Downloaded 485 times
Uploaded byRichard Brown
Coma Bp
1. The document provides guidelines for evaluating and managing unconscious patients, outlining stages of consciousness from conscious to death and diagnostic tests and treatments. 2. Key factors include assessing airway, breathing, circulation, disability level using the Glasgow Coma Scale, and identifying potential causes such as trauma, stroke, infection, toxins or metabolic disturbances. 3. Structured neurological examination including vital signs, pupil response, motor response and diagnostic tests can help identify structural or toxic/metabolic causes and guide emergency treatment and management.
More Related Content
Coma Bp
- 1. MANAGEMENT OF UNCONSCIOUSPATIENT DR. B. PRAKASH. Prof. M.B. PRANESH DEPT. OF NEUROLOGY KG HOSPITAL AND POSTGRADUATE INSTITUTE, COIMBATORE – INDIA
- 2. INTRODUCTION Unconscious patientmakes everybody anxious Requires structured way of approach Should act Urgently / Appropriately / Accurately Conscious> Drowsy> Unconscious> ?Death / Permanent Brain Damage
- 3. STAGES OF CONSCIOUSNESSConscious: Awareness of self and surroundings. Clouding of Consciousness: Reduced attention span with irritability. Confusion: Mild lowering of consciousness. Lethargy : Drowsy but arousable. Obtundation: Drowsy, slow reaction, gives appropriate answers, back asleep on leaving alone. Stupor: Roused by vigorous repetitive stimuli, moans without proper answering. Light coma: Unarousable, disorganized primitive motor responses. Deep Coma: Absence of response to most painful stimuli.
- 4. Eye opening 4 Spontaneous 3 To speech 2 To pain 1 None Best motor response 6 Obeying 5 Localizing pain 4 Withdrawal 3 Abnormal flexing 2 Extensor response 1 None GLASGOW COMA SCALE Best verbal response 5 Oriented 4 Confused conversation 3 Inappropriate words 2 Incomprehensible sounds 1 None USED MOSTLY FOR HEAD INJURY PATIENTS RATHER THAN STROKE (HEMIPLEGIA,APHASIA)
- 5. Algorhythm COMA Airway/?IntubateIV Line CFCD Tests-Eme History-Eme CBC, ESR Sugar,RFT ABG,Lytes CXR,ECG Ca,Mg, Toxic Scr’n TRAUMA CT Scan No Trauma Neu.Surg Stiff Neck CT Scan Normal SAH LP Meningitis Toxin Alc->Thiamine 100mg / 50% Dextose 50 ml Opiate -> Inj.Naloxone 0.4-0.8mg IV BenzDia ->Inj.Flumazenil 0.2-1 mg IV Others -> Stomach wash / Antidote / Sympt Supple CNS Exam Normal Lateralising Metabolic CT Scan
- 6. SELECTIVE HISTORY TAKINGFriend /Relative /Observer When was he Last seen? How was he discovered? What is the mode & evolution of Coma ? What are the past Illness? What drugs he is on? Is any past mental history? Trauma Drug / Toxins Head ache Vomiting Seizures Giddiness Fever Chest pain
- 7. SELECTIVE EXAMINATION VITALSIGNS: HTN – Structural /HT.E Hypo – Shock SKIN : Trauma / Needle Marks Rashes / Cherry redness Jaundice BREATH: Alcohol /Acetone Fetor Hepaticus HEAD Hematoma/#/Lacer’ns ENT: CSF otorrhea/Rhinorrhea Hemotympanum Tongue Biting NECK: Do not Move if injured Neck Stiffness (Meningitis / SAH)
- 8. Gen. Phy. ExamFever: Syst infection / Meningitis / Encephalitis Hyperthermia: Heat stroke / Anticholinergic intoxcn. Hypothermia : Cold exp / Alcohol / Barb /Phenoth’z Sedative/ Hypo Glycemia/ HypoThyroid/ Per.cir.Fail Tachypnea : Acidosis / Pneumonia Aberrant Respiratory Patterns: BS disorders Marked HTN : HT.E / SAH / ICP / Head injury Hypotension : Alcohol / Barb / Int.bleed / AMI / Sepsis / HypoThyroidism / Addison’s crisis Petechiae: TTP/ Meningococcemia/ Bld’g Diathesis
- 9. NEUROLOGIC EXAMINATION 1.Gen. Appearance 2. Level of Cons’ss 3. Respiration 4. Fields 5. Fundi 6. Corneal Reflex To asses the Depth of COMA To localize/Lateralize the lesion 7.Gag Reflex 8.Pupils 9.Ocular Movements 10.Motor Response 11.Sensory Resp’se 12.Reflexes
- 10. NEU.EXAM-1.GEN.APPEAR’CE Open Eyelids/ Slack Jaw – Deep Coma Head & Gaze deviation – Ipsi.Hemi.Lesion Myoclonus –BS Lesion / Metabolic Focal Seizures – Contra.Lesion / Hyperglycemia NEU.EXAM- 2.LEVEL OF CONS. Document the response to specific Stimulus Quantify with Glasgow Coma Scale
- 11. NEU.EXAM- 3.RESPIRATION. Depressed – Any deep Coma Chyne-stokes – Bihemisp / Metabolic Hypervent’n – Met.Aci/ Hep.Enc/ BS les/ Coning Apneustic – Pontine Damage Cluster – Pontine/ Cerebellar damage Ataxic (Biot’s) – Medullary Lesion
- 12. NEUROLOGIC EXAMINATION 4.Fields– By Menace Reflex 5.Fundii –Papilledema - >12 hrs of ↑ ICT Subhyloid H’ge – Asst’d č SAH 6.Corneal Reflex – Aff: CrV / Eff: CrVII 7.Gag Reflex – Absent in BS Les / Deep coma 11.Sensory Response – Lateralizing Sensory Loss 12.Deep T.Reflex – Helps in Lateralizing 13.Plantar Reflex -- Helps in Lateralizing -- ↑ ↑ Structural / Metabolic
- 13. Symmetrical Reacting pupils– intact midbrain Normal pupils + Absent Dolls – Metabolic / Sedatives Fixed Mid position pupil – Focal Midbrain Lesion Pinpoint Reactive – Pontine Damage / Opiate / OPC / Hydrocephalus / Thalamic Hemorrhage Unil / Dil / Fixed – Uncal Herniation - same/opposite Bil / Dil / Fixed – Central Herniation / Hypoxia / Atropine or Barbiturate Poisoning / Mydriatics Eccentric oval - Early midbrain / III n Compression Unil / Small (Horner) – Large Cerebral Hemorrhage Affecting Thalamus NEU.EXAM- 8.PUPILS.
- 14. Frontal Eye fieldsdrive horiz. Gaze to opp.side Pontine Gaze Centres drive gaze to same side Midbrain tegmentum & Lower diencephalon mediates vertical gaze movements Oculocephalic & Oculovestibular Reflexes act via semicircular canals / CrVIII / Vestibular and 3,4&6 th N Nuclei -- in eliciting gaze movements in comatose patients Normal gaze indicate Intact Cr III – VIII (MB & PONS) NEU.EXAM- 9.Ocular Movements.
- 15. (A) POSITION OFTHE EYES AT REST : Gaze away from Hemi paresis – Contra lateral Hemispherical lesion Gaze towards Hemi paresis – Contra lateral Pontine Lesion / Contra lateral Seizure Activity Forced down gaze – Mid Brain Tectal / Thalamic Lesion Slow roving gaze – Bihemisperical Lesion Ocular bob (Slow upward Brisk Downward & Loss of Horizontal eye movements) – Bil. Pontine gaze centre dysfunction Ocular Dip ( Slow Arrhythmic Downward And fast Upward eye movement with normal Dolls) – Diffuse cortical Axonal Damage Saccadic (Fast) movements in Coma – Psychological Horizontal divergent eyes – Drowsiness Bilateral Abducted eyes – 3 rd N Dysfunction Bilateral Adducted eyes – 6 th N Dysfunction (ICP) NEU.EXAM- 9.Ocular Movements.
- 16. (B)OCULOCEPHALIC (DOLLS) REFLEX: Turn the head briskly side to side – Conjugate opposite eye movements are normal (Could not be elicited in normal persons due to supranuclear control) Normal reflex in coma indicates bihemispherical / metabolic abnormality Absent dolls due to (upper) brainstem lesion NEU.EXAM- 9.Ocular Movements.
- 17. (C) OCULOVESTIBULAR (CALORIC)REFLEX : Flex the Head 30 ° -- Lavage the ear with cold ( 30 °C) water -30 ml – Observe for 30 sec – Opp. Side Nystagmus is normal response (COWS) – Tonic Eye deviation to same side No Nystagmus but normal tonic phase – Bihemispherical Absent Response – Deep Coma / BS dysfunction Asymmetric Response – BS lesion Conjugate gaze paresis -- Hemispherical / Pontine NEU.EXAM- 9.Ocular Movements.
- 18. NEU.EXAM–MOTOR RESPONSES Bestindicator for the severity of coma Observe Spontaneous movements for symmetry and purpose Check tone for symmetry / Bil LL ↑ tone favors Herniation. Induce increasing stimuli & observe symmetry 1. Verbal command -(open eyes, Show 2 fingers) 2.Sternal rub / pressure- (Purposeful / Gross localizing responses)
- 19. 3.Nailbed Pressure :a) Withdrawl – Motor cortex b) Decortication (Flexion of the Elbow & wrist with supination of the arm)– Deep Hemisphere / Upper midbrain level inv of pyramidal tract c) Decerebration (Extension of Elbows Wrist & Pronation) – Pons / Upper medullary lesion NEU.EXAM–MOTOR RESPONSES
- 20. DIAGNOSTIC TESTING 1.Head CT (or MRI) Scan : Great boon for the Diagnosis of structural lesions. Mostly CT is enough & is Quick for the Patient & Doctor. All types of ICH, Tumor & Hydrocephalus. Bihemispherical Infarcts, BS lesion, DAI, Meningitis, Encephalitis, isodense SDH & CVT may be missed by CT Scan. Contrast when required / Bone window - Trauma 2. Lumbar Puncture : Exclude ICT / Mass effect by CT Scan Before LP To Diagnose Meningitis /Encephalitis / SAH Do not postpone Treatment for Men’s if LP is delayed
- 21. 3. EEG: Progressivelyincreasing background slowing corresponds to the level of consciousness. Triphasic waves in hepatic (other) Encephalopathies. Asymmetric slowing in hemispherical lesion. Alpha coma : Alpha waves all over – pontine / Diff.Cort Excessive Beta waves in Sedative Intoxication. Electrical Status in Non-Convulsive SE. Normal Alpha Activity seen in Locked in syndrome & Hysteria. DIAGNOSTIC TESTING
- 22. EMERGENCY TREATMENT FORCOMA 1. ICSOL: Surgical intervention 2. INCREASED ICP (For buying time): a. Head Elevation b. Intubation / Hyperventilation c. Sedation if Agitated (midazolam) d. 20% Mannitol 1gm/kg e. Dexamethasone 10mg IV Q6H 3. ENCEPHALITIS (HSE): Acyclovir 10mg/kg IV Q8H 4. MENINGITIS : Ceftriaxone +Ampicillin
- 23. CAUSES OF STUPORAND COMA 1. STRUCTURAL a)Trauma i.ICH ii.Diff Axon Injury iii.Concussion b)CVA i.ICH / SAH ii.Hemisp / BS Inf iii.CVT iv.HTN’ve Encep’thy c)Infection i.Meningitis ii.Encephalitis iii.Abscess d)Inflammatory i.Autoimmune Vasculitis ii.Demyelination e)Neoplasm f)Hydrocephalus 2. TOXIC / METABOLIC a)Global Hypoxia / Ischemia b)Elec’te / Acid-Base Disorders i.pH Disturbances ii. Hyper/Hypo Natremia iii. Hyper/Hypo Glycemia iv. Hyper/Hypo Calcemia c)Drug intoxic’n / Withdrawl d)Temp’re (Hyper/Hypo thermia) e)Organ System Dysfunction i.Liver ii.Kidney iii.Thyroid iv.Adrenal v.Cardiac /Respiratory f)Seizures and Post-ictal states g)Thiamine / B12 Deficiency 3. PSYCOGENIC COMA
- 24. CEREBRO VASCULAR ACCIDENT10% of coma are due to CVA Variable depth of coma with Hemiplegia Large infarct / ICH -Facial / Limb Weakness IVH -Decerebration / Meningismus Brain Stem Infarct - BS Signs VBI - Loss of Bl.Supply to RAS - Drop attack SAH - Th’rclap HA , Mening’s , Focal deficits HT.E - Blindness,Fits,Paps,Retino/Nephro’y CVT-Fits,HA,ICT,Mening’s,Focal Deficits Small vessel occl’n-SLE,SBE,DIC,TTP
- 25.
- 26.
- 27.
- 28.
- 29. ANEURYSM & SAH10 / 1,00,000 PER YEAR Frequently in females Age, HTN, Smoking, Alcohol –risk 70% gets Warning leaks 45% Manifest as COMA at the onset Suspicion, CT & LP are Diagnostic methods MRA, CT Angio & DSA for confirmation Close monitor’g, rest, sedate, Vol.expaners, AED, Avoid Vasospasm, Anti HTN, & Dulcolax Plan Surgery at the earliest
- 30.
- 31. 13% of comaare due to trauma History & Evidences of external Injury Concussion – Immediate / Late Coma Contusion / Laceration – Foc.def / Seiz’s EDH (MMA H’ge) - Lucid Interval SDH – Delayed Symptoms Monitor T,P,BP,ICP,CT, MRI,C.Spine for all Trauma. TRAUMA
- 32. Contusion / Concussion/ DAI / SAH
- 33. Common Cause ofComa Flushed face, Conj.inj., Bounding pulse, Dil’d pp, Alcohol from Breath, Stomach & Blood ICH, Trauma, SDH, Wernicke’s Encp’thy Urgent CT, LFT, Coag’ln profile Inj.B1 & 50% Dextrose if hypoglycemic AED if H/O seizures ALCOHOL INTOXICATION
- 34. Tongue bite, Froath,Bloody sputum, Injury Etiology of convulsion may be different Confusion & Irritability Brief stupor and profound sleep To rule out Non-Convulsive Status Post ictal state DIABETES Hypo is worse so give IV dextrose Dec DTR, T, BP, Hyd’n, / Inc P, R Smell of Acetone
- 35. Suicidal/ Homicidal/ AccidentalDrugs and Toxins History / Physical findings Lavage/ Symptomatic/ Antidote/ Tt Compl No Lateralizing signs Depth of coma Acc to Strength & Amount Poisoning Meningitis HA, Fever, LOC, Meningismus (not in age extremes & Imm. supp), ICP ENT infection, SBE, Rash in mening.meng’s Do CT before LP
- 36. ENCEPHALITIS Present withFever, Meningismus, Altered sensorium, seizures and focal Deficits. Usually the Seizures are difficult to control EEG& CSF are better diagnostic tools than Imaging HSE affects FT regions asymmetrically present with focal seizures EEG may show PLEDs, Focal epileptic activity or slowing MRI shows signal alterations in inferior FT regions asymmetrically IV Acyclovir is the Treatment of choice with full dose AED
- 37.
- 38. PSEUDOCOMA 1. PSYCHOGENICCOMA Negativistic Behavior (Resists opening eye) Avoidance Behavior (Hand avoids face on dropping) Intact Saccades / Normal Caloric response Recovery on very painful stimuli 2. LOCKED IN SYNDROME Complete paralysis except for vertical eye movements Pt usually alert and can communicate thru’ EOM Due to bilateral Pontine Damage (Infarct) 3. AKINETIC MUTISM (Motionless, Mindless Wakefulness) Extreme psychomotor retardation- Appears awake Show Delayed Limited responses Due to Extensive Thalamic / Frontal Damage
- 39. VEGETATIVE STATE Lossof Awareness of self and surroundings. Normal sleep wake cycles & BS reflexes. Normal metabolic and circulatory functions. Normal eye opening / closure & Swallowing. Eye movements & Sensory Localization – Poor. Doesn’t obey requ’s / No comprehensible words. Preserved Hypothalamic & Autonomic fns. Above findings lasting > 1 month – PVS. CVA, SAH, Trauma, Toxin, Injury, Infn, Arrest etc., Low amplitude irregular Delta in EEG. Cortical necrosis, multi-infarcts, Diffuse neuronal loss and gliosis of neocortex, hippocampus thalamus & purkinje cells – BS relatively intact.
- 40. GENERAL CARE FORCOMATOSE PTS Protect airway / Adeq. Vent’n & O2 / NPO Good Hydration – Prefer isotonic Saline Nasogatric adeq. calorie feed with smaller tube Prevent Bedsore – Q2H Position / Water bed Protect Eyes by keeping closed / Lubricants Ranitin to prevent Stress ulcer / Stool softener Aseptic Catherization / Intermittent catheteris’n Passive Limb Exercises to prevent Contractures Calf exe / Stocking / Heparin to avoid DVT
- 41. BRAIN DEATH Stateof cessation of cerebral activity with normal Heart function, Respiration being maintained by Ventilators. Brain death is the Death of the Individual Three Essential elements for Dx 1. Widespread Cortical Destruction (Unresponsive to all stimuli) 2.Global BS Damage (Loss of all BS reflexes) 3.Lower BS destruction – Complete Apnea Exclude Drug induced / Hypothermic CNS Depression
- 42.