CRACKCast E204 – Depressed Consciousness and Coma

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This updated episode of CRACKCast covers Rosen’s Chapter 013, Depressed Consciousness and Coma (9th Ed.). Obtaining a reliable history from an unresponsive patient is next to impossible, especially if the patient arrives to the ED alone. The podcast will give you the knowledge to rapidly identify the cause of your patient’s unresponsiveness and give you the tools to intervene on your next shift.

This episode features Haley Cochrane, graduating EM resident at the University of Saskatchewan.

Shownotes – PDF here


Rosen’s in Perspective

We are back at it again and you all know what that means: we are jumping into the episode with a case:

You are working the afternoon shift at a community hospital when you get paged by the charge nurse to come to the triage desk. There is an 84-year-old female with a PMHx of mild cognitive impairment, hypertension, and hypercholesterolemia that is being brought into the ED by EMS. She was found by her daughter and was noted to be more somnolent than usual. En route, BP 95/85, HR 110, Temp 35.9 degrees Celsius, RR 25, SpO2 93% RA. Her GCS is 13-14. Yesterday, she was her normal self with no specific complaints.

You look down at your shoes, take a breath, and get ready. You think about all of the things that could cause this presentation. You reach a differential list of 4000 diagnoses and you mind breaks a bit. You begin to get a little confused yourself and start to feel a bit panicked. What are you going to do?

Answer: Don’t sweat it. As always we got your back.

This post will have everything you need to quell your anxiety. We will give you the tools to be able to organize that mammoth list into a concise table in your mind. Additionally, we will give you a good run down of the relevant elements on history and physical exam to elicit in your next altered patient. These are patients you will be seeing A LOT of in the ED, so having a solid approach will help you immeasurably. Most of the people will have a toxic ingestion or metabolic derangement as the cause of their depressed LOC, but structural brain lesions, infections, and other things can cause your patients to be a little stuporous.

This podcast will be a keeper, but as we always say, read the chapter. Use our resources to supplement your learning, because as good as we think we are, we know that repeated exposure to core content in Emergency Medicine is key.

With that said, grab your coffee, settle in, and take a listen.


Core Questions:


[1] Define coma and differentiate coma from lethargy and stupor.

Coma is defined by Rosen’s Emergency Medicine (9th Edition) to be the following:

  • “A state of profoundly decreased arousal, resembling sleep”
    • These patients, by definition, will not be able to be aroused by external stimuli
    • It is important to note that these patients can have variable reflex behaviours present and still be comatose
  • When you consider lethargy and stupor, these people will have diminished level of consciousness, but they are aroused by external stimuli

[2] Name five neuroanatomic structures involved in maintaining arousal.

Tight list for you guys. Here we go:

  1. Brainstem nuclei
  2. Hypothalamus
  3. Thalamus
  4. Ascending Reticular Activating System (ARAS)
  5. Basal forebrain

The ARAS is the most important structure to consider. The neurons are located in the pons and midbrain. Their projections extend through the thalamus and into the cortices

Aside from equipping you for your next Neuro pimp session, knowing this content will allow you to help localize potential lesions causing depressed LOC. Any insult that affects the aforementioned structures or the cortices bilaterally will produce coma, so look for other signs on physical exam to either confirm or refute your clinical suspicions of lesion in this area.

[3] List five critical and five emergent causes of depressed consciousness. (see Table 13.1)

Critical DiagnosesHypoglycemiaDiaphoresis, insulin pumpD50W, 50 ml
Hyperglycemia (DKA/HHNKS)Tachypnea, N+V, abdo pain, dehydrationIsotonic fluids, insulin
BeriberiHypothermia, hypotensionThiamine 100 mg IV
Adrenal CrisisWeakness, weight loss, hypotension, hyperpigmentationD5NS, correct low gluc, hydrocortisone 100 mg IVLook for hyperK+
Pituitary ApoplexyHA, visual impairment, multiple hormone dysfunctionTreat electrolyte abnormalities, IV hydrocort 100 mg IVMay have pit adenoma; consult NeuroSx
SepsisSIRS criteria, poor end-organ perfusion, deliriumABX + isotonic fluids
Emergent DiagnosesWernicke’s EncephalopathyCN III or VI palsies, sluggish pupils, anisocoria, gait instability, peripheral neuropathyThiamine replacementAlcoholics or malnourish; rare in Hyperemesis Gravidarum
HyponatremiaProgressive confusion, HA, anorexia, seizureFluid restriction, hypertonic saline if seizingThink med ADE
HyperammonemiaLethargy, irritability, vomiting, seizures, poor feedingMonitor protein intake, dialysisSeen in liver disease, IEM’s, ADE valproic acid, complication of bariatric Sx
HypercalcemiaLethargy, polyuria, AKI, constipationIsotonic fluidsCauses nephrogenic DI, suspect malignancy
UremiaN+V, anorexia, fatigue, ammonia breathTreat hyperkalemia, dialysisCheck EKG for hyperK changes
Hepatic EncephalopathyFetor hepaticus, asterixis, ascites, stigmata of cirrhosisLactuloseRule out sepsis, GIB, SBP
ThyrotoxicosisFever, tachycardia, sweating, diarrheaIsotonic fluids, propranolol 1 mg IV, PTU 600 mg POMay need to treat adrenal insuff
Myxedema ComaSluggish, weight gain, edema, depression, hair loss, constipationThyroxine 500 ug IV; hydrocortisone 100 mg IVSearch for acute precipitant
Heat StrokeHyperpyrexia (<41.1 Celsius), flushing, exertion in heat, dehydrationIsotonic fluid, evaporative coolingLook at elderly unable to seek cool environment
HACERapid ascent, HA, confusion, psychosisRapid descent, hyperbaric O2, dexamethasone 10 mg IVMore common above 3500 m
Critical DiagnosesHypoglycemic AgentsOlder adult with poor renal function, intentional ODD50W; octreotide 50-100 ug IV q 8h if refractoryFrequent OPCK in peds; admit all
OpioidsStupor, apnea, miosis, needle tracksNaloxone 0.4 mg IV, up to 10 mg IVCheck skin for fent patches
Simple AsphyxiantsSudden lightheadedness, collapse, syncope100% O2Leaking CO2 tank in enclosed space; also helium, nitrogen, argon gas
COCombustion of fuel in enclosed space, HA, confusion, malaise, nausea100% O2, hyperbaric O2 per toxicologyLook for others involved; think of pregnant patients carefully
Histotoxic HypoxiaConfusion, seizure, H2S with rotten egg smell, cyanide with bitter almond scent; may result from products of combustion100% oxygen; hydroxocobalam 70 mg/kg (or 5 g) for CNConsider CN in any house or car fire
MethHgBUse of meds, cyanosis, pulse ox 85%100% O2, methylene blue 1-2 mg/kg IVCan be caused by diarrhea in children
Emergent DiagnosesSedativesAlcohol, benzos, may othersSupportiveAvoid flumazenil
Toxic OH’sN+V, early osmolar gap then AGMA, renal failureFomepizole; 15 mg/kg IV load; correct electrolytes, isotonic fluid at 500 cc/hrConsult Nephro and Tox for hemodialysis
InhalantsYoung, paint on hands/face, diplopia, slurred speech, arrhythmiasCheck EKG; definitive airway if lip or tongue edemaConsider frostbite causing airway edema
Psychiatric MedsHypotension, prolonged QRSNaHCO3 for TCA’s
AnticonvulsantsConfusion, slurred speech, elevated levelsSupportive measuresHyperammo. with Valproate
AnticholinergicsHyperpyrexia, pupil dilation, urinary retention, visual hallucinationsPyridostigmine rarely used; benzos for severe agitation
ClonidineBradycardia, hypotension, somnolenceNaloxone up to 10 mg IV, then infusion 2-4 mg/h
Beta BlockersBradycardia, hypotension, hypoglycemia, seizureGlucagon 5 mg IV, epi 1-4 ug per min; atropine 0.5 mg IV; pacingDiscuss IV lipid infusion with Tox
SalicylatesN+V, tinnitus, delirium, hyperpnea, AGMA + mixed resp alkD5W with 150 mEq/L NaHCO3; correct hypoK+, consider hemodialysisConsider oil of wintergreen
NMSHyperpyrexia, rigidity, delirium, autonomic instabilityCooling, isotonic fluids, benzosMay need to paralyze with ND agent
Serotonin SyndromeMultiple agents, hypertension, tachy, hyperreflexia, rigidity, tremor, nausea, diarrheaIsotonic fluids, check CK, cyproheptadine 12 mg PO, benzosMay need to paralyze with ND agent
Critical DiagnosesHemorrhageHA, HTN, sudden onset, neuro deficitsCT w/o contrast, reversal of anticoagulationConsult NeuroSx early
Cortical InfarctSudden neuro deficits (unilateral)CT/CTA, Neuro consultTPA, if no CI’s: 0.8 mg/kg IV, max 90 mg dose; administer 10% over 1 min, then rest over 60 min
Cerebellar InfarctSudden vertigo, nausea, ataxia, dysarthriaConsider TPANeuroSx

[4] Describe your approach to the history and physical examination for the patient with depressed consciousness.


Point One: As you most you would likely assume, getting a history from an obtunded patient is not necessarily easy. Additionally, salient points on history from these patients may also be unreliable. Thus, it is important to stress that the VAST MAJORITY of the history in patients with altered LOC will come from collateral sources. Valuable sources for health information include the following:

  • Family, friends, bystanders
  • EMS (these people are trained to gather information at the scene; ask them what is what like during the extrication)
  • First responders (e.g., police services)
  • Electronic medical records

Point Two: It is important to contextualize the events leading up to the diminished LOC, the time period when the person became altered, and the patient’s course after being discovered. Make sure to establish points of chronology:

  • When were they last seen normal?
  • How was their health prior to being altered?
  • Had they any specific cardiovascular, respiratory, urinary, or neurologic complaints of note?
  • How did they become altered? Was it a sudden event (more indicative or an acute cardiac, neurologic events like CVA or seizure, or toxic ingestion) or was it gradual (more indicative of a metabolic or infectious cause of their symptoms).

Point Three: Do a thorough medication review. These can often cause or contribute to the patient’s altered state. Also, do not forget about OTC and supplements.

  • You can consider contacting the patient’s pharmacy to get more information about their medication history and compliance

Point Four: Look for any information that the patient may be carrying that will help you discern the cause of their cookiness. For example, many elderly persons carry cue cards with relevant PMHx and medication information on them. Medical alert bracelets and tattoos may also help.

Physical Exam:

These guys get a full head-to-toe examination. A wise practitioner of Emergency Medicine once said to undress all of your patients greater than 60 years old. Their AARP membership or Humpty’s Emerald Club Card buys them a strip search.

Relevant structures to assess on physical exam include the following:

Vital Signs – don’t forget a blood glucose

HEENT – look for signs of trauma, hemorrhage, skull fracture; also, look inside the mouth for evidence of tongue laceration to help discern if a seizure too place. Look for goiters and other stigmata of thyrotoxicosis/myxedema coma.

C-Spine – if there is any suspicion that this patient has a C-spine injury, immobilize and treat appropriately

CVS – full exam; listen for murmurs or extra heart sounds

RESP – listen for signs of focal consolidation or diffuse fluid volume overload

ABDO – look for stigmata of chronic liver disease, acute urinary retention, or peritonitis

DERM – look for signs of trauma, infection, and transdermal patches. Additionally, look for purpura or petechiae to support a diagnosis of meningococcemia

NEURO – The breakdown of the NEURO exam is as follows:

  1. GCS
  2. Cranial Nerves
    1. Pay attention to those pupils AND positioning of the eyes; dysconjugate gaze or pupillary abnormalities may indicate pathology intracranially
  3. Motor Exam
    1. Look at gross motor movements
    2. Look for rigidity, spasticity, clonus
    3. Evaluate reflexes
    4. Evaluate posturing
  4. Brainstem Reflexes
    1. Oculocephalic Reflex
    2. Oculovestibular Reflex
    3. Corneal Reflex
    4. Gag Reflex

[5] Outline your exam to accurately assess the Glasgow Coma Scale (GCS). (see Table 13.2)

This is an oldy but a goody. You have to know this stuff well, as knowledge of the GCS will most certainly influence management decisions. While not a perfect test, having a reliable exam is important. It will give you valuable information about disease progression and patient status going forward, and may give you a little more help with your differential and disposition plan.

Parameter Rating Score
Eye Opening
Open before stimulus Spontaneous 4
Open on spoken or shouted request To voice 3
Open to fingertip stimulus To pain 2
No opening at any time, no interfering factor No response 1
Closed by local factor Not testable (NT) NT
Best Verbal Response
Correctly gives name, place, and date Oriented 5
Not oriented but communicates coherently Confused 4
Intelligible single words Inappropriate words 3
Only moans or groans Incomprehensible sounds 2
No audible response, no interfering factor No response 1
Factor interfering with communication NT NT
Best Motor Response
Obeys two-step request Obeys command 6
Moves hand across the body or above clavicle to stimulus Localizes pain 5
Bends arm at elbow rapidly, features not predominantly abnormal Withdraws from pain 4
Bends arm at elbow, features clearly predominantly abnormal Flexion to pain 3
Extends arm at elbow Extension to pain 2
No movement in arms or legs, no interfering factor No response 1
Paralyzed or other limiting factor NT NT

[6] What is the FOUR score, and how is it calculated? (see Table 13.3)

The FOUR score, or the Full Outline of Unresponsiveness score is another tool we can use to assess the level of consciousness in a patient. It has been shown to have a higher interrater reliability than the GCS and has been validated in multiple clinical settings. This score integrates a more detailed assessment of brainstem reflexes. It is, albeit, not commonly used in many centers, but it is still a good tool – so remember it.

It is easy to remember: 4, 4, 4, 4

  • Eye Response
    • 0 – closed to pain
    • 1 – open with pain
    • 2 – open to loud voice
    • 3 – open but not tracking
    • 4 – open or opened, tracking, or blinking to command
  • Motor Response
    • 0 – no response to pain or generalized myoclonus status
    • 1 – extension to pain
    • 2 – flexion to pain
    • 3 – localizing pain
    • 4 – thumbs-up or peace sign
  • Brainstem Reflexes
    • 0 – absent pupillary, corneal, and cough reflex
    • 1 – pupil AND corneal response absent
    • 2 – pupil OR corneal response absent
    • 3 – one pupil wide and fixed
    • 4 – pupil and corneal reflexes present
  • Respiration
    • 0 – breathes at ventilator rate or apnea
    • 1 – breathes above ventilator rate
    • 2 – not intubated, irregular breathing
    • 3 – not intubated, Cheyne- Stokes breathing pattern
    • 4 – not intubated, regular breathing pattern

[7] What ancillary tests should be ordered in the patient with depressed consciousness?

This is a difficult question to answer, as you will select ancillary tests that are appropriate for your patient’s presenting issues. With that being said, however, given that the differential is so broad for altered LOC, consider casting a wide net. Fixation is one of the leading causes of cognitive error in these scenarios, so do not focus on diagnosis too quickly.

According to Rosen’s 9th Edition, consider the following diagnoses:

  • Bedside glucose
  • CBC
  • Electrolytes, Extended Electrolytes
  • VBG with Lactate
  • Co-oximetry
  • INR/aPTT
  • Urinalysis
  • Acetaminophen, ASA
  • Antiepileptic drug serum levels (as appropriate)
  • TSH
  • Blood and urine cultures (if infection is suspected)
  • CSF sampling (if appropriate)
  • CT Scan (contrast versus non-contrast depending on clinical picture)
  • CXR
  • EKG

Other things you can consider are the following:

  • Trops/CK
  • Serum OsM
  • Serum EtOH (Rosen’s states that this is rarely useful, however, we disagree)

[8] Outline your plan of management for the patient with depressed consciousness. (see Figure 13.2)

Rosen’s 9th Edition actually has a decent algorithm that can help guide you through the initial management and work up for the patient with depressed consciousness. We have attempted to summarize it below, but check out the textbook for more details.

  • Step One: Assess ABC’s
  • Step Two: measure glucose at bedside, obtain IV access, maintain SpO2 at approx 97%, initiate cardiac monitoring, obtain portable CXR, EKG, and labs
  • Step Three: administer glucose if hypoglycemic, naloxone if opioid toxicity is suspected, and thiamine if malnourished
  • Step Four: complete physical and neurologic examinations
    • If they improve with initial investigations and the clinical picture is clear, treat and observe
    • If initial management does not improve the patient and the work up at this point does not identify a cause, investigate for other causes
  • Step Five: Determine if brainstem signs are present, secure airway, and administer ABx if infectious cause is suspected
    • If present – CT/CTA
    • If absent, plain CT
  • Step Six: Determine if structural cause is present
    • If present, consult specialist, treat cause, and provide neuroprotective interventions. Also consider ICU admission.
    • If no structural cause is present, run through the DDx again
      • Toxins – labs, antidote/dialysis?
      • Seizure – EEG, anticonvulsant?
      • PRES – MRI, antihypertensive?
      • Infection – LP, antibiotics?
      • Nutrition – thiamine, glucose?
      • Endocrine – thyroid studies, steroids?




[1] What is the best noxious stimulus to apply to evaluate GCS?

Trick question, there are many. Another thing you should know is this: you should be applying two different types of painful stimuli depending on what you are trying to assess. While there is not a lot of high quality evidence surrounding this topic, Critical Care Services Ontario (an organization of hospital administrators and clinicians) recommends the following painful stimuli be used to adequately evaluate GCS:

When attempting to evaluate the patient’s eye opening score on GCS, use a peripheral painful stimulus. Specifically, use interphalangeal pressure to determine this score. To do so, you should:

  • Apply pressure with a pen/pencil to the lateral outer aspect of the proximal or distal interphalangeal joint (lateral aspect of the patient’s finger or toe) for 10 to15 seconds to elicit a response.
  • Note: just because the patient flexes their arm does not mean the person has intact brain functioning; this is a spinal reflex

While attempting to elicit a motor response to assess the Motor score of the GCS, you should use a central stimulus. Specifically, you should use either the trapezius twist (CN XI), supraorbital pressure method (CN V), or jaw margin pressure method (CN V). To do this:

  • Trap Twist – grab two inches of the muscle at the angle where the shoulder meets the neck with your thumb and first two fingers and twist for 10-20 seconds
    • Note: high SCI’s may falsely obscure this finding
  • Supraorbital Pressure Method – place the flat aspect of the thumb over the supraorbital ridge for 10-20 seconds, applying gradually increasing pressure
    • Note: do not use with suspected maxillofacial or head trauma
  • Jaw Margin Pressure Method – apply the flat of your thumb at the maxillomandibular joint and apply gradually increasing pressure for 10-20 seconds
    • Note: use caution in patients with suspected elevated ICP, as this may compress the jugular vein and worsen pressures

This organization does not recommend using sternal rub as a noxious stimulus as the patient is often left with residual pain and injury afterwards. So, be kind to your next sleepy man when assessing GCS.

[2] What are the oculocephalic and oculovestibular reflexes, and what information do they provide?

We are going back to the days of medical school neurology lectures with this one. Strap in tight and enjoy the ride.

Oculocephalic Reflex

  • Otherwise known as the Doll’s Eye Reflex
  • A normal oculocephalic reflex is seen when the patient’s eyes move in the direction opposite the head when rotating the patient’s head laterally. Normally, the eyes will appear to maintain visual fixation on an object
  • Indicative of normal brainstem functioning
  • Testing for the Doll’s Eye reflex is not always possible given potential concern regarding cervical spine injury in altered trauma patients

Oculovestibular Reflex

  • Otherwise known as the Cold Caloric Test
  • More sensitive test for brainstem dysfunction
  • With the patient’s head of the bed elevated at 30 degrees, infusion of ice water into the external auditory canal produced sustained conjugate deviation toward the irrigated ear
  • If the patient is conscious, the patient will also demonstrate nystagmus with the fast phase away from the irrigated ear
    • They will also likely have intense vertigo, nausea, and vomiting
  • Again, an absent conjugate gaze likely indicates brainstem dysfunction; these people will keep their eyes in mid position with respect to the orbits and their eyes will move in unison with their head

[3] Describe decorticate and decerebrate posturing.

Pretty quick one here:

  • Decorticate Posturing
    • Reflexive shoulder adduction, flexion of the elbows, writs, and fingers
  • Decerebrate Posturing
    • Reflexive shoulder adduction, elbow extension, and forearm pronation

Remember, this reflexive posturing is usually seen in patients with focal brain lesions; however, patients with systemic conditions (including toxic ingestions and metabolic derangements) can demonstrate these findings.

[4] What is the utility of serum ammonia testing?

This topic is controversial to say the least. While serum ammonia levels correlate well with the degree of hepatic encephalopathy (up to 2 x the ULN), there are some issues with them

  1. You do not need elevated ammonia levels to make the diagnosis of HE – some patients can have normal ammonia levels and still have HE
  2. Levels can change depending on a multitude of factors, including whether or not a tourniquet was used during the blood draw, whether or not the sample was placed on ice directly after being drawn, and whether or not the patient suffers from another condition that would increase their ammonia levels (e.g., Reye’s Syndrome, cigarette smoking, shock, certain inborn errors of metabolism, GI bleeding)

UptoDate notes that they can be useful in monitoring the effects of ammonia-lowering agents, but does not find them useful when attempting to make the diagnosis of HE or when monitoring patients with chronic cirrhosis. Measuring serum ammonia levels may also be useful in states where acute hyperammonemia is caused by drug ingestion (e.g., valproic acid).

Thus the short answer is this: Their utility is in question, but serum ammonia levels may be useful in some patient


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Owen Scheirer

Owen is a resident in the FRCPC Emergency Medicine program at the University of Saskatchewan. When he's not running around the emergency department, he's hanging out with his wife, new baby girl, and dog. Spare time = climbing and cycling!

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Dillan Radomske

Dillan Radomske is an Emergency Medicine resident at the University of Saskatchewan. He is passionate about technology-enhanced medical education, podcast creation and production, and Indigenous advocacy. He is one of the new CRACKCast hosts, and aspires to continue to contribute to the field of FOAMed in the future.

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