Nontraumatic Coma Glasgow Coma Score and Coma Etiology Ralph L. Sacco, MD;
R.
VanGool, MD; J. P. Mohr, MD; W. A. Hauser,
\s=b\ In 1987 and 1988, we carried out a prospective study of patients older than
10 years with nontraumatic coma in the intensive care units of Columbia-Presbyterian Medical Center, New York, NY. Of 188 patients with Glasgow Coma Scale (GCS) determinations within 72 hours, 61% were dead or in persistent coma by 2 weeks from onset. Age, sex, and ethnicity did not influence outcome. The 2-week outcome for patients with initial GCS of 3 to 5 was 14.8% awake; 85.2% were dead or in persistent coma. For the GCS 6 to 8 group, 53.1% were awake and 46.9% were dead or in persistent coma. Hypoxic or ischemic coma had the worst 2-week outcome (79% dead or comatose); coma caused by metabolic disease or sepsis (68%), focal cerebral lesions (66%), and general cerebral diseases (55%) were intermediate, while drug-induced coma had a favorable outcome (27% dead or comatose). The independent predictors of 2-week outcome were the first GCS and drug-induced coma. The predicted probability of waking at 2 weeks was eight times better for drug-induced coma than other causes when GCS was held constant. Patients with an initial GCS score of 6 to 8 were seven times more likely to waken than those with a score of 3 to 5. The motor subscore alone was a significant independent predictor of 2-week outcome. Modification of coma score to include etiology may give more accurate predictions of 2\x=req-\ week outcome after nontraumatic coma. (Arch Neurol. 1990;47:1181-1184)
the absence of standardized
Scale
(GCS) in
as
Predictors of 2-Week Outcome
MD
1974 in
patients with
in 76% of published head injury stud¬ ies between 1983 and 1985.2 For pa¬ tients with severe head injury, both the type of lesion and the GCS score accurately predict outcome.3 In pa¬ tients with nontraumatic coma, how¬ ever, recovery is also related to the cause of coma4 and the GCS has not been widely used in studies of acute cerebral disorders.3 We have therefore evaluated coma etiology and GCS scores as predictive factors for 2-week outcome of nontraumatic coma.
disturbances in electrolytes, and acid/base disequilibrium; and (5) drug-induced or toxic injury included drug overdose and coma persisting 24 hours after discontinu¬ ation of sedative drugs. The cause of coma was based on clinical and laboratory data from the medical record and, often, discus¬ sion with the admitting physician. The total Glasgow Coma Score was cal¬ culated as the sum of the motor, verbal, and eye subscores (Table 1). No patient was re¬ ceiving paralyzing agents at the time of GCS assessment. The verbal score in intu¬ bated patients was difficult to accurately record and was sometimes based on non¬ verbal communication. For each patient the best response for each item was retained.1
PATIENTS, MATERIALS,
Follow-up
acute head injuries.1 The GCS was used
AND METHODS Patient Selection
For 10 months from September 1,1987, to June 30,1988, we surveyed the six intensive care units of Columbia-Presbyterian Medi¬ cal Center, New York, NY: neurologic, car¬
diac, surgical, medical, cardiac-surgery, and pediatrie. We identified 234 patients in coma, defined broadly as unresponsiveness
than 6 hours. We excluded children because a pediatrie coma scale has been used for patients younger than 10 years.5 We also excluded coma arising from trauma or acute enceph¬ alopathy of unknown cause, and patients seen later than 72 hours after onset of coma because the aim was to analyze nontrau¬ matic coma of known cause and GCS score to external stimuli for
more
at onset. Data Collection
After a 1-month pilot study, we organized surveillance system and a survey form was used to record the following: medical record number, date of birth and age, gen¬ der, ethnicity, location of patient, time of coma onset and time of Glasgow Coma Score assessment, coma etiology, the GCS subscores, and status at 2 weeks. Ethnicity a
as-
sessments, verbal descriptions of
the level of consciousness may lead to ambiguities and misinterpretations when patient information is ex¬ changed between medical personnel, when different treatment methods are compared, or when comparisons are made among different centers or studies. The need for a consistent, re¬ liable, and sensitive scale led to the development of the Glasgow Coma Accepted for publication April 23, 1990. From the Neurological Institute (Drs Sacco, Mohr, and Hauser) and Sergievsky Center of Neuroepidemiology, Columbia-Presbyterian Medical Center (Drs VanGool and Hauser), New York, NY. Reprint requests to the Neurological Institute, 710 W 168th St, New York, NY 10032 (Dr Sacco).
was
categorized
as
white, black, Hispanic,
and other. Time of coma onset was taken from the medical record. Coma etiologies were grouped into five
categories: (1) hypoxic
or
included cardiac arrest,
ischemie injury
cardiopulmonary arrest, myocardial infarction, acute respi¬ ratory failure, congestive heart failure, and chronic obstructive pulmonary disease; (2) focal cerebral injury included brain tumor, brain abscess, brain infarct, or intraparenchymal hemorrhage; (3) general cerebral injury included meningitis, hydrocephalus, intraventricular hemorrhage, and sub¬ arachnoid hemorrhage; (4) metabolic or septic encephalopathy included bacterial or human immunodeficiency virus infection or
Two-week outcome
categorized
was
as
dead, persistent coma, or awake. Awake was defined as eye-opening spontaneously or in response to speech and, either appro¬ priate response to commands, or recogniz¬ able words spoken in response to speech or
pain.6·7
Analyses Two-week outcome was determined for each level of the Glasgow Coma Score, coma etiology, and demographic variables. Sta¬ tistical significance was determined by 2 test for categorical variables and by the unpaired t test for the means of continuous variables. The relationship of the GCS score to 2-week outcome was evaluated af¬ ter stratification by coma etiologic subtype. The overall relationship was evaluated us¬ ing the Mantel-Haenszel 2 statistic. Logistic regression was used to assess the independence of predictors for outcome.8 All independent variables were entered into the model and after backward elimination only factors significant at the .05 level were retained. The dependent variable was 2week outcome: awake vs dead or persistent coma. Using this method, the conditional probability of death or persistent coma (given the values of XI, X2...) was ex¬ pressed as the following function of predic¬ tive factors:
Probability of Death Coma
=
1/1 + e-(B0
+
or
B,X1
+
Persistent B2X2
+
B'Xr>
where BO, BI,... Br are measures to be es¬ timated by maximum likelihood estimation from the data, and the XI, X2,... are the set of values for a particular individual. There was no assumption of multivariate normal¬ ity for these covariates. RESULTS
From
1988,
we
Downloaded From: http://archneur.jamanetwork.com/ by a Indiana University School of Medicine User on 05/12/2015
September 1,1987, to June 30, found 234 patients in coma.
We excluded 26 patients younger than 10 years, 12 with traumatic coma or coma due to acute encephalopathy of undetermined cause, and eight who were not evaluated within 72 hours of onset. We then restricted analysis to 169 patients with a GCS score of 8 and under, a cutoff score used in many
Table 1.—Glasgow Coma Scale*
studies.
Motor Response Obeys commands
Verbal Oriented
Localizes
Disoriented
Withdraws
Inappropriate Incomprehensible
Extension
None
Response
Eye-Opening Response Spontaneous To speech To pain None
None
By 2 weeks, 44.4% had died, 21.5% were in persistent coma, and 33.1%
Numbers indicate
awake (Table 2). The mean age of the cohort was 59.3 years, with a range of 13 to 96 years. There were 87 men and 82 women, comprising 96 (56.8% )
Glasgow Coma Scale
scores.
were
Table 2.—Two-Week Outcome and Demographic Characteristics in Patients With Nontraumatic Coma
whites, 44 (26.0%) blacks, 26 (15.4%) Hispanics, and 3 (1.8%) others (Table 2). Elderly men (age, 70 to 96 years) were more likely to have died by 2 weeks. Hispanics had the worst 2-week outcome with only 23.1% awake at 2 weeks, compared with whites with 38.5% awake. However, neither age, gender, or ethnicity were related to 2-
Variable Mean age Female
or
NS*
60.7
58.9
87 82
34.5 31.7
65.5 1
68.3
/
NS1'
assessed within
Unpaired
tx2
Coma Score
26
23.1
76.9
)
63 16
5 6
9 33 32 16 88 81 169
t test
3-5 6-8 All
-
Awake Dead/Coma
3
8
NSt
.-
4
7
Hispanic
Two-Week %
Outcome, 12.7 18.8
69.8/17.5 68.7/12.5
22.2 51.5
55.6/22.2
50.0 62.5 14.8 53.1 33.1
18.2/30.3 25.0/25.0 18.8/18.7 85.2 46.9 44.4/21.5
—.49. not significant (NS).
with k dl.
onset in 80% of
patients and within 48 hours in 92.3% of patients. Of all patients in coma for 24 hours
Awake
White Black
*
2-Week Outcome coma
Glasgow
169
Other
score was
Initial
Dead/ Coma
All
Relationship of Initial GCS to The GCS
Outcome,
Race, %
week outcome.
24 hours of
Two-
Week, Sex, % Male
Table 3.—Two-Week Outcome of Nontraumatic Coma and Initial Glasgow Coma Score
less at the time of initial
scoring, 64.4% had a poor outcome (dead or in persistent coma) at 2 weeks after coma onset. For patients with an
interval of 24 to 48 hours between coma onset and coma scoring, 71.4% had a poor outcome at 2 weeks. The proportion awake at 2 weeks in¬ creased with higher initial GCS scores, but the increase was not linear. Re¬ gardless of the initial GCS score, there
consistent 20% risk of persistent at 2 weeks. The 2-week outcome for 88 patients with initial GCS score of 3 to 5 was 14.8% awake and 85.2% dead or in persistent coma. For those with GCS of 6 to 8, 53.1% were awake and 46.9% were dead or in persistent coma (Table 3) ( 2 with 1 df < .001). was a coma
Relationship of Coma Subtype to 2-Week Outcome
Hypoxie or ischemie injury was the of coma in 61 (36.1%), focal cerebral lesions in 38 (22.5%), meta¬ bolic or septic in 37 (21.8%), general¬ ized cerebral in 22 (13.0% ), and druginduced or toxic coma in 11 (6.5%). Hypoxie or ischemie coma had the cause
worst 2-week outcome: 54.1%
were
dead and 24.6% were in persistent coma, with 21.3% awake (Table 4). Hypoxie or ischemie coma subtype also had the greatest percentage of pa¬ tients in the deep-coma group (GCS score, 3 to 5). Focal cerebral lesions
and metabolic or septic coma had a better outcome. Generalized cerebral injury had a slightly better outcome, with 36.4% of the patients dead, 18.2% in persistent coma, and 45.4% awake. Drug-induced coma had the most fa¬ vorable outcome: none died, 27.3% were still comatose, and 72.7% were awake. The percentage of patients with persistent coma was similar among the different coma subtypes. After stratifying by coma subtype, the relationship between the initial GCS score and 2-week outcome re¬ mained significant (Cochran-MantelHaenszel 2, < .001) (Table 5). Ex¬ cept for patients with general cerebral injury and patients with drug-induced coma, a higher initial categorical GCS score was associated with a signifi¬ cantly greater chance of waking by 2 weeks. A logistic regression model demon¬ strated that the initial GCS score and drug-induced coma subtype were inde¬ pendent predictors of 2-week outcome (Table 6). Age, gender, ethnicity, and interval between coma onset and coma scoring were not significantly associ¬ ated with outcome. The estimated probability of waking from coma in¬ creased with increasing GCS score, but the risk depended on etiology (Figure). Glasgow Coma Scale was entered as a continuous variable in model 1 or cat¬ egorized as 3 to 5 or 6 to 8 in model 2. Our model estimated that patients in drug-induced coma were eight times
likely to wake at 2 weeks than those with nondrug-induced coma when GCS was held constant. Irrespec¬ tive of coma etiology, patients with GCS scores of 6 to 8 were seven times more likely awake than those with ini¬ tial scores of 3 to 5. In a model to assess individual GCS subscores (model 3), motor score was the only significant independent predictor of 2-week out¬ come. When combined with drug-in¬ duced cause (model 4), the motor score alone was similar to the entire GCS score in predicting 2-week outcome more
(Table 6).
COMMENT
Predictors of coma outcome
are
im¬
portant for allocation of time and ef¬ fort to
patients with a more favorable prognosis and for optimal stratifica¬ tion of patients enrolled in experimen¬ tal treatment protocols. The GCS pro¬ vides adequate information to identify specific levels of consciousness and to categorize the severity of coma. The
GCS is often used as the inclusion cri¬ terion and for follow-up assessment of patients in multicenter studies. In our study of patients with nontraumatic coma, GCS was found to be a reliable predictor of 2-week outcome. Patients with GCS scores of 3 to 5 had a greater risk of death or persistent coma at 2 weeks than patients with higher scores of 6 to 8. The estimated probability of waking from nontraumatic coma by 2 weeks was seven times higher in those
Downloaded From: http://archneur.jamanetwork.com/ by a Indiana University School of Medicine User on 05/12/2015
Table 4.—Two-Week Outcome of Nontraumatic Coma and Coma Two-Week
Coma Etiology Hypoxie or ischemie Metabolic or septic Focal cerebral
General cerebral
Drug-induced All
2
No.
(%) (36.1) 37 (21.8) 38 (22.5) 22 (13.0) 11 (6.5)
Awake
Outcome,
with
a 2-week mortality of 67%, com¬ pared with 20% of those in the 6 to 8
Etiology
group. Duration of coma has been as¬ sociated with poorer outcome in both
%
Dead/Coma
traumatic coma3 and the present se¬ ries. In other studies of nontraumatic coma, in which drug-induced coma was excluded, favorable predictors from the GCS included production of incom¬ prehensible speech, eye-opening after noxious stimuli, and withdrawal mo¬ tor responses (GCS of 8).4-6 After 24
54.1/24.6
61
34.2
47.4/18.4
36.4/18.2 72.7
33.1
169
44.4/21.5
with 8 df.
Table 5.—Two-Week Outcome of Nontraumatic Coma and Initial (GCS) Stratified by Coma Etiology* Two-Week Coma
Hypoxie
Etiology or
Awake
GCS
ischemie
3-5
43
6-8
Metabolic
or
3-5
septic
14.0 38.9
Glasgow Coma Score
Outcome, % Dead/Coma 36.0 1 31.1
Pit
J
100
15 54.6
6-8
Focal cerebral
Drug-induced
i-0
28.6 53.3
71.4 Ì 46 7
3-5
60
40
1
6-8
83.3
16.7
/
All
*NS
indicates not t Stratum specific
/
55.0 General cerebral
NS
/
NS
66.9
169
R.
VanGool, MD; J. P. Mohr, MD; W. A. Hauser,
\s=b\ In 1987 and 1988, we carried out a prospective study of patients older than
10 years with nontraumatic coma in the intensive care units of Columbia-Presbyterian Medical Center, New York, NY. Of 188 patients with Glasgow Coma Scale (GCS) determinations within 72 hours, 61% were dead or in persistent coma by 2 weeks from onset. Age, sex, and ethnicity did not influence outcome. The 2-week outcome for patients with initial GCS of 3 to 5 was 14.8% awake; 85.2% were dead or in persistent coma. For the GCS 6 to 8 group, 53.1% were awake and 46.9% were dead or in persistent coma. Hypoxic or ischemic coma had the worst 2-week outcome (79% dead or comatose); coma caused by metabolic disease or sepsis (68%), focal cerebral lesions (66%), and general cerebral diseases (55%) were intermediate, while drug-induced coma had a favorable outcome (27% dead or comatose). The independent predictors of 2-week outcome were the first GCS and drug-induced coma. The predicted probability of waking at 2 weeks was eight times better for drug-induced coma than other causes when GCS was held constant. Patients with an initial GCS score of 6 to 8 were seven times more likely to waken than those with a score of 3 to 5. The motor subscore alone was a significant independent predictor of 2-week outcome. Modification of coma score to include etiology may give more accurate predictions of 2\x=req-\ week outcome after nontraumatic coma. (Arch Neurol. 1990;47:1181-1184)
the absence of standardized
Scale
(GCS) in
as
Predictors of 2-Week Outcome
MD
1974 in
patients with
in 76% of published head injury stud¬ ies between 1983 and 1985.2 For pa¬ tients with severe head injury, both the type of lesion and the GCS score accurately predict outcome.3 In pa¬ tients with nontraumatic coma, how¬ ever, recovery is also related to the cause of coma4 and the GCS has not been widely used in studies of acute cerebral disorders.3 We have therefore evaluated coma etiology and GCS scores as predictive factors for 2-week outcome of nontraumatic coma.
disturbances in electrolytes, and acid/base disequilibrium; and (5) drug-induced or toxic injury included drug overdose and coma persisting 24 hours after discontinu¬ ation of sedative drugs. The cause of coma was based on clinical and laboratory data from the medical record and, often, discus¬ sion with the admitting physician. The total Glasgow Coma Score was cal¬ culated as the sum of the motor, verbal, and eye subscores (Table 1). No patient was re¬ ceiving paralyzing agents at the time of GCS assessment. The verbal score in intu¬ bated patients was difficult to accurately record and was sometimes based on non¬ verbal communication. For each patient the best response for each item was retained.1
PATIENTS, MATERIALS,
Follow-up
acute head injuries.1 The GCS was used
AND METHODS Patient Selection
For 10 months from September 1,1987, to June 30,1988, we surveyed the six intensive care units of Columbia-Presbyterian Medi¬ cal Center, New York, NY: neurologic, car¬
diac, surgical, medical, cardiac-surgery, and pediatrie. We identified 234 patients in coma, defined broadly as unresponsiveness
than 6 hours. We excluded children because a pediatrie coma scale has been used for patients younger than 10 years.5 We also excluded coma arising from trauma or acute enceph¬ alopathy of unknown cause, and patients seen later than 72 hours after onset of coma because the aim was to analyze nontrau¬ matic coma of known cause and GCS score to external stimuli for
more
at onset. Data Collection
After a 1-month pilot study, we organized surveillance system and a survey form was used to record the following: medical record number, date of birth and age, gen¬ der, ethnicity, location of patient, time of coma onset and time of Glasgow Coma Score assessment, coma etiology, the GCS subscores, and status at 2 weeks. Ethnicity a
as-
sessments, verbal descriptions of
the level of consciousness may lead to ambiguities and misinterpretations when patient information is ex¬ changed between medical personnel, when different treatment methods are compared, or when comparisons are made among different centers or studies. The need for a consistent, re¬ liable, and sensitive scale led to the development of the Glasgow Coma Accepted for publication April 23, 1990. From the Neurological Institute (Drs Sacco, Mohr, and Hauser) and Sergievsky Center of Neuroepidemiology, Columbia-Presbyterian Medical Center (Drs VanGool and Hauser), New York, NY. Reprint requests to the Neurological Institute, 710 W 168th St, New York, NY 10032 (Dr Sacco).
was
categorized
as
white, black, Hispanic,
and other. Time of coma onset was taken from the medical record. Coma etiologies were grouped into five
categories: (1) hypoxic
or
included cardiac arrest,
ischemie injury
cardiopulmonary arrest, myocardial infarction, acute respi¬ ratory failure, congestive heart failure, and chronic obstructive pulmonary disease; (2) focal cerebral injury included brain tumor, brain abscess, brain infarct, or intraparenchymal hemorrhage; (3) general cerebral injury included meningitis, hydrocephalus, intraventricular hemorrhage, and sub¬ arachnoid hemorrhage; (4) metabolic or septic encephalopathy included bacterial or human immunodeficiency virus infection or
Two-week outcome
categorized
was
as
dead, persistent coma, or awake. Awake was defined as eye-opening spontaneously or in response to speech and, either appro¬ priate response to commands, or recogniz¬ able words spoken in response to speech or
pain.6·7
Analyses Two-week outcome was determined for each level of the Glasgow Coma Score, coma etiology, and demographic variables. Sta¬ tistical significance was determined by 2 test for categorical variables and by the unpaired t test for the means of continuous variables. The relationship of the GCS score to 2-week outcome was evaluated af¬ ter stratification by coma etiologic subtype. The overall relationship was evaluated us¬ ing the Mantel-Haenszel 2 statistic. Logistic regression was used to assess the independence of predictors for outcome.8 All independent variables were entered into the model and after backward elimination only factors significant at the .05 level were retained. The dependent variable was 2week outcome: awake vs dead or persistent coma. Using this method, the conditional probability of death or persistent coma (given the values of XI, X2...) was ex¬ pressed as the following function of predic¬ tive factors:
Probability of Death Coma
=
1/1 + e-(B0
+
or
B,X1
+
Persistent B2X2
+
B'Xr>
where BO, BI,... Br are measures to be es¬ timated by maximum likelihood estimation from the data, and the XI, X2,... are the set of values for a particular individual. There was no assumption of multivariate normal¬ ity for these covariates. RESULTS
From
1988,
we
Downloaded From: http://archneur.jamanetwork.com/ by a Indiana University School of Medicine User on 05/12/2015
September 1,1987, to June 30, found 234 patients in coma.
We excluded 26 patients younger than 10 years, 12 with traumatic coma or coma due to acute encephalopathy of undetermined cause, and eight who were not evaluated within 72 hours of onset. We then restricted analysis to 169 patients with a GCS score of 8 and under, a cutoff score used in many
Table 1.—Glasgow Coma Scale*
studies.
Motor Response Obeys commands
Verbal Oriented
Localizes
Disoriented
Withdraws
Inappropriate Incomprehensible
Extension
None
Response
Eye-Opening Response Spontaneous To speech To pain None
None
By 2 weeks, 44.4% had died, 21.5% were in persistent coma, and 33.1%
Numbers indicate
awake (Table 2). The mean age of the cohort was 59.3 years, with a range of 13 to 96 years. There were 87 men and 82 women, comprising 96 (56.8% )
Glasgow Coma Scale
scores.
were
Table 2.—Two-Week Outcome and Demographic Characteristics in Patients With Nontraumatic Coma
whites, 44 (26.0%) blacks, 26 (15.4%) Hispanics, and 3 (1.8%) others (Table 2). Elderly men (age, 70 to 96 years) were more likely to have died by 2 weeks. Hispanics had the worst 2-week outcome with only 23.1% awake at 2 weeks, compared with whites with 38.5% awake. However, neither age, gender, or ethnicity were related to 2-
Variable Mean age Female
or
NS*
60.7
58.9
87 82
34.5 31.7
65.5 1
68.3
/
NS1'
assessed within
Unpaired
tx2
Coma Score
26
23.1
76.9
)
63 16
5 6
9 33 32 16 88 81 169
t test
3-5 6-8 All
-
Awake Dead/Coma
3
8
NSt
.-
4
7
Hispanic
Two-Week %
Outcome, 12.7 18.8
69.8/17.5 68.7/12.5
22.2 51.5
55.6/22.2
50.0 62.5 14.8 53.1 33.1
18.2/30.3 25.0/25.0 18.8/18.7 85.2 46.9 44.4/21.5
—.49. not significant (NS).
with k dl.
onset in 80% of
patients and within 48 hours in 92.3% of patients. Of all patients in coma for 24 hours
Awake
White Black
*
2-Week Outcome coma
Glasgow
169
Other
score was
Initial
Dead/ Coma
All
Relationship of Initial GCS to The GCS
Outcome,
Race, %
week outcome.
24 hours of
Two-
Week, Sex, % Male
Table 3.—Two-Week Outcome of Nontraumatic Coma and Initial Glasgow Coma Score
less at the time of initial
scoring, 64.4% had a poor outcome (dead or in persistent coma) at 2 weeks after coma onset. For patients with an
interval of 24 to 48 hours between coma onset and coma scoring, 71.4% had a poor outcome at 2 weeks. The proportion awake at 2 weeks in¬ creased with higher initial GCS scores, but the increase was not linear. Re¬ gardless of the initial GCS score, there
consistent 20% risk of persistent at 2 weeks. The 2-week outcome for 88 patients with initial GCS score of 3 to 5 was 14.8% awake and 85.2% dead or in persistent coma. For those with GCS of 6 to 8, 53.1% were awake and 46.9% were dead or in persistent coma (Table 3) ( 2 with 1 df < .001). was a coma
Relationship of Coma Subtype to 2-Week Outcome
Hypoxie or ischemie injury was the of coma in 61 (36.1%), focal cerebral lesions in 38 (22.5%), meta¬ bolic or septic in 37 (21.8%), general¬ ized cerebral in 22 (13.0% ), and druginduced or toxic coma in 11 (6.5%). Hypoxie or ischemie coma had the cause
worst 2-week outcome: 54.1%
were
dead and 24.6% were in persistent coma, with 21.3% awake (Table 4). Hypoxie or ischemie coma subtype also had the greatest percentage of pa¬ tients in the deep-coma group (GCS score, 3 to 5). Focal cerebral lesions
and metabolic or septic coma had a better outcome. Generalized cerebral injury had a slightly better outcome, with 36.4% of the patients dead, 18.2% in persistent coma, and 45.4% awake. Drug-induced coma had the most fa¬ vorable outcome: none died, 27.3% were still comatose, and 72.7% were awake. The percentage of patients with persistent coma was similar among the different coma subtypes. After stratifying by coma subtype, the relationship between the initial GCS score and 2-week outcome re¬ mained significant (Cochran-MantelHaenszel 2, < .001) (Table 5). Ex¬ cept for patients with general cerebral injury and patients with drug-induced coma, a higher initial categorical GCS score was associated with a signifi¬ cantly greater chance of waking by 2 weeks. A logistic regression model demon¬ strated that the initial GCS score and drug-induced coma subtype were inde¬ pendent predictors of 2-week outcome (Table 6). Age, gender, ethnicity, and interval between coma onset and coma scoring were not significantly associ¬ ated with outcome. The estimated probability of waking from coma in¬ creased with increasing GCS score, but the risk depended on etiology (Figure). Glasgow Coma Scale was entered as a continuous variable in model 1 or cat¬ egorized as 3 to 5 or 6 to 8 in model 2. Our model estimated that patients in drug-induced coma were eight times
likely to wake at 2 weeks than those with nondrug-induced coma when GCS was held constant. Irrespec¬ tive of coma etiology, patients with GCS scores of 6 to 8 were seven times more likely awake than those with ini¬ tial scores of 3 to 5. In a model to assess individual GCS subscores (model 3), motor score was the only significant independent predictor of 2-week out¬ come. When combined with drug-in¬ duced cause (model 4), the motor score alone was similar to the entire GCS score in predicting 2-week outcome more
(Table 6).
COMMENT
Predictors of coma outcome
are
im¬
portant for allocation of time and ef¬ fort to
patients with a more favorable prognosis and for optimal stratifica¬ tion of patients enrolled in experimen¬ tal treatment protocols. The GCS pro¬ vides adequate information to identify specific levels of consciousness and to categorize the severity of coma. The
GCS is often used as the inclusion cri¬ terion and for follow-up assessment of patients in multicenter studies. In our study of patients with nontraumatic coma, GCS was found to be a reliable predictor of 2-week outcome. Patients with GCS scores of 3 to 5 had a greater risk of death or persistent coma at 2 weeks than patients with higher scores of 6 to 8. The estimated probability of waking from nontraumatic coma by 2 weeks was seven times higher in those
Downloaded From: http://archneur.jamanetwork.com/ by a Indiana University School of Medicine User on 05/12/2015
Table 4.—Two-Week Outcome of Nontraumatic Coma and Coma Two-Week
Coma Etiology Hypoxie or ischemie Metabolic or septic Focal cerebral
General cerebral
Drug-induced All
2
No.
(%) (36.1) 37 (21.8) 38 (22.5) 22 (13.0) 11 (6.5)
Awake
Outcome,
with
a 2-week mortality of 67%, com¬ pared with 20% of those in the 6 to 8
Etiology
group. Duration of coma has been as¬ sociated with poorer outcome in both
%
Dead/Coma
traumatic coma3 and the present se¬ ries. In other studies of nontraumatic coma, in which drug-induced coma was excluded, favorable predictors from the GCS included production of incom¬ prehensible speech, eye-opening after noxious stimuli, and withdrawal mo¬ tor responses (GCS of 8).4-6 After 24
54.1/24.6
61
34.2
47.4/18.4
36.4/18.2 72.7
33.1
169
44.4/21.5
with 8 df.
Table 5.—Two-Week Outcome of Nontraumatic Coma and Initial (GCS) Stratified by Coma Etiology* Two-Week Coma
Hypoxie
Etiology or
Awake
GCS
ischemie
3-5
43
6-8
Metabolic
or
3-5
septic
14.0 38.9
Glasgow Coma Score
Outcome, % Dead/Coma 36.0 1 31.1
Pit
J
100
15 54.6
6-8
Focal cerebral
Drug-induced
i-0
28.6 53.3
71.4 Ì 46 7
3-5
60
40
1
6-8
83.3
16.7
/
All
*NS
indicates not t Stratum specific
/
55.0 General cerebral
NS
/
NS
66.9
169
