The Glasgow Coma Scale: A Tool Stretched Too Far

For decades, the Glasgow Coma Scale (GCS) has been one of the most familiar tools in emergency and critical care medicine. It is quick, somewhat memorable, and widely used. Over time, however, its role has quietly expanded far beyond what it was designed to do. The GCS is now routinely asked to stand in for airway protection, sedation depth, intoxication severity, and even anesthetic effect.

When a tool is stretched far outside its original purpose, it does not become more powerful. It can become misleading.

One of the most visible consequences of this stretch is the long-standing dogma: “GCS < 8, intubate.” But that phrase is not the root problem. It is a symptom of how far we have extrapolated a neurologic communication scale into domains it was never meant to cover.

I think the best place to start is the origin...

Birth of The GCS

Before the mid-1970s, clinicians lacked a shared language to describe consciousness. This made early detection of neurologic deterioration difficult, especially across hospital boundaries. In 1974, Teasdale and Jennett published Assessment of Coma and Impaired Consciousness in The Lancet, introducing what would become the Glasgow Coma Scale.

The scale originated in a neurosurgical unit in Glasgow, UK. Its purpose was straightforward: provide a standardized way to describe and trend neurologic function in patients with acute brain injury. It was particularly useful for traumatic brain injury, stroke, and subarachnoid hemorrhage, where subtle changes in exam mattered.

As Teasdale later emphasized, the need for clear communication between referring hospitals and specialist units was a major driver of the scale’s development.

The GCS was designed to track neurologic injury over time, not to dictate airway management, assess intoxication, or classify levels of sedation or anesthesia.

How a Communication Tool Became a Trigger

Early head injury research identified that patients with lower GCS scores were at increased risk for airway compromise. This observation was never intended as a rigid directive. It was a reminder to be cautious. Over time, risk awareness gradually became a rule. “At risk for airway compromise” became “requires intubation.” The nuance disappeared, and a numeric threshold replaced clinical reasoning. “GCS < 8, intubate” did not emerge because the scale was designed for airway decision-making. It emerged because the scale was easy to remember, easy to teach, and easy to operationalize, even when it was being used outside its intended domain.

The problem is that intubation is not a benign procedure and is definitely not without risk—excellent review by Dr. Domink Jakob here.

The Problem With Using GCS as an Airway Assessment

The Glasgow Coma Scale measures responsiveness, not airway physiology. It does not tell you whether the patient is protecting their airway, able to manage secretions, has appropriate oxygenation and ventilation, or why the level of consciousness is decreased in the first place.

A low GCS can be caused by hypoglycemia, intoxication, postictal states, metabolic derangements, hypoxia, shock, or trauma. Many of these conditions are reversible and do not inherently require intubation.

Using GCS alone to make airway decisions confuses correlation with causation.

Airway Reflexes & GCS

A GCS of 6 or 7 does not automatically mean the loss of airway reflexes. Patients who are maintaining their secretions, pulling away from stimulation, moving air effectively, breathing with an appropriate rate and depth, or able to cough are demonstrating airway protection regardless of the number assigned to them.

Most experienced clinicians have encountered the intoxicated patient labeled “GCS 3” who is snoring loudly yet ventilating adequately, or the postictal patient who is temporarily unresponsive but protecting their airway. These patients often need observation and supportive care, not a laryngoscope and plastic tube.

Before committing a patient to an advanced airway, reversible causes of altered mental status should be addressed.

GCS Was Never a Sedation Scale

The Glasgow Coma Scale was not designed to describe agitation or sedation. It was intended to identify pathologic neurologic changes, not medication-induced alterations in consciousness.

I have yet to see a patient develop decerebrate posturing after receiving midazolam for anxiety during flight. Using pain response or command obedience to describe intentional sedation distorts communication and misrepresents neurologic status.

When GCS is applied outside the context of true neurologic injury:

1. It does not suggest an appropriate intervention

2. It generalizes or distorts communication of sedation depth

3. It limits the ability to detect meaningful changes over time

When we evaluate GCS criteria in the absence of pathological neuro changes (TBI, CVA, Etc.)

1. Does not suggest an intervention.

2. Distorts or generalizes the communication of the actual level of sedation.

3. Allows little room to detect changes.

For these reasons, anesthesiologists and intensivists commonly use the Richmond Agitation-Sedation Scale (RASS) to measure depth of sedation or agitation.

RASS uses a single value centered at zero to represent an alert, calm patient. Positive values describe agitation. Negative values describe sedation. A single number immediately conveys a mental image of the patient’s state and allows for precise trending. Calling a patient RASS −3 or −4 communicates far more helpful information than an additive GCS score ever could.

Sedation, Transport, and Downstream Harm

Deep sedation is sometimes necessary, but it is not benign. Increasing evidence shows that deeper levels of sedation, particularly with benzodiazepines, are associated with higher rates of delirium and increased mortality.

The argument for deep sedation during transport often centers on the noxious environment of ambulances and helicopters. However, simple interventions such as ear protection, reduced lighting, or visual shielding may allow clinicians to target lighter sedation levels while maintaining safety. It is easy to aim for deep sedation and slug paralytics... and sometimes it is therapeutically necessary. However, it may be time to tighten up our evaluation of sedation, explore additional means to reduce noxious stimuli, and hopefully prevent the need for deeper levels of sedation.

Just as unnecessary intubation introduces risk, unnecessary deep sedation carries long-term consequences.

The Bottom Line

The problem is not that the Glasgow Coma Scale is useless. The problem is that it has been asked to do too much.

The phrase “GCS<8, intubate” should be updated to something more accurate:

“GCS <8? = EVALUATE (the airway)."

The Glasgow Coma Scale remains valuable when used for its intended purpose: communicating neurologic injury and trending change over time.

A better approach is to use the right tool for the right question.

References:

Assessment of coma and impaired consciousness. A practical scale.Teasdale, G., & Jennett, B. (1974). The Lancet, 304(7872), 81–84.

Lorazepam is an independent risk factor for transitioning to delirium in intensive care unit patients. Pandharipande, P. P., Shintani, A., Peterson, J. F., Pun, B. T., Wilkinson, G. R., Dittus, R. S., Bernard, G. R., & Ely, E. W. (2006). Anesthesiology, 104(1), 21–26.https://www.ncbi.nlm.nih.gov/pubmed/16394685

The Glasgow Coma Scale at 40 years: Standing the test of time.Teasdale, G., Allan, D., Brennan, P., McElhinney, E., & Mackinnon, L. (2014). The Lancet Neurology, 13(8), 844–854.https://www.ncbi.nlm.nih.gov/pubmed/25030516

Glasgow Coma Scale (GCS) explained for first aiders.First Aid for Free.https://www.firstaidforfree.com/glasgow-coma-scale-gcs-first-aiders/

Intubation in patients with low Glasgow Coma Scale scores: A systematic review.Duncan, R., Thakore, S., & others. (2020). Emergency Medicine Journal.https://pmc.ncbi.nlm.nih.gov/articles/PMC7223660/

The Internet Book of Critical Care: Delirium.Farkas, J.https://emcrit.org/ibcc/delirium/

The Richmond Agitation-Sedation Scale: Validity and reliability in adult intensive care unit patients.Sessler, C. N., Gosnell, M. S., Grap, M. J., Brophy, G. M., O’Neal, P. V., Keane, K. A., Tesoro, E. P., & Elswick, R. K. (2002). American Journal of Respiratory and Critical Care Medicine, 166(10), 133 81344.https://www.ncbi.nlm.nih.gov/pubmed/12421743