The document provides guidance on evaluating and managing a patient presenting with altered sensorium (AS). It defines sensorium and levels of consciousness. Common causes of AS include metabolic disturbances, infections, trauma, medications, and neurological conditions. The approach involves assessing ABCDE, obtaining history, performing a full physical exam including Glasgow Coma Scale, running diagnostic tests, considering various differential diagnoses, and treating reversible causes. The prognosis depends on the underlying etiology, with metabolic/toxic causes having a better outlook than structural injuries or hypoxia.

1. APPROACH TO PATIENT WITH
ALTERED SENSORIUM
MY MENTOR : DR. KAMLESH KUMAR SINGH
MCH NEUROSURGERY
DR. DHEERENDRA KUMAR MISHRA
FAMILY MEDICINE JUNIOR RESIDENT (PGY1)

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 : Arousal 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, sun downing‟
 Perceptual disturbances and misinterpret voices, common objects and
actions of other persons

9. Some Common Terms in Altered Sensorium
 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)
 Psychosis : refers to a mental state often described as
involving a "loss of contact with reality".

10. DIFFERENTIATING DELIRIUM, DEMENTIA AND PSYCHOSIS

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
 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.

14. • 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. Hypo perfusion 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)

15. 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

16. 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, Addison's)
• 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?

17. PHYSICAL EXAM
 VITAL SIGNS
 NEUROLOGIC STATUS
 Level of alertness GCS score or AVPU Content
 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

18.  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?

19. 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.

20. SOME IMPORTANT PHYSICAL EXAMINATION IN DETAIL
 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 : Extreme Tachy / 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 SCORE

22. GLASGOW COMA SCALE : EYE OPENING (E)

23. Glasgow Coma Scale : Verbal response (V)

24. Glasgow Coma Scale : Motor response (M)

25. GLASGOW COMA SCORE
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

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
• HYPOXIA
• SEDATIVE OVERDOSE
• ANTICHOLINERGIC POISONING
PIN POINT • PONTINE LESION
• OPIATES
UNILATERAL FIXED DILATED • OCULOMOTOR NERVE PALSY

30. 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 trans tentorial
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

31. CONDITIONS MIMIC AS/COMA
 Brain death
 Locked-in syndrome
 Vegetative state
 Frontal lobe disease
 Non-convulsive status epilepticus
 Psychiatric disorder (catatonia, depression)

32. 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.

33. 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

34. 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.

36. ALTERNATIVELY, A MNEMONIC THAT IS COMMONLY USED
TO HELP GENERATE A DIFFERENTIAL DIAGNOSIS OF AMS
IS: AS = AEIOU TIPS

37. 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)

38.  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

39. 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

40. 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= Naloxone G= Glucose
‟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.

41. TREATMENT
 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.
 NALOXONE: If opioid toxicity is suspected, naloxone can be used. It
acts as competitive antagonist at opioid receptor and is indicated for
the reversal of CNS and Respiratory system depression caused
by opioids.
 GLUCOSE: Glucose is essential energy source and primary
source of brain. If hypoglycemia is indicated then glucose should
be used.

42.  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,
labetalol or fenoldepam for hypertensive encephalopathy
 Hypertonic saline for profound hyponatremia with seizures
or AS
 Glucocorticoids for metastatic CNS lesions with vasogenic
edema

43. 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 TO THE HOSPITAL
WARD MAY BE BASED ON HEMODYNAMIC STABILITY,
ETIOLOGY OF THE ALTERED SENSORIUM.

44. THANK YOU