http://www.glasgowcomascale.org/self-test/
https://en.wikipedia.org/wiki/Glasgow_Coma_Scale
1 in 10 coma chance 1979-1996: An analysis of the relationship between Glas
gow Coma Scale score and plasma glucose level according to the severity of
hypoglycemia (Kenneth Martin Dolan < 3 hours after meal 51 mg/dl 1987 to 19
89) due to sub-clinical hyperthyroidism
J Intensive Care. 2014; 2(1): 1.
Published online 2014 Jan 3. doi: 10.1186/2052-0492-2-1
PMCID: PMC4267581
An analysis of the relationship between Glasgow Coma Scale score and plasma
glucose level according to the severity of hypoglycemia
Atsushi Kotera,corresponding author Shinsuke Iwashita, Hiroki Irie, Junichi
Taniguchi, Shunji Kasaoka, and Yoshihiro Kinoshita
Author information ► Article notes ► Copyright and License
information ►
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Abstract
Background
The Glasgow Coma Scale (GCS) score of an individual with hypoglycemia is ex
pected to be low due to an insufficient glucose supply to the brain. Howeve
r, we sometimes encounter hypoglycemic patients with high GCS scores. This
study was undertaken to analyze the relationship between the GCS score and
the plasma glucose level.
Methods
Among the patients with neurological impairments admitted to our institutio
n between October 1, 2010 and March 31, 2013, the cases of 41 hypoglycemic
patients were examined in this retrospective cohort study. The defined plas
ma glucose level for mild hypoglycemia was 41–60 mg/dL, that for mo
derate hypoglycemia was 21–40 mg/dL, and that for extreme hypoglyce
mia was below 20 mg/dL. We divided the patients into two groups: those with
mild hypoglycemia (n = 14) and those with moderate/extre
me hypoglycemia (n = 27). We compared the two groups' phy
siological data and assessed the relationship between the GCS score and the
plasma glucose level by Spearman rank correlation (ρ), the significan
ce of which was determined by Spearman's rank sum test. We used the Mann-Wh
itney U-test and the chi-square (χ2) test to test for differences betw
een the two groups when appropriate.
Results
Three hundred twenty-six patients with neurological impairments were admitt
ed during the study period, and 41were eligible hypoglycemic patients. The
GCS scores of the 14 patients with mild hypoglycemia were significantly hig
her than those of the 27 patients with moderate or extreme hypoglycemia (me
cluding autonomic symptoms) between the two groups. Spearman's rank sum tes
t was 0.491 in the total group of 41 hypoglycemic patients, 0.053 in the mi
ld hypoglycemic patients, and 0.493 in the moderately or extremely hypoglyc
emic patients.
Conclusions
The relationship between the GCS score and the plasma glucose level differe
d according to the severity of hypoglycemia. Even when a patient has a high
GCS score, careful assessment of differential diagnosis should be conducte
d and the possibility of hypoglycemia should be considered in light of his
or her neurogenous symptoms.
Keywords: Hypoglycemia, Glasgow Coma Scale, Diabetes mellitus
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Background
The Glasgow Coma Scale (GCS) was developed to describe the level of conscio
usness in patients with traumatic brain injury [1]. It measures the patient
s' best eye, motor, and verbal responses, and it classifies the level of co
nsciousness as mild (score of 14–15), moderate (9–13), or s
evere (3–8) [2]. The GCS is also used for describing the level of c
onsciousness in hypoglycemic patients [3], and it is widely accepted as a t
ool for both trauma and non‒trauma patients.
Hypoglycemic patients commonly have neuroglycopenic symptoms. The GCS score
of hypoglycemic patients is predicted to be low because the glucose supply
to the brain is insufficient. However, we sometimes encounter the hypoglyc
emic patients with high GCS scores. There are few reports concerning the re
lationship between the GCS score and the plasma glucose level in hypoglycem
ic patients. In the present study, we analyzed the relationship between the
se two parameters according to the severity of hypoglycemia and compared th
e physiological data among patients with differing degrees of hypoglycemia.
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Methods
Patients
We investigated patients age 18 and over who were transferred to our instit
ution with neurological impairments between October 1, 2010 and March 31, 2
013. Among those patients, only the hypoglycemic patients were eligible for
the present study. Hypoglycemia was defined as a plasma glucose level belo
w 60 mg/dL, accompanied by a wide variety of symptoms [4]. We also used the
cemia, below 20 mg/dL [4]. We usually perform the sampling of either arteri
al blood or capillary blood rapidly and check the glucose level by arterial
blood gas analyzer or glucose meter. The choice of the material and the de
vice is committed to each emergency physician. On the other hand, we also p
erform the sampling of venous blood without delay, and the plasma glucose l
evel per patient is measured by glucose oxidase method in a central laborat
ory. Thus, in the present study, we used the sample of venous blood.
Protocol design
This was a retrospective cohort study. All data were obtained from medical
charts and did not include any personal information that would identify any
of the patients. Therefore, informed consent from the patients was waived,
based on the Ethical Guidelines for Epidemiological Studies issued jointly
by the Ministry of Health, Labour and Welfare and the Ministry of Educatio
n, Culture, Sports, Science, and Technology of Japan.
Data collection
The data collected from medical charts were age, gender, symptoms, GCS scor
e, renal dysfunction, diabetes mellitus (DM) status, body temperature, hear
t rate, systolic blood pressure, and plasma glucose level. Lucidity was def
ined as GCS score of 15, mild confusion was GCS of 14, moderate confusion w
as GCS of 9–13, and severe confusion or coma was GCS of 3–8
[2]. Estimation of the level of consciousness by the GCS score and samplin
g of the venous blood to measure the plasma glucose level were performed at
the same time as part of the Emergency Room visit.
We divided the patients into two groups: the mild hypoglycemia group and th
e moderate/extreme hypoglycemia group. The physiological data of the two gr
oups were compared. Renal dysfunction was defined as a glomerular filtratio
n rate (GFR) less than 60 mL/min [5]. In our study, the GFR was assessed by
determining the estimated GFR. DM was defined according to the World Healt
h Organization criteria as the presence of either fasting venous plasma glu
cose levels of 7.0 mmol/L (126 mg/dL) or greater, or 2-h venous plasma gluc
ose levels of 11.1 mmol/L (200 mg/dL) or greater, or a 75 g oral glucose to
lerance test result [6].
Statistical analysis
All statistical analyses were performed using the software programs SPSS 17
.0 (SPSS, Chicago, IL, USA) and Excel Tokei 2012 (Social Survey Research In
formation Co., Tokyo, Japan). Intergroup differences were assessed with the
χ2 test with Yates' correlation for continuity in categorical variabl
es. The Mann-Whitney U test was used to test for differences in continuous
variables. We considered p values <0.05 significant. We analyzed the correl
ation between the GCS score and plasma glucose level by Spearman rank corre
lation (ρ), the significance of which was determined by Spearman's ran
k sum test.
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Results
The number of patients with neurological impairments admitted to our instit
ution during the study term was 326 of the 3,514 patients, and 41 of these
326 patients were hypoglycemic. The median plasma glucose level in the 41 p
atients was 32 mg/dL (range, 10–58 mg/dL). The number of patients w
ith mild hypoglycemia was 14, that of patients with moderate hypoglycemia w
as 21, and that of patients with extreme hypoglycemia was 6. Because the nu
mber of patients with extreme hypoglycemia was small, we divided the patien
ts into the two groups of mild hypoglycemia and moderate/extreme hypoglycem
ia.
The symptoms of the two groups were shown in Table 1. The symptoms in the m
ild hypoglycemia group were confusion in ten patients (two mild, seven mode
rate, and one severe), difficulty in speech in one patient, weakness in two
patients, and convulsions in one patient. The symptoms in the moderate/ext
reme hypoglycemia group were confusion in 26 patients (4 mild, 12 moderate,
and 10 severe) and weakness in 1 patient. Several patients complained of v
arious neurological impairments besides confusion.
Table 1
Table 1
The symptoms on arrival between the two groups
The causes of hypoglycemia in the two groups were shown in Table 2. Of the
41 patients, 33 patients had DM, 24 were treated with insulin, and 9 were t
he common causes of hypoglycemia in the diabetic patients were low calorie
intake due to illness or dieting (23/33) and suspected overdose of insulin
or oral anti‒diabetic agents (5/33). The causes in the non‒
diabetic patients were various: malnutrition due to chemotherapy in two pat
ients, and anorexia nervosa, hepatocellular carcinoma secreting insulin-lik
e growth factor II, sudden withdrawal from long-term steroid treatment, dum
ping syndrome, and alcoholism (one patient each). In the mild hypoglycemia
group, 11 patients had DM and the other 3 did not. The moderate/extreme hyp
oglycemia group included 22 patients with DM and 5 without.
Table 2
Table 2
The causes of hypoglycemia in the two groups
The groups' physiological data (in medians and ranges) are provided in Tabl
e 3. There were no significant differences between the two hypoglycemia gro
ups in age, gender, renal dysfunction, rate of DM, body temperature, heart
rate, or systolic blood pressure. However, the GCS scores in the mild hypog
lycemia group were significantly higher than those in the moderate/extreme
Table 3
Table 3
The physiological data on admission between the two groups
Figures 1 and and22 demonstrate the relationship between the GCS s
cores and the plasma glucose levels. The GCS scores were significantly corr
elated with the plasma glucose levels in the total hypoglycemic patients (F
igure 1a, ρ = 0.491, p < 0.01) and i
roup, the GCS scores were not correlated with plasma glucose levels (Figure
1c, ρ = 0.053, p = 0.857). The re
the non‒diabetic patients; nevertheless, the value of Spearman's ra
Figure 1
Figure 1
Scatter graph demonstrating the relationship between the GCS scores and the
plasma glucose levels. (a) The value of the Spearman's rank sum test was s
tatistically high (ρ = 0.493) in the total hypoglyce
mic patients. (b) The ...
Figure 2
Figure 2
Scatter graph demonstrating the relationship between the GCS scores and the
plasma glucose levels. Closed circles indicate the patients who had recurr
ent hypoglycemic episodes. Open circles indicate the patients who had no hy
poglycemic episodes. Open ...
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Discussion
The relationship between the GCS scores and the plasma glucose levels was s
ignificant in the total hypoglycemic patients and in the moderate/extreme h
ypoglycemia group. However, the number of patients in the mild hypoglycemia
group is small and the relationship was not significant. We considered the
mechanisms that might underlie this discrepancy.
In general, neuroglycopenic symptoms are observed when an individual's plas
ma glucose level reaches approximately 50–60 mg/dL [7]. It was repo
rted that the plasma glucose level at which cognitive dysfunction was obser
ved was approximately 57 mg/dL [8], the level for neurogenous symptoms was
approximately 55 mg/dL, the level for disorders of mental function was 46 m
g/dL, and the level for convulsions or coma was 27 mg/dL [9]; however, thes
e levels varied among the patients [9]. Of the strictly regulated diabetic
patients in that study, almost all had experienced hypoglycemia previously,
and the plasma glucose levels at the onset of neuroglycopenic symptoms mig
ht have declined further [9]. In addition, recurrent hypoglycemic episodes
can weaken the adrenalin and glucagon response to decreased plasma glucose
levels, and severe hypoglycemia can be induced [9]. This weakened response
was recently named hypoglycemia-associated autonomic failure (HAAF), and it
was described as a potential risk factor for ‘hypoglycemia unaware
ness’ [9–11]. Conversely, in the poorly controlled diabetic
patients of the same study, the plasma glucose levels at the onset of neur
oglycopenic symptoms became higher [9, 12].
In the 33 diabetic patients, 27 had recurrent hypoglycemic episodes, 3 had
no episodes, and 3 were unclear. The median (range) GCS scores and plasma g
lucose levels in the diabetic patients with versus (vs.) without recurrent
hypoglycemic episodes were 11 (3–15) and 33 mg/dL (18–58 mg
/dL) vs. 10 (3–12) and 28 mg/dL (25–47 mg/dL) (not signific
ant). The number of diabetic patients without recurrent hypoglycemic episod
es was small, and it was difficult to elucidate the effect of recurrent hyp
oglycemic episodes statistically in the diabetic patients.
The hemoglobinA1c (HbA1c) level indicates whether DM is well controlled or
date on which a hypoglycemic episode occurred was not measured in 9 of the
patients, and the analysis was not enough to predict whether DM was well c
ontrolled or not.
iabetic agents. The median (range) daily insulin dosage was 0.56 U/kg (0.28
–1.14 U/kg) in the 24 patients treated with insulin, and the dosage
was equivalent to that in other studies [14, 15]. Indeed, hypoglycemia ind
uced by the overdose of insulin therapy or oral anti‒diabetic agent
s was observed in five patients, and almost all of the diabetic patients ha
d experienced recurrent hypoglycemic episodes. Furthermore, the median plas
ma glucose level in the diabetic patients of the present study was lower th
an that in the poorly controlled diabetic patients of the other study (33 v
s. 78 mg/dL) [12]. Considering these data, it appears that almost all of th
e diabetic patients in the present study are thought to be strictly control
led.
In the eight non‒diabetic patients, four had recurrent hypoglycemic
episodes and four did not have. The median (range) GCS scores and plasma g
lucose levels in the patients with vs. without recurrent hypoglycemic episo
e significantly lower in the patients with recurrent hypoglycemic episodes
(p = 0.0421), but there was no significant difference in
the GCS scores. The number of patients is small; however, we can construct
the hypothesis that the plasma glucose levels at the onset of neuroglycopen
The recurrent hypoglycemic episodes and the strict management for DM would
shift the plasma glucose levels at the onset of neuroglycopenic symptoms to
the lower levels, and that may have contributed to the discrepancy in the
Spearman's rank sum test. When the plasma glucose levels were 41–60
mg/dL, the levels were not low enough to cause severe neurogenous symptoms
and the GCS scores did not correlate with the plasma glucose levels. Conve
rsely, when the plasma glucose levels were below 40 mg/dL, the levels were
low enough to cause severe neurogenous symptoms in almost all of the patien
ts and the GCS scores were significantly correlated with the plasma glucose
levels. The cause of the declined plasma glucose levels at the onset of ne
hypoglycemia had contributed to the high value of Spearman's rank sum test
in the diabetic and non-diabetic patients. In the future, even when a pati
ent has a high GCS score, a careful assessment of differential diagnosis sh
ould be made, and the treating physicians should consider the possibility o
f hypoglycemia in light of the patient's various neurogenous symptoms.
Hypoglycemia also causes autonomic symptoms that show dependence on the acc
ording to plasma glucose levels [7, 9]. The increased levels of glucagon an
d adrenaline could cause tachycardia or hypertension. The reported plasma g
lucose levels of each autonomic symptom were as follows: increased glucagon
secretion at 69 mg/dL, increased adrenalin secretion at 66 mg/dL, and incr
eased cortisol secretion at 57 mg/dL [9]. There were no significant differe
nces in heart rate or systolic blood pressure between the two groups. Heart
rate or systolic blood pressure was influenced by anti‒hypertensiv
e drugs. Indeed, in the present study, 24 of the 41 patients were medicated
with anti‒hypertensive drugs. The level of adrenalin, glucagon, an
d cortisol were not measured in our patients, and we could not detect any d
ifferences in autonomic symptoms according to the plasma glucose levels. We
will conduct such an analysis in the future.
There are several limitations in this study. The sample size of patients wa
s small, and the data reflect the experience of a single center. Thus, the
results may not be generalized for the population as a whole. Ongoing trial
s and reexamination with a large number of patients at several centers are
necessary to test the results in the present study. In addition, the study
was a retrospective investigation. Further examinations are needed to evalu
ate the results after measuring the adrenaline, glucagon, and cortisol leve
ls in hypoglycemic patients. Finally, Inoue et al. [16] reported the differ
ence of the accuracy of blood-glucose measurements between arterial blood g
as analyzers and glucose meters by using arterial blood or capillary blood.
It should be noted that a choice of the blood sample or the device could i
nfluence the blood glucose levels.
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Conclusions
The relationship between the GCS scores and the plasma glucose levels diffe
red according to the severity of the patients’ hypoglycemia. Even w
hen a patient has a high GCS score, his or her differential diagnosis shoul
d be carefully evaluated and the possibility of hypoglycemia should be cons
idered in light of various neurogenous symptoms.
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Acknowledgements
We thank all of the staff members of the Department of Emergency and Genera
l Medicine and the Department of Intensive Care Medicine, Kumamoto Universi
ty Hospital, who participated in the treatment of the reported patients. We
also acknowledge the staff of the Department of Metabolic Medicine who adv
ised us regarding the treatment plan for the patients. This study was not s
upported by any grants.
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Footnotes
Competing interests
All authors declare that they have no competing interests.
Authors’ contributions
AK conceived the study, analyzed the results, researched the literature, an
d drafted the manuscript. SI contributed to the study design. HI participat
ed in the data collection. JT collated the results and supervised the testi
ng and data collection. SK critically reviewed the manuscript and offered g
uidance. YK contributed to the study design and helped draft the manuscript
. All authors reviewed this manuscript and approved the final submitted ver
sion.
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Contributor Information
Atsushi Kotera, Email: pj.en.yojne.3ih@229dpft30w.
Shinsuke Iwashita, Email: pj.ca.u-otomamuk.huk.cf@iekusnihs.
Hiroki Irie, Email: pj.ca.u-otomamuk.huk.cf@eiri-ikorih.
Junichi Taniguchi, Email: pj.ca.u-otomamuk.huk.cf@nujinat.
Shunji Kasaoka, Email: pj.ca.u-otomamuk.huk.cf@akoasak.
Yoshihiro Kinoshita, Email: pj.ca.u-otomamuk.huk.cf@ponik.
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References
1. Barlow P. A practical review of the Glasgow Coma Scale and score. Surgeo
n. 2012;10:114–119. doi: 10.1016/j.surge.2011.12.003. [PubMed] [Cro
ss Ref]
2. Mena JH, Sanchez AI, Rubiano AM, Peitzman AB, Sperry JL, Gutierrez MI, P
uyana JC. Effect of the modified Glasgow Coma Scale score criteria for mild
traumatic brain injury on mortality prediction: comparing classic and modi
fied Glasgow Coma Scale model scores of 13. J Trauma. 2011;71:1185–
1193. doi: 10.1097/TA.0b013e31823321f8. [PMC free article] [PubMed] [Cross
Ref]
3. Moore C, Woollard M. Dextrose 10% or 50% in the treatment of hypoglycemi
a out of hospital? A randomised controlled trial. Emerg Med J. 2005;22:512
–515. doi: 10.1136/emj.2004.020693. [PMC free article] [PubMed] [Cr
oss Ref]
4. Rozance PJ, Hay WW. Describing hypoglycemia—definition or operat
ional threshold? Early Hum Dev. 2010;86:275–280. doi: 10.1016/j.ear
lhumdev.2010.05.002. [PMC free article] [PubMed] [Cross Ref]
5. Levey AS, Levin A, Kellum JA. Definition and classification of kidney di
seases. Am J Kidney Dis. 2013;61:686–688. doi: 10.1053/j.ajkd.2013.
03.003. [PubMed] [Cross Ref]
6. Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabe
tes mellitus and its complications. Part 1: diagnosis and classification of
diabetes mellitus provisional report of a WHO consultation. Diabet Med. 19
98;15:539–553. doi: 10.1002/(SICI)1096-9136(199807)15:7<539::AID-DI
A668>3.0.CO;2-S. [PubMed] [Cross Ref]
7. Service FJ. Hypoglycemic disorders. N Eng J Med. 1995;27:1144–11
52. doi: 10.1056/NEJM199504273321707. [PubMed] [Cross Ref]
8. Frier BM. Defining hypoglycemia: what level has clinical relevance? Diab
etologia. 2009;52:31–34. doi: 10.1007/s00125-008-1209-3. [PubMed] [
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9. Bakatselos SO. Hypoglycemia unawareness. Diabetes Res Clin Pract. 2011;9
3:92–96. doi: 10.1016/S0168-8227(11)70020-1. [PubMed] [Cross Ref]
10. Oyer DS. The science of hypoglycemia in patients with diabetes. Curr Di
abetes Rev. 2013;9:195–208. doi: 10.2174/15733998113099990059. [Pub
Med] [Cross Ref]
11. Cryer PE. Mechanisms of hypoglycemia-associated autonomic failure and i
ts component syndromes in diabetes. Diabetes. 2005;54:3592–3601. do
i: 10.2337/diabetes.54.12.3592. [PubMed] [Cross Ref]
12. Boyle PJ, Schwartz NS, Shah SD, Clutter WE, Cryer PE. Plasma glucose co
ncentrations at the onset of hypoglycemic symptoms in patients with poorly
13. Saudek CD, Derr RL, Kalyani RR. Assessing glycemia in diabetes using se
14. Hirsch IB, Bergenstal RM, Parkin CG, Wright E, Jr, Buse JB. A real-worl
d approach to insulin therapy in primary care practice. Clin Diabetes. 2005
;23:78–86. doi: 10.2337/diaclin.23.2.78. [Cross Ref]
15. Papa G, Baratta R, Cali V, Degano C, Iurato MP, Licciardello C, Maioran
a R, Finocchiaro C. Factors that influence basal insulin requirement in typ
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12-0372-7. [PubMed] [Cross Ref]
16. Inoue S, Egi M, Kotani J, Morita K. Accuracy of blood-glucose measureme
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Articles from Journal of Intensive Care are provided here courtesy of BioMe
d Central
Glasgow Coma Scale
From Wikipedia, the free encyclopedia
Not to be confused with Glasgow Outcome Scale.
Glasgow Coma Scale
Diagnostics
MeSH D015600
[edit on Wikidata]
Glasgow Coma Scale (GCS) is a neurological scale which aims to give a relia
ble and objective way of recording the conscious state of a person for init
ial as well as subsequent assessment. A patient is assessed against the cri
teria of the scale, and the resulting points give a patient score between 3
(indicating deep unconsciousness) and either 14 (original scale) or 15 (th
e more widely used modified or revised scale).
GCS was initially used to assess level of consciousness after head injury,
and the scale is now used by first responders, EMS, nurses and doctors as b
eing applicable to all acute medical and trauma patients. In hospitals it i
s also used in monitoring chronic patients in intensive care.
The scale was published in 1974 by Graham Teasdale and Bryan J. Jennett, pr
ofessors of neurosurgery at the University of Glasgow's Institute of Neurol
ogical Sciences at the city's Southern General Hospital.
GCS is used as part of several ICU scoring systems, including APACHE II, SA
PS II, and SOFA, to assess the status of the central nervous system, as it
was designed for. The initial indication for use of the GCS was serial asse
ssments of patients with traumatic brain injury[1] and coma for at least 6
hours in the neurosurgical ICU setting, though it is commonly used througho
ut hospital departments. A similar scale, the Rancho Los Amigos Scale is us
ed to assess the recovery of traumatic brain injury patients.
Contents [hide]
1 Elements of the scale
1.1 Eye response (E)
1.2 Verbal response (V)
1.3 Motor response (M)
2 Interpretation
3 Revisions
4 Controversy
5 See also
6 References
7 External links
Elements of the scale[edit]
Glasgow Coma Scale
1 2 3 4 5 6
Eye Does not open eyes Opens eyes in response to painful stimuli Opens eyes
in response to voice Opens eyes spontaneously N/A N/A
Verbal Makes no sounds Incomprehensible sounds Utters incoherent words Conf
used, disoriented Oriented, converses normally N/A
Motor Makes no movements Extension to painful stimuli (decerebrate response
) Abnormal flexion to painful stimuli (decorticate response) Flexion / With
drawal to painful stimuli Localizes painful stimuli Obeys commands
Note that a motor response in any limb is acceptable.[2] The scale is compo
sed of three tests: eye, verbal and motor responses. The three values separ
ately as well as their sum are considered. The lowest possible GCS (the sum
) is 3 (deep coma or death), while the highest is 15 (fully awake person).
Eye response (E)[edit]
There are four grades starting with the most severe:
No eye opening
Eye opening in response to pain stimulus. (a peripheral pain stimulus, such
as squeezing the lunula area of the patient's fingernail is more effective
than a central stimulus such as a trapezius squeeze, due to a grimacing ef
fect).[3]
Eye opening to speech. (Not to be confused with the awakening of a sleeping
person; such patients receive a score of 4, not 3.)
Eyes opening spontaneously
Verbal response (V)[edit]
There are five grades starting with the most severe:
No verbal response
Incomprehensible sounds. (Moaning but no words.)
Inappropriate words. (Random or exclamatory articulated speech, but no conv
ersational exchange. Speaks words but no sentences.)
Confused. (The patient responds to questions coherently but there is some d
isorientation and confusion.)
Oriented. (Patient responds coherently and appropriately to questions such
as the patient’s name and age, where they are and why, the year, mo
nth, etc.)
Motor response (M)[edit]
There are six grades:
No motor response
Decerebrate posturing accentuated by pain (extensor response: adduction of
arm, internal rotation of shoulder, pronation of forearm and extension at e
lbow, flexion of wrist and fingers, leg extension, plantarflexion of foot)
Decorticate posturing accentuated by pain (flexor response: internal rotati
on of shoulder, flexion of forearm and wrist with clenched fist, leg extens
ion, plantarflexion of foot)
Withdrawal from pain (Absence of abnormal posturing; unable to lift hand pa
st chin with supraorbital pain but does pull away when nailbed is pinched)
Localizes to pain (Purposeful movements towards painful stimuli; e.g., brin
gs hand up beyond chin when supraorbital pressure applied.)
Obeys commands (The patient does simple things as asked.)
Interpretation[edit]
Individual elements as well as the sum of the score are important. Hence, t
he score is expressed in the form "GCS 9 = E2 V4 M3 at 07:35".
Generally, brain injury is classified as:
Severe, with GCS < 8–9
Moderate, GCS 8 or 9–12 (controversial)[4]
Minor, GCS ≥ 13.
Generally when a patient is in a decline of their GCS score, the nurse or m
edical staff should assess the cranial nerves and determine which of the tw
elve have been affected.
Tracheal intubation and severe facial/eye swelling or damage make it imposs
ible to test the verbal and eye responses. In these circumstances, the scor
e is given as 1 with a modifier attached e.g. "E1c" where "c" = closed, o
r "V1t" where t = tube. A composite might be "GCS 5tc". This would mean,
for example, eyes closed because of swelling = 1, intubated = 1, leavin
g a motor score of 3 for "abnormal flexion". Often the 1 is left out, so th
e scale reads Ec or Vt.
The GCS has limited applicability to children, especially below the age of
36 months (where the verbal performance of even a healthy child would be ex
pected to be poor). Consequently, the Pediatric Glasgow Coma Scale, a separ
ate yet closely related scale, was developed for assessing younger children
.
Revisions[edit]
Glasgow Coma Scale: While the 15-point scale is the predominant one in use,
this is in fact a modification and is more correctly referred to as the Mo
dified Glasgow Coma Scale. The original scale was a 14-point scale, omittin
g the category of "abnormal flexion". Some centres still use this older sca
le, but most (including the Glasgow unit where the original work was done)
have adopted the modified one.
The Rappaport Coma/Near Coma Scale made other changes.
Meredith W., Rutledge R, Fakhry SM, EMery S, Kromhout-Schiro S have propose
d calculating the verbal score based on the measurable eye and motor respon
ses.
The most widespread revision has been the Simplified Motor and Verbal Scale
s which shorten the respective sections of the GCS without loss of accuracy
.[5]
The GCS for intubated patients is scored out of 10 as the verbal component
falls away
Controversy[edit]
The GCS has come under pressure from some researchers who take issue with t
he scale's poor inter-rater reliability and lack of prognostic utility.[6]
Although there is no agreed-upon alternative, newer scores such as the Simp
lified motor scale and FOUR score have also been developed as improvements
to the GCS.[7] Although the inter-rater reliability of these newer scores h
as been slightly higher than that of the GCS, they have not gained consensu
s as replacements.[8]
See also[edit]
AVPU scale
Blantyre Coma Scale
Early warning score
Paediatric Glasgow Coma Scale
Rancho Los Amigos Scale
Revised Trauma Score
Triage
References[edit]
Jump up ^ Teasdale G, Jennett B (1974). "Assessment of coma and impaired co
nsciousness. A practical scale.". Lancet. 2 (7872): 81–4. doi:10.10
16/S0140-6736(74)91639-0. PMID 4136544.
Jump up ^ Hutchinson’s clinical methods 22nd edition
Jump up ^ "The Glasgow Coma Scale: clinical application in Emergency Depart
ments". Emergency Nurse. 14 (8): 30–5. 2006. doi:10.7748/en2006.12.
14.8.30.c4221.
Jump up ^ http://www.cdc.gov/masstrauma/resources/gcs.pdf
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External links[edit]
Website to calculate the Glasgow Coma Scale
Glasgow Coma Scale Calculator
Glasgow Coma Scale at the US National Library of Medicine Medical Subject H
eadings (MeSH)
Dr. Graham Teasdale speaks with The Lancet - podcast, August 2014
Glasgow Coma Scale at 40
Simplified Motor Score
Glasgow Coma Scale Calculator for OS Android
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