Abstract
Negative pressure pulmonary edema (NPPE) may result in respiratory
failure refractory to conventional management strategies. Venovenous
extracorporeal membrane oxygenation (VV ECMO) can serve as a rescue
therapy in cases of severe respiratory failure. Rapid initiation of VV
ECMO can decrease morbidity and mortality while facilitating early
liberation from mechanical ventilation and promoting early
rehabilitation. We describe the successful utilization of VV ECMO as
rescue therapy for severe NPPE-induced hypoxic respiratory failure and
peri-arrest state in the post-anesthesia care unit (PACU) in a patient
with post-extubation airway obstruction after undergoing patellar tendon
repair.
Glossary of Terms:
Negative Pressure pulmonary edema: NPPE
Veno-venous extracorporeal membrane oxygenation: VV ECMO
Post-anesthesia care unit: PACU
Systemic anticoagulation: SA
Membrane pressure gradient: dP
Chest radiograph: CXR
Oxygen delivery: DO2
Introduction
Negative Pressure pulmonary edema (NPPE), also known as postobstructive
pulmonary edema, is a rare life-threatening etiology of acute
respiratory failure. Classically NPPE develops as a result of upper
airway obstruction from post-extubation laryngospasm after surgery,
upper airway infections, or tumors1.
Conventional treatment of severe NPPE is focused on relieving the upper
airway obstruction, positive pressure ventilation, and medication
therapy including diuretics, with resolution of most cases. Case reports
have described the need for delayed veno-venous extracorporeal membrane
oxygenation (VV ECMO) in cases of refractory hypoxia not responding to
initial therapies 2, 3, 4, 5. However, the use of VV
ECMO as acute rescue therapy in the post anesthesia care unit (PACU) for
NPPE-induced severe hypoxic respiratory failure, shock, and peri-arrest
physiology is yet to be described in the literature.
We describe the utilization of VV ECMO in the PACU as a rescue therapy
for severe NPPE induced hypoxic respiratory failure and profound shock
in a patient with post extubation airway obstruction after undergoing
elective patellar tendon repair. Additionally, we discuss the challenges
of systemic anticoagulation (SA) in the immediate postoperative period,
early mechanical ventilation liberation facilitated by VV ECMO support,
and the consideration of VV ECMO as part of the difficult airway
management algorithm 6.
This manuscript adheres to the Consensus-based Clinical Case Reporting
Guidelines 7. Written Health Insurance Portability and
Accountability Act authorization has been obtained for the publication
of this case report
Case Description
A 29-year-old ASA II male with history of post-traumatic stress disorder
(PTSD) underwent elective open patellar tendon repair under general
anesthesia at an outside hospital. The case was uneventful and the
patient was extubated prior to transfer to the PACU. On arrival to the
PACU, he was noted to be apneic with concern for airway obstruction. Bag
mask ventilation and narcan was administered. Despite these
interventions the patient developed worsening respiratory distress,
profound hypoxemia (SpO2 <85%), and copious pulmonary edema.
Reintubation required several attempts due to regurgitation of profuse
pulmonary edema. The patient was given 120 mg of furosemide for
diuresis. Multiple modes of ventilation, including inverse ratio
ventilation, were attempted without success and hypoxemia persisted.
Ventilator settings were maximized on a volume targeted
pressure-controlled mode with PEEP of 24 cmH2O and 100% FIO2 with a
prolonged inspiratory time.
Despite maximal medical optimization he had severe refractory hypoxia
with subsequent circulatory shock. The patient required high dose
vasopressor support including norepinephrine, epinephrine, and
vasopressin infusions, along with bolus dosing of vasopressors to
maintain adequate blood pressure. Given this, the ECMO team was
consulted for emergent VV ECMO cannulation. The patient was deemed a
suitable candidate for ECMO cannulation. Given the hemodynamic
instability the decision was made to initiate ECMO therapy in the PACU.
A right femoral 25 french multistage venous access cannula and a 22
french right internal jugular venous return cannula were placed with
subsequent ECMO initiation via a Cardiohelp system. ECMO flow was set to
5 liters at 3460 RPMS and a sweep gas of 8 liters. Prior to leaving the
PACU, the HLS circuit was noted to have a rapidly rising membrane
pressure gradient (dP), from 20 mmHg to 80 mmHg, necessitating a circuit
exchange due to concern for oxygenator thrombosis. The patient received
5000 units of heparin at the time of cannulation and an additional 5000
units followed by a heparin infusion at the time of oxygenator exchange.
Subsequent dP maintained within acceptable range of 20-30 mmHg.
The patient was then transferred to the intensive care unit at our
institution (Table 1), where he was transitioned to pressure control
ventilation with PEEP of 15 cmH2O and inspiratory pressures of 16 cmH2O.
Despite these settings, tidal volumes of only 20 ml to 70 ml could be
achieved due to the poor pulmonary compliance. Initial chest radiograph
(CXR) demonstrated complete opacification of bilateral lung fields
(Figure 1). Within 24 hours of cannulation the patient demonstrated a
rapid improvement in his oxygenation (Table 2). Vasopressor requirements
dramatically declined and he was weaned off all vasopressor support.
Transthoracic echocardiogram revealed hyperdynamic left ventricular
function, ejection fraction >70%, and normal right
ventricular function. The acute kidney injury present on admission
rapidly resolved, and he required diuresis for the first 48 hours.
Forty-eight hours post cannulation, he was able to be extubated with
ongoing support via VV ECMO despite his CXR demonstrating persistent
extensive bilateral airspace opacities (Figure 2). Anticoagulation for
the ECMO circuit was maintained with heparin infusion targeting aPTT
goal of 40 seconds. A small amount of bleeding from the cannulation site
occurred but resolved with suturing. No other hemorrhagic complications
were experienced including at the operative site.
On day 5, he tolerated a sweep trial and was subsequently liberated from
ECMO. He briefly required oxygen via nasal cannula but was weaned to
room air within the next 48 hours with drastic improvements in his CXR
(Figure 3). He was transferred to the floor on day 7. On day 8, he was
discharged home-neurologically intact without a supplemental oxygen
requirement (Table 1).
Discussion
This case illustrates the feasibility of early initiation of ECMO
support in the perioperative period. In this case, ECMO therapy was
initiated while the patient was in extremis with profound hemodynamic
instability and shock secondary to severe hypoxemia. In the presence of
severe hypoxemia, an inability to match the high myocardial oxygen
demand leads to hypotension and arrest if the cycle is not interrupted.
Rapid institution of VV ECMO in the PACU allowed our team to interrupt
this vicious cycle preventing cardiac arrest and anoxic brain injury.
When initiating VV ECMO in the immediate postoperative period, the need
for systemic anticoagulation (SA) poses a myriad of challenges. SA is
generally required during ECMO therapies as blood exposed to foreign
materials triggers the inflammatory response/coagulation cascade leading
to prothrombotic state 9, 10The risks of
thromboembolic events such as circuit thrombosis, oxygenator failure,
and venous thromboembolism must be weighed against the potential risks
of major bleeding with SA in the postoperative period. With heparin
bonded extracorporeal tubing and newer generation centrifugal pumps
there has been increased interest in minimizing SA in these patients and
literature supports the feasibility of an anticoagulation free approach
with no increased risk of thrombosis 11, 12.
Unfortunately, our patient had a rapidly rising dP immediately post
cannulation, raising concern for oxygenator thrombosis necessitating a
circuit exchange. Given the concerns for a prothrombotic state, SA with
heparin infusion was initiated and maintained until decannulation. The
patient had no further significant oxygenator thrombosis with stable dPs
and no post decannulation venous thromboembolism. Additionally, the
patient had no hemorrhagic complications despite his recent orthopedic
surgery.
Severe NPPE can significantly impair lung compliance making maintenance
of lung protective ventilation while promoting adequate gas exchange a
considerable challenge.
Utilization of VV ECMO not only allows for lung protective ventilation,
but also facilitates early extubation with gas exchange supported by
ECMO 13. Additionally, early liberation from
mechanical ventilation and associated sedation can minimize risk of
delirium, critical illness myopathy/polyneuropathy, diaphragmatic
dysfunction, and ventilator associated pneumonia 14.
Early extubation also facilitates patient interaction which is often an
under-appreciated benefit that can not only minimize patient anxiety and
discomfort but also facilitate better care as patients can relay their
symptoms to better inform care 14. This case
demonstrated the ability to successfully liberate our patient from the
ventilator within 36 hours of the initial insult while supporting him on
VV ECMO till he had recovered gas exchange. Early extubation facilitated
removal of sedation, minimized deconditioning in the setting of his
patellar tendon repair, and allowed for enhanced patient interaction
which was especially important to this patient in the setting of his
history of PTSD.
The profuse pulmonary edema in this case created a difficult airway for
reintubation. The difficult airway algorithm historically relied on an
invasive emergency cricothyrotomy as a last resort for a difficult
airway if intubation or other airway adjuvants failed6. In the 2022 update of the American Society of
Anesthesiologists Practice Guidelines for Management of the Difficult
Airway, ECMO is now considered a vital part of the algorithm for
management of the difficult airway. The guidelines reinforce the
importance of minimizing time where a patient cannot be ventilated or
oxygenated 6. Research has shown that anoxic brain
damage can occur within minutes without oxygen and death shortly after,
making early intervention imperative 15. Rapid
institution of VV ECMO, as in this case, can be lifesaving and is an
important resource that should be part of every difficult airway
algorithm for a patient that cannot be ventilated or oxygenated.
In cases of severe NPPE with refractory hypoxia, despite conventional
treatment with positive pressure ventilation, rapid initiation of VV
ECMO in the postoperative is not only feasible but can also decrease
morbidity and mortality. VV ECMO facilitates lung protective ventilation
as well as early liberation from mechanical ventilation thus minimizing
risk of delirium, critical illness myopathy/polyneuropathy,
diaphragmatic dysfunction, and ventilator associated pneumonia while
promoting early rehabilitation. Early initiation of ECMO therapy should
be incorporated into any clinical algorithm when presented with
refractory respiratory failure.
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Tables
Table 1 Title: Timeline of Relevant Clinical Events