Approach to Altered Sensorium

Dr. Sudhir Dev

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:

What is Sensorium?

Ability of the brain to receive and interpret sensory stimuli.

Good Sensorium = Alertness + Awareness

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).

Altered Sensorium

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

Presentation of Patient with AS:

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)

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

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

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".

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 consciousness

Altered Normal Variable

HallucinationsVisual (related to external stimuli)

RareAuditory (related to internal stimuli)

Physical exam Often abnormal Often normal Often normal

PrognosisPoor if cause not treated

Progressive Variable

Underlying cause Organic (myriad)Organic (degenerative)

Functional

Dementia VS Confusional state

Dementia– Longstanding nature

– Varies little from time to time

– Memory problem

Confusional state– Acute

– Fluctuate

– Clouding of consciousness

Approach to Altered Sensorium

Initial Actions and Primary Survey

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).

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.

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 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

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?

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 reflexesCommon in withdrawal states or metabolic derangements

Physical Exam

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?

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 the change in mental status.

Some Important Physical Examination in Detail

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.

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- None2 - Incomprehensible sounds

3 - Abnormal flexion posturing

1 - No Sounds2 - Abnormal extension posturing

1 - None

Glasgow Coma Scale : Eye opening (E)

Glasgow Coma Scale : Verbal response (V)

Glasgow Coma Scale : Motor response (M)

Notes

1. scoring from the best response

2. verbal response will not correct in the condition of aphasia, intubation and facial injury

3. sensory loss may interfere painful stimulation

4. eye opening may be interfered by orbital swelling and 3rd CN palsy

5. arm movements may be impaired from local trauma or cervical cord lesion

GLASGOW COMA SCORE

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

Decorticate posture results from damage to one or both corticospinal

tracts

Decerebrate posture results from damage to the upper brain stem

Pupils in comatose patients

DESCRIPTIONSINTERPRETATION

Small, reactive Metabolic causesDiencephalic lesion

Midposition, fixed Mid brain lesion

large, fixed Extensive brain stem lesion hypoxiaSedative overdoseAnticholinergic poisoning

Pin point Pontine lesion Opiates

Unilateral fixed dilated Oculomotor nerve palsy

Doll’s eye maneuver

(Oculocephalic reflex)

Cold caloric test (Oculovestibular

reflex)

Ocular Movement

Medial Longitudinal Fasciculus

Eye movements

ConditionAwakeCerebral dysfunction, brainstem intactBrain stem lesion

Doll’s eyesNegativePositive Negative

ConditionAwakeCerebral dysfunction, brainstem intactBrain stem lesion

Cold caloricsNystagmus, N/V, painSlow deviation toward waterNegative

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.

Conditions mimic AS/Coma

Brain death Locked-in syndrome Vegetative state Frontal lobe disease Non-convulsive status epilepticus Psychiatric disorder (catatonia,

depression)

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.

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

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

Metabolic and Autoregulatory

Pharmacologic/Toxic Infectious others

Tumors

- Primary- MetastaticHemorrhage- Spontaneous- TraumaticEdema- HTN enceph- Obstructive hydrocephalusSeizure- Post-ictal state- Todd's paralysisDementia- Degenerative- Multi-infarct

Hypo/hyper-glycemia-natremia-calcemia-thyroid-thermiaHypercapniaHypoxemia

Medication effects- HTN- Steroids- Sedatives - Analgesics- Sleep aids- Anticholinergics- PolypharmacyAlcohols- ETOH- methanol/ethylene glycolWithdrawal- Benzodiazepine- Narcotic

Primary CNS- Meningitis- Encephalitis- AbscessesOther site of Infection- UTI- Pneumonia- Skin/decub ulcer- Intra-abdominal- Viral syndrom

Hypoperfusion states- Cardiogenic- Hypovolemic- Hemorrhagic- Distributive

Complicated migraine

Psychiatric dosorder- Acute - Chronic

AS/COMA

LOCALIZING SIGN NO LOCALIZING SIGN

SUPRATENTORIAL INFRATENTORIAL

NO STIFF NECK

STIFF NECK

- CVD- TUMOUR- ABSCESS

STRUCTURAL DAMAGE FUNCTIONAL NEURONAL DEPRESSION

- HYPOXIA- CARDIAC ARREST- ENCEPHALITIS

- HEPATIC- URAEMIC- POST ICTAL STATE- FLUID ELECTROLYTE IMBALANCE- DRUGS

- SAH- MENINGITIS

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

SShock, Stroke, Subarachnoid Hemorrhage and Space-Occupying Lesion

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)

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

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

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=oxygenN= 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.

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.

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

DispositionThe 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 to the hospital ward may be based on hemodynamic stability, etiology of the AS

Thank you