The Journal
of Emergency
Medicine.
Vol 10, pp 753-75.5,
1992
Printed in the USA
Copyright
0 1992 Pergamon
Press Ltd.
VITAMIN H AND WHEN TO USE IT Once again, I cannot resist joining in an argument that I find very interesting. I suspect that if all the physicians could sit down and discuss the subject in a single room, there would not be much disagreement among them and that perhaps what is happening here is a difference in style compounded by an unintended meaning from an original text. It is my contention that the Drs. Kuchinski (l), Walls (2), and Neal and Pollock (3) are struggling to solve some of the most difficult problems in trauma patient care. These not only include what is the best way to actively manage the airway of the trauma patient, but what is the best way to chemically control the combative trauma patient who has not yet been screened for serious injury. A further problem concerns what is the best way to prevent surges of intracranial hypertension that lead to cerebral edema and probably account for much of the permanent and serious morbidity of acute closed head injury. There is much concern for the management of the airway, and I believe that we are coming to a consensus that oral intubation is permissible even before the cervical spine has been cleared so long as hyperextension, hyperflexion, and hyperdistraction are avoided. I further believe that most institutions are coming around to my opinion that oral intubation is safe even in the presence of cervical spine injury so long as the three hypers are avoided (4). I do not find consensus for either how to chemically control the combative patient or how to protect the brain. I don’t think that anyone would argue against controlled rapid sequence sedation, paralysis, intubation, and hyperventilation of the patient with serious closed head injury. The argument over the exact level of Glascow Coma Score to select for mandatory intubation is silly, since it ignores how the Glascow Coma Score was originally defined. Specifically, it was not intended to be used as a field, emergency department, or trauma resuscitation score, since there is no way to accurately apply the Glascow Coma Score when there are drugs or alcohol present that confuse the neurologic picture. Moreover, it was intended as
a prognosticating device rather than as a clinical monitor. That it has found widespread use as a clinical monitor is interesting and fortuitous, but we all must remember the limitations of the Glascow Coma Score’s initial accuracy. Nevertheless, I believe there is good consensus that any patient with serious alteration in neurologic performance that would cause a score of 8 or less to be derived should be intubated under rapid sequence control (5). The problem, then, is the patient who cannot be defined as a Glascow Coma Score alteration of more than one or two points, but who is too combative to evaluate safely without some kind of chemical control. If the patient has frontal contusion and a modest amount of alcohol, he will often be as combative as if he had a large amount of alcohol and a winsome personality disorder rather than a head injury. Short of time, there is no way to tell. But in trying to acquire the time to allow these differentiations to be made, the patient may well have converted himself from a cervical skeletal injury to a spinal cord quadriplegia. As unsuccessful as I have been in documenting a case of quadriplegia caused by oral intubation of an unknown status cervical spine, I have encountered at least three cases of patients who started with normal function and ended up with quadriplegia or paraplegia from uncontrolled combativeness in the resuscitation room. I believe that it is for this group of patients that we need to examine our modalities of control. If a head injury is suspected, then I suspect all would agree that rapid sequence induction, intubation with paralysis, and subsequent intense diagnostics with CT scan and observation would be in order. It is for the patient who we think is probably just intoxicated with alcohol, cocaine, amphetamines, or all of the above who is the problem case. I think that such patients are best managed without active intubation, but that they do need chemical control. While our neurosurgeons prefer morphine, 0736-4679/92 $5.00 + .OO 753
754 I think it requires a large amount of opiate to get control. Like all sedatives, morphine in small dosage can have a paradoxical stimulating or dysphoric effect; hardly a solution to the problem in question. In large dosage, not only is respiration likely to be compromised, thereby again eventuating in active airway management, but vomiting is likely to be induced, and there may be profound autonomic effects in the event of volume depletion that are very hard to reverse even with the opiate antagonist Naloxone. Fentanyl is a preferable opiate for sedation and trauma analgesia, but while it has less effect on blood pressure, it is too short-acting to be effective for this kind of patient. Repeated doses to maintain control can lead to a total body rigidity, including laryngospasm, that will require muscle paralysis and intubation; again, the very procedure that I would like to avoid in these patients. Benzodiazepines can sometimes be effective sedatives, especially in a patient whose agitation comes from alcohol withdrawal, or in the postictal phase of a seizure, but in addition to having the same paradoxical stimulating effect in small dosages referred to above, they frequently cause respiratory arrest in patients with alcohol present, thereby again necessitating intubation. Moreover, the benzodiazepines are potent inducers of amnesia. While this is usually transient, it can last as long as several days and, in the elderly patient, as long as a week. It then becomes very hard to distinguish who has a head injury and who has a drug effect. Finally, in the presence of volume depletion, they also may have profound autonomic effects. The drug that I have seen and personally used for over 20 years, and which my colleagues reported upon at UAEMS, is Haloperidol(6). In fact, we have given so much, so often, and so effectively that the housestaff refer to Haldol as Vitamin H, and the combative patient as being Vitamin H deficient. Its onset is rapid (within 2 to 5 minutes of a single intravenous dose 95% of the time); its effect profound (within thirty minutes, most patients who have required four-point restraints can be released from the restraints); and rather than masking neurologic status, it frequently enables one to evaluate that status. It can cause hypotension, but does so very infrequently (7). It does not cause respiratory arrest and, while it purportedly lowers the seizure threshold in experimental animals, I have never seen Haldol induce a seizure in the human. It lasts for eight to twelve hours, but during that period the patient is rousable, and usually back in control. The dose schedule I prefer is lo-milligram intravenous push. If no response in 5 minutes, I repeat and
The Journal
of Emergency
Medicine
often double the dose. I have given as much as 120 milligrams to achieve control. It can cause neuroleptic malignant syndrome, and this does not appear to be dose-related. The only case I have observed in over 500 administrations was mild, and occurred in a patient who was already taking Haldol for psychosis. It does cause extrapyramidal reactions in about 10% of patients. This is preventable with Benadryl. I have never seen the reaction in less than 24 hours, so it really does not interfere with initial evaluation. The advantage is quick control; no need for intubation; often no need for a CT scan; and the ability to distinguish the patient with a drug or alcohol acute organic brain syndrome from the patient with closed head injury. I therefore suggest that the solution to the problem stated above is best achieved, for the patient who is thought not to have a head injury, through the use of intravenous haloperidol. If the patient is thought to have a head injury, then I would utilize the rapid sequence technique of intubation using Fentanyl as the sedating agent, anectine as the paralyzing agent, and hyperventilation as the immediate cerebral edema controlling agent. I would intubate the patient orally, and I would accept the reality that I will not be able to intubate every patient, and that there will be some patients who require cricothyrotomy. I will also accept the reality that I will not be perfect in my assessments and that some patients who have head injury will receive Haldol, and some patients who are simply intoxicated will receive rapid sequence induction. I further accept the reality that there will inevitably be technical errors committed in the performance of intubation. I hope that I am lucky enough to recognize an esophageal intubation, but the reality is that there is not enough luck to go around, and some patients will not thrive despite our best efforts to care for them. I would not use rapid sequence intubation merely to control the combative patient, since I think there is a satisfactory alternative: specifically, Haldol. I’m sure this will merely serve to muddy the waters even more badly, but if we don’t discuss the problems, we cannot achieve consensus. Let us try to find the path to common management and not confuse style differences with negligent practice. It goes without saying that anyone who fails to recognize and accept my practice recommendations is very silly and doesn’t know anything about the management of trauma. Peter Rosen, MD Editor-in-Chief
Editorial
755 REFERENCES
1. Kuchinski J, Tinkoff G, Rhodes M, Becher JW Jr. Emergency intubation for paralysis of the uncooperative trauma patient. J Emerg Med. 1991;9:9-12. 2. Walls RM. The combative trauma patient: a paradigm of trauma leadership. J Emerg Med. 1991;9:67-8. 3. Neal JM, Pollock JE. Letter to the Editor. J Emerg Med. 1992; lO:OOO-000. 4. Rosen P, Wolfe RE. Therapeutic legends of emergency medicine. J Emerg Med. 1989;7:387-9.
5. Rosen P, Barkin R, Sternbach CL. Airway management. In: Rosen P, Barkin R, Sternbach CL, eds. Essentials of emergency medicine (chapter 2). St Louis: CV Mosby: 1991. 6. Silverstein S, Frommer DA, Marx JA, Rosen P. Haloperidol in combative patients: a prospective study. Ann Emerg Med. 1986; 15:636. 7. McCarron MM, Schulze BW, Thompson GA, et al. Acute phencyclidine intoxication: clinical patterns, complications, and treatment. Ann Emerg Med. 1981;10:290.
of Emergency
Medicine.
Vol 10, pp 753-75.5,
1992
Printed in the USA
Copyright
0 1992 Pergamon
Press Ltd.
VITAMIN H AND WHEN TO USE IT Once again, I cannot resist joining in an argument that I find very interesting. I suspect that if all the physicians could sit down and discuss the subject in a single room, there would not be much disagreement among them and that perhaps what is happening here is a difference in style compounded by an unintended meaning from an original text. It is my contention that the Drs. Kuchinski (l), Walls (2), and Neal and Pollock (3) are struggling to solve some of the most difficult problems in trauma patient care. These not only include what is the best way to actively manage the airway of the trauma patient, but what is the best way to chemically control the combative trauma patient who has not yet been screened for serious injury. A further problem concerns what is the best way to prevent surges of intracranial hypertension that lead to cerebral edema and probably account for much of the permanent and serious morbidity of acute closed head injury. There is much concern for the management of the airway, and I believe that we are coming to a consensus that oral intubation is permissible even before the cervical spine has been cleared so long as hyperextension, hyperflexion, and hyperdistraction are avoided. I further believe that most institutions are coming around to my opinion that oral intubation is safe even in the presence of cervical spine injury so long as the three hypers are avoided (4). I do not find consensus for either how to chemically control the combative patient or how to protect the brain. I don’t think that anyone would argue against controlled rapid sequence sedation, paralysis, intubation, and hyperventilation of the patient with serious closed head injury. The argument over the exact level of Glascow Coma Score to select for mandatory intubation is silly, since it ignores how the Glascow Coma Score was originally defined. Specifically, it was not intended to be used as a field, emergency department, or trauma resuscitation score, since there is no way to accurately apply the Glascow Coma Score when there are drugs or alcohol present that confuse the neurologic picture. Moreover, it was intended as
a prognosticating device rather than as a clinical monitor. That it has found widespread use as a clinical monitor is interesting and fortuitous, but we all must remember the limitations of the Glascow Coma Score’s initial accuracy. Nevertheless, I believe there is good consensus that any patient with serious alteration in neurologic performance that would cause a score of 8 or less to be derived should be intubated under rapid sequence control (5). The problem, then, is the patient who cannot be defined as a Glascow Coma Score alteration of more than one or two points, but who is too combative to evaluate safely without some kind of chemical control. If the patient has frontal contusion and a modest amount of alcohol, he will often be as combative as if he had a large amount of alcohol and a winsome personality disorder rather than a head injury. Short of time, there is no way to tell. But in trying to acquire the time to allow these differentiations to be made, the patient may well have converted himself from a cervical skeletal injury to a spinal cord quadriplegia. As unsuccessful as I have been in documenting a case of quadriplegia caused by oral intubation of an unknown status cervical spine, I have encountered at least three cases of patients who started with normal function and ended up with quadriplegia or paraplegia from uncontrolled combativeness in the resuscitation room. I believe that it is for this group of patients that we need to examine our modalities of control. If a head injury is suspected, then I suspect all would agree that rapid sequence induction, intubation with paralysis, and subsequent intense diagnostics with CT scan and observation would be in order. It is for the patient who we think is probably just intoxicated with alcohol, cocaine, amphetamines, or all of the above who is the problem case. I think that such patients are best managed without active intubation, but that they do need chemical control. While our neurosurgeons prefer morphine, 0736-4679/92 $5.00 + .OO 753
754 I think it requires a large amount of opiate to get control. Like all sedatives, morphine in small dosage can have a paradoxical stimulating or dysphoric effect; hardly a solution to the problem in question. In large dosage, not only is respiration likely to be compromised, thereby again eventuating in active airway management, but vomiting is likely to be induced, and there may be profound autonomic effects in the event of volume depletion that are very hard to reverse even with the opiate antagonist Naloxone. Fentanyl is a preferable opiate for sedation and trauma analgesia, but while it has less effect on blood pressure, it is too short-acting to be effective for this kind of patient. Repeated doses to maintain control can lead to a total body rigidity, including laryngospasm, that will require muscle paralysis and intubation; again, the very procedure that I would like to avoid in these patients. Benzodiazepines can sometimes be effective sedatives, especially in a patient whose agitation comes from alcohol withdrawal, or in the postictal phase of a seizure, but in addition to having the same paradoxical stimulating effect in small dosages referred to above, they frequently cause respiratory arrest in patients with alcohol present, thereby again necessitating intubation. Moreover, the benzodiazepines are potent inducers of amnesia. While this is usually transient, it can last as long as several days and, in the elderly patient, as long as a week. It then becomes very hard to distinguish who has a head injury and who has a drug effect. Finally, in the presence of volume depletion, they also may have profound autonomic effects. The drug that I have seen and personally used for over 20 years, and which my colleagues reported upon at UAEMS, is Haloperidol(6). In fact, we have given so much, so often, and so effectively that the housestaff refer to Haldol as Vitamin H, and the combative patient as being Vitamin H deficient. Its onset is rapid (within 2 to 5 minutes of a single intravenous dose 95% of the time); its effect profound (within thirty minutes, most patients who have required four-point restraints can be released from the restraints); and rather than masking neurologic status, it frequently enables one to evaluate that status. It can cause hypotension, but does so very infrequently (7). It does not cause respiratory arrest and, while it purportedly lowers the seizure threshold in experimental animals, I have never seen Haldol induce a seizure in the human. It lasts for eight to twelve hours, but during that period the patient is rousable, and usually back in control. The dose schedule I prefer is lo-milligram intravenous push. If no response in 5 minutes, I repeat and
The Journal
of Emergency
Medicine
often double the dose. I have given as much as 120 milligrams to achieve control. It can cause neuroleptic malignant syndrome, and this does not appear to be dose-related. The only case I have observed in over 500 administrations was mild, and occurred in a patient who was already taking Haldol for psychosis. It does cause extrapyramidal reactions in about 10% of patients. This is preventable with Benadryl. I have never seen the reaction in less than 24 hours, so it really does not interfere with initial evaluation. The advantage is quick control; no need for intubation; often no need for a CT scan; and the ability to distinguish the patient with a drug or alcohol acute organic brain syndrome from the patient with closed head injury. I therefore suggest that the solution to the problem stated above is best achieved, for the patient who is thought not to have a head injury, through the use of intravenous haloperidol. If the patient is thought to have a head injury, then I would utilize the rapid sequence technique of intubation using Fentanyl as the sedating agent, anectine as the paralyzing agent, and hyperventilation as the immediate cerebral edema controlling agent. I would intubate the patient orally, and I would accept the reality that I will not be able to intubate every patient, and that there will be some patients who require cricothyrotomy. I will also accept the reality that I will not be perfect in my assessments and that some patients who have head injury will receive Haldol, and some patients who are simply intoxicated will receive rapid sequence induction. I further accept the reality that there will inevitably be technical errors committed in the performance of intubation. I hope that I am lucky enough to recognize an esophageal intubation, but the reality is that there is not enough luck to go around, and some patients will not thrive despite our best efforts to care for them. I would not use rapid sequence intubation merely to control the combative patient, since I think there is a satisfactory alternative: specifically, Haldol. I’m sure this will merely serve to muddy the waters even more badly, but if we don’t discuss the problems, we cannot achieve consensus. Let us try to find the path to common management and not confuse style differences with negligent practice. It goes without saying that anyone who fails to recognize and accept my practice recommendations is very silly and doesn’t know anything about the management of trauma. Peter Rosen, MD Editor-in-Chief
Editorial
755 REFERENCES
1. Kuchinski J, Tinkoff G, Rhodes M, Becher JW Jr. Emergency intubation for paralysis of the uncooperative trauma patient. J Emerg Med. 1991;9:9-12. 2. Walls RM. The combative trauma patient: a paradigm of trauma leadership. J Emerg Med. 1991;9:67-8. 3. Neal JM, Pollock JE. Letter to the Editor. J Emerg Med. 1992; lO:OOO-000. 4. Rosen P, Wolfe RE. Therapeutic legends of emergency medicine. J Emerg Med. 1989;7:387-9.
5. Rosen P, Barkin R, Sternbach CL. Airway management. In: Rosen P, Barkin R, Sternbach CL, eds. Essentials of emergency medicine (chapter 2). St Louis: CV Mosby: 1991. 6. Silverstein S, Frommer DA, Marx JA, Rosen P. Haloperidol in combative patients: a prospective study. Ann Emerg Med. 1986; 15:636. 7. McCarron MM, Schulze BW, Thompson GA, et al. Acute phencyclidine intoxication: clinical patterns, complications, and treatment. Ann Emerg Med. 1981;10:290.
