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INFLUENCE OF BOLUS DOSES OF PHENOPERIDINE ON INTRACRANIAL PRESSURE AND SYSTEMIC ARTERIAL PRESSURE IN TRAUMATIC COMA
Br. J. Anaesth. (1987), 59, 592-595
INFLUENCE OF BOLUS DOSES OF PHENOPERIDINE ON INTRACRANIAL PRESSURE AND SYSTEMIC ARTERIAL PRESSURE IN TRAUMATIC COMA
Narcotic analgesics are administered commonly to those patients in traumatic coma requiring mechanical ventilation—to provide analgesia (particularly in the presence of multiple injuries) and to suppress spontaneous, asynchronous ventilatory movements. Since the maintainance of cerebral perfusion pressure (CPP) is fundamental to successful management in such patients, the influence of narcotics on intracranial pressure (ICP) and mean arterial pressure (MAP) is of particular relevance. Although a number of investigations have suggested that narcotics have little effect on ICP (Barker et al., 1968; Fitch et al., 1969; Misfeldt et al.j 1976), these were performed on patients undergoing elective neurosurgical procedures, in many of whom ICP was normal, whereas in others intracranial hypertension was secondary to focal space-occupying lesions. Consequently, the results of these studies may not be directly applicable to patients with severe head injury. This view is supported by a recent case report which described significant increases in ICP following the administration of bolus doses of phenoperidine i.v. to a patient in traumatic coma (Grummitt and Goat, 1984). The purpose of this study was to examine further the influence of i.v. bolus doses of the narcotic analgesic phenoperidine on ICP, mean arterial pressure and cerebral perfusion pressure in head-injured patients.
R. M. BlNGHAM, B.SC., M.B., F.F.A.R.C.S.; C. J. HlNDS, M.B., M.R.C.P., F.F.A.R.CS.; Department of Anaesthesia and Intensive Care, St Bartholomew's Hospital, London EC1A 7BE. Accepted for Publication: August 7, 1986.
SUMMARY The effects of bolus doses of phenoperidine 1-2 mg i. v. either alone, or combined with pancuronium 2-4 mg, were investigated in seven patients in traumatic coma. Phenoperidine alone significantly reduced mean arterial pressure {MAP) by a mean (±SEM) of 13.2(±2.8) mm Hg. Overall there was no significant change in intracranial pressure (ICP) despite the decreases in MAP and, consequently, cerebral perfusion pressure (CPP) decreased (14.0±2.4 mm Hg) on all but one occasion. In some instances these decreases were considerable (maximum 38mmHg). Similar results were obtained when phenoperidine was combined with pancuronium. These findings suggest that the bolus administration of phenoperidine and probably other opiates should be avoided in traumatic coma.
PATIENTS AND METHODS
Patients Seven consecutive patients (two female) admitted to the Intensive Care Unit with severe head injury (Glasgow Coma Score < 8) were studied. Their ages were in the range 11-37 yr. Evacuation of intracranial haematoma was performed in three patients (one intxacerebral, one extradural, one subdural). Three had diffuse swelling and the remaining patient had predominantly left hemisphere oedema. Monitoring Indwelling Teflon cannulae were placed in a radial artery and in the right internal jugular vein
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
R. M. BINGHAM AND C. J. HINDS
PHENOPERIDINE AND ICP
Clinical management
All patients received intermittent positive pressure ventilation to maintain PaCOt between 3.4 and 4.7 kPa. Inspired oxygen concentration was adjusted to maintain arterial oxygen saturation greater than 90 %. Patients were sedated using a continuous i.v. infusion of etomidate (initially 5 ug kg"1 min"1) supplemented with bolus doses to control any acute increases in ICP, and before stimulating procedures. Phenoperidine 1-2 mg i.v. with or without pancuronium 2-4 mg i.v. was administered, if necessary, to prevent the patient resisting the ventilator. Mannitol 0.3 g kg"1 every 6 h was also used to control ICP. However, if on any occasion the ICP failed to decrease following the administration of mannitol, its use was discontinued. All but two patients received a dose of mannitol at some stage during their treatment and four required repeated administrations. Fluid intake was restricted to 5% dextrose 1 ml kg"1 h"1. Colloidal solutions (Haemaccel or plasma protein fraction) were administered, as required, to maintain the circulating fluid volume. Prophylactic anti-convulsant therapy (phenobarbitone 60 mg i.m. 8-hourly in adults) was given to all patients (supplemented with diazepam and phenytoin if seizures occurred). All events, drug administrations and procedures were noted on the 4-channel chart recording, which was continued for the duration of ICP monitoring (up to 7 days). The effects of bolus doses of phenoperidine (with or without pancuronium) on ICP and MAP were determined by retrospective analysis of the chart records. Analysis was restricted to those occasions when the bolus doses were not accompanied by the administration of any other drug nor by any stimulating procedure. Statistical comparisons were performed using the two-sample t test.
RESULTS
Bolus doses of phenoperidine, with or without pancuronium, induced significant decreases in MAP (mean(±SEM) = 16.6(±4.3)mmHg(P < 0.005) and 13.2( + 2.8)mmHg (P < 0.0001), respecTABLE I. Mean changes (±SEM) in MAP, ICP and CPP following bolus doses of phenoperidine(± pancuronium')
AMAP (mm Hg) AICP (mm Hg) ACPP (mm Hg)
Phenoperidine alone (n = 16)
Phenoperidine with pancuronium (n = 18)
-13.2 (±2.8)
-16.6 (±4.3)
+ 0.81 (±1.4)
+ 1.89 ( + 2.1)
-14.0 (±2.4)
-18.4 (±3.6)
TABLE II. Changes in MAP, ICP and CPP (mm Hg) following individual bolus closes of phenoperidine with and without pancuronium Change in MAP (mm Hg) Phenoperidine alone -13 -5 -14 -50 -13 -18 -5 -8 -8 0 -8 -10 -20 -13 -11 -15
Change in ICP (mm Hg)
0 7 11 -12 4 10 1 3 1 0 -1 -2 0 -2 -3 -4 Phenoperidine with pancuronium -7 1 1 7 .-4 -13 2 1 -30 -2 -25 -7 -65 -14 -49 -7 -25 -8 -17 1 -13 12 -5 22 -14 15 -20 11 -18 6 -3 0 -3 4 2 0
Change in CPP (mm Hg) -13 -13 -25 -38 -17 -28 -6 -11 -9 0 -7 -8 -20 -11 -8 -11 -8 6 -9 1 -28 -18 -51 -42 -17 -18 -25 -27 -29 -31 -24 -3 -7 -2
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
and used to monitor, respectively, arterial and central venous pressure
593
BRITISH JOURNAL OF ANAESTHESIA
594 40 CO
E o.
o
30 20 10 0
CO
150
X
100 Q_ <
50 0
100 r
~
10
s LL
u 5 0
DISCUSSION
In this study, the administration of phenoperidine virtually always resulted in a decrease in MAP. ICP did not decrease correspondingly; indeed, it was usually unchanged, or even increased, and 15 rrun cerebral perfusion pressure was, therefore, deFIG. 1. Examples of the effects of a phenoperidone bolus and creased. In this respect there was no difference an etomidate bolus on ICP and arterial pressure (AP) in the between the effects of phenoperidine alone or absence of external stimulation. The phenoperidine bolus is followed by an increase in ICP and moderate hypotension: phenoperidine combined with pancuronium. CPP decreases. An attempt to treat the increase in ICP with These results are in agreement with the observaetomidate was successful at the expense of marked hypotension tions of Grummitt and Goat (1984), who which resulted in a further reduction in CPP. Note the marked suggested that phenoperidine may actively indepression of the CFM (cerebral function monitor) associated crease cerebral blood flow (CBF), and therefore with the administration of etomidate. ICP, by inducing cerebral vasodilatation. The results of experimental studies of the effects tively) (table I). MAP decreased on 15 of 16 occasions following phenoperidine alone (on one of narcotic analgesics on CBF are conflicting and occasion MAP was unchanged) (table II), and 15 there are marked species differences (Nilsson and of 18 occasions following phenoperidine combined Ingvar, 1965; Michenfelder and Theye, 1971). with pancuronium. In this latter group MAP in- One human study, in which phenoperidine was creased slightly on two occasions and remained combined with droperidol, found no detectable effect of this combination on CBF (Barker et al., unchanged on a third. Despite the decreases in MAP, ICP increased 1968). Most clinical studies, however, have concenslightly in both groups (0.8(±1.4) mm Hg after phenoperidine alone and 1.9(±2.1) mm Hg after trated on the effects of narcotics on ICP. In phenoperidine combined with pancuronium). spontaneously breathing subjects given opiates,
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
200
[ Etomidate 6 ml Phenoperidine 1mg Pancuronium 2 mg
Seven of the 16 bolus doses of phenoperidine alone and 11 of the 18 bolus doses of phenoperidine combined with pancuronium were followed by an increase in ICP of between 1 and 22 mm Hg. As a result of these changes in ICP and MAP, CPP was reduced significantly overall by 14.0(±2.4) mm Hg after phenoperidine alone ( P < 0.0001) and by 18.4(±3.6) mm Hg after phenoperidine and pancuronium combined (P < 0.0001) (table I, fig. 1). CPP was unchanged on one occasion after the administration of phenoperidine alone, and on two occasions slight increases in CPP, secondary to unexplained increases in MAP, followed the administration of phenoperidine combined with pancuronium. All the remaining bolus doses of phenoperidine (with or without pancuronium) decreased CPP. In both groups very large decreases in CPP were occasionally identified (maximum of 38 mm Hg with phenoperidine alone, and 51 mmHg with phenoperidine and pancuronium combined). These were usually associated with marked hypotension (MAP decreased by 50 mm Hg and 65 mm Hg in the above examples). There were no significant differences between the changes in MAP, ICP or CPP between the two groups.
PHENOPERIDINE AND ICP
be a cerebral vasoconstrictor (Michenfelder and Theye, 1971). The explanation for the increases in ICP associated with more than half of the bolus doses of phenoperidine in our patients is uncertain. It is possible that, as Drs Grummitt and Goat suggest, phenoperidine results in active cerebral vasodilatation. Alternatively, however, cerebral vasodilatation may occur as an autoregulatory response to arterial hypotension, in which case cerebral blood flow might be maintained despite the reduction in CPP. Whatever the mechanism of the ICP changes, the arterial hypotension which almost always followed the administration of phenoperidine is likely to be detrimental in this group of patients. It is conceivable that analgesia would be better provided in such patients by the continuous infusion of an appropriate narcotic analgesic.
REFERENCES Barker, J., Harper, A. M., McDowall, D. G., Fitch, W., and Jennett, W. B. (1968). Cerebral blood flow, cerebrospinal fluid pressure and E.E.G. activity during neuroleptanalgesia induced with dehydrobenzperidol and phenoperidine. Br.J. Anaesth., 40, 143. Fitch, W., Barker, J., Jennett, W. B., and McDowall, D. G. (1969). The influence of neuroleptanalgesic drugs on cerebrospinal fluid pressure. Br. J. Anaesth., 41, 800. Grummitt, R. M., and Goat, V. A. (1984). Intracranial pressure after phenoperidine. Anaesthesia, 39, 565. Michenfelder, J. D., and Theye, R. A. (1971). Effects of fentanyl, droperidol and Innovar on canine cerebral metabolism and blood flow. Br. J. Anaesth., 43, 630. Misfeldt, B. B., Jorgensen, P. B., Spotoft, H., and Ronde, F. (1976). The effects of droperidol and fentanyl on intracranial pressure and cerebral perfusion pressure in neurosurgical patients. Br. J. Anaesth., 48, 963. Moss, E., Powell, D., Gibson, R. M., and McDowall, D. G. (1978). Effects of fentanyl on intracranial pressure and cerebral perfusion pressure during hypocapnia. Br. J. Anaesth., 50, 799. Nilsson, E., and Ingvar, D. H. (1965). Cerebral blood flow during neurolept-analgesia in the cat. Acta Anaesthesiol. Scand., 10, 47.
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
ICP is increased secondary to ventilatory depression and hypercapnia, but when the arterial carbon dioxide tension is maintained constant the results are variable. Fitch and colleagues (1969) found that the administration of fentanyl and dropendol to patients with or without intracranial hypertension significantly reduced ICP. In the former group, however, CPP was reduced as a consequence of associated arterial hypotension. In the same study there was no significant reduction in ICP following phenoperidine combined with dropendol in patients with normal CSF pathways. This finding led the authors to postulate that there was a difference between the effects of fentanyl and phenoperidine on CBF and cerebral metabolic rate. Similar results were obtained by Moss and co-workers (1978), who studied the combination of fentanyl and droperidol. Although the changes in ICP were small, CPP always decreased—on two occasions to less than 50 mm Hg. In contrast, Misfeldt's group found that fentanyl (also combined with droperidol) increased ICP in five of eight patients; CPP was again reduced in all patients (Misfeldt et al., 1976). Finally, Barker and colleagues (1968) found that CSF pressure was unchanged following the administration of phenoperidine and droperidol. These findings may not, however, be applicable to patients with severe head injuries, since they were all performed on patients with focal intracranial lesions before elective neurosurgical procedures. In many of these patients ICP was normal and intracranial compliance may have been sufficient to allow some increase in intra-cranial volume without change in ICP. Furthermore, the narcotics were commonly given following the induction of anaesthesia with a barbiturate and the institution of controlled ventilation, both of which are likely to have attenuated any subsequent increases in ICP. In addition, they were always given in combination with droperidol which is known to
595
INFLUENCE OF BOLUS DOSES OF PHENOPERIDINE ON INTRACRANIAL PRESSURE AND SYSTEMIC ARTERIAL PRESSURE IN TRAUMATIC COMA
Narcotic analgesics are administered commonly to those patients in traumatic coma requiring mechanical ventilation—to provide analgesia (particularly in the presence of multiple injuries) and to suppress spontaneous, asynchronous ventilatory movements. Since the maintainance of cerebral perfusion pressure (CPP) is fundamental to successful management in such patients, the influence of narcotics on intracranial pressure (ICP) and mean arterial pressure (MAP) is of particular relevance. Although a number of investigations have suggested that narcotics have little effect on ICP (Barker et al., 1968; Fitch et al., 1969; Misfeldt et al.j 1976), these were performed on patients undergoing elective neurosurgical procedures, in many of whom ICP was normal, whereas in others intracranial hypertension was secondary to focal space-occupying lesions. Consequently, the results of these studies may not be directly applicable to patients with severe head injury. This view is supported by a recent case report which described significant increases in ICP following the administration of bolus doses of phenoperidine i.v. to a patient in traumatic coma (Grummitt and Goat, 1984). The purpose of this study was to examine further the influence of i.v. bolus doses of the narcotic analgesic phenoperidine on ICP, mean arterial pressure and cerebral perfusion pressure in head-injured patients.
R. M. BlNGHAM, B.SC., M.B., F.F.A.R.C.S.; C. J. HlNDS, M.B., M.R.C.P., F.F.A.R.CS.; Department of Anaesthesia and Intensive Care, St Bartholomew's Hospital, London EC1A 7BE. Accepted for Publication: August 7, 1986.
SUMMARY The effects of bolus doses of phenoperidine 1-2 mg i. v. either alone, or combined with pancuronium 2-4 mg, were investigated in seven patients in traumatic coma. Phenoperidine alone significantly reduced mean arterial pressure {MAP) by a mean (±SEM) of 13.2(±2.8) mm Hg. Overall there was no significant change in intracranial pressure (ICP) despite the decreases in MAP and, consequently, cerebral perfusion pressure (CPP) decreased (14.0±2.4 mm Hg) on all but one occasion. In some instances these decreases were considerable (maximum 38mmHg). Similar results were obtained when phenoperidine was combined with pancuronium. These findings suggest that the bolus administration of phenoperidine and probably other opiates should be avoided in traumatic coma.
PATIENTS AND METHODS
Patients Seven consecutive patients (two female) admitted to the Intensive Care Unit with severe head injury (Glasgow Coma Score < 8) were studied. Their ages were in the range 11-37 yr. Evacuation of intracranial haematoma was performed in three patients (one intxacerebral, one extradural, one subdural). Three had diffuse swelling and the remaining patient had predominantly left hemisphere oedema. Monitoring Indwelling Teflon cannulae were placed in a radial artery and in the right internal jugular vein
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
R. M. BINGHAM AND C. J. HINDS
PHENOPERIDINE AND ICP
Clinical management
All patients received intermittent positive pressure ventilation to maintain PaCOt between 3.4 and 4.7 kPa. Inspired oxygen concentration was adjusted to maintain arterial oxygen saturation greater than 90 %. Patients were sedated using a continuous i.v. infusion of etomidate (initially 5 ug kg"1 min"1) supplemented with bolus doses to control any acute increases in ICP, and before stimulating procedures. Phenoperidine 1-2 mg i.v. with or without pancuronium 2-4 mg i.v. was administered, if necessary, to prevent the patient resisting the ventilator. Mannitol 0.3 g kg"1 every 6 h was also used to control ICP. However, if on any occasion the ICP failed to decrease following the administration of mannitol, its use was discontinued. All but two patients received a dose of mannitol at some stage during their treatment and four required repeated administrations. Fluid intake was restricted to 5% dextrose 1 ml kg"1 h"1. Colloidal solutions (Haemaccel or plasma protein fraction) were administered, as required, to maintain the circulating fluid volume. Prophylactic anti-convulsant therapy (phenobarbitone 60 mg i.m. 8-hourly in adults) was given to all patients (supplemented with diazepam and phenytoin if seizures occurred). All events, drug administrations and procedures were noted on the 4-channel chart recording, which was continued for the duration of ICP monitoring (up to 7 days). The effects of bolus doses of phenoperidine (with or without pancuronium) on ICP and MAP were determined by retrospective analysis of the chart records. Analysis was restricted to those occasions when the bolus doses were not accompanied by the administration of any other drug nor by any stimulating procedure. Statistical comparisons were performed using the two-sample t test.
RESULTS
Bolus doses of phenoperidine, with or without pancuronium, induced significant decreases in MAP (mean(±SEM) = 16.6(±4.3)mmHg(P < 0.005) and 13.2( + 2.8)mmHg (P < 0.0001), respecTABLE I. Mean changes (±SEM) in MAP, ICP and CPP following bolus doses of phenoperidine(± pancuronium')
AMAP (mm Hg) AICP (mm Hg) ACPP (mm Hg)
Phenoperidine alone (n = 16)
Phenoperidine with pancuronium (n = 18)
-13.2 (±2.8)
-16.6 (±4.3)
+ 0.81 (±1.4)
+ 1.89 ( + 2.1)
-14.0 (±2.4)
-18.4 (±3.6)
TABLE II. Changes in MAP, ICP and CPP (mm Hg) following individual bolus closes of phenoperidine with and without pancuronium Change in MAP (mm Hg) Phenoperidine alone -13 -5 -14 -50 -13 -18 -5 -8 -8 0 -8 -10 -20 -13 -11 -15
Change in ICP (mm Hg)
0 7 11 -12 4 10 1 3 1 0 -1 -2 0 -2 -3 -4 Phenoperidine with pancuronium -7 1 1 7 .-4 -13 2 1 -30 -2 -25 -7 -65 -14 -49 -7 -25 -8 -17 1 -13 12 -5 22 -14 15 -20 11 -18 6 -3 0 -3 4 2 0
Change in CPP (mm Hg) -13 -13 -25 -38 -17 -28 -6 -11 -9 0 -7 -8 -20 -11 -8 -11 -8 6 -9 1 -28 -18 -51 -42 -17 -18 -25 -27 -29 -31 -24 -3 -7 -2
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
and used to monitor, respectively, arterial and central venous pressure
593
BRITISH JOURNAL OF ANAESTHESIA
594 40 CO
E o.
o
30 20 10 0
CO
150
X
100 Q_ <
50 0
100 r
~
10
s LL
u 5 0
DISCUSSION
In this study, the administration of phenoperidine virtually always resulted in a decrease in MAP. ICP did not decrease correspondingly; indeed, it was usually unchanged, or even increased, and 15 rrun cerebral perfusion pressure was, therefore, deFIG. 1. Examples of the effects of a phenoperidone bolus and creased. In this respect there was no difference an etomidate bolus on ICP and arterial pressure (AP) in the between the effects of phenoperidine alone or absence of external stimulation. The phenoperidine bolus is followed by an increase in ICP and moderate hypotension: phenoperidine combined with pancuronium. CPP decreases. An attempt to treat the increase in ICP with These results are in agreement with the observaetomidate was successful at the expense of marked hypotension tions of Grummitt and Goat (1984), who which resulted in a further reduction in CPP. Note the marked suggested that phenoperidine may actively indepression of the CFM (cerebral function monitor) associated crease cerebral blood flow (CBF), and therefore with the administration of etomidate. ICP, by inducing cerebral vasodilatation. The results of experimental studies of the effects tively) (table I). MAP decreased on 15 of 16 occasions following phenoperidine alone (on one of narcotic analgesics on CBF are conflicting and occasion MAP was unchanged) (table II), and 15 there are marked species differences (Nilsson and of 18 occasions following phenoperidine combined Ingvar, 1965; Michenfelder and Theye, 1971). with pancuronium. In this latter group MAP in- One human study, in which phenoperidine was creased slightly on two occasions and remained combined with droperidol, found no detectable effect of this combination on CBF (Barker et al., unchanged on a third. Despite the decreases in MAP, ICP increased 1968). Most clinical studies, however, have concenslightly in both groups (0.8(±1.4) mm Hg after phenoperidine alone and 1.9(±2.1) mm Hg after trated on the effects of narcotics on ICP. In phenoperidine combined with pancuronium). spontaneously breathing subjects given opiates,
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
200
[ Etomidate 6 ml Phenoperidine 1mg Pancuronium 2 mg
Seven of the 16 bolus doses of phenoperidine alone and 11 of the 18 bolus doses of phenoperidine combined with pancuronium were followed by an increase in ICP of between 1 and 22 mm Hg. As a result of these changes in ICP and MAP, CPP was reduced significantly overall by 14.0(±2.4) mm Hg after phenoperidine alone ( P < 0.0001) and by 18.4(±3.6) mm Hg after phenoperidine and pancuronium combined (P < 0.0001) (table I, fig. 1). CPP was unchanged on one occasion after the administration of phenoperidine alone, and on two occasions slight increases in CPP, secondary to unexplained increases in MAP, followed the administration of phenoperidine combined with pancuronium. All the remaining bolus doses of phenoperidine (with or without pancuronium) decreased CPP. In both groups very large decreases in CPP were occasionally identified (maximum of 38 mm Hg with phenoperidine alone, and 51 mmHg with phenoperidine and pancuronium combined). These were usually associated with marked hypotension (MAP decreased by 50 mm Hg and 65 mm Hg in the above examples). There were no significant differences between the changes in MAP, ICP or CPP between the two groups.
PHENOPERIDINE AND ICP
be a cerebral vasoconstrictor (Michenfelder and Theye, 1971). The explanation for the increases in ICP associated with more than half of the bolus doses of phenoperidine in our patients is uncertain. It is possible that, as Drs Grummitt and Goat suggest, phenoperidine results in active cerebral vasodilatation. Alternatively, however, cerebral vasodilatation may occur as an autoregulatory response to arterial hypotension, in which case cerebral blood flow might be maintained despite the reduction in CPP. Whatever the mechanism of the ICP changes, the arterial hypotension which almost always followed the administration of phenoperidine is likely to be detrimental in this group of patients. It is conceivable that analgesia would be better provided in such patients by the continuous infusion of an appropriate narcotic analgesic.
REFERENCES Barker, J., Harper, A. M., McDowall, D. G., Fitch, W., and Jennett, W. B. (1968). Cerebral blood flow, cerebrospinal fluid pressure and E.E.G. activity during neuroleptanalgesia induced with dehydrobenzperidol and phenoperidine. Br.J. Anaesth., 40, 143. Fitch, W., Barker, J., Jennett, W. B., and McDowall, D. G. (1969). The influence of neuroleptanalgesic drugs on cerebrospinal fluid pressure. Br. J. Anaesth., 41, 800. Grummitt, R. M., and Goat, V. A. (1984). Intracranial pressure after phenoperidine. Anaesthesia, 39, 565. Michenfelder, J. D., and Theye, R. A. (1971). Effects of fentanyl, droperidol and Innovar on canine cerebral metabolism and blood flow. Br. J. Anaesth., 43, 630. Misfeldt, B. B., Jorgensen, P. B., Spotoft, H., and Ronde, F. (1976). The effects of droperidol and fentanyl on intracranial pressure and cerebral perfusion pressure in neurosurgical patients. Br. J. Anaesth., 48, 963. Moss, E., Powell, D., Gibson, R. M., and McDowall, D. G. (1978). Effects of fentanyl on intracranial pressure and cerebral perfusion pressure during hypocapnia. Br. J. Anaesth., 50, 799. Nilsson, E., and Ingvar, D. H. (1965). Cerebral blood flow during neurolept-analgesia in the cat. Acta Anaesthesiol. Scand., 10, 47.
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on July 10, 2015
ICP is increased secondary to ventilatory depression and hypercapnia, but when the arterial carbon dioxide tension is maintained constant the results are variable. Fitch and colleagues (1969) found that the administration of fentanyl and dropendol to patients with or without intracranial hypertension significantly reduced ICP. In the former group, however, CPP was reduced as a consequence of associated arterial hypotension. In the same study there was no significant reduction in ICP following phenoperidine combined with dropendol in patients with normal CSF pathways. This finding led the authors to postulate that there was a difference between the effects of fentanyl and phenoperidine on CBF and cerebral metabolic rate. Similar results were obtained by Moss and co-workers (1978), who studied the combination of fentanyl and droperidol. Although the changes in ICP were small, CPP always decreased—on two occasions to less than 50 mm Hg. In contrast, Misfeldt's group found that fentanyl (also combined with droperidol) increased ICP in five of eight patients; CPP was again reduced in all patients (Misfeldt et al., 1976). Finally, Barker and colleagues (1968) found that CSF pressure was unchanged following the administration of phenoperidine and droperidol. These findings may not, however, be applicable to patients with severe head injuries, since they were all performed on patients with focal intracranial lesions before elective neurosurgical procedures. In many of these patients ICP was normal and intracranial compliance may have been sufficient to allow some increase in intra-cranial volume without change in ICP. Furthermore, the narcotics were commonly given following the induction of anaesthesia with a barbiturate and the institution of controlled ventilation, both of which are likely to have attenuated any subsequent increases in ICP. In addition, they were always given in combination with droperidol which is known to
595