Αρχική σελίδα A & A Practice An Unusual Cause of Intraoperative Hemodynamic Instability Complicating Elective Mastectomy With...

An Unusual Cause of Intraoperative Hemodynamic Instability Complicating Elective Mastectomy With Immediate Free Flap Reconstruction

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14
Περιοδικό:
A & A Practice
DOI:
10.1213/XAA.0000000000001157
Date:
February, 2020
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E CASE REPORT

An Unusual Cause of Intraoperative Hemodynamic
Instability Complicating Elective Mastectomy With
Immediate Free Flap Reconstruction: A Case Report
Bruce Young, FRCA, Christos Chamos, MD, DESA, Ben Fitzwilliams, FRCA, and Neel Desai, FRCA
Extrinsic compression of the heart consequent to intrapleural fluid is a rare cause of cardiac
tamponade. Cases of massive hemothorax resulting in external cardiac tamponade due to injury
of the internal thoracic artery (ITA) following blunt or penetrating trauma have been described in
the literature. Here, we present a case of iatrogenic injury to the right ITA complicating mastectomy and deep inferior epigastric perforator flap reconstruction. It manifested as hemodynamic
instability that persisted despite aggressive fluid resuscitation. Investigation with an intraoperative transesophageal echocardiogram demonstrated cardiac tamponade secondary to a massive hemothorax which resolved following surgical placement of an intercostal drain.  (A&A
Practice. 2020;14:102–5.)
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GLOSSARY
CT = computed tomography; DIEP = deep inferior epigastric perforator; ITA = internal thoracic
artery; LA = left atrium; LV = left ventricle; PF = pleural fluid; RA = right atrium; RV = right ventricle;
TEE = transesophageal echocardiogram

A

cute cardiac tamponade is a life-threatening condition that necessitates immediate diagnosis and
treatment.1 Extrinsic compression causes a progressive constriction of the heart chambers, impairing diastolic
compliance and resulting in a reduction of end-diastolic and
stroke volumes.2,3 Cardiac tamponade is most commonly
secondary to an increase in intrapericardial pressure due to
the accumulation of fluid, blood, pus, or air within the pericardium, but this is not the only mechanism.3 It can rarely
occur secondary to large unilateral or bilateral pleural effusions even in the absence of pericardial fluid.; 4 This has been
demonstrated in animal studies3 and described in patients
with pleural effusions of various etiologies5–7 including
cases of traumatic hemothoraces.8,9
Here, we present what the authors believe is the first
reported case of an intraoperative external cardiac tamponade due to damage to the internal thoracic artery
(ITA) and secondary massive hemothorax. Written consent for publication of this case report was obtained from
the patient.

CASE DESCRIPTION
A 57-year-old woman with intermediate-grade ductal
breast carcinoma in situ and multifocal grade 1 invasive
cancer of the upper outer quadrant of the right breast presented for an elective right mastectomy with immediate
From the Department of Anaesthetics, Guy’s and St Thomas’ NHS Foundation Trust, London, United Kingdom.
Accepted for publication November 20, 2019.
Funding: None.
The authors declare no conflicts of interest.
Address correspondence to Bruce Young, FRCA, Department of
Anaesthetics, Guy’s and St Thomas’ NHS Foundation Trust, Westminster
Bridge Rd, London, SE1 7EH, United Kingdom. Address e-mail to bruce.
young1@nhs.net.
Copyright © 2019 International Anesthesia Research Society
DOI: 10.1213/XAA.0000000000001157

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reconstruction using a deep inferior epigastric perforator
(DIEP) free flap. Her background included hypertension,
but there was no other significant anesthetic or medical history. She had a body mass index of 34 and her preoperative
hemoglobin was 12.8 g/dL, with the rest of her blood panel
found to be unremarkable.
After establishing electrocardiographic, pulse oximetric,
and noninvasive blood pressure monitoring, anesthesia was
induced and maintained with total intravenous anesthesia
using propofol and remifentanil, and a tracheal tube followed by an arterial line were inserted. Following transfer from the anesthetic room to the operating theater and
patient positioning, surgery commenced uneventfully until
completion of the right mastectomy. It was at this point that,
while preparing the recipient vessels for the DIEP flap, an
injury occurred to the ITA and pleura, giving rise to a brisk
and large external bleed of approximately 1100 mL. The
injury was repaired by the plastic surgeons within minutes
and no further hemorrhage was visualized.
In response to this, the patient became increasingly
tachycardic and hypotensive with the highest heart rate
and lowest blood pressure, respectively, recorded as 124
beats/min and 65/40 mm Hg. Fluid resuscitation was
immediately started with 2000 mL of Hartmann solution, 4
units of packed red blood cells, and 4 units of fresh frozen
plasma. Moreover, 1 g of tranexamic acid was administered.
Subsequent to the first unit of packed red blood cells having been administered, an arterial blood gas demonstrated
the hemoglobin to be 6.6 g/dL. Despite fluid resuscitation
and support of cardiovascular parameters with metaraminol in divided doses of 0.5 mg, only transient hemodynamic
improvement could initially be achieved with slowly recurring tachycardia and hypotension. Later, even though the
post-transfusion arterial blood gas revealed a hemoglobin
of 8.3 g/dL, lactate of 3.1 mmol/L, and negative base excess
of 4.5, the hemodynamics of the patient no longer improved
with fluid resuscitation and showed minimal response to
February 15, 2020 • Volume 14 • Number 4

Copyright © 2019 International Anesthesia Research Society. Unauthorized reproduction of this article is prohibited.

Figure 1. Images from an intraoperative transesophageal echocardiogram. Midesophageal 4-chamber view (A) and midesophageal view with
clockwise probe rotation (B) demonstrating extrinsic compression and collapse of the right atrium (A) and a right pleural effusion (B). LA indicates left atrium; LV, left ventricle; PF, pleural fluid; RA, right atrium; RV, right ventricle.

escalating doses of metaraminol either administered as a
bolus or peripheral infusion.
It was clear to the clinical team that, in the absence of
continuing obvious bleeding, the patient was not responding in the expected manner to the management strategy that
had been instituted hence far. In light of this, other concomitant diagnoses were considered, such as acute heart failure
due to fluid overload, hemothorax, and pneumothorax. Of
note, there had not been a decrease in the oxygen saturation or an increase in the airway peak pressure, and the trachea remained central with evidence of bilateral anterior air
entry.
The clinical team requested assistance from a cardiac
anesthetist to perform an on-table transesophageal echocardiogram (TEE) in order to assess her left ventricular
function. It demonstrated an underfilled left ventricle with
no regional wall motion abnormalities, but the most striking finding was significant compression of the right atrium
(Figure 1A). Furthermore, a large right intrathoracic fluid
collection and a very small pericardial collection were
shown (Figure 1B). These findings were in keeping with
external cardiac tamponade secondary to a massive rightsided hemothorax.
In view of this, after a preprocedural ultrasound scan
performed by a radiologist, an intercostal drain insertion
was performed by a cardiothoracic surgeon. Seven hundred milliliters of fresh blood was drained over the next 15
minutes, adequate to relieve extrinsic cardiac compression
(Figure 2), and a rapid return of hemodynamic stability was
observed, sufficient to facilitate discontinuation of peripheral vasopressors. It was at this time that the cardiothoracic
surgeon was able to visually inspect the repair of the pleura
and the ITA.
Given that the DIEP flap had already been prepared earlier on in the operation and there were no signs of further
bleeding, extrinsic cardiac compression, or hemodynamic
instability, a multidisciplinary decision was made to complete the surgery. Unfortunately, her postoperative recovery
was complicated by flap failure and she was reoperated on
overnight for attempted salvage before eventual removal of
the flap.

February 15, 2020 • Volume 14 • Number 4

Figure 2. Midesophageal 4-chamber view from a transesophageal
echocardiogram demonstrating relief of the cardiac tamponade after
drainage of the right hemothorax. LA indicates left atrium; LV, left
ventricle; RA, right atrium; RV, right ventricle.

On the first day in the postoperative intensive recovery
unit, a chest radiograph demonstrated a large and persistent collection within the right hemithorax (Figure 3).
Further imaging with computed tomography of her chest
showed a significant residual hemothorax (Figure 4A, B).
This was treated by video-assisted thoracoscopic surgery
where 1200 mL of residual liquid and clotted blood was
washed out (Figure 5). Subsequent to tracheal extubation,
removal of chest drains and a period of rehabilitation, she
was discharged from hospital 11 days following the original
operation.

DISCUSSION
Breast reconstruction with a DIEP flap necessitates the exposure and preparation of the recipient vessels. Due to their
propensity for excellent flow of 15–35 mL/min and low
rate of subsequent atheroma formation, the ITAs are commonly selected.10,11 Iatrogenic damage of the artery, pleura,
or vein, however, are all potential complications. In the case
described here, the ITA and pleural were simultaneously

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injured, providing the conditions required for the development of a massive hemothorax.
Cardiac tamponade can be diagnosed by either clinical
assessment or medical imaging alone or in combination.12
Clinical signs vary13 and the eponymous Beck triad of
tachycardia, hypotension, and raised jugular venous pressure is found in only 10%–40% of patients.2 Pulsus paradoxus, defined as a decrease of >10 mm Hg in the systolic
blood pressure during the inspiratory phase of respiration,
is present in 77% of cases.2 It can be subtle in hypovolemia
and may be absent or reversed, respectively, in left ventricular dysfunction and positive pressure ventilation.3,9 In
general, a picture of increased sympathetic drive and progressive dyspnea is likely,2 but the latter cannot be evaluated in an anesthetized patient. As cardiac output falls,
signs of decreased end-organ perfusion such as confusion,
a progressive metabolic acidosis, and reduced urine output
develop. In patients who are ventilated, as was the case
here, hemodynamic compromise can present more readily as the negative intrapleural pressure generated during
spontaneous inspiration is replaced by positive intrathoracic pressure, further reducing venous return.11
Diagnosis of external cardiac tamponade, caused by the
pressure exerted by fluid in the pleural rather than pericardial space, can be more challenging. Published reports of

Figure 3. Chest radiograph showing diffuse and increased opacification of the right hemithorax. The orange arrow indicates the intercostal drain and the white arrows point to the breast tissue expander.

massive pleural effusions occurring due to cardiac failure
or liver disease describe an insidious onset of respiratory
symptoms preceding cardiovascular collapse.5 If external
cardiac tamponade is a result of massive hemothorax, then
cardiovascular compromise may occur early secondary to
acute hemorrhage.8 Resuscitation with intravenous fluid
and blood products to replenish the circulating volume can
transiently increase cardiac output or, depending on the
severity of cardiac tamponade, the patient may remain in
fluid refractory hypotension.
In this particular case, the presence of both obvious and
occult bleeding made the diagnosis even more difficult for
the clinical team to establish. Initial hemodynamic instability was thought to be due to hypovolemia, yet when it did
not improve following the cessation of visible hemorrhage
and appropriate resuscitation, the differential diagnosis was
reconsidered, prompting the need for further investigation.
Rescue echocardiography is a valuable modality in
the assessment of persistent or unexplained hypotension.
Operators can interrogate for hypovolemia, ventricular
dysfunction, valvular pathology, signs consistent with
pulmonary embolism, and pericardial or pleural effusion
with or without signs of cardiac tamponade. If right atrial
collapse is present, as was the case here, its persistence for
over a third of the cardiac cycle has a 94% sensitivity and
100% specificity for cardiac tamponade.14,15 Should cardiac
tamponade be found, it is sensible to image for a pleural
effusion as there is otherwise a potential for inappropriate
attempts at pericardiocentesis to be undertaken.4
Emergency treatment of external cardiac tamponade
must include attempts to decrease intrathoracic pressure,
most commonly achieved by the insertion of an intercostal
drain. In our case, the initial intercostal drainage of blood
was adequate to resolve intraoperative hemodynamic instability. It should be remembered, however, that each hemithorax will accommodate a large volume of blood before
the pressure increases to the point of causing cardiac tamponade. In view of this, cardiothoracic review and imaging
should be sought as soon as possible to confirm the complete drainage of any residual blood and the integrity of
vascular repair to avoid subsequent complications.
In conclusion, the intraoperative development of external cardiac tamponade secondary to hemothorax is rare in
noncardiac surgery. If iatrogenic damage to intrathoracic

Figures 4. Computed tomography (CT) of the chest showing a large right residual hemothorax with contralateral shift of the mediastinum. The
orange arrow indicates the intercostal drain and the white arrows point to the breast tissue expander.

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Figure 5. Chest radiograph showing decreased volume in the right
hemithorax and a small residual pleural effusion following videoassisted thoracoscopic surgery. The orange arrows indicate the
intercostal drains.

vessels is a possible complication, the authors suggest that
consideration should be given to external cardiac tamponade as a cause of refractory hemodynamic compromise. E
DISCLOSURES
Name: Bruce Young, FRCA.
Contribution: This author helped prepare and write the manuscript.
Name: Christos Chamos, MD, DESA.
Contribution: This author helped revise the manuscript.
Name: Ben Fitzwilliams, FRCA.
Contribution: This author helped revise the manuscript.
Name: Neel Desai, FRCA.
Contribution: This author helped write and revise the manuscript.
This manuscript was handled by: Kent H. Rehfeldt, MD.
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