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Vasodepressor reaction in an unsedated patient undergoing colonoscopy and observing the video display
taken to avoid bile spillage by vigorous suction. The cholecystotomy was then closed with the Multifire Endo Hernia Instrument (United States Surgical Corporation, Norwalk, Conn.), and cholecystectomy proceeded in the usual manner. When facilities exist, and particularly when early cholecystectomy is not contemplated, extracorporeal shock wave lithotripsy can be used to fragment the impacted stone, thereby allowing the basket to be closed and withdrawn. 3 However, a risk remains that the stone fragments may subsequently become symptomatic. W.T. Ng, MD M.K. Yiu, MD K. Lee, MD Department of Surgery Princess Margaret Hospital Lai King Hill Road Hong Kong
REFERENCES 1. Cutler AF, Hassig WM, Schubert TT. Basket impaction at the pancreatic head [Letter]. Gastrointest Endosc 1992;38:520-1. 2. Martin DF, Tweedle DEF. Endoscopic management of common duct stones without cholecystectomy. Br J Surg 1987;74:209-11. 3. Merett M, Desmond P. Removal of impacted endoscopic basket and stone from the common bile duct by extracorporeal shock waves. Endoscopy 1990;20:92.
Vasodepressor reaction in an unsedated patient undergoing colonoscopy and observing the video display To the Editor: The performance of an endoscopic examination exposes the patient to several potential precipitators of a vasodepressor (vasovagal) episode: emotional upset and distress, somatic or visceral pain, mild dehydration, and a warm, crowded environment. 1 Video display of gastrointestinal endoscopy is being increasingly used and may expose the patient to an often powerful additional stimulus for vasodepressor syncope: the sight of blood, bodily fluids, and visceral tissues. This is a report of a severe vasodepressor reaction that occurred during colonoscopy in an unsedated patient who was watching his examination on a video display. The patient, a 51-year-old man, underwent colonoscopy during a hospital admission to evaluate a several-week history of scant hematochezia, increased frequency of loose stools, and mild lower abdominal cramping relieved by defecation. He had no history of cardiovascular disease, was in good medical health, and his only medication was cimetidine 300 mg twice daily for symptoms of gastroesophageal reflux (pyrosis). The admission electrocardiogram, complete blood count, and electrolyte and SMA-12 tests showed normal results. Physical examination was unremarkable. Preparation of the colon was made with an oral electrolyte lavage solution (Golytely). Just before colonoscopy, the patient was alert and oriented, with a pulse of 64 beats/min, respiration of 20 218
breaths/min, and blood pressure of 110/80 mm Hg. An intravenous infusion of crystalloid solution had been established 48 hours previously. A pulse oximetry device was attached to monitor pulse and oxygen saturation. A cardiac monitor was not used. No preoperative or intraoperative medication was administered. The patient was able to observe the video monitor throughout the procedure. The colonoscope was introduced and easily advanced through the rectosigmoid colon. The presence of mild to moderate ulcerative proctosigmoiditis was observed and was noted by the patient. The instrument was then advanced without difficulty to the region of the hepatic flexure, with the patient remaining alert, responsive, and comfortable. Pulse was noted to remain in the range of 60 to 70 beats/min throughout this period. The hepatic flexure was negotiated easily, and the instrument quickly advanced into the cecum. The patient did not indicate verbally or nonverbally that he was experiencing any discomfort throughout the procedure. The entire colonoscopy was performed without technical difficulty. During efforts to visualize the cecum clearly, with the patient observing and hearing efforts to suction the green, fecal-laden fluid present, various hemodynamic changes occurred. During the course of approximately 1 minute, the pulse dropped from between 60 and 70 beats/min to 40 to 45 beats/min. The patient became pale, slow to respond, and less verbal and when questioned admitted that he "felt bad." Within the next 10 to 15 seconds, the patient, although conscious, became unresponsive and the pulse was noted to be between 20 and 30 beats/min. The pulse oximeter immediately indicated asystole. At that point, the patient was unconscious, dusky, apneic, and without pulse. The back and neck began to hyperextend. The period of asystole and apnea lasted approximately 10 seconds, during which time we considered calling a "code blue" resuscitation. However, the patient regained a slow pulse and began to breathe spontaneously. Blood pressure was noted to be 60 mm Hg/palpable with an Sao2 of 91 % and pulse between 50 and 60 beats/min. The patient soon began to respond to verbal commands. He was placed in Trendelenburg's position, and intravenous crystalloid solution was rapidly infused. Pulse rate and blood pressure rose gradually during the next 20 to 25 minutes to 60 to 70 beats/min and 96/60 mm Hg with an Sao2 of 96 %. He indicated that he "felt fine" and that "sometimes I have this reaction to the sight of blood." He denied having had any significant pain during the procedure and recalled only that he had felt light-headed. An electrocardiogram obtained after completion of the procedure was found to be normal. The patient remained hemodynamically stable during the next 48 hours and was discharged with plans for a Holter monitor study, which showed normal results when completed on an outpatient basis. He later indicated that he had experienced transient episodes of sudden weakness, tremor, diaphoresis, and pale coloration and occasional episodes of syncope since his late teenage years and noted that some of these episodes appeared to have been stress related. With the widespread use of video endoscopy, patients undergoing colonoscopy may be increasingly provided with the option of observing their own procedure. Therefore, those patients who are predisposed to vasodepressor syncope may GASTROINTESTINAL ENDOSCOPY
be at particular risk of having a syncopal episode with the addition of an additional precipitator of vasodepressor syncope. Vasodepressor (or vasovagal) syncope is primarily a hemodynamic derangement during which a profound decrease in peripheral vascular resistance caused by skeletal muscle bed vasodilation is not compensated by an increase in the cardiac output. 1, 2 The pathophysiologic bases of (1) the initial vasodilatory response and (2) the lack of a compensatory increase in cardiac output and peripheral vasoconstriction are not well understood. Evidence suggests that the lack of appropriate sympathetically mediated pressor effects may be related to central nervous system parasympathetic inhibition of sympathetic efferents to the heart and the vascular bed of peripheral muscle. 3-5 Because the primary hemodynamic derangement in vasodepressor syncope is a loss of peripheral resistance, administration of atropine, although it increases heart rate, does relatively little to increase systemic pressures. 1, 2 The recumbent position used in most endoscopic procedures may help explain why vasodepressor episodes are rarely encountered, inasmuch as the recumbent position allows for good central venous return even if peripheral resistance decreases. The arching of neck and back seen in our patient is typical of anoxic convulsion and is a common occurrence during vasodepressor syncope. 6 It results from the disinhibition of bulbopontine reticular formation from the anoxia-sensitive cerebral cortex and basal ganglia. Occurrence of such an anoxic seizure does not necessarily signify a subclinical neurologic disorder. A dramatic vasodepressor episode such as this can result from an exaggerated emotional response to normal stimuli,
VOLUME 39, NO.2, 1993
such as blood, injury, or illness. A true vasodepressor episode in response to appropriate stimuli can indicate blood-injury-illness phobia. 7 Physicians who use video endoscopy should consider the potential risk of creating a vasodepressor response before encouraging patients to observe the video screen. Particular caution may be indicated in patients with a history of fainting, syncope, or blood-injury-illness phobia. Philip S. Shore, MD, PhD William B. Salt II, MD Robert Guthrie, MD The Ohio State University and Mount Carmel Hospital Columbus, Ohio
REFERENCES 1. Brandenburg RO, Fustner V, Giuliani ER, McGoon DC, eds. Cardiology: fundamentals and practice. Chicago: Year Book Medical Publishers, 1987:689. 2. Selleger R, Adamec A, Morabia A, Zimmerman M. Vasovagal syncope during rectosigmoidoscopy: report of a case. PACE Pacing Clin Electrophysiol1988;11:346-8. 3. Hurst JW, Schlant RC, eds. The heart, arteries, and veins. 7th ed. New York: McGraw Hill, 1990:583. 4. Goldstein DS, Spanarkel M, Pitterman A, et al. Circulatory control mechanisms in vasodepressor syncope. Am Heart J 1982;104:1071-5. 5. Wallin BG, Sundloff G. Sympathetic outflow to muscles during vasovagal syncope. J Auton Nerv Syst 1982;6:287-91. 6. Adams RD, Victor M. Principles of neurology. 4th ed. New York: McGraw Hill, 1989:292. 7. Kaplan HI, Sidock BJ. Comprehensive textbook of psychiatry. Baltimore: Williams and Wilkins, 1989:978.
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REFERENCES 1. Cutler AF, Hassig WM, Schubert TT. Basket impaction at the pancreatic head [Letter]. Gastrointest Endosc 1992;38:520-1. 2. Martin DF, Tweedle DEF. Endoscopic management of common duct stones without cholecystectomy. Br J Surg 1987;74:209-11. 3. Merett M, Desmond P. Removal of impacted endoscopic basket and stone from the common bile duct by extracorporeal shock waves. Endoscopy 1990;20:92.
Vasodepressor reaction in an unsedated patient undergoing colonoscopy and observing the video display To the Editor: The performance of an endoscopic examination exposes the patient to several potential precipitators of a vasodepressor (vasovagal) episode: emotional upset and distress, somatic or visceral pain, mild dehydration, and a warm, crowded environment. 1 Video display of gastrointestinal endoscopy is being increasingly used and may expose the patient to an often powerful additional stimulus for vasodepressor syncope: the sight of blood, bodily fluids, and visceral tissues. This is a report of a severe vasodepressor reaction that occurred during colonoscopy in an unsedated patient who was watching his examination on a video display. The patient, a 51-year-old man, underwent colonoscopy during a hospital admission to evaluate a several-week history of scant hematochezia, increased frequency of loose stools, and mild lower abdominal cramping relieved by defecation. He had no history of cardiovascular disease, was in good medical health, and his only medication was cimetidine 300 mg twice daily for symptoms of gastroesophageal reflux (pyrosis). The admission electrocardiogram, complete blood count, and electrolyte and SMA-12 tests showed normal results. Physical examination was unremarkable. Preparation of the colon was made with an oral electrolyte lavage solution (Golytely). Just before colonoscopy, the patient was alert and oriented, with a pulse of 64 beats/min, respiration of 20 218
breaths/min, and blood pressure of 110/80 mm Hg. An intravenous infusion of crystalloid solution had been established 48 hours previously. A pulse oximetry device was attached to monitor pulse and oxygen saturation. A cardiac monitor was not used. No preoperative or intraoperative medication was administered. The patient was able to observe the video monitor throughout the procedure. The colonoscope was introduced and easily advanced through the rectosigmoid colon. The presence of mild to moderate ulcerative proctosigmoiditis was observed and was noted by the patient. The instrument was then advanced without difficulty to the region of the hepatic flexure, with the patient remaining alert, responsive, and comfortable. Pulse was noted to remain in the range of 60 to 70 beats/min throughout this period. The hepatic flexure was negotiated easily, and the instrument quickly advanced into the cecum. The patient did not indicate verbally or nonverbally that he was experiencing any discomfort throughout the procedure. The entire colonoscopy was performed without technical difficulty. During efforts to visualize the cecum clearly, with the patient observing and hearing efforts to suction the green, fecal-laden fluid present, various hemodynamic changes occurred. During the course of approximately 1 minute, the pulse dropped from between 60 and 70 beats/min to 40 to 45 beats/min. The patient became pale, slow to respond, and less verbal and when questioned admitted that he "felt bad." Within the next 10 to 15 seconds, the patient, although conscious, became unresponsive and the pulse was noted to be between 20 and 30 beats/min. The pulse oximeter immediately indicated asystole. At that point, the patient was unconscious, dusky, apneic, and without pulse. The back and neck began to hyperextend. The period of asystole and apnea lasted approximately 10 seconds, during which time we considered calling a "code blue" resuscitation. However, the patient regained a slow pulse and began to breathe spontaneously. Blood pressure was noted to be 60 mm Hg/palpable with an Sao2 of 91 % and pulse between 50 and 60 beats/min. The patient soon began to respond to verbal commands. He was placed in Trendelenburg's position, and intravenous crystalloid solution was rapidly infused. Pulse rate and blood pressure rose gradually during the next 20 to 25 minutes to 60 to 70 beats/min and 96/60 mm Hg with an Sao2 of 96 %. He indicated that he "felt fine" and that "sometimes I have this reaction to the sight of blood." He denied having had any significant pain during the procedure and recalled only that he had felt light-headed. An electrocardiogram obtained after completion of the procedure was found to be normal. The patient remained hemodynamically stable during the next 48 hours and was discharged with plans for a Holter monitor study, which showed normal results when completed on an outpatient basis. He later indicated that he had experienced transient episodes of sudden weakness, tremor, diaphoresis, and pale coloration and occasional episodes of syncope since his late teenage years and noted that some of these episodes appeared to have been stress related. With the widespread use of video endoscopy, patients undergoing colonoscopy may be increasingly provided with the option of observing their own procedure. Therefore, those patients who are predisposed to vasodepressor syncope may GASTROINTESTINAL ENDOSCOPY
be at particular risk of having a syncopal episode with the addition of an additional precipitator of vasodepressor syncope. Vasodepressor (or vasovagal) syncope is primarily a hemodynamic derangement during which a profound decrease in peripheral vascular resistance caused by skeletal muscle bed vasodilation is not compensated by an increase in the cardiac output. 1, 2 The pathophysiologic bases of (1) the initial vasodilatory response and (2) the lack of a compensatory increase in cardiac output and peripheral vasoconstriction are not well understood. Evidence suggests that the lack of appropriate sympathetically mediated pressor effects may be related to central nervous system parasympathetic inhibition of sympathetic efferents to the heart and the vascular bed of peripheral muscle. 3-5 Because the primary hemodynamic derangement in vasodepressor syncope is a loss of peripheral resistance, administration of atropine, although it increases heart rate, does relatively little to increase systemic pressures. 1, 2 The recumbent position used in most endoscopic procedures may help explain why vasodepressor episodes are rarely encountered, inasmuch as the recumbent position allows for good central venous return even if peripheral resistance decreases. The arching of neck and back seen in our patient is typical of anoxic convulsion and is a common occurrence during vasodepressor syncope. 6 It results from the disinhibition of bulbopontine reticular formation from the anoxia-sensitive cerebral cortex and basal ganglia. Occurrence of such an anoxic seizure does not necessarily signify a subclinical neurologic disorder. A dramatic vasodepressor episode such as this can result from an exaggerated emotional response to normal stimuli,
VOLUME 39, NO.2, 1993
such as blood, injury, or illness. A true vasodepressor episode in response to appropriate stimuli can indicate blood-injury-illness phobia. 7 Physicians who use video endoscopy should consider the potential risk of creating a vasodepressor response before encouraging patients to observe the video screen. Particular caution may be indicated in patients with a history of fainting, syncope, or blood-injury-illness phobia. Philip S. Shore, MD, PhD William B. Salt II, MD Robert Guthrie, MD The Ohio State University and Mount Carmel Hospital Columbus, Ohio
REFERENCES 1. Brandenburg RO, Fustner V, Giuliani ER, McGoon DC, eds. Cardiology: fundamentals and practice. Chicago: Year Book Medical Publishers, 1987:689. 2. Selleger R, Adamec A, Morabia A, Zimmerman M. Vasovagal syncope during rectosigmoidoscopy: report of a case. PACE Pacing Clin Electrophysiol1988;11:346-8. 3. Hurst JW, Schlant RC, eds. The heart, arteries, and veins. 7th ed. New York: McGraw Hill, 1990:583. 4. Goldstein DS, Spanarkel M, Pitterman A, et al. Circulatory control mechanisms in vasodepressor syncope. Am Heart J 1982;104:1071-5. 5. Wallin BG, Sundloff G. Sympathetic outflow to muscles during vasovagal syncope. J Auton Nerv Syst 1982;6:287-91. 6. Adams RD, Victor M. Principles of neurology. 4th ed. New York: McGraw Hill, 1989:292. 7. Kaplan HI, Sidock BJ. Comprehensive textbook of psychiatry. Baltimore: Williams and Wilkins, 1989:978.
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