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Altered sensorium

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Dr Sudhir (BPKIHS GPEM)

Dr Sudhir (BPKIHS GPEM)

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  • 1. Approach to Altered Sensorium Dr. Sudhir Dev
  • 2. Objectives: Recognize the importance of historical factors in diagnosing causes of AS Identify dementia, delirium and psychosis as the three most common classifications of AS Articulate a differential diagnosis of AS Construct an approach to the diagnostic workup and management of a patient with AS Describe initial management of many causes of AS Discuss the disposition of a patient with AS
  • 3. What is Sensorium? Ability of the brain to receive and interpret sensory stimuli Good Sensorium = Alertness + Awareness
  • 4. Altered Sensorium Altered Sensorium is not a disease: It is a symptom. Causes could be easily reversible (hypoglycemia) to permanent (stroke) and from the relatively benign (alcohol intoxication) to life threatening (meningitis or encephalitis).
  • 5. Presentation of Patient with AS: Unfortunately, there is no classic presentation for a patient with Altered Sensorium. Presentations can range from CNS depression to confusion, agitation, etc. Altered sensorium can be determined by evaluating level of Consciousness
  • 6. Level of Consciousness Alert : Normal awake and responsive state Drowsiness : State of apparent sleep, briefly arousal with oral command Lethargic : Resembles sleepiness, but not becoming fully alert, slow verbal response and inattentive. Unable to adequately perform simple concentration task (such as counting 20 to 1)
  • 7. Level of Consciousness Somnolent : Easily aroused by voice or touch; awakens and follows commands; required stimulation to maintain arousal Obtunded/Stuporous : Arousable only with repeated and painful stimulation; verbal output is unintelligible or nil; some purposeful movement to noxious stimulation Comatose : No arousal despite vigorous stimulation, no purposeful movement- only posturing, brainstem reflexes often absent
  • 8. Some Common Terms in Altered Sensorium Confusion : – impaired attention and concentration, manifest disorientation in time, place and person, impersistent thinking, speech and performance, reduced comprehension and capacity to reason – Fluctuate in severity, typically worse at night „sundowning‟ – Perceptual disturbances and misinterpret voices, common objects and actions of other persons
  • 9.  Delirium : confusion and associated agitation, hallucination, convulsion and tremor Amnesia : a loss of past memories and to an ability to form new ones, despite alert and normal attentiveness Dementia the progressive deterioration in cognitive function - the ability to process thought (intelligence). Phychosis refers to a mental state often described as involving a "loss of contact with reality".
  • 10. Differentiating Delirium, Dementia and Phychosis Finding Delirium Dementia Psychosis Onset Rapid Slow Variable Course Fluctuating Progressive Variable Vital signs Often abnormal Usually normal Usually normal Level of Altered Normal Variable consciousness Visual (related to Auditory (related Hallucinations Rare external stimuli) to internal stimuli) Physical exam Often abnormal Often normal Often normal Poor if cause not Prognosis Progressive Variable treated Organic Underlying cause Organic (myriad) Functional (degenerative)
  • 11. Dementia VS Confusional state Dementia  Confusional state – Longstanding nature – Acute – Varies little from time to – Fluctuate time – Memory problem – Clouding of consciousness
  • 12. Approach to Altered Sensorium
  • 13. Initial Actions and Primary Survey All emergency department patients require an initial assessment for immediate threats. The “ABCDE approach” also provides a good opportunity to check for quickly reversible causes of Altered sensorium. A- Check to see that the airway is open and protected. Hypoxia is a potentially reversible cause of Altered Sensorium. B- Assess breathing. Inadequate ventilation will lead to elevated levels of CO2 (respiratory acidosis) and can cause AS. C- Assess circulatory status. Hypoperfusion starves the brain of oxygen and glucose and leads to AS. D- Check for neurologic disability. Use GCS or AVPU scale for a quick assessment of level of consciousness. Look for seizure activity. Are the pupils equal and reactive? Pay attention to spontaneous movements. Lack of movement on one side of the body night indicate stroke while lack of movement below a certain level of the body could indicate spinal cord injury. If there is any suspicion of trauma the cervical spine should be stabilized. E- Expose (fully undress) and perform a rapid head to toe look for signs of trauma, transdermal drug patches, dialysis access, infectious sources (such as catheters)
  • 14.  As we proceed through ABCDE , keep in mind rapidly reversible causes for the Altered Sensorium . Hypoglycemia and narcotic overdose are very common causes of Altered Sensorium and can easily be managed with dextrose and naloxone respectively.At a minimum, all Altered Sensorium patients deserve: Assessment of the ABCs Cardiac monitoring and pulse oximetry Supplemental oxygen Bedside glucose testing Intravenous access Evaluation for signs of trauma and consider c-spine stabilization Consider naloxone administration if narcotic overdose is suspected
  • 15. Detailed History and Physical Exam Patients with an AS are difficult to derive a comprehensive and detailed history from. Family, friends, caretakers, nursing home workers, witnesses are all invaluable sources of information. Make the effort to contact them to ascertain the nature of the change in mental status.Many medical conditions manifest as AS when decompensated. Look for a history of: diabetes (DKA, HONK), hypertension (hypertensive encephalopathy or medication overdose) endocrine disease (thyroid, Addisons) renal failure cancer (paraneoplastic syndromes, Na+, Ca++) cardiovascular and cerebrovascular disease seizure (atypical?) psychiatric issues Medication effects are also very common causes of AS in the elderly. A detailed review of medications (including non prescription, health supplements, home remedies) is critical. Has the patient recently started or stopped any medications?
  • 16. Physical Exam Vital signs Neurologic status Level of alertness GCS score or AVPU Content of thought and speech Does the patient stay focused? Is their speech tangential? Is the patient appropriately oriented? Does the patient keep asking the same questions over and over (perseveration)? Are they reacting to internal stimuli? Assess for focal motor findings Is there weakness or pronator drift? Cranial nerve exam (especially pupils) Evaluate for tremulousness or abnormal reflexes Common in withdrawal states or metabolic derangements
  • 17. Cardiovascular exam Are there arrhythmias (a-fib) that predispose to embolic strokes? Is there a murmur? endocarditis? Is there evidence of good peripheral circulation? Are there pulmonary findings that indicate pneumonia (sepsis) or pulmonary edema (hypoxia)? Are there bruits over the carotid arteries?Abdominal exam Is there ascites, caput medusa, liver enlargement or tenderness (hepatic encephalopathy)? Is the abdomen tender (appendicitis, intussusception, abdominal sepsis source, mesenteric ischemia)? Genitourinary and rectal exam Is the patient making urine (uremic encephalopathy)? Are there signs or urinary, vaginal, prostatic or perineal infection? Is there melena or blood in the stool?
  • 18. Skin, extremity, musculoskeletal exam Are there petechiae (meningococcemia)? Is there a dialysis graft (uremic encephalopathy)? Are there track marks from injection drug abuse? Are there transdermal drug patches? Is the skin jaundiced (hepatic encephalopathy)? Is there nuchal rigidity or meningismus (CNS infection)? Are there signs of trauma (raccoons eyes, Battle „s sign, hemotympanum)? Are there infectious sources noted (decubitus ulcers, cellulitis, abscesses)? Are there masses or lymphadenopathy that might indicate cancer History and physical exam findings are usually enough to help you categorize the change in mental status.
  • 19. Some Important Physical Examination in Detail
  • 20. General physical examination Vital sign – Temperature  Fever (High grade can Cause Acute febrile Encephalopathy which may lead to AS and even Coma)  Hypothermia -- <31 C causes coma – Pulse : Extereme Trachy / Brady can lead to AS and Even Coma – Respiratory rate and pattern ( Hypoxia/ Hypercapnia) – Blood pressure (HTN Encephalopathy or Shock lead to AS and Coma.
  • 21. GLASGOW COMA SCOREEyes Opening Verbal Motor4 - Spont 5 - Oriented 6 - Obeys3 – Response Verbal 4 - Confused 5 - Localizes to pain command2 - To Pain 3 - Inapprop words 4 - Withdraws to pain 2 - Incomprehensible 3 - Abnormal flexion1- None sounds posturing 2 - Abnormal extension 1 - No Sounds posturing 1 - None
  • 22. Glasgow Coma Scale : Eye opening (E)
  • 23. Glasgow Coma Scale : Verbal response (V)
  • 24. Glasgow Coma Scale : Motor response (M)
  • 25. GLASGOW COMA SCORENotes1. scoring from the best response2. verbal response will not correct in the condition of aphasia, intubation and facial injury3. sensory loss may interfere painful stimulation4. eye opening may be interfered by orbital swelling and 3rd CN palsy5. arm movements may be impaired from local trauma or cervical cord lesion
  • 26. Neurologic assessment Observe – Movement : restless, twitching, multifocal myoclonus, asterixis – Decorticate rigidity Suggest severe bilateral damage rostral to midbrain – Decerebrate rigidity Indicate damage to motor tracts in the midbrain or caudal diencephalon
  • 27. Decorticate posture results fromdamage to one or both corticospinal tracts
  • 28. Decerebrate posture results fromdamage to the upper brain stem
  • 29. Pupils in comatose patients DESCRIPTIONS INTERPRETATIONSmall, reactive Metabolic causes Diencephalic lesionMidposition, fixed Mid brain lesionlarge, fixed Extensive brain stem lesion hypoxia Sedative overdose Anticholinergic poisoningPin point Pontine lesion OpiatesUnilateral fixed dilated Oculomotor nerve palsy
  • 30. Ocular Movement Doll’s eye Cold caloric test maneuver (Oculovestibular(Oculocephalic reflex) reflex)
  • 31. MedialLongitudinalFasciculus
  • 32. Eye movementsCondition Doll’s eyesAwake NegativeCerebral dysfunction, Positivebrainstem intactBrain stem lesion NegativeCondition Cold caloricsAwake Nystagmus, N/V, painCerebral dysfunction, Slow deviation towardbrainstem intact waterBrain stem lesion Negative
  • 33. Respiratory pattern Cheyne-Stokes respiration : abnormal respiration in which periods of shallow and deep breathing alternate. a/w bilateral cortical or bilateral thalamic lesions, metabolic disturbances, incipient transtentorial herniation Hyperventilation : midbrain or pons lesions Apneusis : lateral tegmentum of lower half of pons Cluster : a breathing pattern in which a closely grouped series of respirations is followed by apnea. a/w lower pontine or high medullary lesions Ataxic : is an abnormal pattern of breathing characterized by complete irregularity of breathing, with irregular pauses and increasing periods of apnea . a?/w dorsomedial medulla lesion Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly DKA
  • 34. Conditions mimic AS/Coma Brain death Locked-in syndrome Vegetative state Frontal lobe disease Non-convulsive status epilepticus Psychiatric disorder (catatonia, depression)
  • 35. Vegetative state An awake but unresponsive state Extensive damage in both cerebral hemisphere Retained respiratory and autonomic functions Cardiac arrest and head injury are the most common causes.
  • 36. Locked-in state Awake patient has no means of producing speech or volitional limb, face and pharyngeal movements Vertical eye movement and lid elevation remain unimpaired Infarction or hemorrhage of the ventral pons
  • 37. Differential DiagnosisFollowing table organizes causes of AS occurring as a result of a structurallesion or primary CNS dysfunction, toxic, metabolic or infectious insults. Primary Metabolic and Pharmacologic/Toxic Infectious others CNS/Structural AutoregulatoryTumors Hypo/hyper Medication effects Primary CNS Hypoperfusion -glycemia - HTN - Meningitis states- Primary -natremia - Steroids - Encephalitis - Cardiogenic- Metastatic -calcemia - Sedatives - Abscesses - HypovolemicHemorrhage -thyroid - Analgesics Other site of Infection - Hemorrhagic- Spontaneous -thermia - Sleep aids - UTI - Distributive- Traumatic Hypercapnia - Anticholinergics - PneumoniaEdema Hypoxemia - Polypharmacy - Skin/decub ulcer Complicated- HTN enceph Alcohols - Intra-abdominal migraine- Obstructive - ETOH - Viral syndromhydrocephalus - methanol/ethylene PsychiatricSeizure glycol dosorder- Post-ictal state Withdrawal - Acute- Todds - Benzodiazepine - Chronicparalysis - NarcoticDementia- Degenerative- Multi-infarct
  • 38. AS/COMA LOCALIZING SIGN NO LOCALIZING SIGNSUPRATENTORIAL INFRATENTORIAL STIFF NECK - CVD - SAH - TUMOUR NO STIFF NECK - MENINGITIS - ABSCESS STRUCTURAL DAMAGE FUNCTIONAL NEURONAL DEPRESSION - HYPOXIA - HEPATIC - CARDIAC - URAEMIC ARREST - POST ICTAL STATE - ENCEPHALITIS - FLUID ELECTROLYTE IMBALANCE - DRUGS
  • 39. Alternatively, a mnemonic that is commonly used tohelp generate a differential diagnosis of AMS is: AS = AEIOU TIPS A Alcohol E Epilepsy, Electrolytes, and Encephalopathy I Insulin O Opiates and Oxygen U Uremia T Trauma and Temperature I Infection P Poisons and Psychogenic Shock, Stroke, Subarachnoid Hemorrhage and Space- S Occupying Lesion
  • 40. Diagnostic Testing Metabolic or Endocrine causes – Rapid glucose – Serum electrolytes (Na+, Ca+) – ABG or VBG (with co-oxymetry for carboxy- or met-hemoglobinemia) – BUN/Creatinine – Thyroid function tests – Ammonia level – Serum cortisol level Toxic or medication causes – Levels of medications (anticonvulsants, digoxin, theophylline, lithium, etc.) – Drug screen (benzodiazepines, opioids, barbiturates, etc.) – Alcohol level – Serum osmolality (toxic alcohols)
  • 41.  Infectious causes – CBC with differential – Urinalysis and culture – Blood cultures – Chest X-ray – Lumbar puncture (with opening pressure) – Always CT first if you suspect increased ICP. Traumatic causes – Head CT/ cervical spine CT Neurologic causes – Head CT (usually start without contrast for trauma or CVA) – MRI (if brainstem/posterior fossa pathology suspected) – EEG (if non-convulsive status epileptics suspected) Hemodynamic instability causes – ECG – Cardiac enzymes (silent MI) – Echocardiogram – Carotid/vertebral artery ultrasound
  • 42. Prognosis of AS/Coma Recovery depends primarily on the causes Intoxication and metabolic causes carry the best prognosis Coma from traumatic head injury far better than those with coma from other structural causes Coma from global hypoxic-ischemic carries least favorable prognosis At 3rd day, no papillary light reflex or GCS < 5 is associated with poor prognosis
  • 43. TreatmentBeyond interventions required for the immediate life threats such asimpending cardiopulmonary collapse, treatment should be geared towardscorrecting / treating the underlying pathologyIf the Cause of Coma/AS is unknown, what is often called a "coma cocktail"is given to the patient. This cocktail consists of T=Thiamine, O=oxygenN= Naloxene G= GlucoseThe „‟TONG‟‟ describes the sequence the cocktail should be given.Thiamine: Thiamine converts pyruvic acid to acetyl coenzyme. WithoutThiamine the energy contained in glucose couldn‟t be obtained. Alcoholintake interferes with absorption of thiamine. Hence thiamine should alwaysbe given prior to glucose if alcohol is suspected cause of coma.
  • 44. Oxygen: Oxygen is essential for cellular functioning. Indication foroxygen would be any clinical situation in which ventilation is notadequate or oxygen carrying capacity is diminished.Naloxene: If opoid toxicity is suspected, naloxene can be used. Itacts as competitive antagonist at opoid receptor and is indicated forthe reversal of CNS and Respiratory system depression caused byopoids. It is less common in Nepal. Recomended dose is mg andincreasing the dose slowly at - minutes interval. At total ofmg can be goven. If there is no response then opoid toxity is ruledout.Glucose: Glucose is essential energy source and primary source ofbraid. If hypoglycemia is indicated then glucose should be used.
  • 45. Rx Contd..... •Supportive care and sedation for agitated withdrawal states •Intravenous fluids for dehydration, hypovolemia, hypotension or hyperosmolar states or hypernatremia •Empiric antibiotics for suspected meningitis, urosepsis, pneumonia, etc. •Rewarming or aggressive cooling for temperature extremes •Fomepazole, pyridoxine, digoxin-fab fragments or other antidotes for specific toxins •Controlled reduction of blood pressure with nitroprusside, labetolol or fenoldepam for hypertensive encephalopathy •Hypertonic saline for profound hyponatremia with seizures or AS •Glucocorticoids for metastatic CNS lesions with vasogenic edema
  • 46. DispositionThe majority of patients with an AS will require hospitalization. Sometimes,however, patients with acute alterations in consciousness that are easilyreversed and observed to be stable in the emergency department can safelybe discharged home.The decision to admit the patient to the hospital ward may be based onhemodynamic stability, etiology of the AS
  • 47. Thank you