coma..approachand assessmentof coma-181206152425.pptx

Comatose Child

1. Comatose child Dr. Sarfaraz Ahmad Assistant Professor Department Of pediatrics MMIMSR, MULLANA Etiology, Clinical approach & Management

2. Anatomy Cerebral Cortex Reticular Activating System

3. State of arousal (wakefulness) with awareness of self and environment. It has 2 components: Arousal (RAS) Awareness (Cortex) Consciousness

4. Anatomy of Consciousness Ascending Reticular Activating System (RAS) is a system of fibers which arises from the reticular formation of the brainstem and projects to the thalamus . Neurons in the reticular formation receive collaterals from the ascending spinothalamic pathways and then project diffusely to the entire cerebral cortex .

5. Sensory stimuli are involved not only with sensory perception but also play role in the maintenance of consciousness through their connections with the RAS. Stimulation of RAS produces arousal and destruction of RAS produces coma . Hypothalamus is an important component of consciousness, Stimulation of posterior hypothalamic region causes arousal . The degree of alteration in consciousness is roughly proportional to the volume of brain tissue involved in the process.

6. States of impaired consciousness

7. Clouding of Consciousness: Mild form of altered mental status. Patient has reduced wakefulness or awareness. Include hyper- excitibility or irritability alternating with drowsiness . Confusional state More profound deficit including disorientation and difficulty in following commands due to focal deficit of cognitive function. Coma. State of ‘unarousable unresponsiveness’. Coma is characterized by sustained, pathologic, eyes-closed, unarousable unresponsiveness. Even strong exteroceptive stimuli fail to elicit recognisable psychologic response; unresponsive to pain

8. Lethargy is a state of reduced wakefulness with attentional deficits. Obtundation is characterized by blunted alertness and diminished interaction with the environment. Stupor – Spontaneous unarousability interruptive only by vigorous, direct external stimulation ; responsive only to pain. Delirium – An acute or subacute reduction in awareness, attention, orientation and perception (clouding of consciousness), associated with abnormal sleep/wake patterns and often psychomotor disturbances. Syncope – Brief loss of consciousness caused by global failure of cerebrovascular perfusion

9. Locked in Syndrome: Ventral brainstem destruction sparing the RAS. Patient is mute and quadriplegic but not comatose , with variable preservation of consciousness. Patient is awake but speechless & motionless with little response to stimuli and Sustained eye opening along with aphonia or hypophonia. Persistant Vegetative state: complete loss of cognition, with sleep/wake cycles and other autonomic functions being relatively intact; patient is unaware of self and environment Patient have massive bilateral hemisphere damage with intact brainstem. In PVS, patient is awake but unaware of environment.

10. Causes of COMA Structural Non- Structural (Focal) (Diffuse or metabolic)

11. Traumatic causes Vascular etiologies Intracranial hemorrhage ( EDH,SDH,SAH,intraparenchymal) Acute arterial infarct Venous sinus thrombosis Vasculitis Carotid or vertebral artery dissection Vascular malformations Mass lesions Primary neoplasm Brain metastasis Abscess Granuloma Hydrocephalus Cerebral contusion Intracranial hemorrhage ( EDH,SDH,SAH,intraparenchymal) Structural Causes of coma

12. Non Structural (Diffuse, Metabolic or Multifocal causes of Coma) A. Deprivation of oxygen, substrate or metabolic cofactors Hypoxia Ischaemia Hypoglycemia Cofactor deficiency (thiamine, niacin, pyridoxine,folate, b12) . B. Toxicity of Endogenous products Due to organ failure (hepatic coma, uremic coma,porphyrias, reyes syndrome,IEMs) Due to hyper or hypofunction of endocrine organs.

13. C. Toxicity of Exogenous poisoning Medications Environmental toxins Acid poisons/ poisons with acid breakdown Psychotropic drugs and illicit substances Infections or inflammation of CNS: Meningitis Encephalitis Vasculitis E. Psychiatric causes. F. others like hypothermia, sepsis, electrolyte imbalances,Diffuse axonal injury,HPE,PRES, Seizures,hypertensive encephalopathy.

14. Approach to An Unconscious Patient.. History.. (Whenever possible from relatives, friends, reliable attenders) Make sure to ask: Onset: (abrupt, gradual) Recent complaints: (headache, weight gain/ loss, fever, depression (suicidal ideas), focal weakness, trauma) Previous medical illness: (diabetes, hypertension, chronic lung diseases, renal failure, thyroid disease, heart disease) Drug intake history: (prescription drugs, insulin, thyroxine, recreational drugs) Family History: (similar complains, to r/o environmental toxicity/ food poisoning etc.) Travel History: (to malaria/ Japanese encephalitis etc. endemic regions. or contact with STD’s)

15. Examination.. (Brief but thorough) Vital signs: Pulse, BP, Temperature, RR,GCS GPE: Habitus, Pallor, Icterus, Cyanosis, Clubbing, Lymphadenopathy, Oedema, Thyroid swelling. Evidence of Trauma: bruises/ laverations/ fracures/ bleeding from ear or nose/ abd distension Evidence of Drug use: Needle marks/ smell from breath/ pupils/ unkempt and poor hygiene/ parasympathetic symptoms Evidence of previous suicide attempts: cut marks Systemic Exam: Respiratory/ Cardiac/ Abdomen/ Neurological. (Esp. look for Meningeal signs, Pupils, Fundus )

16. Changes in Pupils with lesions at different levels of brain that can cause Coma Diencephalon: Thalamus Hypothalamus Pituitary Pretectum : Lies at the junction of mid and fore brain. Made up of atleast 7 nuclei Main role:  initiation of optokinetic reflexes, also nociception and REM sleep . Hippus : Pupillary athetosis . Irregular alternating dilation and contraction of the pupil in response to light.

17. Coma Evaluation Scales Glasgow Coma Scale Graham Teasdale and Bryan Jennet, Neurosurgery professors, at the University of Glasgow , Developed this scale in 1974 15 point scale, used to test best motor response (6), best verbal response (5) and best eye response (4). Score ranges from 3 (deep coma or death) to 15 (fully awake ). Limitations: Failure to assess verbal score in intubated patients. Inability to test brainstem reflexes Person to person variation (a 2005 trial in the US, showed only 30% ER docs, 38% Neurosurgeons Concur) Does not take physical debility into account ( eg . eyes swollen shut after head injury, broken bones causing painful movements)

18. Glasgow Coma Scale GCS Developed to define outcome in adult patients with head injury Coma: score of 8 or less There is a modified scale used for infants and children

19. Glasgow Score Eye opening Motor Response Spontaneous 4 obeys commands 6 To command 3 localizes pain 5 To pain 2 withdraws to pain 4 None 1 abnormal flexion 3 Verbal abnormal extension 2 Oriented 5 none 1 Confused 4 Inappropriate words 3 TOTAL 3-15 Incomprehensible sounds 2 None 1

20. MODIFIED GLASGOW COMA SCORE For Infants Eye opening Motor spontaneous 4 normal 6 To speech 3 withdraws to touch 5 To pain 2 withdraws to pain 4 None 1 abnormal flexion 3 Verbal abnormal extension 2 Coos 5 none 1 Irritable cries 4 Cries to pain 3 Moans to pain 2 None 1

21. GCS Individual elements as well as the sum of the score are important. The score is expressed in the form " GCS 9 = E 2 V 4 M 3 at 07:35 Generally, coma is classified as: Severe , with GCS ≤ 8 Moderate , GCS 9 - 12 Minor , GCS ≥ 13.

22. Newer Scales for Prognosis of Coma: FOUR (Full O utline of UnResponsiveness ) SCALE New Coma Scale is devised in 2005, Four components (Eye, Motor, Brainstem, Respiration ) Each component has maximum of score of Four. AVPU A lertness, response to  V erbal stimuli, response to  P ainful stimuli, or U nresponsive ACDU A lertness ,  C onfusion ,  D rowsiness , and  U nresponsiveness Grady Scale:   Scale of I to V along a scale of Confusion , Stupor , Deep stupor,  abnormal Posturing , and Coma . Wijdicks E, Bamlet WR et al. Validation of New Coma Scale: The Four Scale. Ann Neurol 2005; 58: 585 – 593.

23. Investigations.. (But don’t wait to start stabilising the patient) Laboratory: Routine: CBC, LFT, RFT, U/E, CRP, ESR Specific: ABG’s, Amylase, TFT, Calcium, Lactate, Cultures, CSF, Toxicology screen Radiological: X- Rays: Chest/ Abdomen/ Skull/ Bones Ultrasound: Abdomen CT Brain: Plain/ With Contrast MRI: If CT inconclusive

24. Stages of Coma Grade I - Individuals who respond with recognition when their name is called and do not lapse into sleep when left undisturbed. Grade II - The person lapses into sleep when undisturbed and is aroused only when a pin is tapped gently over the chest wall. Grade III - Patient who winces in response to deep pain stimulus . Deep pain stimulus may result in abnormal postural reflexes either unilateral or bilateral. Grade IV – Deep pain stimulus may result in decorticate or decerebrate posturing. Grade V - The patient who maintains a state of flaccid unresponsiveness inspite of deep pain stimulation .

25. Turn the patient frequently to prevent aspiration,sore,hypostasis – Skin care – Bladder care – Bowel care 2. If the General condition stablilized , do CT head scan to detect organic lesion – Infract can’t be seen immediately,can see at least 6-8 hr – Haemorrhage can be seen immediately-do CT scan immediately – Tumour -can see as SOL Treatment

26. 3 . CT head - Normal -do LP – If infection present - treat 4. CT & LP - normal - treat metabolic (if consider metabolic) – If deteriorate ,consider expansion of disease, new lesion and metabolic 5. Increased ICP - osmotic diuresis – Mannitol - 20% in 200cc N/S within 20min. 6. Evaculation of Haemorrhage - refer to neurosurgery 7. Infract - symptomatic treatment Prognosis – Can be determined by GCS & Head injury – If there is no improvement within 48 hr, prognosis is bad.

27. Consisting of High Flow Oxygen, dextrose , flumazenil, naloxone , thiamine, activated charcoal is sometimes used in the management of an orphan comatose patient. Coma cocktail

28. TO RECAP...

29. TAKE HOME MESSAGES.... Even before detailed history & examination, it is important to start emergency measures such as correction of possible deficiencies in glucose, oxygenation and blood pressure. After determination of vital signs, attention should be towards ensuring an adequate airway, oxygenation and intravenous access . Immediately after obtaining blood samples, 50 cc of 50% glucose followed by 100 mg of thiamine should be given.

30. Naloxone and flumazenil may be given if there is suspicion of opiate or benzodiazepine overdose. Preparation for intubation , respiratory support , and for use of pressor agents should be made, as it may become necessary. Always assume a cervical spine injury may be present, and immobilise the neck until a fracture can be ruled out . Never forget to check ECG/RBS/ TFT’s in an unconscious patient.

31. APPROACH TO ETIOPATHOLOGY COMA STRUCTURAL LESIONS (FOCAL) Supratentorial (Hemispheric) Infratentorial (Brainstem) SYSTEMIC DISORDERS (DIFFUSE , SYMMETRIC)