Keywords
transnasal transsphenoidal pituitary surgery - negative pressure pulmonary edema -
nasal packing
Introduction
Negative pressure pulmonary edema (NPPE) is a bilateral, noncardiogenic flash pulmonary
edema manifesting as hyperacute respiratory failure. It occurs when a patient spontaneously
generates strong negative intrathoracic force against an obstructed airway. The stated
incidence is 0.1 to 11%, although the actual occurrence is presumed much higher.[1]
[2] Underreporting is attributed to a lack of clinical awareness, delayed recognition,
and masking of manifestations. However, NPPE must be addressed as a life-threatening
emergency and managed expeditiously to prevent avoidable consequences. We report successful
management of NPPE following endoscopic transnasal-transsphenoidal (TNTS) pituitary
surgery for nonfunctional pituitary tumor (NFPT). Patient provided written consent
and CARE (CAse REport) guidelines were referenced in writing this case report.
Case Report
A 43-year-old, 150 cm tall, 50 kg woman with body mass index of 22.22 kg/m2, without any comorbidities presented with headache and gradual visual loss. Magnetic
resonance imaging of brain revealed a mass measuring 22 × 17 × 21 mm along planum
sphenoidale, extending into suprasellar region. Preoperative hormonal workup and blood
tests were unremarkable. The patient was scheduled for endoscopic resection of NFPT
through TNTS approach.
Preoperatively, the patient was positioned supine, and standard monitors were applied.
Following propofol, fentanyl, and vecuronium induced anesthesia, the patient was intubated.
Intraoperatively, propofol and dexmedetomidine infusions were used to achieve target
entropy values between 40 and 60. Vitals remained stable and arterial blood gas (ABG)
levels were normal. Surgery lasted 2 hours. In total, 1,000 mL intravenous fluid were
used, 150 mL blood loss, and 300 mL urine output was noted. After completion, surgeon
performed bilateral nasal packing using absorptive nasal packs. Propofol and dexmedetomidine
infusions were stopped. Analgesics and antiemetic drugs were administered. Intravenous
neostigmine 2.5 mg and glycopyrrolate 0.5 mg were given to reverse neuromuscular blockade
(NMB) when train-of-four ratio (TOFR) was 0.7. A smooth extubation was performed after
awakening the patient, once entropy values were > 80 and TOFR was 0.9.
After extubation, the patient appeared stable and could obey commands. There were
no episodes of coughing or laryngospasm or kinking of endotracheal tube. Oxygen supplementation
was continued. The patient gradually exhibited labored breathing and became agitated.
She was propped up and jaw-thrust was given to assist breathing. Oxygen saturation
began to drop and fell to a minimum of 90%. Blood pressure and heart rate increased
dramatically. On auscultation, crepitations were heard in basal lung fields bilaterally.
ABG revealed hypercarbia and mild hypoxemia. Due to deteriorating clinical condition,
patient's trachea was reintubated. On reintubation, pinkish frothy secretions appeared
in the endotracheal tube. Diagnosis of pulmonary edema was considered, and 20 mg furosemide
was administered. Subsequently, patient was sedated, paralyzed, and shifted to intensive
care unit. Positive pressure ventilation (PPV) with positive end-expiratory pressure
of 8 cm H2O was continued. X-ray chest revealed bilateral homogenous diffuse opacities ([Fig. 1A]). Echocardiography showed an ejection fraction of 55% with normal valvular morphology.
Vital signs and ABG were normal. Diagnosis of NPPE was made considering clinical presentation,
ABG analysis, chest imaging, and exclusion of other causes of pulmonary edema. PPV
was continued for the next 24 hours.
Fig. 1 (A) Chest X-ray depicts features of pulmonary edema following intubation. (B) Chest X-ray depicts resolution of pulmonary edema.
Subsequent X-ray chest demonstrated reduced haziness ([Fig. 1B]). Oxygen saturation of 100% was maintained on 30% fraction of inspired oxygen. Both
nasal packs were removed. Patient was gradually weaned off and extubated. On the second
postoperative day, the chest radiograph was normal; the patient was mobilized to the
ward.
Discussion
NPPE is a dilemmatic diagnosis, usually by exclusion, because of its indeterminate
myriad of etiologies, masked manifestations, overlapping symptoms, and lack or delay
in clinical suspicion. It is more prevalent in men and healthier patients, presumably
due to greater propensity to generate more negative intrathoracic pressure against
a closed upper airway.[1]
[2]
Pathogenically, NPPE is transudative edema caused by high negative intrathoracic pressure
that translates into augmented pulmonary venous hydrostatic pressure and increased
pulmonary capillary permeability leading to flooding of alveoli. Hypoxemia and respiratory
acidosis further increase pulmonary vascular resistance and contribute to pulmonary
capillary membrane injury, setting up a vicious cycle.
Many cases of NPPE following compact nasal packing after rhinoplasty have been reported
in the literature, but its occurrence after TNTS surgery for NFPT has not been reported.[3]
[4] Nishino and Kochi demonstrated that adults under the effect of sedation lose ability
to shift from nasal to oral breathing due to a lack of conscious control of palatal
muscles.[5] This finding can be extrapolated to patients emerging from general anesthesia, as
in our case. We believe that bilaterally packed nares acted as obstruction in indexed
case. Instead of breathing through the oral cavity, the patient attempted to breathe
through the nose, exerting excessive negative intrathoracic pressure, which led to
the development of type-I NPPE. Type-I NPPE is caused by acute obstruction of upper
airway, whereas type-II is observed following resolution of chronically obstructed
upper airway.
Nasal packing helps in hemostasis, supports the reconstruction site, prevents synechiae
formation, and temporarily seals off the intracranial cavity. It is also linked with
patient discomfort and theoretical risk for infection (i.e., toxic shock syndrome).
Hence, foregoing nasal packing or partially packed sphenoid cavity, without packing
the nasal cavity is significantly more comfortable and does not alter recovery.[6]
[7]
Few reports mentioned NPPE occurrence after TNTS for functional pituitary tumors.[8] The functional tumor produces structural changes in the airway and hormonal imbalance
which further causes increased pulmonary capillary permeability and aberrant fluid
distribution, hence increases the likelihood of developing NPPE. Even though no hormonal
abnormalities were found in our case, there might have been some underlying subclinical
imbalances owing to the pituitary gland dysfunction, which was the primary site of
pathology.
Other differentials for acute NPPE include aspiration pneumonitis, fluid overload,
sepsis, and anesthetic and nonanesthetic drugs. Neostigmine, a drug used to reverse
the NMB, is occasionally implicated with NPPE by its ability to impair upper airway
dilator muscle activity.[9]
NPPE responds expeditiously with appropriate therapy, such as lung protective PPV
and supportive care. Diuretics are administered to reverse hydrostatic gradient across
pulmonary capillary membranes and hasten recovery, although their role is debatable.[10] Refractory respiratory failure is managed by paralyzing and ventilating, and prone
positioning.
To conclude, a high index of suspicion of NPPE may be warranted following TNTS surgery
for NFPT secondary to bilateral nasal packing. Whenever possible, avoid nasal packing
unless there is structural impairment or an active nasal bleed is present.
