503789
research-article2013
AOPXXX10.1177/1060028013503789Annals of Pharmacotherapy
Article
Sustained Hypotension Following Intravenous Metoclopramide
Annals of Pharmacotherapy XX(X) 1–4 © The Author(s) 2013 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1060028013503789 aop.sagepub.com
Tammy T. Nguyen, PharmD1 and Renee M. Petzel Gimbar, PharmD1
Abstract Objective: To report a case of sustained hypotension associated with the use of intravenous metoclopramide. Case Summary: A 50-year-old woman developed a hypotensive episode lasting approximately 90 minutes after the administration intravenous metoclopramide for the treatment of a migraine. The patient presented to the emergency department after she woke up with a severe headache that was much worse than her normal migraine headaches. Her past medical history included migraines, diabetes type 2, hypertension, and hyperlipidemia. Fifteen minutes after the administration of intravenous metoclopramide 10 mg, the patient’s systolic blood pressure decreased from 138 to 84 mmHg (a mean arterial pressure decrease of 40.7 mmHg). The patient was given 1 L of intravenous NaCl 0.9% that had minimal effect on blood pressure. The patient did not reapproach her baseline systolic blood pressure until 90 minutes after the metoclopramide administration when it was measured at 138 mmHg. Subsequent contrast tomography of the head was negative and the patient’s headache was successfully treated with butalbital/acetaminophen/caffeine. The patient was discharged home the same day. Discussion: There are few published case reports of metoclopramide-induced hypotension in the current literature. Of those published, all showed transient hypotension with metoclopramide, lasting seconds to minutes. An objective causality assessment for drug-associated adverse drug reaction showed metoclopramide as a probable cause of the patient’s hypotension (Naranjo score of 5). In this case, several indicators of metoclopramide induced hypotension were evident, including the timing of the hypotension after drug administration and the lack of any other possible causes of hypotension. This is the first published case report of sustained hypotension due to intravenous metoclopramide. Conclusion: Intravenous metoclopramide may cause sustained episodes of hypotension. Keywords Metoclopramide induced hypotension Received August 13, 2013; revised MONTH XX, XXXX; Accepted MONTH XX, XXXX.
Introduction Metoclopramide is a 4-amino-5-chloro-2-methoxy-N-(2diethyl-aminoethyl) benzamide that is structurally related to procainamide, but differs by its reported negligible cardiac effects.1 It blocks dopamine and serotonin receptors in the chemoreceptor trigger zone, in addition to enhancing the effects of acetylcholine in the upper gastrointestinal tract, promoting gastric motility. Because of its various mechanisms, metoclopramide is considered a therapeutic mainstay in the emergency department (ED) for the treatment of migraines with patients reporting decreased pain and nausea/vomiting and minimal safety concerns.2 The most common adverse effects include drowsiness and dystonic reactions. However, there has been limited information concerning the potential cardiovascular effects of metoclopramide. In this case report, we present a patient treated
with metoclopramide 10 mg slow intravenous push (IVP) over 3 to 5 minutes who experienced an episode of sustained hypotension lasting approximately 90 minutes that was minimally responsive to fluids.
Case Report A 50-year-old Caucasian woman (height 165.1 cm, weight 102.04 kg) with a past medical history of transient ischemic 1
University of Illinois Hospital and Health Sciences System, Chicago, IL, USA Corresponding Author: Renee Petzel Gimbar, Clinical Assistant Professor, Department of Pharmacy Practice, University of Illinois College of Pharmacy, 833 S. Wood Street (RM 164, MC 886), Chicago, IL 60612, USA. Email: [email protected]
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
2
Annals of Pharmacotherapy XX(X)
Table 1. Vital Signs and Medications Administered. Date/Time
BP (mmHg)
MAP (mmHg)
Pulse (beats/min)
RR (breaths/min)
09/25 09:58 09/25 10:19 09/25 10:28 09/25 11:00
128/69 171/88 149/82
88.7 115.7 104.3
114 110 105
20 18 16
09/25 11:04 09/25 11:16 09/25 11:49 09/25 12:31 09/25 12:36
138/84 84/50 92/55 138/78
102 61.3 67.3 98
103 109 88 82
16 18 16 18
Medications Diphenhydramine 25 mg PO ξ1 Metoclopramide 10 mg IV ξ1 NaCl 0.9% 1000 mL bolus started NaCl 0.9% 1000 mL bolus completed Butalbital/acetaminophen/caffeine 2 tabs PO ξ1
Abbreviations: BP, blood pressure; MAP, mean arterial pressure; RR, respiratory rate; PO, per oral; IV, intravenous.
attack (2003), migraines, diabetes, hypertension, and hyperlipidemia presented to the ED at 10 AM with complaints of worsening headache for 2 days. Patient stated that the morning of ED presentation the headache became more severe than her normal migraine. Her medications included benazepril 40 mg orally (PO) daily, calcium and vitamin D supplementation, clopidogrel 75 mg PO daily, insulin glargine 90 units subcutaneously (SC) twice a day, insulin lispro 50 units SC 3 times a day before meals, levothyroxine 300 mcg PO daily, metformin 1000 mg PO twice a day, paroxetine 40 mg PO daily, and simvastatin 40 mg PO before bedtime. The patient stated she took the morning dose of her medications at 8 am before coming into the ED. She denied any recent changes in medications (dose or timing), or taking any other prescription, over the counter, or herbal medications. Patient stated that she was adherent to her medication. In the ED, all labs, including basic metabolic panel, liver function tests, complete blood cell count, and cardiac enzymes were all within normal limits or negative, except for a blood glucose of 266 mg/dL. Physical exam showed she was alert and oriented to person, place, and time, normal motor strength in all extremities. Initial electrocardiogram showed sinus tachycardia with a ventricular rate of 110 beats/min, QRS of 46 ms, and QTc of 465 ms. No further electrocardiograms were ordered in the ED. As migraine was high on the differential, the patient was treated with metoclopramide 10 mg slow IVP over 3 to 5 minutes and diphenhydramine 25 mg PO once 1 hour after ED presentation. Fifteen minutes after the patient received the metoclopramide, her blood pressure (BP) unexpectedly dropped from 138/84 to 84/50 mmHg, a mean arterial pressure decrease of 40%, and she had a new complaint of light headedness (see Table 1). An intravenous bolus of NaCl 0.9% 1000 mL was run wide open over 30 minutes with minimal effect. A contrast tomography scan of the head was negative for any acute intracranial process. The patient’s BP returned to normal approximately 90 minutes later when it increased to 138/78 mmHg.
After the resolution of her hypotension, the patient’s headache persisted. As a result, she was treated with butalbital/acetaminophen/caffeine 2 tabs PO one time only resulting in complete resolution of her headache. Patient was discharged from the ED the same day with a prescription for butalbital/acetaminophen/caffeine.
Discussion As previously mentioned, the evidence supporting metoclopramide induced hypotension is scarce. Search terms in PubMed such as “metoclopramide induced hypotension” and “metoclopramide AND hypotension” resulted in only 4 published reports of metoclopramide-induced reductions of blood pressure.3-6 The first case published by Park3 in 1978 describes 4 patients undergoing surgery for repair of a ruptured intracranial aneurysm. Patients were being administered metoclopramide 10 mg IVP one time for prophylaxis of postoperative emesis. After administration, patients experienced a mean arterial pressure decrease of 10 to 30 mmHg and an increase in heart rate (HR) of 2 to 7 beats/min without normalization for as long as 100 seconds. Central venous pressure decreased in 1 patient, remained unchanged in the other 2 patients, and was unknown in the fourth. This case study led Park4 to look at metoclopramide’s cardiovascular effect in 6 healthy, conscious volunteers. The trial was double blind, where volunteers were given metoclopramide 10 mg IVP or 10 mL of normal saline IV over a period of 15 seconds. None of the volunteers saw a change in BP or HR with placebo. However, when 10 mg of metoclopramide was given intravenously, all patients saw a decrease in systolic BP ranging from 5 to 15 mmHg and a HR increase of 8 to 30 beats per minute, which normalized within 90 seconds. Park was not the only author to see this transient hemodynamic change associated with metoclopramide. A case series of 16 consecutive patients, undergoing various elective neurosurgical operations, found that patients who
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
3
Nguyen and Petzel Gimbar received metoclopramide 10 mg IVP over a period of 10 seconds had an average SBP drop of 22% over 44 seconds with normalization occurring within 96 seconds.5 The mechanism of metoclopramide-induced hypotension is unknown. Park3 postulated that because of its similar structure to the antiarrhythmic procainamide, metoclopramide may result in both cardiac depression and peripheral vasodilation. Hughes6 actually found metoclopramide as a possible cause of a dysrhythmia in a previously healthy 40-year-old patient who was anaesthetized for a hysterectomy. After receiving metoclopramide 10 mg IVP over 10 seconds for postoperative emesis prophylaxis, the patient developed bigeminy with a heart rate of 44 beats/min and an unmeasurable BP. Per operating room reports, the patient’s wound also stopped oozing blood. However, when atropine 0.6 mg IVP was administered, the patient had restoration to normal sinus rhythm within 30 seconds with a BP of 110/70 mmHg and her wound began bleeding profusely again. Hughes’s case provides further evidence that metoclopramide has a widely unrecognized cardiovascular effect. The number of published metoclopramide-induced hypotension case reports is small and encompasses only a limited number of patients.3-6 In addition, all these reports were published in the 1970s to 1980s when the rapid administration of metoclopramide over 10 to 15 seconds was widely accepted. In our ED, metoclopramide is administered slow IVP over 3 to 5 minutes to minimize possible cardiovascular and musculoskeletal adverse effects. This is comparable to the package insert recommendation of 1 to 2 minutes.7 It is possible that previous reports of metoclopramide-induced hypotension may reflect the fast administration rate. This case report is the first describing sustained, transient hypotension due to metoclopramide reported in the literature. Our patient experienced a systolic BP drop of 40 to 50 mmHg with symptoms of hypotension (new onset lightheadedness) lasting for 90 minutes. Other possible etiologies for the patient’s hypotension were investigated. No reports of oral diphenhydramine-induced hypotension could be found, patient denied any recent changes to her home medications, and labs did not show any signs of dehydration. A drug interaction check found that metoclopramide and paroxetine in combination could result in neuroleptic malignant hyperthermia and in turn autonomic instability.7,8 However, the patient was never found to have altered mental status, hyperthermia, or muscle cramping/tremors while in the ED. Although diabetes has been reported to cause orthostatic hypotension through autonomic neuropathy, this patient’s hypotension was persistent and not positional.9 Finally, it should also be noted that migraines themselves may cause hypotension; however, patient denied ever having previous episodes of lightheadedness. Because of the above findings, metoclopramide was considered the most likely culprit of this patient’s hypotensive episode. The
Naranjo adverse drug reaction probability scale was used with a calculated score of 5, showing that metoclopramide was a probable cause of the patient’s sustained hypotension.10 Potential score variability based on clinician view of subjective information may result in +/-1 of the Naranjo score. Resultant scores still show metoclopramide as a probable or possible cause of the patient’s hypotension. As there is no antidotal therapy available for the reversal of metoclopramide, 1000 mL of normal saline IV was the only treatment administered for the patient’s hypotension in the ED, with minimal response. No vasopressors were initiated because the patient’s only symptom was lightheadedness, her systolic BP remained stable in the 80 mmHg range, and her tachycardia of 109 beats/min resolved to the 80s despite the sustained hypotensive episode. The patient maintained baseline mental status, was alert and oriented to person, place, and time, and considered stable. In the future, we do not advocate treatment beyond fluid boluses because of the transient nature of the hypotension unless the patient has clinically significant signs and symptoms, including, but not limited to, altered mental status, cardiac abnormalities, and poor peripheral perfusion. The underreporting of metoclopramide-induced hypotension in the literature may be due to the quick and spontaneous resolution of hypotension within 90 seconds as previously reported. It is also questionable whether these drops in BP are normally clinically significant. In the light of this case and previous literature, we propose that caution be used when metoclopramide is administered via slow IVP in the ED, especially in patients who may already be at risk for hypotension. Acknowledgment The authors would like to thank John Williams, MD, FACEP, at the University of Illinois Hospital and Health Sciences System.
Declaration of Conflicting Interests The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
References 1. Metoclopramide. DRUGDEX System [database online]. Greenwood Village, CO: Thomson Reuters (Healthcare), Inc; 2013. http://www.thomsonhc.com/hcs/librarian. Accessed January 14, 2013. 2. Coleman I, Brown MD, Innes GD, Grafstein E, Roberts TE, Rowe BH. Parenteral metoclopramide for acute migraine: meta-analysis of randomized controlled trials. BMJ. 2004;329:1369-1373.
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
4
Annals of Pharmacotherapy XX(X)
3. Park GR. Hypotension following metoclopramide administration during hypotensive anaesthesia for intracranial aneurysm [letter]. Br J Anaesth. 1978;50:1268-1269. 4. Park GR. Hypotension following the intravenous injection of metoclopramide [letter]. Anaesthesia. 1981;36:75-76. 5. Pegg MS. Hypotension following metoclopramide injection [letter]. Anaesthesia. 1980;35:615. 6. Hughes RL. Hypotension and dysrhythmia following intravenous metoclopramide [letter]. Anaesthesia. 1984; 39:720. 7. Metoclopramide [package insert]. Lake Forest, IL: Hospira, Inc; June 2012.
8. Micromedex Healthcare Series [database online]. Greenwood Village, CO: Thomson Reuters (Healthcare), Inc; 2013. http:// www.thomsonhc.com/hcs/librarian. Accessed January 14, 2013. 9. Vinik AI, Maser RE, Mitchell BD, Freeman R. Daibetic autonomic neuropathy. Diabetes Care. 2003;26:1553-1579. 10. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30:239-245.
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
research-article2013
AOPXXX10.1177/1060028013503789Annals of Pharmacotherapy
Article
Sustained Hypotension Following Intravenous Metoclopramide
Annals of Pharmacotherapy XX(X) 1–4 © The Author(s) 2013 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1060028013503789 aop.sagepub.com
Tammy T. Nguyen, PharmD1 and Renee M. Petzel Gimbar, PharmD1
Abstract Objective: To report a case of sustained hypotension associated with the use of intravenous metoclopramide. Case Summary: A 50-year-old woman developed a hypotensive episode lasting approximately 90 minutes after the administration intravenous metoclopramide for the treatment of a migraine. The patient presented to the emergency department after she woke up with a severe headache that was much worse than her normal migraine headaches. Her past medical history included migraines, diabetes type 2, hypertension, and hyperlipidemia. Fifteen minutes after the administration of intravenous metoclopramide 10 mg, the patient’s systolic blood pressure decreased from 138 to 84 mmHg (a mean arterial pressure decrease of 40.7 mmHg). The patient was given 1 L of intravenous NaCl 0.9% that had minimal effect on blood pressure. The patient did not reapproach her baseline systolic blood pressure until 90 minutes after the metoclopramide administration when it was measured at 138 mmHg. Subsequent contrast tomography of the head was negative and the patient’s headache was successfully treated with butalbital/acetaminophen/caffeine. The patient was discharged home the same day. Discussion: There are few published case reports of metoclopramide-induced hypotension in the current literature. Of those published, all showed transient hypotension with metoclopramide, lasting seconds to minutes. An objective causality assessment for drug-associated adverse drug reaction showed metoclopramide as a probable cause of the patient’s hypotension (Naranjo score of 5). In this case, several indicators of metoclopramide induced hypotension were evident, including the timing of the hypotension after drug administration and the lack of any other possible causes of hypotension. This is the first published case report of sustained hypotension due to intravenous metoclopramide. Conclusion: Intravenous metoclopramide may cause sustained episodes of hypotension. Keywords Metoclopramide induced hypotension Received August 13, 2013; revised MONTH XX, XXXX; Accepted MONTH XX, XXXX.
Introduction Metoclopramide is a 4-amino-5-chloro-2-methoxy-N-(2diethyl-aminoethyl) benzamide that is structurally related to procainamide, but differs by its reported negligible cardiac effects.1 It blocks dopamine and serotonin receptors in the chemoreceptor trigger zone, in addition to enhancing the effects of acetylcholine in the upper gastrointestinal tract, promoting gastric motility. Because of its various mechanisms, metoclopramide is considered a therapeutic mainstay in the emergency department (ED) for the treatment of migraines with patients reporting decreased pain and nausea/vomiting and minimal safety concerns.2 The most common adverse effects include drowsiness and dystonic reactions. However, there has been limited information concerning the potential cardiovascular effects of metoclopramide. In this case report, we present a patient treated
with metoclopramide 10 mg slow intravenous push (IVP) over 3 to 5 minutes who experienced an episode of sustained hypotension lasting approximately 90 minutes that was minimally responsive to fluids.
Case Report A 50-year-old Caucasian woman (height 165.1 cm, weight 102.04 kg) with a past medical history of transient ischemic 1
University of Illinois Hospital and Health Sciences System, Chicago, IL, USA Corresponding Author: Renee Petzel Gimbar, Clinical Assistant Professor, Department of Pharmacy Practice, University of Illinois College of Pharmacy, 833 S. Wood Street (RM 164, MC 886), Chicago, IL 60612, USA. Email: [email protected]
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
2
Annals of Pharmacotherapy XX(X)
Table 1. Vital Signs and Medications Administered. Date/Time
BP (mmHg)
MAP (mmHg)
Pulse (beats/min)
RR (breaths/min)
09/25 09:58 09/25 10:19 09/25 10:28 09/25 11:00
128/69 171/88 149/82
88.7 115.7 104.3
114 110 105
20 18 16
09/25 11:04 09/25 11:16 09/25 11:49 09/25 12:31 09/25 12:36
138/84 84/50 92/55 138/78
102 61.3 67.3 98
103 109 88 82
16 18 16 18
Medications Diphenhydramine 25 mg PO ξ1 Metoclopramide 10 mg IV ξ1 NaCl 0.9% 1000 mL bolus started NaCl 0.9% 1000 mL bolus completed Butalbital/acetaminophen/caffeine 2 tabs PO ξ1
Abbreviations: BP, blood pressure; MAP, mean arterial pressure; RR, respiratory rate; PO, per oral; IV, intravenous.
attack (2003), migraines, diabetes, hypertension, and hyperlipidemia presented to the ED at 10 AM with complaints of worsening headache for 2 days. Patient stated that the morning of ED presentation the headache became more severe than her normal migraine. Her medications included benazepril 40 mg orally (PO) daily, calcium and vitamin D supplementation, clopidogrel 75 mg PO daily, insulin glargine 90 units subcutaneously (SC) twice a day, insulin lispro 50 units SC 3 times a day before meals, levothyroxine 300 mcg PO daily, metformin 1000 mg PO twice a day, paroxetine 40 mg PO daily, and simvastatin 40 mg PO before bedtime. The patient stated she took the morning dose of her medications at 8 am before coming into the ED. She denied any recent changes in medications (dose or timing), or taking any other prescription, over the counter, or herbal medications. Patient stated that she was adherent to her medication. In the ED, all labs, including basic metabolic panel, liver function tests, complete blood cell count, and cardiac enzymes were all within normal limits or negative, except for a blood glucose of 266 mg/dL. Physical exam showed she was alert and oriented to person, place, and time, normal motor strength in all extremities. Initial electrocardiogram showed sinus tachycardia with a ventricular rate of 110 beats/min, QRS of 46 ms, and QTc of 465 ms. No further electrocardiograms were ordered in the ED. As migraine was high on the differential, the patient was treated with metoclopramide 10 mg slow IVP over 3 to 5 minutes and diphenhydramine 25 mg PO once 1 hour after ED presentation. Fifteen minutes after the patient received the metoclopramide, her blood pressure (BP) unexpectedly dropped from 138/84 to 84/50 mmHg, a mean arterial pressure decrease of 40%, and she had a new complaint of light headedness (see Table 1). An intravenous bolus of NaCl 0.9% 1000 mL was run wide open over 30 minutes with minimal effect. A contrast tomography scan of the head was negative for any acute intracranial process. The patient’s BP returned to normal approximately 90 minutes later when it increased to 138/78 mmHg.
After the resolution of her hypotension, the patient’s headache persisted. As a result, she was treated with butalbital/acetaminophen/caffeine 2 tabs PO one time only resulting in complete resolution of her headache. Patient was discharged from the ED the same day with a prescription for butalbital/acetaminophen/caffeine.
Discussion As previously mentioned, the evidence supporting metoclopramide induced hypotension is scarce. Search terms in PubMed such as “metoclopramide induced hypotension” and “metoclopramide AND hypotension” resulted in only 4 published reports of metoclopramide-induced reductions of blood pressure.3-6 The first case published by Park3 in 1978 describes 4 patients undergoing surgery for repair of a ruptured intracranial aneurysm. Patients were being administered metoclopramide 10 mg IVP one time for prophylaxis of postoperative emesis. After administration, patients experienced a mean arterial pressure decrease of 10 to 30 mmHg and an increase in heart rate (HR) of 2 to 7 beats/min without normalization for as long as 100 seconds. Central venous pressure decreased in 1 patient, remained unchanged in the other 2 patients, and was unknown in the fourth. This case study led Park4 to look at metoclopramide’s cardiovascular effect in 6 healthy, conscious volunteers. The trial was double blind, where volunteers were given metoclopramide 10 mg IVP or 10 mL of normal saline IV over a period of 15 seconds. None of the volunteers saw a change in BP or HR with placebo. However, when 10 mg of metoclopramide was given intravenously, all patients saw a decrease in systolic BP ranging from 5 to 15 mmHg and a HR increase of 8 to 30 beats per minute, which normalized within 90 seconds. Park was not the only author to see this transient hemodynamic change associated with metoclopramide. A case series of 16 consecutive patients, undergoing various elective neurosurgical operations, found that patients who
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
3
Nguyen and Petzel Gimbar received metoclopramide 10 mg IVP over a period of 10 seconds had an average SBP drop of 22% over 44 seconds with normalization occurring within 96 seconds.5 The mechanism of metoclopramide-induced hypotension is unknown. Park3 postulated that because of its similar structure to the antiarrhythmic procainamide, metoclopramide may result in both cardiac depression and peripheral vasodilation. Hughes6 actually found metoclopramide as a possible cause of a dysrhythmia in a previously healthy 40-year-old patient who was anaesthetized for a hysterectomy. After receiving metoclopramide 10 mg IVP over 10 seconds for postoperative emesis prophylaxis, the patient developed bigeminy with a heart rate of 44 beats/min and an unmeasurable BP. Per operating room reports, the patient’s wound also stopped oozing blood. However, when atropine 0.6 mg IVP was administered, the patient had restoration to normal sinus rhythm within 30 seconds with a BP of 110/70 mmHg and her wound began bleeding profusely again. Hughes’s case provides further evidence that metoclopramide has a widely unrecognized cardiovascular effect. The number of published metoclopramide-induced hypotension case reports is small and encompasses only a limited number of patients.3-6 In addition, all these reports were published in the 1970s to 1980s when the rapid administration of metoclopramide over 10 to 15 seconds was widely accepted. In our ED, metoclopramide is administered slow IVP over 3 to 5 minutes to minimize possible cardiovascular and musculoskeletal adverse effects. This is comparable to the package insert recommendation of 1 to 2 minutes.7 It is possible that previous reports of metoclopramide-induced hypotension may reflect the fast administration rate. This case report is the first describing sustained, transient hypotension due to metoclopramide reported in the literature. Our patient experienced a systolic BP drop of 40 to 50 mmHg with symptoms of hypotension (new onset lightheadedness) lasting for 90 minutes. Other possible etiologies for the patient’s hypotension were investigated. No reports of oral diphenhydramine-induced hypotension could be found, patient denied any recent changes to her home medications, and labs did not show any signs of dehydration. A drug interaction check found that metoclopramide and paroxetine in combination could result in neuroleptic malignant hyperthermia and in turn autonomic instability.7,8 However, the patient was never found to have altered mental status, hyperthermia, or muscle cramping/tremors while in the ED. Although diabetes has been reported to cause orthostatic hypotension through autonomic neuropathy, this patient’s hypotension was persistent and not positional.9 Finally, it should also be noted that migraines themselves may cause hypotension; however, patient denied ever having previous episodes of lightheadedness. Because of the above findings, metoclopramide was considered the most likely culprit of this patient’s hypotensive episode. The
Naranjo adverse drug reaction probability scale was used with a calculated score of 5, showing that metoclopramide was a probable cause of the patient’s sustained hypotension.10 Potential score variability based on clinician view of subjective information may result in +/-1 of the Naranjo score. Resultant scores still show metoclopramide as a probable or possible cause of the patient’s hypotension. As there is no antidotal therapy available for the reversal of metoclopramide, 1000 mL of normal saline IV was the only treatment administered for the patient’s hypotension in the ED, with minimal response. No vasopressors were initiated because the patient’s only symptom was lightheadedness, her systolic BP remained stable in the 80 mmHg range, and her tachycardia of 109 beats/min resolved to the 80s despite the sustained hypotensive episode. The patient maintained baseline mental status, was alert and oriented to person, place, and time, and considered stable. In the future, we do not advocate treatment beyond fluid boluses because of the transient nature of the hypotension unless the patient has clinically significant signs and symptoms, including, but not limited to, altered mental status, cardiac abnormalities, and poor peripheral perfusion. The underreporting of metoclopramide-induced hypotension in the literature may be due to the quick and spontaneous resolution of hypotension within 90 seconds as previously reported. It is also questionable whether these drops in BP are normally clinically significant. In the light of this case and previous literature, we propose that caution be used when metoclopramide is administered via slow IVP in the ED, especially in patients who may already be at risk for hypotension. Acknowledgment The authors would like to thank John Williams, MD, FACEP, at the University of Illinois Hospital and Health Sciences System.
Declaration of Conflicting Interests The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
References 1. Metoclopramide. DRUGDEX System [database online]. Greenwood Village, CO: Thomson Reuters (Healthcare), Inc; 2013. http://www.thomsonhc.com/hcs/librarian. Accessed January 14, 2013. 2. Coleman I, Brown MD, Innes GD, Grafstein E, Roberts TE, Rowe BH. Parenteral metoclopramide for acute migraine: meta-analysis of randomized controlled trials. BMJ. 2004;329:1369-1373.
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
4
Annals of Pharmacotherapy XX(X)
3. Park GR. Hypotension following metoclopramide administration during hypotensive anaesthesia for intracranial aneurysm [letter]. Br J Anaesth. 1978;50:1268-1269. 4. Park GR. Hypotension following the intravenous injection of metoclopramide [letter]. Anaesthesia. 1981;36:75-76. 5. Pegg MS. Hypotension following metoclopramide injection [letter]. Anaesthesia. 1980;35:615. 6. Hughes RL. Hypotension and dysrhythmia following intravenous metoclopramide [letter]. Anaesthesia. 1984; 39:720. 7. Metoclopramide [package insert]. Lake Forest, IL: Hospira, Inc; June 2012.
8. Micromedex Healthcare Series [database online]. Greenwood Village, CO: Thomson Reuters (Healthcare), Inc; 2013. http:// www.thomsonhc.com/hcs/librarian. Accessed January 14, 2013. 9. Vinik AI, Maser RE, Mitchell BD, Freeman R. Daibetic autonomic neuropathy. Diabetes Care. 2003;26:1553-1579. 10. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30:239-245.
Downloaded from aop.sagepub.com at Universitats-Landesbibliothek on December 2, 2013
