Case Report
VV ECMO Rescue of Silicone Syndrome
Arthur F Ng* and Elie M Elmann
Department of Cardiology, Hackensack Meridian University Medical Center, USA
*Corresponding author: Arthur Ng, Department of Cardiology, Hackensack Meridian University Medical Center, 20 Prospect Ave, Suite 900 20 Prospect Ave, Suite 900, NJ 07601, USA
Published: 19 Sep, 2018
Cite this article as: Ng AF, Elmann EM. VV ECMO Rescue
of Silicone Syndrome. Ann Clin Case
Rep. 2018; 3: 1546.
Abstract
Silicone Embolism Syndrome can cause an acute life threatening pneumonitis. It is usually seen after illicit injections of silicone. We report a case wherein the silicone use was medically sanctioned but resulted in pneumonitis severe enough to require use of a membrane oxygenator (VV ECMO).
Case Presentation
The patient is a 64 year old woman physician who 30 years prior had had bilateral cosmetic
subcutaneous silicone implants performed abroad. Six months prior she started to feel ill and
required multiple hospitalizations. Her symptoms included right sided chest pain, capsular
contractures from her implants, back discomfort, dyspnea, fatigue and persistent fevers. Implant
rupture was diagnosed on the basis of CT scan (Figure 1 and 2). During her work up she was found
to have a right coronary stenosis for which a drug eluting stent was placed. A transthoracic ECHO
showed a normal ejection fraction of 55-60%- no LVH, normal valve and right ventricle function.
A CXR and CT were otherwise unremarkable. She underwent rheumatologic evaluation for fever
of unknown origin up to Tmax 102ºC. She was anemic, ESR was elevated to 90 mm/hr, and CRP
120 mg/L to 130 mg/L. Her work up was ongoing when three months prior to our encounter she
began self-medicating with high dose steroids (prednisone 40 mg). She reportedly felt ‘great’ and
blood assays showed that her ESR and CRP levels returned to normal. She was scheduled for elective
implant removal/revision. Her preoperative testing was unremarkable; she had self- tapered to 5 mg
prednisone.
At the operation, the silicone and ruptured prostheses were found to be encapsulated allowing
for a relatively clean removal of the foreign material. Both implants were removed and a new sub
muscular implant was placed on the right. While working to reimplant the left and at this point,
approximately three hours after induction, the patient experienced VT/VF arrest then PEA in the
setting of extreme hypoxia. Return of spontaneous circulation was achieved after 21 minutes of
CPR. The left breast was packed, the surgery terminated and the patient brought to the ICU. In the
ICU she experienced continued hypoxia and a second PEA arrest but with relatively quick return
of circulation. Her caregivers requested emergent transfer to our institution as part of thrombosispage
for acute myocardial infarction.
Upon arrival patient was on 26mcg/min levophed and 8mcg epinephrine, bedside ECHO
was consistent with mild global cardiac stunning, cardiac catheterization was notable for normal
coronaries, CVP 20 mmHg, and LVEDP 28 mmHg. CT head negative, CT Chest angiogram revealed
no evidence of pulmonary embolism, bilateral alveolar consolidation of the lungs especially at the
bases and scattered areas of ground glass opacities. She was in florid pulmonary edema with copious
frothy hemorrhagic secretions. Initial ABG on FiO2 1.0 and 16 mmHg PEEP; pH 7.079/pCO2 24.6/
pO2 59.6/O2 sat 75.5%/ BE -20.7. Serum lactate 10 (ref. 0.5 mmol/L to 2.2 mmol/L), anion gap 21.7,
troponin 2.37 (ref. 0 ng/ml -0.20 ng/ml).
In a hybrid OR she underwent emergent percutaneous placement of 27F Avalon Dual Lumen
right internal jugular vein catheter and initiation of VV ECMO at flows of 3L/min. A right common
femoral 5F vascular sheathe was placed to allow rapid escalation to V-AV ECMO in the event that
it was needed. Heparin was administered to an ACT target of 200-240s. Meanwhile, her metabolic
acidosis was treated. Corrective resuscitative measures were taken including the initiation of inhaled
nitric oxide, correction of metabolic acidosis, downgrading of vasopressors/inotropes and resetting
of ventilator in accordance with a lung protective strategy. The patient left the OR an hour post
ECMO initiation with the ABG pH 7.36/pCO2 44.7/pO2 91.8/O2 sat 94.8%. TEE documented
unloading of the right ventricle and some early improvement to left ventricle function.
Over the next several days the patient’s respiratory status improved, she gained full neurologic and cardiac recovery, underwent bilateral pleural effusions drainage,
full explant of her breast prosthesis with closure and was weaned off
ECMO on day 9 (Figure 3). She was discharged to rehabilitation on
day 14. She was seen in six month follow up earlier this year. The
above described events have left her with little long term morbidity.
Figure 1
Figure 2
Discussion
Medical silicones belong to a polymer class characterized by
alternating silicon-oxygen atoms. They are chemically and thermally
stable, non-immunogenic and, as such, considered biologically inert.
As a result they have been used in a number of human implants,
most notably breast implants. Anecdotal reports have linked silicone
breast implants to a number of recognized rheumatologic diseases
(Sjogren’s syndrome, Lupus Erythematosus and scleroderma) and
to otherwise unexplained symptoms that appear to be auto immune
in origin [1]. While a 2000 meta-analysis failed to demonstrate an
increased incidence of specific rheumatologic diseases among silicone
breast implant patients, serologic studies have linked the HLA-DR53
genotype and the formation of B-cell autoantibodies to symptomatic
recipients [2,3]. Our patient during the time that she was discovered
to have ruptured implants began to complain of a number of nonspecific
ailments that were associated with elevated inflammatory
markers (ESR and CRP). Rheumatologic evaluation failed to identify
a specific rheumatologic illness or explanation for her fever of
unknown origin but prednisone did ameliorate the majority of her
symptoms. We may speculate that silicone exposure sensitized her
immune system but have no confirmation and are unclear as to
whether this may have played a role in the severity of her reaction to
silicone embolization.
On the day of surgery she experienced the described acute events
while under the careful supervision of an operation. That she became
severely hypoxic arrested after the manipulation of her ruptured
implants and well after anesthetic induction is most consistent with
a diagnosis of Silicone Embolism Syndrome (SES). Moreover, her
work up excluded the majority of alternate causes. The migration
of silicone, introduced from various perivascular spaces to the
pulmonary microcirculation can cause acute inflammation, increase
capillary permeability, alveolar edema and alveolar hemorrhage [4].
Lung imaging usually shows bilateral patchy alveolar infiltrates and
scattered ground glass opacities. Clinically an acute form occurring
within hours or days of inoculation and a more latent form up to six
months after injection have been described. Dyspnea, hypoxia and
acute respiratory failure are the most common symptoms. Treatment
consists of rest, supplemental oxygen and mechanical ventilation
if necessary. The role of corticosteroids is unclear. Most patients
recovering from the acute phase do so without sequela.
The patient presented represents a case of severe acute
pneumonitis resulting from silicone embolism syndrome. Despite
maximal medical therapy within an intensive hospital setting the
patient’s hypoxia failed to correct and she experienced two PEA
arrests. VV ECMO with VA standby was successfully used to rescue,
stabilize and recover this patient. In our review of the literature we
identified two case reports of patients requiring ECMO support for
recovery from silicone embolism syndrome, in each case after the
illegal injection of liquid silicone for cosmetic purposes [5,6]. This,
to our knowledge, is the first case of ECMO used to successfully
recover a patient from silicone embolism syndrome sustained during
a medically sanctioned silicone implant/explant procedure.
Figure 3
Figure 3
Sequential chest radiographs: day of admission, hospital day (HD)
4 and day of ECMO explants (HD 9).
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