A 3-month-old (39 weeks postconceptual age) male infant weighing 2.9 kg was scheduled
for laser photocoagulation with a diagnosis of retinopathy of prematurity. He was
born at 27 weeks gestation with a birth weight of 970 g. He had been mechanically
ventilated from birth for 20 days for respiratory insufficiency due to respiratory
distress syndrome (RDS) and bronchopulmonary dysplasia (BPD). A chest X-ray performed
before the subsequent ligation of the patent ductus arteriosus showed bilateral haziness
in the entire lung field due to the RDS and BPD during tracheal intubation. The infant
required ventilation with a high concentration of oxygen and received surfactant therapy.
Twenty days after birth, patent ductus arteriosus (PDA) ligation was done under general
anesthesia in which induction was achieved with inhalation of sevoflurane and 1 mg
of rocuronium. The operation proceeded uneventfully and the extubation was performed
five days after the surgery. After extubation, the infant was able to breathe spontaneously
with an incubator oxygen supply, and the oxygen saturation was maintained above 90%.
After PDA ligation, the infant was diagnosed with retinopathy of prematurity, and
he was then scheduled for laser photocoagulation. On the chest X-ray, improvement
of haziness was observed from five days before the operation. After consultation with
pediatrics, the decision was made to operate.
Upon arrival in the operating room, electrocardiography, pulse oximetry, and noninvasive
blood pressure were monitored, and the patient's vital signs were stable. Induction
of anesthesia was achieved with thiopental (15 mg), rocuronium (2 mg), and sevoflurane.
The tracheal intubation was performed with an uncuffed 3.5 mm internal diameter endotracheal
tube, but there was no capnogram trace after three breaths. At this time, the oxygen
saturation rapidly dropped to below 80%. The endotracheal tube was removed because
the anesthesiologist suspected esophageal intubation and the patient was ventilated
with 100% oxygen via face mask. Mask ventilation was not performed well, and peak
inspiratory pressure was revealed to be above 25 mmHg. The anesthesiologist suspected
stiff lungs, which suggested bronchospasm. Hydrocortisone sodium succinate (Solu-Cortef®,
Pfizer Inc., New York, NY, USA) 20 mg was intravenously injected. Five minutes later,
oxygen saturation slowly increased up to 99% and reintubation was attempted. Although
it was confirmed by direct laryngoscopy that the tube had passed between the vocal
cords, proper ventilation of the lungs was not achieved. No expired carbon dioxide
was noted on the capnograph, and chest auscultation was equivocal. The oxygen saturation
was then in the low sixties. After sevoflurane was administered by inhalation, a slight
chest movement was noted, and oxygen saturation increased up to 80%. During that time,
a portable chest radiograph was taken which revealed severe consolidation with air
bronchograms (Fig. 1A). Despite ventilatory support for 10 minutes, the oxygen saturation
failed to increase beyond 80%. Hydrocortisone sodium succinate 20 mg was then intravenously
injected once more. Afterwards, SaO2 was maintained at 88-93%. The surgery was cancelled,
and glycopyrrolate 0.2 mg and pyridostigmine 0.2 mg were intravenously administered.
The intubated patient was transferred to the neonatal intensive care unit (NICU) with
Ambu bag ventilation for further management. While in transit to the NICU, the patient's
vital signs were stable, and oxygen saturation was maintained above 90%.
In the NICU, another chest radiograph was taken after the patient was stabilized,
and this showed an improved state of consolidation (Fig. 1B). After the patient's
spontaneous breathing completely returned and became regular, extubation was performed.
The patient recovered without complications.
We experienced a case in which severe bronchospasm caused ventilation failure in a
3-month-old premature pediatric patient with a previous history of mechanical ventilation
and incompletely resolved consolidation with underlying bronchopulmonary dysplasia.
In this case, the onset of symptoms was rapid, including extreme stiffness of the
lungs, and there was an absence of the end-tidal carbon dioxide trace noted immediately
after intubation. During the event, the chest radiography revealed severe consolidation
with air bronchograms.
Fatal contraction of airway smooth muscle can be observed spontaneously or by agonist.
Thus, even within the first days of life, bronchospasm can occur in preterm infants
Bronchospasm associated with anesthesia presents with an expiratory wheeze with/without
auscultation, prolonged expiration and rising end-tidal carbon dioxide, increasing
circuit pressure, increased pressures of inflation during positive pressure ventilation,
and/or desaturation .
Wheeze cannot be audible either with or without auscultation because it is caused
by gas flow in the patient's airways. Thus, in cases of severe bronchospasm such as
our case, the chest may be silent or equivocal on auscultation and the diagnosis may
be delayed on appropriate assessment of increased inflation pressures. However, wheeze
may occur as bronchospasm but can be heard with a misplaced endotracheal tube, such
as in bronchial or esophageal intubation, and with acute respiratory distress syndrome
or pulmonary edema. We also make a wrong diagnosis because the patient had no detectable
end-tidal carbon dioxide or chest movement. Thus, extubation was conducted and optimal
management was delayed. In the same way, wheezing was not a typical symptom for diagnosis
of bronchospasm, and the wheezing of our patient was not distinct because the patient
underwent severe airway obstruction.
Increased inspiratory pressures may develop not only with bronchospasm but also with
obstruction of a natural airway or any component of a breathing circuit and decreased
compliance of the lungs or chest such as atelectasis, hemo-pneumothorax, or fentanyl
induced rigidity . Accordingly, the anesthesiologist takes a systematic approach
to the diagnosis and treatment of bronchospasm in relation to anesthesia.
In our case, airway irritation from direct laryngoscopy and passage of the endotracheal
tube is suspected to have caused bronchospasm during intubation. This procedure is
noted for profoundly painful stimuli and is related to bronchospasm and/or laryngospasm.
In particular, a patient who has a previous respiratory history is closely connected
to an increased risk for perioperative desaturation, bronchospasm, laryngospasm, or
airway obstruction . Furthermore, our patient underwent long-term mechanical ventilation.
Therapy with high inspired oxygen concentrations or mechanical ventilation with high
positive airway pressures leads to inflammation, fibrosis, or smooth muscle hypertrophy
in the airways of premature infants , which might result in our patient having
an increased vulnerability to bronchospasm.
We suggest that the anesthesiologist should carefully consider respiratory complications
such as bronchospasm during the induction of anesthesia with a premature infant who
has a previous history of mechanical ventilation and underlying respiratory diseases.
In addition, we keep in mind the respiratory complications throughout general anesthesia.