Massive Verapamil Pharmacobezoar Resulting In
for Disease Control/Emory University/Georgia Poison
Professor, Dept. of Emergency Medicine
Medical Toxicology Fellowship
Int J Med Toxicol 2004; 7(1): 4
previous reports, sustained release calcium channel blocker (CCB)
pharmacobezoars have been anatomically located in the stomach or
found in polyethylene glycol rectal effluent. We report the first
case of a CCB esophageal pharmacobezoar.
61-year-old female overdosed on 100 verapamil SR (240 mg) tablets.
Emergency medical service personnel performed endotracheal
intubation and transported the patient to the emergency department.
Several attempts were made by hospital personnel to pass a
nasogastric tube to begin whole bowel irrigation. After the last
attempt, air insufflation could not be auscultated over the stomach,
but a kidney-ureter-bladder radiograph demonstrated the nasogastric
tube below the diaphragm. Direct esophagoscopy revealed an
obstructing mass of pills. Thoracoabdominal computerized axial
tomography revealed that the esophagus was completely casted with
debris. The nasogastric tube was identified within the mediastinum
with associated mediastinal emphysema, and free contrast material
was seen within the pelvis indicating peritoneal perforation. The
patient was taken to surgery where opening of the esophagus revealed
a massive bezoar of verapamil tablets, which was manually
disimpacted, and an esophageal perforation was found. The patient
report the first case of esophageal CCB pharmacobezoar complicated
by nasogastric tube perforation of the esophagus.
term "bezoar" is used to describe any indigestible concretion of
foreign material in the gastrointestinal tract. Pharmacobezoar is
used to describe concretions formed from ingested medications.
Pharmacobezoars have been reported following the ingestion of a
variety of agents including sustained release calcium channel
blockers (CCB). Previous anatomical locations of CCB bezoars have
included the stomach, small and large bowel and in polyethylene
glycol rectal effluent. (1-3). We report the first case of a CCB
pharmacobezoar in the esophagus.
61-year-old female was brought to the emergency department after
presumed polysubstance overdose including up to 100 verapamil SR (240 mg)
tablets. Other potential ingested agents included quinine
sulfate, paroxetine, zolpidem, famotidine, alprazolam, torasemide,
valproate, captopril, and celecoxib. The patient was intubated by
prehospital personnel for apnea.
emergency department arrival the patient was unresponsive with a
heart rate of 40/min and systolic blood pressure of 55 mmHg. The ECG
showed a sinus bradycardia with peaked T waves and a QRS complex of
158 msec. The chest radiograph revealed good position of the
endotracheal tube and clear lung fields.
Initial therapy included dopamine titrated to 20
mcg/kg/min, four grams calcium chloride, 150 mEqs of sodium bicarbonate, and 1 mg of
glucagon intravenously. The Georgia Poison Center was contacted. The
recommendations included nasogastric tube placement for polyethylene
glycol administration. Several attempts to pass the nasogastric tube
were unsuccessful. Eventually, the tube was felt to pass into the
stomach, but air insufflation could not be auscultated over the
stomach when checking for tube placement. A repeat chest radiograph
demonstrated the nasogastric tube was below the diaphragm.
performed by ENT revealed an obstructing mass in the
esophagus. The patient's hemodynamic status had improved with
axial tomography revealed that the esophagus was completely casted
with debris (Figure
1). The nasogastric tube was visualized within the
mediastinum with associated mediastinal emphysema (Figure 1,
arrowhead). Free contrast was seen within the pelvis indicating
left exploratory thoracotomy was performed. There was considerable
air and fluid within the mediastinum. No transmural perforation of
the esophagus was apparent. Upon opening of the esophagus a massive
bezoar of verapamil tablets was discovered and manually disimpacted
2). The nasogastric tube was found to
have exited the proximal esophageal lumen through a mucosal tear,
dissecting down the entire esophageal wall between the muscular
layers, and perforated the peritoneal cavity to lie posterior to the
posterior peritoneal tear was repaired and the esophagus was diverted
via left neck esophagostomy. Serum levels obtained on admission were
verapamil 77 ng/ml (reference range 100-600 ng/ml), norverapamil 90 ng/ml (reference range
100-400 ng/ml) and valproate 41 mg/ml. The patient was maintained on
J tube feedings while the esophagus healed. The esophagus was
eventually reanastamosed and the patient made a complete
sheer volume of our patient's ingestion most likely resulted in the
impaction of the pill mass in the esophagus and formation of the
pharmacobezoar. The patient had no history of esophageal disease,
strictures or gastrointestinal motility disorder. The inability to
pass the nasogastric tube through the bezoar led to repetitive
attempts and the subsequent esophageal perforation. The failure to
confirm nasogastric tube placement by auscultation resulted in
further evaluation with esophagoscopy and thoracoabdominal
computerized axial tomography, ultimately leading to the diagnosis
of a pharmacobezoar and peritoneal perforation.
low serum levels of verapamil and norverapamil are most likely
explained by the "containment" of most of the ingested tablets in
the esophagus. The patient's initial bradycardia, hypotension and
electrocardiographic abnormalities were most likely the result of
co-ingestants since the verapamil and norverapamil levels were
subtherapeutic. Possibilities include quinine, captopril and
and Manning hypothesized that the local effects of calcium channel
blocker toxicity on the gastrointestinal tract may include
vasodilatory compromise of mesenteric blood flow leading to mucosal
ulceration or even mucosal infarct. (1) In our case, false passage
of the nasogastric tube through a shallow, proximal esophageal
mucosal ulceration, down the esophageal wall to perforate the
peritoneum posterior to the stomach was decidedly unique and
unfortunate. The role that local esophageal vasodilatory effect
played in this iatrogenic complication is unknown.
mechanisms of pharmacobezoar formation include novel drug delivery
systems, characteristics of the pill coating or matrix, pH
responsiveness of the formulation, hygroscopic properties, and
volume and rate of ingestion or administration.
mechanisms include pharmaceutically-slowed gastrointestinal
motility, fixed anatomic alterations of the gastrointestinal tract,
mechanical motility disorders, and neuromuscular motility
formation may be considered in any poisoned patient with persistent
symptoms of toxicity, physical, radiographic, or laboratory evidence
of obstructed gastrointestinal function, or ingestion of a compound
known to form bezoars by intrinsic mechanisms.
should consider the possibility of esophageal pharmacobezoar
formation following ingestion of sustained release products.
Pharmacobezoar formation requires adaptation on the part of the
toxicologist with respect to diagnostic testing and therapeutic
interventions. Repetitive attempts at nasogastric placement
in patients with esophageal pharmacobezoars can result in esophageal
Sporer KA, Manning JJ. Massive ingestion of sustained-release
verapamil with a concretion and bowel infarction. Ann Emerg Med.
Rankin, RJ;Edwards, IR. Overdose of sustained release verapamil. N Z
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Buckley, N; Dawson, AH; Howarth, D; Whyte, IM. Slow-release
verapamil poisoning. Med. J. Aust. 1993;158(3):202-4
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