Negative pressure pulmonary edema in the prone position: a case report
Hesham Omar
2
Jaya Kolla
1
Amrat Anand
0
Willem Nel
0
Devanand Mangar
1
Enrico Camporesi
3
0
Florida Gulf to Bay Anesthesiology Associates
,
PA, Tampa, Florida
,
USA
1
Research Associate, Tampa General Hospital, Florida Gulf to Bay Anesthesiology Associates
,
PA, Tampa, Florida
,
USA
2
Department of Cardiovascular Medicine, Cairo University Hospital, Cairo, Egypt, Visiting Scholar at Tampa General Hospital, Florida Gulf to Bay Anesthesiology Associates
,
PA, Tampa, Florida
,
USA
3
Department of Surgery/Anesthesiology, University of South Florida, Tampa, FL and Florida Gulf to Bay Anesthesiology Associates
,
PA, Tampa, Florida
,
USA
Acute airway obstruction can result in life - threatening pulmonary edema. It can develop rapidly, without warning, in otherwise healthy patients. Negative pressure pulmonary edema has been described after acute airway obstruction in situations when a patient is breathing against an obstructed airway such as croup, epiglottitis or laryngospasm. In the following case, we observed a rare occurrence of pulmonary edema in a female following sedation in the prone position.
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Case presentation
A 49-year-old Caucasian female, with a long history of heavy
cigarette smoking and a previous diagnosis of
supraventricular tachycardia, for which cardiac ablation was
performed 2 years ago, was admitted to the hospital for an
elective sacral neuromodulator lead change to treat urinary
incontinence. In the operating room, the patient received
monitored anesthesia care (MAC) in the prone position.
During the procedure she required increasing sedation
(IV propofol infusion) and after thirty minutes the patient
showed progressive hypercapnia from the nasal cannula
sample line, while receiving supplemental oxygen (4 L/min).
An oral airway was placed, but end-tidal CO2 ranged from
65 to 75 mmHg and did not improve. It was then decided to
place a laryngeal mask and to supply positive pressure
ventilation; however no improvement of the hypercapnia
ensued and we could not provide adequate ventilation. The
patient was then emergently intubated to secure an airway
and provide adequate ventilation. This required interruption
of surgery, turning the patient supine, ventilating oxygen by
mask and a succinylcholine bolus. During the intubation
process, marked edema above the vocal cords was noticed by
an experienced anesthesiologist, allowing only for a smaller
sized endotracheal tube to be inserted (6 mm with difficulty,
but not a 7 mm tube). The patient was given dexamethasone
8 mg and diphenhydramine 25 mg for the airway edema.
Following intubation and after securing the tube in place, we
started positive pressure ventilation and returned the patient
to the prone position, and the end tidal CO2 returned within
normal range. However, within a few minutes, the patient
developed bibasilar rales, with abundant frothy, blood
tinged secretions appearing in the tube. We maintained the
patient prone while the surgical procedure was concluded.
The edema fluid was adequately suctioned and abated after
10 minutes of positive pressure ventilation. Postoperatively
the patient remained intubated and sedated on a propofol
infusion. While in recovery, an arterial blood gas obtained
on Synchronized Intermittent Mechanical Ventilation
(SIMV) and FiO2 of 30%, showed a PO2 of 92 mmHg,
PCO2 of 46 mmHg, pH of 7.34 and HCO3 of 25 mEq/L with
a SaO2 of 97%. Chest X-ray performed after surgery indicated
clear lung fields with normal size heart and no evidence of
pulmonary edema. The patients condition steadily
improved and she was subsequently extubated two hours
later but continued to be closely monitored overnight
and was discharged the following day without requiring an
ICU stay.
Discussion
In this case report we describe a case of NPPE following
supraglottic obstruction with deepening sedation in the
prone position. Supraglottic obstruction was possibly
induced by intense inspiratory effort in a patient who was
sedated and hypoventilating leading to airway obstruction
and subsequently pulmonary edema. Another possibility is
malpositioning (or biting) of the LMA causing inspiratory
efforts against an obstructed airway, which could be the
cause for the observed supraglottic swelling. The apparent
absence of gastric contents in the pulmonary edema fluid,
the absence of left ventricular dysfunction in a previously
performed echocardiogram and the sequence of the
described symptoms make the diagnosis of acute NPPE
likely.
NPPE is a relatively uncommon intra-operative and
postoperative complication and is still a diagnosis by exclusion
of other factors. Generally, NPPE occurs when inspiratory
effort against an obstruction creates a large
intrapulmonary negative pressure which can increase venous return
with subsequent increase in the pulmonary capillary
hydrostatic pressure. The transudation of fluid from the
pulmonary vasculature causes edema formation into
the alveolar space [1,2]. Normal inspiratory pleural
pressure rang (...truncated)