NIFEDIPINE IN RENAL COLIC Importance of plasma levels /20~dipine
serum
bevel { n g / m l ) . . . . . . . . . . . . . . . . . . . . . . . . . . .
I00 80 60
$ ÷
40
$ 20 0
........
i ............................ RESPONDERS
t" NON-RESPONDERS
GROUPS
edipine in relieving pain related to acute renal colic. T h e authors did not observe any significant difference in pain relief b e t w e e n nifedipine and placebo administration. We w o u l d l i k e to r e p o r t the r e s u l t s of a p r e l i m i n a r y open study t h a t was conducted in our e m e r g e n c y d e p a r t m e n t and i n c l u d e d d e t e r m i n a t i o n s of nifedipine levels in serum. After informed consent had been obtained, patients w h o w e r e d e v o i d of c o n t r a i n d i c a t i o n s to c a l c i u m c h a n n e l blockers and who presented to the ED w i t h renal colic
were asked to c h e w t w o capsules of nifedipine (20 mg) and t h e n to s w a l l o w it w i t h 150 m L water. T h e y were also asked to assess their pain s e v e r i t y (4, severe; 3, mild; 2, endurable; 1, n o pain) before and ten, 20, and 40 m i n u t e s after n i f e d i p i n e a d m i n i s t r a t i o n . T h e y w e r e c o n s i d e r e d a responder if t h e pain score decreased two points w i t h i n 20 minutes. N o n r e s p o n d e r s (after 20 minutes) were a d m i t t e d to the usual r e g i m e n of t r e a t m e n t . Nifedipine levels w e r e d e t e r m i n e d at 30 m i n u t e s . T w e l v e p a t i e n t s w i t h subseq u e n t l y c o n f i r m e d n e p h r o l i t h i a s i s were i n c l u d e d in t h e data analysis, The results of n i f e d i p i n e d e t e r m i n a t i o n s in serum are s h o w n in t h e Figure, w h i c h c l e a r l y d e m o n s t r a t e s t h a t higher levels were o b s e r v e d in responders. We thus suggest that the i n a b i l i t y of n i f e d i p i n e to relieve renal colic in some patients m a y be r e l a t e d to an erratic absorption a n d ' to the v a r i a b i l i t y in p l a s m a levels. We conclude that the unreliable effect of n i f e d i p i n e precludes a routine clinical use in this painful c o n d i t i o n .
P Lheureux, M D R Askenasi, MD, PhD Emergency Department D Gangi, MD Clinical Pharmacology Erasme University Hospital Brussels, Belgium
Aneurysm Alert To the Editor: Dr F o n t a n a r o s a , in his article, " R e c o g n i t i o n of Subarachnoid H e m o r r h a g e " [November 1989;18:1199-1205], is correct in d i r e c t i n g a t t e n t i o n to t h e w a r n i n g h e a d a c h e t h a t occurs in about one half of cases of intracranial saccular a n e u r y s m shortly before rupture. T h e challenge facing t h e e m e r g e n c y p h y s i c i a n e v a l u a t i n g a p a t i e n t w i t h headache is recognizing an a n e u r y s m as the cause of the headache. Surgical a t t a c k on the u n r u p t u r e d lesion results in a generally excellent outcome, I, 2 b u t if the a n e u r y s m ruptures, the overall m o r t a l i t y is about 50%. A c o m p u t e d t o m o g r a p h y (CT) scan perhaps followed by a l u m b a r puncture, looking for blood in the subarachnoid space, is r e c o m m e n d e d in t h e literature3A to evaluate the w a r n i n g headache; this has become the practice of m a n y e m e r g e n c y p h y s i c i a n s . However, a n e g a t i v e u n e n h a n c e d CT scan and a negative l u m b a r p u n c t u r e do n o t exclude saccular a n e u r y s m as the cause of the p a t i e n t ' s s y m p t o m s . T h e w a r n i n g headache is n o t necessarily due to leakage of b l o o d b u t m a y r e s u l t from h e m o r r h a g e i n t o or s u d d e n tearing and expansion of the still i n t a c t a n e u r y s m wall. S y m p t o m s also could result from cortical i s c h e m i a due to spasm of the involved artery. As D a y and R a s k i n 5 have emphasized, absence of blood does n o t exclude a sympt o m a t i c aneurysm. E m e r g e n c y c o n t r a s t - e n h a n c e d CT scan w i t h m u l t i p l e t h i n cuts (CECT/MTC) through the sella is a t e c h n i q u e that should detect m o s t saccular a n e u r y s m s of the circle 19:7 July 1990
of Willis. Twelve years ago, Katada et al 6 reported successful v i s u a l i z a t i o n b y t h i s m e t h o d of 27% of a n e u r y s m s smaller than 5 m m , 70% of those 5 to 10 m m , and all a n e u r y s m s larger t h a n 10 r a m . More recently, Schmid and associates 7 used C E C T / M T C to d e m o n s t r a t e 74 of 76 cons e c u t i v e a n g i o g r a p h i c a l l y or a u t o p s y - p r o v e n i n t r a c r a n i a l aneurysms d o w n to 3 m m in diameter. Other groupsS, 9 also have described the t e c h n i q u e and confirm its usefulness in detecting u n r u p t u r e d aneurysms. T h e objective in the e m e r g e n c y e v a l u a t i o n of the pat i e n t w i t h headache s h o u l d be the direct v i s u a l i z a t i o n of the a n e u r y s m itself. We therefore r e c o m m e n d that such patients be regarded as p o s s i b l y harboring an expanding or tearing cerebral a n e u r y s m and t h a t they be sent to t h e CT laboratory for e m e r g e n c y C E C T / M T C .
Merrill A Cohen, MD Ronald S Benenson, MD York Hospital York, Pennsylvania 1. Mount LA, Brisman R: Treatment of multiple and asymptomatic aneurysms, in Schmidek Hid, Sweet WH [eds): Current Techniquesin Operative Neurosurgery. New York, Grune & Stratton, 1982, vol 2, p 765-769. 2. Wirth FP, Laws ER Jr, Piepgras D, et al: Surgical treatment of incidental intracranial aneurysms. Neurosurgery 1983;12:507-5tl. 3. Adams HP, Jergenson DE), Kassell NF, et al: Pitfalls in the recognition of subarachnoid hemorrhage. JAMA 1980;244:794-796.
Annals of Emergency Medicine
842/159
CORRESPONDENCE
4. LeblancR: The minor leak precedingsubarachnoidhemorrhage. J Neurosurg 1987;66:35-39. 5. Day JW, Raskin NH: Thunderclapheadache: Symptoms of unruptured cerebral aneurysm. Lancet 1986;2:1247-1248. 6. Katada K, Kanno T, Sano H, et al: CT in evaluation of the circle of willis. Neuroradiology 1978;16:337-339. 7. SchmidUD, Steiger HJ, Huber P: Accuracyof high resolution computed
tomography in direct diagnosis of cerebral aneurysms. Neuroradiology 1987;29:152-159. 8. Asari S, Satoh T, Sakurai M, et al: Delineation of unruptured cerebral aneurysms by computerized angiotomography. J Neurosurg 1982~57: 527-534. 9. YamamotoY, Asari S, Sunami N, et al: Computed angiotomographyof unruptured cerebral aneurysms. J Comput Assisted Tomogr 1986;10: 21-27.
Managed Care Plans & Denial of Care To the Editor: In the J a n u a r y issue, Shaw and colleagues [1990;19: 59-62[ describe w i t h r e m a r k a b l e candor w h a t h a p p e n e d w h e n their emergency d e p a r t m e n t conspired with a m a n aged care plan to deny ED care to indigent "plan" patients who presented requesting care but the plan's "gatekeeper" physician refused to authorize the visit. Predictably, the experience (particularly for the patients) was not good. To their credit, the managers of this ED reversed their policy and n o w "no longer deny care i n the emergency departm e n t to c h i l d r e n " w h e n the m a n a g e d care plan's gatekeeping physician denies authorization for the visit. It is i m p o r t a n t to r e m e m b e r that the "gatekeepers" for managed care plans cannot deny patients care in the ED. The gatekeepers can deny authorization for care, which m e a n s that they can deny payment, b u t only we can deny care to patients. It has always been a moral obligation and n o w is a legal obligation for EDs to provide, for every patient, at least that level of evaluation that is adequate to determine that no "emergency" exists. To reliably do so requires both a n u r s i n g assessment and an evaluation by a physician. C o m m o n sense demands that an adequate record of this interaction be made. By the time one does all this, one m i g h t as well just see the patient. This calculation is particularly c o n v i n c i n g w h e n one factors in the lia-
bility risk that will accrue w h e n (inevitably) a triage error is made and someone who needs care is denied it. In our department, we take the approach that the discussion regarding authorization for p a y m e n t for ED care is a matter to be settled between the managed care plan and the subscriber. O u r p e r s o n n e l will m a k e the t e l e p h o n e call and place the subscriber i n c o n t a c t w i t h the gatekeeper. If after talking with the patient or parent the gatekeeper denies authorization, we make it crystal clear to the patient that we will not deny t h e m care, but that on the contrary we will be pleased to see them. I r e c o m m e n d this approach as the most appropriate for EDs to follow. It has long been a c o n t e n t i o n of emergency physicians that the list of valid definitions of an emergency m u s t include situations i n which the patient feels a need for prompt evaluation and t r e a t m e n t for some sympt o m that he or she finds alarming. We should stick to that and not change our principles with the financial winds.
Marshall T Morga±l, M D Emergency Medicine Center UCLA Medical Center Los Angeles
Opioid Action of Analgesic Nitrous Oxide To the Editor: I read w i t h interest "Nitrous Oxide Analgesia in a Pediatric Emergency D e p a r t m e n t " [February 1989;18:177-181[ by G a m i s et al and agree totally w i t h their c o n t e n t i o n that physicians who use this technique should, like dentists, be specifically trained for the technique of n i t r o u s oxide analgesia. However, these authors also state in their article that "To date, its m e c h a n i s m of action r e m a i n s unk n o w n . " There is n o w considerable evidence that n i t r o u s oxide analgesia is a m u l t i p o t e n t opioid receptor agonist, 1,2 w h i c h like m o r p h i n e also acts by the release of endogenous opioid system agonists.1 From b i n d i n g studies it has been shown to act directly at m u 3,4 and delta sites1, 5 with evidence for actions at kappa,~,2, 6 sigma, l,2,6 and epsilon z sites possibly by the release of e n d o g e n o u s opioid agonists. From the work quoted above it would seem that the analgesic I and emetic 8 actions of nitrous oxide analgesia are 160/843
mediated by interactions with the endogenous opioid system. Mark A Gillman South African Brain Research Institute Johannesburg 1. Gilhnan MA: Analgesic(subanesthetic)nitrous oxide interacts with the endogenous opioid system: A review of the evidence. Life Sei 1986; 39:1209-1211. 2. Gillman MA: Nitrous oxide an opioid addictive agent. Am J Med 1986;81:97-102. 3. Daras C, Cantrill RC, Gilhnan MA: 3 (H) Naloxone displacement:Evidence for nitrous oxide as opioid receptor agonist. Eur J Pharmacol 1983;89:177-t78. 4. Ori C, Ford-RiceF, LondonED: Effects of nitrous oxide and halothane on mu and kappa opioid receptors in guinea-pig brain. Anesthesiology 1989;70:541-544.
Annals of Emergency Medicine
19:7 July 1990
serum
bevel { n g / m l ) . . . . . . . . . . . . . . . . . . . . . . . . . . .
I00 80 60
$ ÷
40
$ 20 0
........
i ............................ RESPONDERS
t" NON-RESPONDERS
GROUPS
edipine in relieving pain related to acute renal colic. T h e authors did not observe any significant difference in pain relief b e t w e e n nifedipine and placebo administration. We w o u l d l i k e to r e p o r t the r e s u l t s of a p r e l i m i n a r y open study t h a t was conducted in our e m e r g e n c y d e p a r t m e n t and i n c l u d e d d e t e r m i n a t i o n s of nifedipine levels in serum. After informed consent had been obtained, patients w h o w e r e d e v o i d of c o n t r a i n d i c a t i o n s to c a l c i u m c h a n n e l blockers and who presented to the ED w i t h renal colic
were asked to c h e w t w o capsules of nifedipine (20 mg) and t h e n to s w a l l o w it w i t h 150 m L water. T h e y were also asked to assess their pain s e v e r i t y (4, severe; 3, mild; 2, endurable; 1, n o pain) before and ten, 20, and 40 m i n u t e s after n i f e d i p i n e a d m i n i s t r a t i o n . T h e y w e r e c o n s i d e r e d a responder if t h e pain score decreased two points w i t h i n 20 minutes. N o n r e s p o n d e r s (after 20 minutes) were a d m i t t e d to the usual r e g i m e n of t r e a t m e n t . Nifedipine levels w e r e d e t e r m i n e d at 30 m i n u t e s . T w e l v e p a t i e n t s w i t h subseq u e n t l y c o n f i r m e d n e p h r o l i t h i a s i s were i n c l u d e d in t h e data analysis, The results of n i f e d i p i n e d e t e r m i n a t i o n s in serum are s h o w n in t h e Figure, w h i c h c l e a r l y d e m o n s t r a t e s t h a t higher levels were o b s e r v e d in responders. We thus suggest that the i n a b i l i t y of n i f e d i p i n e to relieve renal colic in some patients m a y be r e l a t e d to an erratic absorption a n d ' to the v a r i a b i l i t y in p l a s m a levels. We conclude that the unreliable effect of n i f e d i p i n e precludes a routine clinical use in this painful c o n d i t i o n .
P Lheureux, M D R Askenasi, MD, PhD Emergency Department D Gangi, MD Clinical Pharmacology Erasme University Hospital Brussels, Belgium
Aneurysm Alert To the Editor: Dr F o n t a n a r o s a , in his article, " R e c o g n i t i o n of Subarachnoid H e m o r r h a g e " [November 1989;18:1199-1205], is correct in d i r e c t i n g a t t e n t i o n to t h e w a r n i n g h e a d a c h e t h a t occurs in about one half of cases of intracranial saccular a n e u r y s m shortly before rupture. T h e challenge facing t h e e m e r g e n c y p h y s i c i a n e v a l u a t i n g a p a t i e n t w i t h headache is recognizing an a n e u r y s m as the cause of the headache. Surgical a t t a c k on the u n r u p t u r e d lesion results in a generally excellent outcome, I, 2 b u t if the a n e u r y s m ruptures, the overall m o r t a l i t y is about 50%. A c o m p u t e d t o m o g r a p h y (CT) scan perhaps followed by a l u m b a r puncture, looking for blood in the subarachnoid space, is r e c o m m e n d e d in t h e literature3A to evaluate the w a r n i n g headache; this has become the practice of m a n y e m e r g e n c y p h y s i c i a n s . However, a n e g a t i v e u n e n h a n c e d CT scan and a negative l u m b a r p u n c t u r e do n o t exclude saccular a n e u r y s m as the cause of the p a t i e n t ' s s y m p t o m s . T h e w a r n i n g headache is n o t necessarily due to leakage of b l o o d b u t m a y r e s u l t from h e m o r r h a g e i n t o or s u d d e n tearing and expansion of the still i n t a c t a n e u r y s m wall. S y m p t o m s also could result from cortical i s c h e m i a due to spasm of the involved artery. As D a y and R a s k i n 5 have emphasized, absence of blood does n o t exclude a sympt o m a t i c aneurysm. E m e r g e n c y c o n t r a s t - e n h a n c e d CT scan w i t h m u l t i p l e t h i n cuts (CECT/MTC) through the sella is a t e c h n i q u e that should detect m o s t saccular a n e u r y s m s of the circle 19:7 July 1990
of Willis. Twelve years ago, Katada et al 6 reported successful v i s u a l i z a t i o n b y t h i s m e t h o d of 27% of a n e u r y s m s smaller than 5 m m , 70% of those 5 to 10 m m , and all a n e u r y s m s larger t h a n 10 r a m . More recently, Schmid and associates 7 used C E C T / M T C to d e m o n s t r a t e 74 of 76 cons e c u t i v e a n g i o g r a p h i c a l l y or a u t o p s y - p r o v e n i n t r a c r a n i a l aneurysms d o w n to 3 m m in diameter. Other groupsS, 9 also have described the t e c h n i q u e and confirm its usefulness in detecting u n r u p t u r e d aneurysms. T h e objective in the e m e r g e n c y e v a l u a t i o n of the pat i e n t w i t h headache s h o u l d be the direct v i s u a l i z a t i o n of the a n e u r y s m itself. We therefore r e c o m m e n d that such patients be regarded as p o s s i b l y harboring an expanding or tearing cerebral a n e u r y s m and t h a t they be sent to t h e CT laboratory for e m e r g e n c y C E C T / M T C .
Merrill A Cohen, MD Ronald S Benenson, MD York Hospital York, Pennsylvania 1. Mount LA, Brisman R: Treatment of multiple and asymptomatic aneurysms, in Schmidek Hid, Sweet WH [eds): Current Techniquesin Operative Neurosurgery. New York, Grune & Stratton, 1982, vol 2, p 765-769. 2. Wirth FP, Laws ER Jr, Piepgras D, et al: Surgical treatment of incidental intracranial aneurysms. Neurosurgery 1983;12:507-5tl. 3. Adams HP, Jergenson DE), Kassell NF, et al: Pitfalls in the recognition of subarachnoid hemorrhage. JAMA 1980;244:794-796.
Annals of Emergency Medicine
842/159
CORRESPONDENCE
4. LeblancR: The minor leak precedingsubarachnoidhemorrhage. J Neurosurg 1987;66:35-39. 5. Day JW, Raskin NH: Thunderclapheadache: Symptoms of unruptured cerebral aneurysm. Lancet 1986;2:1247-1248. 6. Katada K, Kanno T, Sano H, et al: CT in evaluation of the circle of willis. Neuroradiology 1978;16:337-339. 7. SchmidUD, Steiger HJ, Huber P: Accuracyof high resolution computed
tomography in direct diagnosis of cerebral aneurysms. Neuroradiology 1987;29:152-159. 8. Asari S, Satoh T, Sakurai M, et al: Delineation of unruptured cerebral aneurysms by computerized angiotomography. J Neurosurg 1982~57: 527-534. 9. YamamotoY, Asari S, Sunami N, et al: Computed angiotomographyof unruptured cerebral aneurysms. J Comput Assisted Tomogr 1986;10: 21-27.
Managed Care Plans & Denial of Care To the Editor: In the J a n u a r y issue, Shaw and colleagues [1990;19: 59-62[ describe w i t h r e m a r k a b l e candor w h a t h a p p e n e d w h e n their emergency d e p a r t m e n t conspired with a m a n aged care plan to deny ED care to indigent "plan" patients who presented requesting care but the plan's "gatekeeper" physician refused to authorize the visit. Predictably, the experience (particularly for the patients) was not good. To their credit, the managers of this ED reversed their policy and n o w "no longer deny care i n the emergency departm e n t to c h i l d r e n " w h e n the m a n a g e d care plan's gatekeeping physician denies authorization for the visit. It is i m p o r t a n t to r e m e m b e r that the "gatekeepers" for managed care plans cannot deny patients care in the ED. The gatekeepers can deny authorization for care, which m e a n s that they can deny payment, b u t only we can deny care to patients. It has always been a moral obligation and n o w is a legal obligation for EDs to provide, for every patient, at least that level of evaluation that is adequate to determine that no "emergency" exists. To reliably do so requires both a n u r s i n g assessment and an evaluation by a physician. C o m m o n sense demands that an adequate record of this interaction be made. By the time one does all this, one m i g h t as well just see the patient. This calculation is particularly c o n v i n c i n g w h e n one factors in the lia-
bility risk that will accrue w h e n (inevitably) a triage error is made and someone who needs care is denied it. In our department, we take the approach that the discussion regarding authorization for p a y m e n t for ED care is a matter to be settled between the managed care plan and the subscriber. O u r p e r s o n n e l will m a k e the t e l e p h o n e call and place the subscriber i n c o n t a c t w i t h the gatekeeper. If after talking with the patient or parent the gatekeeper denies authorization, we make it crystal clear to the patient that we will not deny t h e m care, but that on the contrary we will be pleased to see them. I r e c o m m e n d this approach as the most appropriate for EDs to follow. It has long been a c o n t e n t i o n of emergency physicians that the list of valid definitions of an emergency m u s t include situations i n which the patient feels a need for prompt evaluation and t r e a t m e n t for some sympt o m that he or she finds alarming. We should stick to that and not change our principles with the financial winds.
Marshall T Morga±l, M D Emergency Medicine Center UCLA Medical Center Los Angeles
Opioid Action of Analgesic Nitrous Oxide To the Editor: I read w i t h interest "Nitrous Oxide Analgesia in a Pediatric Emergency D e p a r t m e n t " [February 1989;18:177-181[ by G a m i s et al and agree totally w i t h their c o n t e n t i o n that physicians who use this technique should, like dentists, be specifically trained for the technique of n i t r o u s oxide analgesia. However, these authors also state in their article that "To date, its m e c h a n i s m of action r e m a i n s unk n o w n . " There is n o w considerable evidence that n i t r o u s oxide analgesia is a m u l t i p o t e n t opioid receptor agonist, 1,2 w h i c h like m o r p h i n e also acts by the release of endogenous opioid system agonists.1 From b i n d i n g studies it has been shown to act directly at m u 3,4 and delta sites1, 5 with evidence for actions at kappa,~,2, 6 sigma, l,2,6 and epsilon z sites possibly by the release of e n d o g e n o u s opioid agonists. From the work quoted above it would seem that the analgesic I and emetic 8 actions of nitrous oxide analgesia are 160/843
mediated by interactions with the endogenous opioid system. Mark A Gillman South African Brain Research Institute Johannesburg 1. Gilhnan MA: Analgesic(subanesthetic)nitrous oxide interacts with the endogenous opioid system: A review of the evidence. Life Sei 1986; 39:1209-1211. 2. Gillman MA: Nitrous oxide an opioid addictive agent. Am J Med 1986;81:97-102. 3. Daras C, Cantrill RC, Gilhnan MA: 3 (H) Naloxone displacement:Evidence for nitrous oxide as opioid receptor agonist. Eur J Pharmacol 1983;89:177-t78. 4. Ori C, Ford-RiceF, LondonED: Effects of nitrous oxide and halothane on mu and kappa opioid receptors in guinea-pig brain. Anesthesiology 1989;70:541-544.
Annals of Emergency Medicine
19:7 July 1990
