- Email: [email protected]
Ventilatory status early after head injury
ORIGINAL CONTRIBUTION head injury, ventilatory status
Ventilatory Status Early After Head Injury The ventilatory status of patients within the first f e w hours following head injury has not been well established. We prospectively studied 63 patients who presented to an urban trauma center with varying severity of head injury to determine whether any trend toward hypo- or hyperventilation existed within the first two hours following injury. Arterial blood gas analysis done on emergency presentation showed that 14 patients with severe head injury (Glasgow coma scale ~ 4) had mean pH values of 7.29 and mean PaC02 of 41.86 torr. IWenty patients categorized as moderate head injury (GCS = 5-11) had mean pH values of 7.38 with a mean PaC02 of 34.1 torr. T~venty-nine patients with GCS >I 12 had mean pH and PaC02 values of 7.4 and 31.8 torr, respectively. These differences in pH and PaC02 were statistically significant between the GCS groups with mild and severe head injury (P ~ .01 pH), (P = .05 PC02), and could not be explained on the basis of hypoxemia, blood alcohol level, hypotension, or associated chest injury. It is concluded that patients with severe craniocerebral trauma show an early trend toward hypercapnea and acidosis. Immediate control of airway and assisted ventilation is necessary in order to reduce PaC02 to optimal levels in patients with severe head injury. [Vicario SL Coleman R, Cooper MA, Thomas DM: Ventilatory status early after head injury. Ann Emerg Med 12:145-148, March 1983.]
Salvator J. Vicario, MD Royce Coleman Mary Ann Cooper, MD, FACEP Donald M. Thomas, MD Louisville, Kentucky From the Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky. Presented at the University Association for Emergency Medicine Annual Meeting in Salt Lake City, Utah, April 1982. Address for reprints: Salvator J. Vicario, MD, Department of Emergency Medicine, University of Louisville, 323 East Chestnut Street, Louisville, Kentucky 40202.
INTRODUCTION The ventilatory status of patients who have sustained a head injury has not been well established. Previous studies regarding ventilatory adequacy of these patients have been conflicting. 1-4 Much of this discrepancy can be attributed to patient selection and delays in observation. North and Jennett s were able to show abnormal breathing patterns in 60% of acutely braindamaged patients at some time during the course of the illness. They also noted a significant overlay in different breathing patterns in the same patient at different times. Despite the obvious importance of this subject, the authors could find little literature which addressed the respiratory status of head-injured patients within the first few hours following such trauma. We therefore initiated this study to determine the ventilatory status of head injury patients within the first two hours following their injury. We were especially interested in delineating trends toward hypo- or hyperventilation in patients with varying severity of head injury. METHODS The study population included 63 patients with varying severity of head injury who presented to the emergency department of the University of Louisville Hospital in Louisville, Kentucky, from June through August 1981. All patients were assigned a Glasgow coma score (GCS) on arrival to the emergency department and at 30-minute intervals. In addition, vital signs were recorded on arrival and blood ethanol and arterial blood gases were drawn within five minutes after arrival in the emergency department. The majority of seriously injured patients were transported by ambulance with oxygen administered by mask or nasal cannula at varying flow rates. Ventilation was assisted prehospital by bag-valve mask at the discretion of the para12:3 March 1983
Annals of Emergency Medicine
145/39
HEAD INJURY Vicario et al
medical personnel. Any patient who could not be scored within two hours from time of insult, or who required endotracheal intubation or cardiopulmonary resuscitation prior to arrival and blood gas analysis, was not included in the study. Arterial blood gases were obtained by percutaneous radial or femoral artery puncture and specimens were analyzed using a Coming 175 Autoanalyzer (Coming, Medfield, MA) within 15 minutes of being obtained. Blood ethanol levels were drawn by venipuncture and analyzed quantitatively using the DuPont ACA instrument (DuPont Co, Wilmington, DE). Based on the GCS on arrival to the emergency department, patients were categorized into three separate groups. Group I included patients with GCS i> 12; Group II, GCS 5-11; and Group III, GCS ~ 4. Demographic data, vital signs, and laboratory values were tabulated for each group and analyzed statistically by Student t test and chisquare analysis. RESULTS During the study period, 316 patients were admitted to the emergency department with varying severity of head injury. The majority were minor, and were excluded from the study population because blood gases and ethanol levels were not clinically indicated. The distribution of the study population of 63 patients included 29 Category I patients, 20 in Category II, and 14 in Category III. Demographical data are shown (Table 1). Vital signs, including heart rate (HR), mean arterial pressure (MAP), and respiratory rate, of each patient category are also given (Table 2). Mean arterial pressures were calculated using the formula: 2 (Systolic - Diastolic) + Diastolic 3 There was no significant difference b e t w e e n groups in age and MAP, while heart rate (P ~ .001) and respiratory rate (P ~ .01) were both decreased significantly in the severely head injured group when compared to those patients with GCS i> 12. Arterial blood gas results are illustrated (Table 3, Figure). No patient category s h o w e d h y p o x e m i a , but those patients with GCS ~ 4 were significantly more hypercapneic than were those with GCS /> 12 (mean PaCO2 = 42 vs 31.8) (P = .05). The mean PaCO2 of Group II patients was 40/146
TABLE 1. Demographics Group I (GCS /> 12)
Group II (GCS = 5-11)
Group III (GCS ~< 4)
29 (46%)
20 (32%)
14 (22%)
Number Mean Age Female/Male (%)
30
32
33
35/65
33/67
14/86
TABLE 2. GCS and vital signs (mean +_ SEM) GCS
MAP
HR
Respirations
/> 12
92 _+ 4
106 _+ 3
21 _+ 1
5-11
90 _+ 8
93 -+ 6
18 __ 2
~<4
94 _+ 36
80 -+ 6*
15 _+ 2 ~
* P ~ . 0 0 1 GCS/> 12vsGCS ~<4. ~-P ~< .01 GCS/> 12 vs GCS ~< 4.
TABLE 3. GCS vs arterial blood gas and ethanol level (mean +- SEM) GCS
No.
pH
I> 12 5-11 ~<4 ~<4CT~
29 20 14 3
7.4 _+ .01 7.38 _+ .02 7.29 _+ .03* 7.30
PCO2
PO2
31.8 _+ 1 88.9 -+ 5 34.1 _+ 1 100 _+ 9 42.0 _+ 5 t 138 _+ 36 41 164
HCO3
Ethanol
19.4 _+ 1.61 20,43 _+ 1.37 20.33 _+ 1.4
0.17 0,23 0,13
*P ~< .01 GCS I> 12 vs GCS ~< 4. tp ~< .05 GCS I> 12 vs GCS ~< 4. ~Three patients with GCS ~< 4 had significant chest trauma but insignificant deviation of pH and PaCO2 measurements.
s o m e w h a t e l e v a t e d c o m p a r e d to Group I patients, but the difference was not statistically significant. The mean pH of patients with severe head injury (GCS ~ 4) was significantly lower (P = .01) when compared to Group I patients (pH = 7.29 vs pH = 7.4). Bicarbonate values were similarly decreased, and mean ethanol levels were elevated in all patient categories. Major thoracic injuries were present in three patients with GCS ~ 4, but mean pH and PaCOz measurements were similarly abnormal to others in the group.
DISCUSSION Although several authors have reported on respiratory patterns and acid-base status in patients with cerebral insults, we are aware of no study that has been directed at delineating ventilatory status within the first two hours following head injury. AddiAnnals of Emergency Medicine
tionally previous studies have failed to separate these patients on the basis of severity of injury other than to grossly classify patients as survivors or nonsurvivors. In an effort to clarify the issue, we used the Glasgow coma score, which has been determined to be a useful and reproducible scoring system for patients who have sustained cranial trauma. 6'7 It has also been found to correlate s o m e w h a t with severity of injury. 7 Most authors 8 "10 recommend hyperventilation of head-injured patients to PaCO2 levels equal to 25 to 30 m m Hg on the theoretical grounds that this will reduce intracranial pressure and increase oxygenation and perfusion of damaged or potentially anoxic cerebral tissue. It is also proposed that the hyperventilation m a y partially compensate for lower intracerebral pH. '11 Our results illustrate that pat i e n t s w i t h GCS ~ 4 tend to be 12:3 March 1983
pH
PCO2
P02
7.45
45
175
7.40
40
150
7.35
35
125
7.30
30
100
] T
7.25 °
~
pH
hypoventilatory and acidotic within the first two hours following craniocerebral trauma, as evidenced by increased PaCO2 and decreased pH, compared to patients with less severe head injury. We may only speculate about the reasons for depressed respiration, but this may be related to elevation of intracranial pressure or to primary brain insult. Associated chest injuries, including pneumothorax or flail chest, did not alter mean pH and PaCO2 values significantly. Ethanol can cause reduced respiratory rate, but given the similarly elevated serum levels in all three patient categories, it would be difficult to incriminate this drug alone. Unfortunately no other potential respiratory depressants, such as benzodiazepines or narcotics, were measured. The significantly decreased pH in Group III patients appeared to be secondary to a mixed respiratory and metabolic acidosis. 1 The etiology of 12:3 March 1983
75
25 II
A\
A~
II
V/
8(_9
8(.9
8
PC02
the metabolic component is not readily explainable, for no lactate measurements were done nor was there any significant difference in MAP on arrival. The acidosis may have been secondary to seizure activity or to hypotension that was corrected by crystalloid infusion prior to arrival. The data, however, do illustrate that patients with GCS ~ 4 were unable to compensate for the metabolic component of the acidosis. All patient groups were adequately oxygenated with supplemental oxygen. Patients in the group with GCS 4 had higher PO2 levels secondary to higher supplemental FIO2. However, any attempt to reduce PaCO~ to recommended levels wassuboptimal in the prehospital phase of care. Patients who were intubated were excluded, so no comment on the efficacy of this modality can be made at present. Conscious patients (GCS / 12) were able to ventilate adequately on their A n n a l s of E m e r g e n c y Medicine
O3
8(..9
-~-
ir
v/
8(D
(D (D
PO2
Fig. GCS and arterial blood gases. own or to be assisted with bag-valve m a s k devices. G r o u p II p a t i e n t s tended to have more elevated PaCO2 levels than did Group I patients, and m a y also benefit from additional efforts to assist ventilation to reduce PaCO~ levels to the 30-mm-Hg range. CONCLUSION Previous studies have given little attention to the early ventilatory status of head injury patients. Our study illustrates that patients with GCS ~ 4 show a significant tendency toward hypoventilation and concomitant acidosis. This state is undoubtedly detrimental if not reversed as soon as possible. We conclude that early intubation and ventilatory assistance of patients with severe head injury is necessary to optimize care. Future studies are needed to determine if, in147/41
HEAD INJURY Vicario et al
deed, patient survival and f u n c t i o n a l r e c o v e r y are i m p r o v e d w h e n c o n trolled v e n t i l a t i o n is i n s t i t u t e d soon after head injury.
juries. Br J Anaesth 40:354, 1968.
REFERENCES
5. North JB, Jennett S: Abnormal breathing patterns associated with acute brain damage. Arch Neurol 31:338-344, 1974.
1. Cook AW, Browder EJ, Lyons HA: Alterations in acid-base equilibrium in craniocerebral trauma, f Neurosurg 18:366, 1961. 2. Katsurada K, Ryohei Y, Tsayoshi S: Respiratory insufficiency in patients with severe head injury. Surgery 73:191-199, 1973. 3. Fromam C: Alterations of respiratory function in patients with severe head in-
4. Naerra N: Blood-gas analyses in unconscious neurosurgical patients on admission to hospital. Acta Anaesth Scand 7:191-199, 1963.
6. Teasdale G, Jennett B: Assessment of coma and impaired consciousness. A practical scale. Lancet 2:81-84, 1974. 7. Rimmel R, Jane JA, Edlich RF: An injury severity scale for comprehensive management of central nervous system trauma. JACEP 8:64-67, 1979.
8. Shields CB, Miles JP, Albright L, et al: Early management of head injuries. J Ky Med Assoc 78:9-13, 1980. 9. Paul RL, Polanco O, Turney SS: Intracranial pressure responses to alterations in arterial carbon dioxide pressures in patients with head injuries. J Neurosurg 36: 714-720, 1972. 10. Becker DP, Miller JD, Ward JD, et al: The outcome from severe head injury with early diagnosis and intensive management. J Neurosurg 47:491-502, 197Z 11. Cold GE, Jensen F, Malmros R: The cerebrovascular CO2 reactivity during the acute phase of brain injury. Acta Anaesth Scand 21:222-231, 1971.
Call for Abstracts: AMA Commission on Emergency Medical Services A national meeting hosted by the American Medical Association's Commission on Emergency Medical Services will be jointly sponsored by the American Medical Association and the American Hospital Association November 4-5, 1983, at the downtown Chicago Marriott Hotel. The meeting will be devoted to the subject of medical control and accountability of prehospital emergency medical services systems. The program will include presentations on particular aspects of medical control and accountability, as well as presentations from individuals responsible for medical control and accountability programs in various communities/regions throughout the nation. Interested individuals are invited to submit abstracts for review by a Program Committee, composed of members of the Commission on Emergency Medical Services, for inclusion in the meeting program. Authors of the selected ab- . stracts will be contacted approximately one month following the deadline for abstract submission, and will be requested to submit a complete manuscript two weeks prior to the day of presentation. These manuscripts will be included in the published proceedings of the meeting. The deadline for submission of abstracts is April 1, 1983. Abstracts should be limited to 250 words and typed double-spaced on 81/2- by 11-inch paper. A cover sheet should be attached to the abstracts and should include the full names, titles, and addresses of the authors. A notation must be included indicating which author will present the paper at the meeting should it be selected. P{esentations will be limited to 20 minutes. Please mail abstracts to Department of Health Care Resources~ American Medical Association, 535 North Dearborn Street, Chicago, IL 60610. Further information may be obtained by writing to this address or by calling 312/751-6781.
42/148
Annals of Emergency Medicine
12:3 March 1983
Ventilatory Status Early After Head Injury The ventilatory status of patients within the first f e w hours following head injury has not been well established. We prospectively studied 63 patients who presented to an urban trauma center with varying severity of head injury to determine whether any trend toward hypo- or hyperventilation existed within the first two hours following injury. Arterial blood gas analysis done on emergency presentation showed that 14 patients with severe head injury (Glasgow coma scale ~ 4) had mean pH values of 7.29 and mean PaC02 of 41.86 torr. IWenty patients categorized as moderate head injury (GCS = 5-11) had mean pH values of 7.38 with a mean PaC02 of 34.1 torr. T~venty-nine patients with GCS >I 12 had mean pH and PaC02 values of 7.4 and 31.8 torr, respectively. These differences in pH and PaC02 were statistically significant between the GCS groups with mild and severe head injury (P ~ .01 pH), (P = .05 PC02), and could not be explained on the basis of hypoxemia, blood alcohol level, hypotension, or associated chest injury. It is concluded that patients with severe craniocerebral trauma show an early trend toward hypercapnea and acidosis. Immediate control of airway and assisted ventilation is necessary in order to reduce PaC02 to optimal levels in patients with severe head injury. [Vicario SL Coleman R, Cooper MA, Thomas DM: Ventilatory status early after head injury. Ann Emerg Med 12:145-148, March 1983.]
Salvator J. Vicario, MD Royce Coleman Mary Ann Cooper, MD, FACEP Donald M. Thomas, MD Louisville, Kentucky From the Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky. Presented at the University Association for Emergency Medicine Annual Meeting in Salt Lake City, Utah, April 1982. Address for reprints: Salvator J. Vicario, MD, Department of Emergency Medicine, University of Louisville, 323 East Chestnut Street, Louisville, Kentucky 40202.
INTRODUCTION The ventilatory status of patients who have sustained a head injury has not been well established. Previous studies regarding ventilatory adequacy of these patients have been conflicting. 1-4 Much of this discrepancy can be attributed to patient selection and delays in observation. North and Jennett s were able to show abnormal breathing patterns in 60% of acutely braindamaged patients at some time during the course of the illness. They also noted a significant overlay in different breathing patterns in the same patient at different times. Despite the obvious importance of this subject, the authors could find little literature which addressed the respiratory status of head-injured patients within the first few hours following such trauma. We therefore initiated this study to determine the ventilatory status of head injury patients within the first two hours following their injury. We were especially interested in delineating trends toward hypo- or hyperventilation in patients with varying severity of head injury. METHODS The study population included 63 patients with varying severity of head injury who presented to the emergency department of the University of Louisville Hospital in Louisville, Kentucky, from June through August 1981. All patients were assigned a Glasgow coma score (GCS) on arrival to the emergency department and at 30-minute intervals. In addition, vital signs were recorded on arrival and blood ethanol and arterial blood gases were drawn within five minutes after arrival in the emergency department. The majority of seriously injured patients were transported by ambulance with oxygen administered by mask or nasal cannula at varying flow rates. Ventilation was assisted prehospital by bag-valve mask at the discretion of the para12:3 March 1983
Annals of Emergency Medicine
145/39
HEAD INJURY Vicario et al
medical personnel. Any patient who could not be scored within two hours from time of insult, or who required endotracheal intubation or cardiopulmonary resuscitation prior to arrival and blood gas analysis, was not included in the study. Arterial blood gases were obtained by percutaneous radial or femoral artery puncture and specimens were analyzed using a Coming 175 Autoanalyzer (Coming, Medfield, MA) within 15 minutes of being obtained. Blood ethanol levels were drawn by venipuncture and analyzed quantitatively using the DuPont ACA instrument (DuPont Co, Wilmington, DE). Based on the GCS on arrival to the emergency department, patients were categorized into three separate groups. Group I included patients with GCS i> 12; Group II, GCS 5-11; and Group III, GCS ~ 4. Demographic data, vital signs, and laboratory values were tabulated for each group and analyzed statistically by Student t test and chisquare analysis. RESULTS During the study period, 316 patients were admitted to the emergency department with varying severity of head injury. The majority were minor, and were excluded from the study population because blood gases and ethanol levels were not clinically indicated. The distribution of the study population of 63 patients included 29 Category I patients, 20 in Category II, and 14 in Category III. Demographical data are shown (Table 1). Vital signs, including heart rate (HR), mean arterial pressure (MAP), and respiratory rate, of each patient category are also given (Table 2). Mean arterial pressures were calculated using the formula: 2 (Systolic - Diastolic) + Diastolic 3 There was no significant difference b e t w e e n groups in age and MAP, while heart rate (P ~ .001) and respiratory rate (P ~ .01) were both decreased significantly in the severely head injured group when compared to those patients with GCS i> 12. Arterial blood gas results are illustrated (Table 3, Figure). No patient category s h o w e d h y p o x e m i a , but those patients with GCS ~ 4 were significantly more hypercapneic than were those with GCS /> 12 (mean PaCO2 = 42 vs 31.8) (P = .05). The mean PaCO2 of Group II patients was 40/146
TABLE 1. Demographics Group I (GCS /> 12)
Group II (GCS = 5-11)
Group III (GCS ~< 4)
29 (46%)
20 (32%)
14 (22%)
Number Mean Age Female/Male (%)
30
32
33
35/65
33/67
14/86
TABLE 2. GCS and vital signs (mean +_ SEM) GCS
MAP
HR
Respirations
/> 12
92 _+ 4
106 _+ 3
21 _+ 1
5-11
90 _+ 8
93 -+ 6
18 __ 2
~<4
94 _+ 36
80 -+ 6*
15 _+ 2 ~
* P ~ . 0 0 1 GCS/> 12vsGCS ~<4. ~-P ~< .01 GCS/> 12 vs GCS ~< 4.
TABLE 3. GCS vs arterial blood gas and ethanol level (mean +- SEM) GCS
No.
pH
I> 12 5-11 ~<4 ~<4CT~
29 20 14 3
7.4 _+ .01 7.38 _+ .02 7.29 _+ .03* 7.30
PCO2
PO2
31.8 _+ 1 88.9 -+ 5 34.1 _+ 1 100 _+ 9 42.0 _+ 5 t 138 _+ 36 41 164
HCO3
Ethanol
19.4 _+ 1.61 20,43 _+ 1.37 20.33 _+ 1.4
0.17 0,23 0,13
*P ~< .01 GCS I> 12 vs GCS ~< 4. tp ~< .05 GCS I> 12 vs GCS ~< 4. ~Three patients with GCS ~< 4 had significant chest trauma but insignificant deviation of pH and PaCO2 measurements.
s o m e w h a t e l e v a t e d c o m p a r e d to Group I patients, but the difference was not statistically significant. The mean pH of patients with severe head injury (GCS ~ 4) was significantly lower (P = .01) when compared to Group I patients (pH = 7.29 vs pH = 7.4). Bicarbonate values were similarly decreased, and mean ethanol levels were elevated in all patient categories. Major thoracic injuries were present in three patients with GCS ~ 4, but mean pH and PaCOz measurements were similarly abnormal to others in the group.
DISCUSSION Although several authors have reported on respiratory patterns and acid-base status in patients with cerebral insults, we are aware of no study that has been directed at delineating ventilatory status within the first two hours following head injury. AddiAnnals of Emergency Medicine
tionally previous studies have failed to separate these patients on the basis of severity of injury other than to grossly classify patients as survivors or nonsurvivors. In an effort to clarify the issue, we used the Glasgow coma score, which has been determined to be a useful and reproducible scoring system for patients who have sustained cranial trauma. 6'7 It has also been found to correlate s o m e w h a t with severity of injury. 7 Most authors 8 "10 recommend hyperventilation of head-injured patients to PaCO2 levels equal to 25 to 30 m m Hg on the theoretical grounds that this will reduce intracranial pressure and increase oxygenation and perfusion of damaged or potentially anoxic cerebral tissue. It is also proposed that the hyperventilation m a y partially compensate for lower intracerebral pH. '11 Our results illustrate that pat i e n t s w i t h GCS ~ 4 tend to be 12:3 March 1983
pH
PCO2
P02
7.45
45
175
7.40
40
150
7.35
35
125
7.30
30
100
] T
7.25 °
~
pH
hypoventilatory and acidotic within the first two hours following craniocerebral trauma, as evidenced by increased PaCO2 and decreased pH, compared to patients with less severe head injury. We may only speculate about the reasons for depressed respiration, but this may be related to elevation of intracranial pressure or to primary brain insult. Associated chest injuries, including pneumothorax or flail chest, did not alter mean pH and PaCO2 values significantly. Ethanol can cause reduced respiratory rate, but given the similarly elevated serum levels in all three patient categories, it would be difficult to incriminate this drug alone. Unfortunately no other potential respiratory depressants, such as benzodiazepines or narcotics, were measured. The significantly decreased pH in Group III patients appeared to be secondary to a mixed respiratory and metabolic acidosis. 1 The etiology of 12:3 March 1983
75
25 II
A\
A~
II
V/
8(_9
8(.9
8
PC02
the metabolic component is not readily explainable, for no lactate measurements were done nor was there any significant difference in MAP on arrival. The acidosis may have been secondary to seizure activity or to hypotension that was corrected by crystalloid infusion prior to arrival. The data, however, do illustrate that patients with GCS ~ 4 were unable to compensate for the metabolic component of the acidosis. All patient groups were adequately oxygenated with supplemental oxygen. Patients in the group with GCS 4 had higher PO2 levels secondary to higher supplemental FIO2. However, any attempt to reduce PaCO~ to recommended levels wassuboptimal in the prehospital phase of care. Patients who were intubated were excluded, so no comment on the efficacy of this modality can be made at present. Conscious patients (GCS / 12) were able to ventilate adequately on their A n n a l s of E m e r g e n c y Medicine
O3
8(..9
-~-
ir
v/
8(D
(D (D
PO2
Fig. GCS and arterial blood gases. own or to be assisted with bag-valve m a s k devices. G r o u p II p a t i e n t s tended to have more elevated PaCO2 levels than did Group I patients, and m a y also benefit from additional efforts to assist ventilation to reduce PaCO~ levels to the 30-mm-Hg range. CONCLUSION Previous studies have given little attention to the early ventilatory status of head injury patients. Our study illustrates that patients with GCS ~ 4 show a significant tendency toward hypoventilation and concomitant acidosis. This state is undoubtedly detrimental if not reversed as soon as possible. We conclude that early intubation and ventilatory assistance of patients with severe head injury is necessary to optimize care. Future studies are needed to determine if, in147/41
HEAD INJURY Vicario et al
deed, patient survival and f u n c t i o n a l r e c o v e r y are i m p r o v e d w h e n c o n trolled v e n t i l a t i o n is i n s t i t u t e d soon after head injury.
juries. Br J Anaesth 40:354, 1968.
REFERENCES
5. North JB, Jennett S: Abnormal breathing patterns associated with acute brain damage. Arch Neurol 31:338-344, 1974.
1. Cook AW, Browder EJ, Lyons HA: Alterations in acid-base equilibrium in craniocerebral trauma, f Neurosurg 18:366, 1961. 2. Katsurada K, Ryohei Y, Tsayoshi S: Respiratory insufficiency in patients with severe head injury. Surgery 73:191-199, 1973. 3. Fromam C: Alterations of respiratory function in patients with severe head in-
4. Naerra N: Blood-gas analyses in unconscious neurosurgical patients on admission to hospital. Acta Anaesth Scand 7:191-199, 1963.
6. Teasdale G, Jennett B: Assessment of coma and impaired consciousness. A practical scale. Lancet 2:81-84, 1974. 7. Rimmel R, Jane JA, Edlich RF: An injury severity scale for comprehensive management of central nervous system trauma. JACEP 8:64-67, 1979.
8. Shields CB, Miles JP, Albright L, et al: Early management of head injuries. J Ky Med Assoc 78:9-13, 1980. 9. Paul RL, Polanco O, Turney SS: Intracranial pressure responses to alterations in arterial carbon dioxide pressures in patients with head injuries. J Neurosurg 36: 714-720, 1972. 10. Becker DP, Miller JD, Ward JD, et al: The outcome from severe head injury with early diagnosis and intensive management. J Neurosurg 47:491-502, 197Z 11. Cold GE, Jensen F, Malmros R: The cerebrovascular CO2 reactivity during the acute phase of brain injury. Acta Anaesth Scand 21:222-231, 1971.
Call for Abstracts: AMA Commission on Emergency Medical Services A national meeting hosted by the American Medical Association's Commission on Emergency Medical Services will be jointly sponsored by the American Medical Association and the American Hospital Association November 4-5, 1983, at the downtown Chicago Marriott Hotel. The meeting will be devoted to the subject of medical control and accountability of prehospital emergency medical services systems. The program will include presentations on particular aspects of medical control and accountability, as well as presentations from individuals responsible for medical control and accountability programs in various communities/regions throughout the nation. Interested individuals are invited to submit abstracts for review by a Program Committee, composed of members of the Commission on Emergency Medical Services, for inclusion in the meeting program. Authors of the selected ab- . stracts will be contacted approximately one month following the deadline for abstract submission, and will be requested to submit a complete manuscript two weeks prior to the day of presentation. These manuscripts will be included in the published proceedings of the meeting. The deadline for submission of abstracts is April 1, 1983. Abstracts should be limited to 250 words and typed double-spaced on 81/2- by 11-inch paper. A cover sheet should be attached to the abstracts and should include the full names, titles, and addresses of the authors. A notation must be included indicating which author will present the paper at the meeting should it be selected. P{esentations will be limited to 20 minutes. Please mail abstracts to Department of Health Care Resources~ American Medical Association, 535 North Dearborn Street, Chicago, IL 60610. Further information may be obtained by writing to this address or by calling 312/751-6781.
42/148
Annals of Emergency Medicine
12:3 March 1983