Altered sensorium

Dr Sudhir (BPKIHS GPEM)

1. Approach to Altered Sensorium Dr. Sudhir Dev

2. 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 Objectives:

3. What is Sensorium? A bility of the brain to receive and interpret sensory stimuli . Good Sensorium = Alertness + Awareness

4. Altered Sensorium is not a disease: I t 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). Altered Sensorium

5. Unfortunately, there is no classic presentation for a patient with Altered Sensorium. P resentations can range from CNS depression to confusion, agitation, etc . Altered sensorium can be determined by evaluating level of Consciousness Presentation of Patient with AS:

6. Level of Consciousness Alert  : N ormal awake and responsive state Drowsiness : S tate of apparent sleep, briefly arousal with oral command Lethargic  : R esembles 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 :  E asily aroused by voice or touch; awakens and follows commands; req uired stim ulation to maintain arousal Obtunded/Stuporous  : A rousable only with repeated and painful stimulation; verbal output is unintelligible or nil; some purposeful movement to noxious stimulation Comatose : N o arousal despite vigorous stim ulation , 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 D ementia P sychosis Onset Rapid Slow Variable Course Fluctuating Progressive Variable Vital signs Often abnormal Usually normal Usually normal Level of consciousness Altered Normal Variable Hallucinations Visual (related to external stimuli) Rare Auditory (related to internal stimuli) Physical exam Often abnormal Often normal Often normal Prognosis Poor if cause not t reated Progressive Variable Underlying cause Organic (myriad) Organic (degenerative) Functional

11. Dementia VS Confusional state Dementia Longstanding nature Varies little from time to time Memory problem Confusional state Acute Fluctuate Clouding of consciousness

12. Approach to Altered Sensorium

13. Initial Actions and Primary Survey A- Check to see that the airway is open and protected. Hypoxia is a potentially reversible cause of A ltered 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) . 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 A ltered sensorium.

14. As we proceed through ABCDE , keep in mind rapidly reversible causes for the A ltered S ensorium . Hypoglycemia and narcotic overdose are very common causes of A ltered S ensorium and can easily be managed with dextrose and naloxone respectively. At a minimum, all A ltered S ensorium patients deserve: Assessment of the ABC's 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, H O NK), 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. V ital 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 Physical Exam

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 (raccoon's 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 th e 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 pres sure (HTN Encephalopathy or Shock lead to AS and Coma.

21. GLASGOW COMA SCORE Eyes Opening Verbal Motor 4 - Spont 5 - Oriented 6 - Obeys 3 – Response Verbal command 4 - Confused 5 - Localizes to pain 2 - To Pain 3 - Inapprop words 4 - Withdraws to pain 1- None 2 - Incomprehensible sounds 3 - Abnormal flexion posturing 1 - No Sounds 2 - Abnormal extension 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. Notes scoring from the best response verbal response will not correct in the condition of aphasia, intubation and facial injury sensory loss may interfere painful stimulation eye opening may be interfered by orbital swelling and 3 rd CN palsy arm movements may be impaired from local trauma or cervical cord lesion GLASGOW COMA SCORE

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 from damage to one or both corticospinal tracts

28. Decerebrate posture results from damage to the upper brain stem

29. Pupils in comatose patients DESCRIPTIONS INTERPRETATION Small, reactive Metabolic causes Diencephalic lesion Midposition, fixed Mid brain lesion large, fixed Extensive brain stem lesion hyp oxia S edative overdose A nticholinergic poisoning Pin point Pontine lesion Opiates Unilateral fixed dilated Oculomotor nerve palsy

30. Doll’s eye maneuver (Oculocephalic reflex) Cold caloric test (Oculovestibular reflex) Ocular Movement

31. M edial L ongitudinal F asciculus

32. Eye movements Condition Awake Cerebral dysfunction, brainstem intact Brain stem lesion Doll’s eyes Negative Positive Negative Condition Awake Cerebral dysfunction, brainstem intact Brain stem lesion Cold calorics Nystagmus, N/V, pain Slow deviation toward water 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/C oma 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 Diagnosis Following table organizes causes of AS occurring as a result of a structural lesion or primary CNS dysfunction, toxic, metabolic or infectious insults . Primary CNS/Structural M etabolic and Autoregulatory Pharmacologic/Toxic Infectious others Tumors - Primary - Metastatic Hemorrhage - Spontaneous - Traumatic Edema - HTN enceph - Obstructive hydrocephalus Seizure - Post- ictal state - Todd's paralysis Dementia - Degenerative - Multi-infarct Hypo/hyper - glycemia - natremia - calcemia -thyroid - thermia Hyperca pnia Hypoxemia Medication effects - HTN - Steroids - Sedatives - Analgesics - Sleep aids - Anticholinergics - Polypharmacy Alcohols - ETOH - m ethanol/ethylene glycol Withdrawal - Benzodiazepine - Narcotic Primary CNS - Meningitis - Encephalitis - Abscesses Other site of I nfection - UTI - Pneumonia - Skin/ decub ulcer - Intra-abdominal - Viral syndrom Hypoperfusion states - Cardiogenic - Hypovolemic - Hemorrhagic - Distributive Complicated migraine Psychiatric dosorder - Acute - Chronic

38. AS/ COMA LOCALIZING SIGN NO LOCALIZING SIGN SUPRATENTORIAL INFRATENTORIAL NO STIFF NECK STIFF NECK - CVD - TUMOUR - ABSCESS STRU C TURAL DAMAGE FUNCTIONAL NEURONAL DEPRESSION - HYPOXIA - CARDIAC ARREST - ENCEPHALITIS - HEPATIC - URAEMIC - POST ICTAL STATE - FLUID ELECTROLYTE IMBALANCE - DRUGS - SAH - MENINGITIS

39. Alternatively, a mnemonic that is commonly used to help 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 S Shock, Stroke, Subarachnoid Hemorrhage and Space-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/C oma 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 3 rd day, no papillary light reflex or GCS < 5 is associated with poor prognosis

43. Treatment : Beyond interventions required for the immediate life threats such as impending cardiopulmonary collapse, treatment should be geared towards correcting / treating the underlying pathology . If 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=oxygen N= Naloxene G= Glucose The ‘’TONG’’ describes the sequence the cocktail should be given. Thiamine : Thiamine converts pyruvic acid to acetyl coenzyme. Without Thiamine the energy contained in glucose couldn’t be obtained. Alcohol intake interferes with absorption of thiamine. Hence thiamine should always be given prior to glucose if alcohol is suspected cause of coma.

44. Oxygen: Oxygen is essential for cellular functioning. Indication for oxygen would be any clinical situation in which ventilation is not adequate or oxygen carrying capacity is diminished. Naloxene: If opoid toxicity is suspected, naloxene can be used. It acts as competitive antagonist at opoid receptor and is indicated for the reversal of CNS and Respiratory system depression caused by opoids. It is less common in Nepal. Recomended dose is 0.1 mg and increasing the dose slowly at 2-3 minutes interval. At total of 10 mg can be goven. If there is no response then opoid toxity is ruled out . Glucose: Glucose is essential energy source and primary source of braid. 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. Disposition The majority of patients with an AS will require hospitalization. Sometimes, however, patients with acute alterations in consciousness that are easily reversed and observed to be stable in the emergency department can safely be discharged home. The decision to admit the patient t o the hospital ward may be based on hemodynamic stability, etiology of the A S

47. Thank you