1. COMA Introduction-etiology-pathophysiology Introduction-etiology-pathophysiology Dr. David Williams Dr. David Williams Asst. Professor of Paediatrics Asst. Professor of Paediatrics

2. Definition Def: It is a state in which the patient makes no meaningful response to external stimulus or innerneed. Def: It is a state in which the patient makes no meaningful response to external stimulus or innerneed. States of decreased consiouness.lethargy-difficult to maintain aroused state.obtundation-response to stimulation other than pain.stupor-response only to pain.coma-unresponsive to pain. States of decreased consiouness.lethargy-difficult to maintain aroused state.obtundation-response to stimulation other than pain.stupor-response only to pain.coma-unresponsive to pain. Coma is a disorder of arousability. Coma is a disorder of arousability.

3. Coma scales Glasgow coma scale Glasgow coma scale Modified coma scale Modified coma scale Adelaid coma scale Adelaid coma scale Blantyre coma scale Blantyre coma scale Infant face scale Infant face scale AVPU score AVPU score

4. Coma scales Every Scale consists of 3 main components Every Scale consists of 3 main components Eye opening Eye opening Best motor response Best motor response Best verbal response Best verbal response

5. Different coma scales Eye opening GCS Modified GCS Adelaid coma scale Spontaneous444 Response to speech 333 Response to pain 222 None111

6. Different coma scales Best motor response GCS Modified GCS Adelai d CS Obeys commands 666 Localises pain 555 Withdrawal of limb 444 Flexion to pain 333 Extension to pain 222 Nil111

7. Best verbal response GCS Modified GCS Adelaid coma scale score Oriented Coos, babbles oriented5 Confused Irritable cry Words4 Inappropriatewords Cries to pain Vocal sounds 3 Incomprehensiblewords Moans to pain Cries2 NilNilNil1

8. Infant face scale It relies on objective behavioral observation. Uses cortical as well as brain stem function. It parallels GCS in score & based on infant appropriate behavior. It can be applied even in intubated patients. It relies on objective behavioral observation. Uses cortical as well as brain stem function. It parallels GCS in score & based on infant appropriate behavior. It can be applied even in intubated patients. Eye opening,motor & verbal responses are tested. Defined either almost perfect or sustained. Eye opening,motor & verbal responses are tested. Defined either almost perfect or sustained.

9. Blantyre coma scale ResponseFindingsscore Bestmotor response localizes painful stimulus (pressure with blunt end of pencil on sternum or supraorbital ridge) 2 withdraws limb from painful stimulus (pressure with horizontal pencil on nail bed of finger or toe) 1 no response or inappropriate response 0 Best verbal response cries inappropriately with painful stimulus, or, if verbal, speaks 2 moan or abnormal cry with painful stimulus 1 no vocal response to painful stimulus 0 Eye mov. watches or follows (e.g., mother's face) 1 fails to watch or follow 0

10. Interpretation of Blantyre Coma Scale Interpretation of Blantyre Coma Scale Maximum score – 5 ( good) Maximum score – 5 ( good) Minimum score – 0 (poor) Minimum score – 0 (poor) Abnormal score <=4 Abnormal score <=4

11. Other scores AVPU score : AVPU score : A – Alert A – Alert V – Response to voice V – Response to voice P – Response to pain P – Response to pain U – Unresponsive U – Unresponsive

12. Etiology of coma in children Infections – Infections – Meningitis Meningitis Encephalitis Encephalitis Cerebral malaria Cerebral malaria Intra cerebral absess Intra cerebral absess Sub dural empyema Sub dural empyema Epi dural empyema Epi dural empyema Gram –ve septicemia Gram –ve septicemia Sepic shock, Typhoid encephalopathy, Shigella encephalpathy, Dengue shock syndrome. Sepic shock, Typhoid encephalopathy, Shigella encephalpathy, Dengue shock syndrome. Rare causes -burn enchalopathy,lyme disease, Rare causes -burn enchalopathy,lyme disease,

13. Etiology Hypoxia-ischemia*; hypoxia –normal cerebral blood flow, hypo ventilation, methemoglobinemia, ischemia –decreased cerebral blood flow. Hypoxia-ischemia*; hypoxia –normal cerebral blood flow, hypo ventilation, methemoglobinemia, ischemia –decreased cerebral blood flow. Drug induced or over dosage. Barbiturate *,transquilisers*,opiates,anti cholinergics.

14. Etiology Supra tentorial lesions- cerebral haemorrhage,cerebral infarction,sub dural haematoma,epidural haematoma,cerebral absess,cerebral edema,pitutary apoplexy,tumors,contusion –laceration, Supra tentorial lesions- cerebral haemorrhage,cerebral infarction,sub dural haematoma,epidural haematoma,cerebral absess,cerebral edema,pitutary apoplexy,tumors,contusion –laceration, Sub tentorial lesions- cerebellar haemorrhage,brain stem infarction,tumors,pontin e haemorrhage,cerebellar absess,tentorial herniation.

15. Etiology Epilepsy: post ictal state, status epilepticus. Epilepsy: post ictal state, status epilepticus. Deficiency states- thiamine, niacin,pyridoxine,vit-b12.

16. Etiology Cardiac causes- decreased cardiac out put due to arrhythmias or valvular disease. Generalised fall of blood pressure-hypovolemia, vaso vagal syncope, carotid sinus massage. Cardiac causes- decreased cardiac out put due to arrhythmias or valvular disease. Generalised fall of blood pressure-hypovolemia, vaso vagal syncope, carotid sinus massage. Vascular causes- hypertensive encephalopathy, polycythemia, emboli,thrombosis,vasculitis,a-v malformations,haemorrh agic diseases.

17. Etiology Metabolic & systemic disorders. Hypoglycemia, diabetic ketoacidosis, hepatic encephalopathy, uraemic encephalopathy,hyper tensive encephalopathy, reyes encephalopathy,ammonia encephalopathy, urea cycle defects, branched chain aa or organic acidemias. Metabolic & systemic disorders. Hypoglycemia, diabetic ketoacidosis, hepatic encephalopathy, uraemic encephalopathy,hyper tensive encephalopathy, reyes encephalopathy,ammonia encephalopathy, urea cycle defects, branched chain aa or organic acidemias. Thyroid disorders,adrenal insuficiecy,medium chain acyl co a dehydrogenase def,theral injury,cardio respiratory failure.

18. Pathophysiology of coma Loss of consciousness – Loss of consciousness – Decreased blood flow to brain, decreased oxygen supply to brain, toxin induced damage. Decreased blood flow to brain, decreased oxygen supply to brain, toxin induced damage. Acute drop of cerebral blood flow from 55ml/min/100g to 25ml/min/100g Acute drop of cerebral blood flow from 55ml/min/100g to 25ml/min/100g Slowing of EEG & syncope Slowing of EEG & syncope

19. Pathophysiology of coma A drop in CBF to <12 -15 ml/min/100g A drop in CBF to <12 -15 ml/min/100g Electrocerebral silence Electrocerebral silence Coma Coma Cessation of metabolic & synaptic functions Cessation of metabolic & synaptic functions O2 consumption of 2 mg/min/100g (app half of normal) O2 consumption of 2 mg/min/100g (app half of normal) Incompatible with alert state Incompatible with alert state

20. Disease process Toxin/effects DKA DKA Uremia Uremia Hepatic coma Hepatic coma Lactic acidosis Lactic acidosis Pulmonary insufficiency Pulmonary insufficiency Hyponatremia Hyponatremia Acetone bodies ( acetone & B-OH butyric acid) Dialyzable toxins NH3 > 5-6 times Arterial PH <7 Hypercapnea Neuronal swelling, loss of KCl from cells

21. Disease process Toxin/effects Gen anesthetics Gen anesthetics Alcohol Alcohol Opiates Opiates Barbiturates Barbiturates Phenytoin Phenytoin Antidepressants Antidepressants Benzodiazepines Benzodiazepines Methyl alcohol Methyl alcohol Ethylene glycol Ethylene glycol Direct effect on neuronal membranes in cerebrum & RAS Metabolic acidosis

22. Disease process Toxin/effects Seizures Seizures Concussion Concussion Local anesthetics Local anesthetics Spread of seizures discharge to deep central structures Rotation of cerebral hemispheres around the axis of upper brainstem Interaction with ligand gated ion channels & alterations in neurotransmittors

23. Pathoanatomy of coma 1. Grossly discernible mass lesion causing lateral displacement of deep central structures ( herniation) 2. Destructive lesion in central structures like thalamus or midbrain 3. Widespread damage to cortex & cerebral white matter

24. THANQ