poor feeding. B) Hypercalcemia – Lethargy, polyuria, AKI, constipation Risk factors Maligancy , gout, chemotherapy drugs. C) Uremia – They present with nausea , vomiting, fatigue, anorexia, ammonia breath, abdominal pain , breathing difficulty.
- 22. Approach in Emergency Department
- 23. • HISTORY • 1:Baseline Cognitive function • 2:Time course of the present illness • 3:Current Medications
- 28. Pathological variables Pupillary light reflex and corneal response Spontaneous eye movements Respratory movements Motor response
- 29. Brain Herniation
- 30. Pupillary reflex • Pupillary pathway is near ARAS • Pupillary pathyway resistant to metabolic insult. • Its single most important physical finding to distinguish structural vs meatbolic disease.
- 31. Pupillary abnormalities 1) Bilaterally enlarged and Unreactive pupils Indicate massive CNS dysfunction( anoxia, drug over dose, poisoning , hypothermia) 2) Pinpoint pupil – indicate pontine hemorrhage,opiates, op poisoning . 3) Unilateral fixed dilated pupil – indicate ipsilateral expanding mass and possible herniation.
- 32. Eye movements • In a light stage of coma, roving side to side movements occur • Persistent deviation to one side may indicate focal seizure activity. • Structural brain stem lesions abolish conjugate eye movements
- 33. Oculocephalic movements(dolls eyes) • Hold eyelids open and rotate head from side to side • Normal response – conjugate deviation of eyes away from direction of head movement .
- 35. Oculovestibular reflex • Elevate head of bed 30 degree and inject 10-15ml of ice water into ear canal. • Normal response is nystagmus with slow phase towards irragated ear and fast beats away. • Unconscious patient with intact brainstem eyes move towards and remain tonically deivated for a minute and slow return to midline.
- 37. Respiratory pattern • Ventilation Is governed by lower pons and medulla . • Modulated by forebrain cortical centers. • Patterns of abnormal respiration A) Cheyne stroke breathing – Hyperapnea (deep and fast ) alternating with apnea B) Central neurogenic hyperventilation – Regular and rapid respiration – Normal pao2 and low paco2 – Midbrain lesion – Brain’s attempt to reduce icp c) Apneustic breathing – Deep , gasping inspiration with a pause at full inspiration followed by a brief insufficient release . – Signifies damage to pons / medulla
- 38. Motor response • Assess muscle strength , tone, and DTRs for normality and symmetry . • Assess if patient can localize motor response to determine level of brain lesion.
- 39. Decorticate posturing – • With elbows , wrists and fingers flexed and legs extended and rotated inwards . • Lesion in the cortex or subcortical white matter . Decerebrate posturing • Rigid extension of arms and legs • Lesion at brainstem and pons.