Delayed Pericardial Tamponade Following Transthoracic Hiatal Hernia Repair
Madhusudan Rao Puchakayala, MBBS, MD, FRCA,* Kenneth Abbey, MD,* Jonathan Haft, MD,† and
Mark B. Orringer, MD†
P ERICARDIAL TAMPONADE is a rare complication fol-
lowing hiatal hernia repair.1,2 The authors report a case of
delayed pericardial tamponade in a patient seen 36 hours after
repair of a recurrent hiatal hernia via the transthoracic ap-
proach. The patient underwent emergency sternotomy, and a
bleeding epicardial artery was identified on the posteroinferior
aspect of the heart. The probable causes for the delayed pre-
sentation are discussed.
CASE REPORT
A 71-year-old obese woman (body mass index, 36) with recurrent
hiatal hernia underwent transthoracic hiatal hernia repair. Past medical
history included hypertension, type 2 diabetes mellitus, and depression.
Relevant surgical history included the original transabdominal fundo-
plication of the hiatal hernia. Medications taken were nicardipine,
amitriptyline, and metformin. The operation was performed with the
patient under general anesthesia through a left posterolateral thoracot-
omy in the sixth intercostal space with a thoracic epidural and a
single-lumen endotracheal tube. The lung was retracted using a moist
sponge and a malleable retractor.
After mobilization of the herniated stomach, an esophageal length-
ening Collis gastroplasty, followed by a 3-cm long Nissen fundoplica-
tion, as described previously,3,4 were performed. The fundoplication
was reduced beneath the diaphragm, and the hiatus was sutured appro-
priately. In the process of mobilizing the large hernia, entry into the
right pleural cavity occurred. Therefore, at the conclusion of the hernia
repair the patient was turned supine for right-sided chest tube place-
ment. Because of her marked obesity and elevated hemidiaphragm,
however, the chest tube was inserted below the diaphragm, resulting in
liver laceration and hemothorax. An emergency laparotomy, suture of
the liver laceration, and right-sided chest tube placement were carried
out. During the operation the total intravenous fluid input included
3500 mL of Ringer’s lactate, 500 mL of hetastarch, and 4 units of
packed red blood cells; the blood loss was 1800 mL.
Extubation was successfully performed at the end of the operation,
and the patient was transferred to the intensive care unit (ICU) for
postoperative monitoring. Chest x-ray studies showed full expansion of
the right lung, with no evidence of hemothorax, and the presence of
bilateral chest tubes.
In the ICU the coagulation profile was normal (prothrombin time,
12.4 seconds; international normalized ratio, 1.2; partial thromboplas-
tin time, 30.3 seconds; and platelet count, 177 ⫻ 109/L). The patient
remained hemodynamically stable, with decreasing bilateral chest tube
drainage (⬍10 mL/h by 24 hours). Approximately 32 hours after
surgery the patient complained of mild dyspnea and anxiety. Chest
auscultation revealed bibasilar crackles. Heart rate was 94 bpm, non-
invasive blood pressure was 121/63 mmHg (mean, 84 mmHg), and
respiratory rate was 18/min. Total fluid balance to this point was
positive by 1200 mL. Furosemide, 40 mg, was administered intrave-
nously, and resulted in diuresis of 500 mL over 2 hours, with clinical
improvement and stable vital signs.
Suddenly, 2 hours later the patient became unresponsive, and non-
invasive blood pressure could not be measured. On examination the
patient was responsive to deep painful stimuli, tachypneic (respiratory
rate, 25/min), and had a weak, thready pulse (heart rate ⬎100 bpm).
The skin was gray and dusky, with clammy extremities.
Immediate resuscitation included airway control with endotracheal
intubation, intravenous fluid resuscitation with 2000 mL of normal
saline solution, transfusion of 2 units of packed red blood cells, and
epinephrine infusion at 0.05 ␮g/kg/min. Invasive vascular access was
Journal of Cardiothoracic and Vascular Anesthesia, Vol 20, No 2 (April), 2006: pp 245-246
established (right subclavian vein catheter, with pulmonary artery cath-
eter and left radial artery catheter). Initial data included heart rate, 112
bpm; blood pressure, 60/44 mmHg (mean, 54 mmHg); pulmonary
artery pressure, 33/27 mmHg (mean, 30 mmHg); and central venous
pressure, 28 mmHg. Arterial blood gases on fraction of inspired oxygen
of 1 revealed pH 7.26; partial arterial carbon dioxide tension, 25
mmHg; partial arterial oxygen tension, 306 mmHg; and bicarbonate, 13
mmol/L. There was only a transient hemodynamic improvement with
fluid boluses and epinephrine infusion. Bedside transesophageal echo-
cardiography (TEE) revealed pericardial tamponade, with diastolic
collapse of the right ventricle.
While awaiting transfer to the operating room, an unsuccessful
attempt was made to aspirate the pericardial sac using a 20-gauge
needle. Multiple intravenous epinephrine boluses (500 ␮g ⫻ 2 doses)
were administered to support blood pressure during transfer to the
operating room.
On arrival in the operating room the patient had a brief period of
pulseless electrical activity prior to surgery during which chest com-
pressions were performed in addition to administration of a 1-mg
intravenous bolus of epinephrine. A sternotomy was performed, and the
pericardial tamponade was decompressed. Approximately 1 L of clot-
ted blood was evacuated from the pericardium. There was a small
bleeding epicardial artery identified on the mid-diaphragmatic surface
of the heart, and that was sutured. The pericardium appeared ecchy-
motic adjacent to the epicardial artery, but appeared intact. Extubation
was successfully performed within 24 hours. Postoperatively the pa-
tient had an uneventful recovery, and was discharged to home 7 days
later.
DISCUSSION
Pericardial tamponade following hiatal hernia repair is a rare
complication that has not been previously described after the
transthoracic approach.1,2 In the literature, only 1 case of peri-
cardial tamponade following hiatal hernia repair has been de-
scribed. This case described a coronary vein laceration with a
staple during an abdominal laparoscopic repair of a large para-
esophageal hernia.1
In the present case, the pericardial tamponade was due to
bleeding from an epicardial artery on the posteroinferior aspect
of the heart along its diaphragmatic surface. The cause of this
injury is uncertain, but could be the result of a torn intraperi-
cardial adhesion during mobilization of the adjacent stomach in
the repeat operation or of inadvertent puncture of the pericar-
dium during placement of the diaphagmatic crural sutures.
From the Departments of *Anesthesiology and Critical Care Medi-
cine, and †Thoracic Surgery, University of Michigan Medical Center,
Ann Arbor, MI.
Address reprint requests to Madhusudan Rao Puchakayala, MBBS,
MD, FRCA, Consultant, Department of Anaesthesia, Guy’s and St.
Thomas’ NHS Foundation Trust, St. Thomas’ Hospital, Lambeth Pal-
ace Road, London SE1 7EH, United Kingdom. E-mail: madhu@
doctors.org.uk
© 2006 Elsevier Inc. All rights reserved.
1053-0770/06/2002-0023$32.00/0
doi:10.1053/j.jvca.2005.01.038
Key words: surgery, hiatal hernia repair, complications, pericardial
tamponade, delayed presentation
245
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Two-lung ventilation and “packing” of the left lung using a
moist sponge and malleable retractor was used for surgical
exposure. It is also possible that the retractor caused blunt
injury to the epicardial vessel. The use of a double-lumen tube
and lung deflation may have provided a better surgical field,
and it might be argued that its use possibly could have pre-
vented this complication. However, at this institution nearly
2,000 of these operations (approximately 250 repeat transhiatal
hernia repairs) have been performed with the “lung retractor,”
and this is the first case of bleeding. Therefore, the authors do
not advocate change of anesthetic practice, because of the
pitfalls of double-lumen tubes, lung deflation, and one-lung
ventilation.5
There was slow intrapericardial bleeding postoperatively un-
til the patient decompensated 36 hours after surgery. The de-
layed presentation is likely multifactorial. The injured vessel
was possibly in some degree of vasospasm during the initial
postoperative period. Furthermore, bleeding may have been
controlled by upright positioning, with elevation of the dia-
phragm from the obese abdomen. This could have compressed
the bleeding epicardial artery temporarily. This can explain
both her deceptively stable hemodynamics initially and the
finding of a large quantity of clotted blood during decompres-
sion. In addition, reducing cardiac preload by diuresis may
have possibly precipitated the symptoms of tamponade and led
to decompensation.
The initial finding in the patient was dyspnea and anxiety,
then leading to hypotension unresponsive to fluids and epineph-
rine infusion. The differential diagnoses in this patient prior to
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PUCHAKAYALA ET AL
TEE included pericardial tamponade and pulmonary embolism.
However, hypotension in the absence of hypoxia excludes
pulmonary embolism.
Needle pericardiocentesis is a risky procedure, and can cause
injury to epicardial vessels. This was attempted unsuccessfully
while awaiting transfer to the operating room only after con-
firmation of the diagnosis at TEE. Had the epicardial artery
been injured, at least a small amount of blood would have been
aspirated, and this was not seen. In addition, only a single
source of bleeding was identified at surgery. Furthermore,
blood clots were mainly evacuated from the pericardial space,
suggesting a slow leak. Thus, it is unlikely that needle pericar-
diocentesis was the cause of epicardial artery injury.
An additional cause of pericardial bleeding can be coagu-
lopathy associated with blood loss and resuscitation with crys-
talloids and packed red blood cells for the traumatic right-sided
chest tube insertion requiring emergency laparotomy. How-
ever, postoperatively the coagulation status was normal, and
there was a decline in the chest tube drainage.
In summary, pericardial tamponade is a rare complication
following transthoracic hiatal hernia repair, and can be delayed
after surgery. In this patient there was injury to the epicardial
artery. The delayed presentation was possibly due to vasospasm
or diaphragmatic compression of epicardial vessels by the
obese abdomen. Early recognition in the ICU, confirming the
diagnosis using TEE and effective multidisciplinary treatment,
expedited therapy and averted a fatal outcome. The diagnosis
should be considered when unexplained hemodynamic collapse
occurs, and treatment must be instituted immediately.
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of the esophagogastric junction. Ann Thorac Surg 25:16-21, 1978
4. Stirling MC, Orringer MB: The combined Collis-Nissen operation for
esophageal reflux strictures. Ann Thorac Surg 45:148-157, 1988
5. Brodsky JB, Lemmens HJM: Left double-lumen tubes: clinical expe-
rience with 1,170 patients. J Cardiothorac Vasc Anesth 17:289-298, 2003