Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
COMA • • • • • • • Coma= State of deep sleep Coma is a profound state of unconsciousness. A person in a coma cannot be awakened Fails to respond normally to pain, light or sound Does not have sleep-wake cycles, and Does not take voluntary actions. A person in a state of coma can be described as comatose. 11/02/2010 Dr. Alka Stoelinga 1 • • • • • Unconsciousness Syncope Brain death Locked-in syndrome Vegetative state • All persons in coma are unconscious, but all who are unconscious are not in coma 11/02/2010 Dr. Alka Stoelinga 2 • Unconsciousness/ loss of consciousness or lack of consciousness, is an alteration of mental state that involves complete or nearcomplete lack of responsiveness to people and other environmental stimuli. – Being in a comatose state or coma is an illustration of unconsciousness. – Fainting due to a drop in blood pressure and a decrease of the oxygen supply to the brain is an illustration of a temporary loss of consciousness. 11/02/2010 Dr. Alka Stoelinga 3 • Syncope is the medical term for fainting, a sudden, usually temporary, loss of consciousness • Generally caused by insufficient oxygen in the brain either by – Cerebral hypoxia – Hypotension 11/02/2010 Dr. Alka Stoelinga 4 • Brain death is the irreversible state when there is no brain activity (including involuntary activity necessary to sustain life) due to total necrosis of the cerebral neurons following loss of brain oxygenation • Reflexes in brain death • Pupillary response – none (fixed pupils) • Oculocephalic reflex- none • Corneal reflex- None • Response to the caloric reflex test- none • Spontaneous respirations- None 11/02/2010 Dr. Alka Stoelinga 5 • Locked-in syndrome is a condition in which a patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eyes. – It is the result of a brain stem lesion in which the ventral (anterior) part of the pons is damaged – Also k/a cerebromedullospinal disconnection, deefferented state, pseudocoma, and ventral pontine syndrome 11/02/2010 Dr. Alka Stoelinga 6 • A vegetative state is a condition of patients with severe brain damage who were in a coma, but progressed to a state of partial awareness. • After four weeks in a Vegetative State (VS), the patient is classified as in a Persistent Vegetative State. • This diagnosis is classified as a Permanent Vegetative State (PVS) after approximately 1 year of being in a Persistent Vegetative State. 11/02/2010 Dr. Alka Stoelinga 7 COMA contd.. • Patients in the deepest level of coma: – Do not respond with any body movement to pain, – Do not have any speech, and – Do not open their eyes • Comas typically last for no more than a few weeks. • However, if the coma continues, the patient is usually considered to be in a persistent vegetative state • Very less chance of awakening after remaining in that state for one year. • Level of consciousness can be measured by GCS 11/02/2010 Dr. Alka Stoelinga 8 Glasgow Coma Scale (GCS) Eye Opening (E) Verbal Response (V) Spontaneous 4 Oriented 5 To loud voice 3 Confused, Disoriented 4 To pain 2 Inappropriate words 3 None 1 Incomprehensible words 2 None 1 Motor Response (M) Obeys commands 6 Localizes pain 5 Withdraws from pain 4 Abnormal flexion posturing 3 Extensor posturing 2 None 1 11/02/2010 Level of consciousness E+M+V Lowest score = 3 (Deep coma) Highest score = 15 (Fully awake or aware) Spontaneous Eye Opening + Obeys command+ Oriented + Dr. Alka Stoelinga 9 CAUSES OF COMA • Vascular • Infectious • Neoplastic • Degenerative • Inflammatory-immunologic • Congenital-developmental • Autoimmune • Toxic/ traumatic • Endocrine/ metabolic 11/02/2010 Dr. Alka Stoelinga 10 Causes of COMA 1. Metabolic disturbances Diabetes- Hypoglycemia/ DKA/ HONK Toxins-> Hepatic Failure (Ammonia)/ Respiratory failure (CO2) Hypothermia/ Hyponatraemia/ Uremia Drug Overdose/ Alcohol 4. Infections Meningitis Encephalitis Cerebral abscess 2. Trauma Cerebral Contusions Extradural/ Subdural hemorrhages hemorrhages 5. Others Epilepsy-> Status Epilepticus Tumor Thiamine deficiency 3. Cerebrovascular diseases SAH/ ICH Brain stem infarction thrombosis Cerebral venous sinus thrombosis 11/02/2010 Dr. Alka Stoelinga 11 History 1. Events from attendance/ visitors focusing on probable causes – Trauma, Drug ingestion, Alcohol – Rapidity with which neurologic symptoms developed – Preceding medical/Neurologic symptoms (Fever, Headache, Vomiting, Seizures, dizziness, Diplopia) – Medical diseases: Hepatic/Renal/cardiac/Respiratory – Past history: TIA, Stroke 11/02/2010 Dr. Alka Stoelinga 12 When approaching a patient with a neurologic disorder look for: Location of the lesion Cerebrum Cerebellum Brainstem Spinal cord Nerve root Peripheral nerve Neuromuscular junction Muscle 11/02/2010 Dr. Alka Stoelinga 13 General physical examination: 1. Vitals: Pulse, BP, Temperature, Respiratory rate and pattern of breathing 2. Oxygen saturation 3. Skin rash 4. Bleeding manifestation 5. Odor 6. Anemia/ Jaundice/ Cyanosis 11/02/2010 Dr. Alka Stoelinga 14 Pattern of Breathing: • • • • • Cheyne-stokes breathing Periods of apnea alternate with periods of hyperapnea seen in Brain damage (bihemispheral damage)due to cerebral hemorrhage or trauma Kussmaul’s respiration Deep and rapid respiration due to stimulation of respiratory center seen in Metabolic acidosis due to Ketoacidosis or Uremia Hyperventilation Rapid and shallow breathing resulting in alkalosis and tetany Ataxic breathing Irregular in time and depth seen in Brain stem damage. Shallow,slow,regular Metabolic/Drug related 11/02/2010 Dr. Alka Stoelinga 15 Neurologic assessment: 1. 2. 3. 4. 5. • • • • • First observe the patient without intervention Assess the level of arousal/Elicited movements Glasgow coma scale Response to noxious stimuli Pupillary light reflex: Normal reactive mid size pupil Excludes mid brain lesion One unreactive and dilated pupil Compression of third cranial nerve Bilateral dilated and unreactive pupil Severe mid brain damage Reactive but bilateral small pupil Metabolic encephalopathy, Deep hemispheric lesion Bilateral pin point pupil Pontine hemorrhage, Barbiturate/ Opoid overdose 11/02/2010 Dr. Alka Stoelinga 16 6.Ocular movements: • Note resting eye position • Look for rectus palsy • Roving movements • Nystigmus 7.Oculocephalic reflex: • Elicited by moving head from side to side • Doll’s eye reflex 8.Oculovestibular reflex: • Caloric stimulation: • Irrigating external auditory canal with either cold or warm water Observe for the tonic deviation of the eyes Remember“COWS” 9.Corneal reflex 11/02/2010 Dr. Alka Stoelinga 17 10.Other Neurologic examination in detail • Cranial nerve • Motor • Meningeal signs • Skull and Spine SYSTEMIC EXAMINATION: • Cardiac • Respiratory • Hepatic • Renal 11/02/2010 Dr. Alka Stoelinga 18 Investigation: 1. Blood: • TC, DC, Hb • Glucose, Electrolytes, Calcium, Urea, Creatinine, ABG, NH3 • Toxicological screening 2. CSF analysis 3. Neuroimaging • CT scan head • MRI head 4. EEG 11/02/2010 Dr. Alka Stoelinga 19 Contraindications of investigations: • Signs and symptoms of raised ICP (Papilloedema, decreased LOC, progressive deficit, headache) due to mass lesion • Do CT first and then proceed to lumbar puncture (LP) if there is no neurologic findings suggestive of localized mass lesion • Obstructive hydrocephalus, or evidence of blood infection at LP site • Coagulopathy (e.g. anticoagulant drugs) or thrombocytopenia • Developmental abnormality (i.e. tethered spinal cord) 11/02/2010 Dr. Alka Stoelinga 20 Diagnostic Tests with CSF: • Opening pressure • Protein • Glucose • Cell counts • Color • VDRL • Viral PCR • IgG levels • Oligoclonal bands • Fungal antigens • Microbiological stains (Gram, ZN, fungal) • Bacterial culture and PCR Correlate with typical CSF Findings in CNS Infections 11/02/2010 Dr. Alka Stoelinga 21 Management: • • Immediate goal: to prevent further brain damage ABC – – – – – Oropharyngeal airway Tracheal intubation Correction of Hypotension Securing IV access/Drawing blood samples Hypo/Hyperthermia 3. Treat the metabolic cause: – Glucose, Electrolytes, Acid Base imbalance 4. Antidotes: – Naloxone (For morphine/ heroin) 5. Assess for head injury/ Cervical spine injury 11/02/2010 Dr. Alka Stoelinga 22 6. 7. 8. Control of Raised ICP Head end elevation:15-30 ̊ Hyperventilation to decrease PaCo2 Osmotic agent: Mannitol, Furosemide, Glycerol Control of seizures Treatment of underlying cause 11/02/2010 Dr. Alka Stoelinga 23 • Advanced Life Support (ALS) – Emergency medical care for sustaining life, including defibrillation, airway management, and drugs and medications • The Basic Life Support (BLS) – Provide a wide variety of healthcare professionals the ability to recognize several life-threatening emergencies, provide CPR, use an Automated External Defibrillator (AED), and relieve choking in a safe, timely and effective manner 11/02/2010 Dr. Alka Stoelinga 24 11/02/2010 Dr. Alka Stoelinga 25 DNR (Do Not Resuscitate) • A do not resuscitate document, often called a living will, is a binding legal document that states resuscitation should not be attempted if a person suffers cardiac or respiratory arrest. 11/02/2010 Dr. Alka Stoelinga 26 • Intracranial pressure (ICP) is the pressure inside the skull [Brain tissue and cerebrospinal fluid (CSF)]. • CSF pressure can be influenced by abrupt changes in intrathoracic pressure during coughing (intraabdominal pressure), valsalva (Queckenstedt's maneuver). • ICP is measured in millimeters of mercury (mmHg) – At rest, is normally 7–15 mmHg for a supine adult – −10 mmHg in the vertical position • At 20–25 mm Hg (The upper limit of normal) treatment to reduce ICP is needed. • Measured by intracranial transducers 11/02/2010 Dr. Alka Stoelinga 27 • Causes of increased intracranial pressure • Increase in venous pressure – Venous sinus thrombosis – Heart failure – Obstruction of superior mediastinal or jugular veins. • Causes are classified by the mechanism in which ICP is increased: • Mass effect – Brain tumor – Infarction with oedema – Contusions, subdural or epidural hematoma, or abscess • Obstruction to CSF flow and/or absorption • Generalized brain swelling – – – – – – Ischemic-anoxia states Acute liver failure Hypertensive encephalopathy Pseudotumor cerebri Hypercarbia These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts. 11/02/2010 Dr. Alka Stoelinga – Hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold-Chiari malformation) – Extensive meningeal disease (e.g., infectious, carcinomatous, granulomatous, or hemorrhagic) – Obstruction in cerebral convexities and superior sagittal sinus (decreased absorption). 28 Signs and Symptoms • • • • • • • • Headache Vomiting without nausea Ocular palsies Altered level of consciousness Back pain Papilloedema Pupillary dilatation Cushing's triad – – – – Increased systolic blood pressure Widened pulse pressure Bradycardia Abnormal respiratory pattern. 11/02/2010 Dr. Alka Stoelinga 29 Treatment • • • • • • Adequate Airway Breathing Oxygenation Maintain circulation Mannitol Treatment of cause 11/02/2010 Dr. Alka Stoelinga 30