(Chest. 1999;115:598-600.)
© 1999
American College of Chest Physicians
Coronary Spasm and Cardiac Arrest From Carcinoid Crisis During Laser Bronchoscopy*
Atul C. Mehta, MBBS, FCCP;
Albert L. Rafanan, MD;
Reginald Bulkley, MD;
Michael Walsh, MD and
Glenn E. DeBoer, MD
*
From the Department of Pulmonary Medicine (Drs. Mehta and Rafanan), and
the Department of Anesthesiology (Drs. Bulkley, Walsh, and DeBoer), Cleveland
Clinic Foundation, Cleveland, OH.
 |
Abstract
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Bronchoscopic manipulation of an endobronchial carcinoid can
precipitate a carcinoid crisis. Coronary artery spasm is an uncommon
manifestation of carcinoid crisis, and has never been reported as a
complication of flexible bronchoscopy. We report a case of a
10-year-old girl who developed coronary artery spasm and cardiac arrest
during neodymium-yttrium aluminum garnet (Nd-YAG) laser photoresection
of an endobronchial carcinoid. Recognition of this unusual presentation
of a carcinoid crisis is important as the treatment approach differs
from standard resuscitation protocols.
Key Words: bronchoscopy • cardiac arrest • carcinoid crisis • carcinoid tumor • laser
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Introduction
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Carcinoid
crisis has been reported to occur with bronchoscopic manipulation of a
carcinoid tumor.1
Frequently reported presentations of an
acute carcinoid crisis include hemodynamic instability, tachycardia,
flushing, diarrhea, bronchoconstriction, and acidosis.1
We
report an unusual life-threatening presentation of a carcinoid crisis
during neodymium-yttrium aluminum garnet (Nd-YAG) laser resection,
wherein an electrocardiographically documented S-T segment elevation
and subsequent ventricular tachycardia and cardiac arrest occurred in a
10-year-old girl. The event was believed to occur from release of
mediators from the carcinoid tumor causing coronary artery spasm.
Coronary artery spasm is an unusual manifestation of carcinoid crisis
and must be recognized by clinicians because the treatment approach to
a carcinoid crisis differs from standard resuscitation
guidelines.2
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Case Report
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A 10-year-old girl presented with a 2-year history of
progressive dyspnea on exercise and a recent episode of hemoptysis. She
had been healthy and physically at par with her peers. She denied
episodes of flushing, nausea, palpitations, diarrhea, or headaches. On
exam, breath sounds were diminished over the right chest and the apical
impulse was displaced to the right parasternal border. The chest
radiograph revealed opacification of the right hemithorax and a
mediastinal shift to the same side. Subsequent bronchoscopy
demonstrated an exophytic tumor occluding the proximal right mainstem
bronchus (RMB) and overriding the carina (Fig 1
).
An endobronchial biopsy revealed a carcinoid tumor. Further diagnostic
testing revealed no evidence of distant metastasis. Laboratory testing
showed a serotonin level of 0.45 µg/mL (normal 0.1 µg/mL) and a
12-hour urinary 5-hydroxyindoleacetic acid (HIAA) level of 4.82 µg/mL
creatinine (normal <3.60 µg/mL creatinine). A CT scan of the chest
indicated that the tumor was arising primarily from the right upper
lobe (RUL). It was then decided to perform laser bronchoscopy to open
up the RMB and to possibly limit the extent of the lung resection.
The patient underwent a smooth halothane-oxygen induction and was
intubated with a 6.5 uncuffed endotracheal tube. During intubation, the
heart rate increased to 130 beats/min and a transient S-T segment
elevation lasting for 90 s in lead II was noted. The blood
pressure and oxygen saturation remained stable during this event. The
halothane was stopped and maintenance anesthesia was continued with
sufentanil, oxygen, vecuronium, and midazolam. The endotracheal tube
was then replaced with a "jet injection cannula" to allow the
flexible bronchoscope (FB) to be passed through the vocal
cords.3
Bronchoscopic laser photoresection was then
started on the endobronchial lesion. Ninety minutes into the case,
another transient S-T segment elevation was noted. The procedure was
temporarily discontinued and the ECG changes resolved spontaneously
(Fig 2
).
Similarly, there were no changes in hemodynamic or respiratory
parameters. It was decided to continue the laser procedure. One hundred
and thirty minutes into the case, a third episode of S-T segment
elevation was noted as the bronchoscopist advanced the FB through the
partially opened intermediate bronchus. At this point, the S-T segment
elevation did not resolve. Subsequently, the patient developed
ventricular tachycardia, ventricular fibrillation, and then asystole.
Cardiopulmonary resuscitation was performed and involved external
cardiac massage, defibrillation, aggressive fluid infusion, atropine,
and intravenous lidocaine. After 12 minutes, the patient regained a
sinus rhythm and a normal blood pressure. The procedure was
discontinued and the patient regained consciousness with no neurologic
sequelae.
Subsequent cardiac enzymes and follow-up ECGs showed no evidence
of a myocardial ischemia or infarction. An echocardiogram revealed
normal valvular and ventricular function. A serum serotonin level and
24-hour urinary 5-HIAA level obtained after the cardiac arrest were
both normal. The S-T segment elevation and cardiac arrest was thought
to be due to coronary spasm from an acute elevation of mediators from
the carcinoid tumor and subsequent carcinoid crisis. The patient was
then started on cyproheptadine (4 mg tid). A week later, a repeat laser
bronchoscopy was performed uneventfully. Near total patency of the RMB
and intermediate bronchus was established, and the carcinoid tumor
seemed to involve only the RUL. The patient was discharged and
instructed to continue taking the cyproheptadine. Weeks later, the
patient returned for a successful RUL sleeve resection. No complication
was noted intraoperatively or postoperatively. Surgical pathology
revealed a carcinoid tumor originating at the bifurcation of the RMB,
with clear resection margins and without hilar and peribronchial lymph
nodes involvement. The patient remained asymptomatic for 48 months of
follow-up.
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Discussion
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Acute carcinoid crisis can occur during FB. The carcinoid
crisis usually involves the development of tachycardia, flushing,
hypertension, or hypotension.1
Coronary artery spasm is an
unusual manifestation of an acute carcinoid syndrome and is not well
recognized. Our patient presented with prolonged S-T segment elevation,
followed by ventricular tachycardia, which is a characteristic of
variant angina. Only two case reports have previously described
coronary spasm with carcinoid syndrome.4
,5
In a similar
manner, both cases reported S-T segment elevation followed by
ventricular arrhythmias and cardiac arrest. In one patient, a graded
exercise test precipitated a carcinoid syndrome with coronary
spasm.4
In the other patient, the coronary spasm occurred
during an episode of flushing.5
In our case, coronary
artery spasm may have been precipitated by tumor manipulation, causing
an acute release of mediators. The patient had a normal serotonin and
urinary 5-HIAA levels after the cardiac arrest. However, it is not
uncommon for patients to have normal levels after an acute carcinoid
crisis.6
It is postulated that the coronary artery spasm occurs from an acute
elevation of serotonin and histamine released by the carcinoid tumor.
In animal studies, both histamine and serotonin have been shown to
provoke coronary artery spasm.7
,8
In humans, histamine has
been experimentally shown to induce coronary artery
spasm.9
Suggested treatment to prevent coronary spasm has
been histamine (H1) receptor blockers or calcium channel
blockers.4
Our patient was pretreated with cyproheptadine,
which is both an antiserotonergic and antihistaminic agent.
Anesthesia involving patients with carcinoid tumors warrants special
attention, as the severity of preoperative symptoms and urinary 5-HIAA
levels do not predict the development of perioperative
complications.6
No anesthetic technique or pharmacologic
regimen has been proven to be especially efficacious. This may be due
to the fact that carcinoid tumors secrete multiple mediators. In
general, the anesthetic approach involves the prevention of mediator
release, preparing for a possible acute carcinoid crisis and avoidance
of factors that can precipitate one. Factors that can trigger a
carcinoid crisis include catecholamines, anxiety, hypercapnia,
hypothermia, hypotension, hypertension, and drugs that release
histamine. Anesthetic drugs that should be avoided include thiopentone,
d-tubocurarine, suxamethonium, and morphine. Several drugs have been
used preoperatively to prevent the release of mediators. Among these
are diphenhydramine, cimetidine, cyproheptadine, aprotinin, and
octreotide.
Complications usually occur during induction of anesthesia, tracheal
intubation, and tumor manipulation.6
In our case, the
patient developed a transient S-T segment elevation with no changes in
hemodynamics immediately following intubation. We wonder if induction
and intubation caused a release of hormones leading to transient
coronary artery spasm. Our failure to recognize this uncommon
presentation of carcinoid crisis led us to proceed with the laser
bronchoscopy.
During refractory hypotension or cardiac arrest from a carcinoid
crisis, emphasis should be placed on volume replacement. The use of
catecholamines should be avoided as it has been shown to stimulate
further hormonal release and paradoxically worsen the
hypotension.2
Intravenous somatostatin in a dosage of 100
to 500 µg has been shown to cause a rapid reversal of the carcinoid
crisis and its hemodynamic complications.10
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Conclusion
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Bronchoscopic manipulation of carcinoid tumors can cause a
life-threatening carcinoid crisis. Coronary artery spasm is an uncommon
presentation of the carcinoid syndrome, and must be recognized by the
clinician as the treatment approach to a carcinoid crisis differs from
standard resuscitation protocols. Hypotension or cardiac arrest should
be treated by aggressive volume replacement and intravenous
somatostatin. Epinephrine should be avoided as it may paradoxically
worsen the hypotension by furthering hormonal release from the
carcinoid tumor. Prevention of coronary spasm from a carcinoid crisis
during FB may be achieved by premedication with cyproheptadine, a
selective histamine (H1) receptor, or calcium channel blocker.
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Footnotes
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Correspondence to: Atul C. Mehta, MBBS, Pulmonary Division A-90,
Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH
44195
Abbreviations: FB = flexible bronchoscope; RMB = right
mainstem bronchus; RUL = right upper lobe
Received for publication July 7, 1998.
Accepted for publication September 14, 1998.
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References
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-
Karmy-Jones, R, Vallieres, E (1993) Carcinoid crisis after biopsy of a bronchial carcinoid. Ann Thorac Surg 56,1403-1405[Abstract]
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Mehta AC, Livingston DR, Levine HL, et al. Ventilatory management during neodyium: yttrium aluminum garnet photoresection of subglottic and higher tracheal lesions. Transactions of the American Broncho-Esophagological Association 1986; 148–153
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Topol, EJ, Fortuin, NJ (1984) Coronary artery spasm and cardiac arrest in carcinoid heart disease. Am J Med 77,950-952[CrossRef][ISI][Medline]
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Petersen, KG, Seemann, WR, Plagwitz, R, et al (1984) Evidence for coronary spasm during flushing in the carcinoid syndrome. Clin Cardiol 7,445-448[ISI][Medline]
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Vaughan, DJ, Brunner, MD (1997) Anesthesia for patients with carcinoid syndrome. Int Anesth Clin 35,129-142[ISI][Medline]
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Bove, AA, Dewey, JD (1983) Effects of serotonin and histamine on proximal and distal coronary vasculature in dogs: comparison with alpha-adrenergic stimulation. Am J Cardiol 52,1333-1339[CrossRef][ISI][Medline]
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Shimokawa, H, Tamoike, H, Nabeyama, S, et al (1983) Coronary artery spasm induced in atherosclerotic miniature swine. Science 221,560-562[Abstract/Free Full Text]
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Ginsburg, R, Bristow, MR, Kantrowitz, N, et al (1981) Histamine provocation of clinical coronary artery spasm: implications concerning pathogenesis of variant angina pectoris. Am Heart J 102,819-822[CrossRef][ISI][Medline]
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TOP
Abstract
Introduction
