U N I L A T E R A L P U L M O N A R Y O E D E M A : A CASE R E P O R T

PATRICK W. KNAPP AN D JOSEPH L. SELTZER

PULMONARY OEDEMA is known to o c c u r secon- along the clavicle. An arterial catheter was placed
dary to a high negative intrathoracic pressure, t-5 to monitor blood gases. Induction proceeded
We present a case o f unilateral p u l m o n a r y with thiopentone and a n a e s t h e s i a was maintained
o e d e m a which we feel was caused by obstruction with meperidine, metocurine and 66 pen- cent
o f the main b r o n c h u s in a s p o n t a n e o u s l y breath- nitrous oxide with o x y g e n . Controlled ventilation
ing patient. was c o m m e n c e d with a v o l u m e o f 750 ml at a rate
o f l0 per minute. Arterial blood g a s e s one horn"
REPORT OF A CASE after induction was Pao2 9.17 kPa (68.6 m m Hg),
Paco2 4.99 kPa (37.5 m m Hg), a n d cH+38.02
A 65-year-old white male with s q u a m o u s cell nmol/I (pH 7.42). Auscultation o f the c h e s t again
c a r c i n o m a o f the larynx was scheduled for a total revealed breath s o u n d s which were equal bilater-
l a r y n g e c t o m y and radical neck dissection. He ally. Fno~ was increased to 0.5. Repeated blood
had a history o f a myocardial infarction compli- gas analysis s h o w e d t h e Pao2 had increased to
cated by congestive heart failure s e v e n years be- 18.75 kPa (141 m m Hg). Several s u b s e q u e n t
fore admission. He was a 50 pack-year cigarette e x a m i n a t i o n s o f the lungs revealed no c h a n g e s
s m o k e r and b e c a m e short o f breath with minimal and the r e m a i n d e r of the a n a e s t h e t i c was un-
exertion. His only medication- was digoxin 0.25 eventful. During the five-hour operation he re-
mg per day. ceived 1850 ml of crystaloid solution 500 ml of
Physical examination revealed an elderly m a n colloid and 500 ml o f whole blood. Muscle relax-
with a barrel chest and increased r e s o n a n c e with alion was reversed with neostigmine 2.5 mg and
decreased breath s o u n d s bilaterally. T h e first a n d atropine 1.2 rag. Although no m e a s u r e m e n t s
s e c o n d heart s o u n d s were regular and distant. were made, respim'ations were j u d g e d to be
and no $3, S+ or m u r m u r were audible. N o j u g u l a r adequate a n d the patient was taken to the ,-eeov-
vein distension or peripheral o e d e m a was noted. ery room. Fifteen minutes after arrival he b e c a m e
An electrocardiogram s h o w e d evidence of an acutely agitated, d y s p n o e i c and cyanotic. Physi-
anterior wall infarction and elevated ST s e g m e n t cal e x a m i n a t i o n o f the c h e s t revealed normal
which persisted on serial cardiograms, suggesting breath s o u n d s and increased r e s o n a n c e on the left
a ventricular a n e u r y s m . T h e preoperative c h e s t side and no breath s o u n d s with dullness to per-
X-ray s h o w e d an enlarged left ventricle without c u s s i o n on the right. A s s i s t e d ventilation was
cardiomegaly, increased interstitial markings begun. Based on the clinical findings, which indi-
bilaterally, and evidence o f p u l m o n a r y h y p e r t e n - cated a total lack o f ventilation of the right side of
sion. Arterial blood g a s e s breathing room air the c h e s t , the tracheal tube was withdrawn until
were Paoa 10.37 kPa (78 m m Hg), Paco2 4.52 kPa the cuff was in view at the s t o m a . This man-
(34 m m Hg), and cH+38.90 nmol/I (pH 7.41). o e u v r e resulted in a rapid i m p r o v e m e n t in the
P u l m o n a r y function tests s h o w e d a vital capacity patient's colour and a return o f bilateral ventila-
o f two litres with a predicted value o f 3.9 litres tion, Coarse rales were n o w heard in the right
and F E V J V C was 0.61. lung. A c h e s t X-ray following this episode
It was elected to do a t r a c h e o s t o m y u n d e r local s h o w e d p u l m o n a r y o e d e m a confined to the fight
a n a e s t h e s i a b e c a u s e o f possible airway obstruc- lung field (Figure I).
tion by the tumour. An 8.0 m m R u s c h anode tube T h e patient was taken to the intensive care unit
was inserted between the s e c o n d and third and c o n t i n u e d on mechanical ventilation with VR
tracheal rings. Breath s o u n d s were equal bilater- 800, I M V 10 a n d P E E P 3 cm HzO. Four h o u r s
ally. T h e t u b e was secured by t w o s u t u r e s placed later a c h e s t X+ray s h o w e d less fluid on the right
side and arterial blood g a s e s on FUo= o f 0.5 were
Patrick W. Knapp+ M+D., Resident in Anesthesiol- Pao~ I 1.92 kPa (91 m m Hg), Paco= 5.05 kPa (38
ogy;Joseph L. Seltzer, M.D,, Assistant Professor. De-
partment of Anesthesiology. State University of New m m Hg), and cH+40.74 nmolt'l (pH 7.39). T h e
York, Upstate Medical Center, Syracuse, New York. next morning, a c h e s t X-ray s h o w e d almost total
13,210. clearing o f the right-sided infiltrate (Figure 2) a n d
437
Canad. Anaesth. Soc. J+, vol. 26, no+ 5. September 1979
438 CANADIAN ANAESTHETISTS" SOCIETYJOURNAL
FIGURE I The chest X-ray obtained in the recovery
room shows a generalized hazy density in the right lung.
FIGURE 2 The morning of the first postoperative
day there had been good resolution of the densities seen
on the chest film taken in the recovery room.
arterial blood gases when breathing 40 per cent
oxygen through a treacheostomy collar were
Paoz 27.82 kPa (134 ram Hg), Paco2 5.29 kPa (39
mm Hg), and cH+37.15 nmol/I (pH 7.43). The
patient was confused for several days but eventu-
ally returned to his pre-operative level of con-
sciousness and was discharged to home on the
15th postoperative day.
DISCUSSION
Our patient had several conditions which pre-
disposed him to develop pulmonary oedema. He
had chronic lung disease and pulmonary hyper-
tension, a history of previous myocardial infarc-
tion and congestive heart failure. In addition, he
was anesthetized by a technique that might have
mild negative inotropic action and had received
2850 ml of fluid during operation. However, the
oedema was limited to one lung and did not de-
velop until after the patient had been breathing
spontaneously for several minutes. Based on the
sequence of events and the physical examination
in the recovery room, it would appeal that his
inspiratory effort caused the tracheal tube to
move to a position which effectively blocked the
right main bronchus. The resulting high negative
pressure in the right hemi-thorax with his vigor-
ous inspiratory efforts resulted in the develop-
ment of pulmonary oedema in that obstructed
lung.
This complication probably could have been
avoided by better management of the tracheal
tube placement. Since we do not have an expla-
nation for the hypoxia during operation it is pos-
sible that the tip of the tube was near the carina
throughout the procedure, As the head and neck
were repositioned during the operation the fixa-
tion points, which were far from the trachostomy
stoma, allowed intermittent movement of the
tube. When the patient began to breathe spon-
taneously, his inspiratory effort moved the tube
so that the right main bronchus became
obstructed, We suggest that tracheal tubes intro-
duced through a tracheostomy during operation
should be securely fixed at a proper length and
changed to a standard laryngectomy tube before
the patient is transferred fiom the care of the
anaesthetist,
SUMMARY
We have presented a case of unilateral pulmo-
nary oedema which we feel is secondary to
obstruction of the right main bronchus during
spontaneous respiration. An anode tracheal tube
was introduced through a tracheostomy during
operation in a man with pre-existing pulmonary
and cardiac disease. At the end of the anaesthe-
tic+ acute obstruction to ventilation of the right
main bronchus developed with the tube still in
place and the patient breathing spontaneously.
The obstruction was relieved, by repositioning of
the tracheal tube, but not before the patient de-
veloped right unilateral pulmonary oedema.
RI~SUM/~
Une sonde trach6ale m6tallis6e fut introduite
par trach6otomie chez un vieillard atteint de
maladies cardiaque et pulmonaire. A la fin de
l'anesth6sie, une obstruction aigue de la bronche
souche droite s'est produite alors que le malade
respirait spontan6ment. Le retrait de la sonde a
 KNAPP & SELTZER: U N I L A T E R A L PULMONARY OEDF.MA
permis de corriger robstruction mais le malade
etait d6jh en crise d'0ed/~me aigu du poumon droit
seul. En 6tudiant la s6quence des 6v~nements e't
parce que I'ted~me se limitait ~ un seul poumoa,
les auteurs concluent que la cause en dtait
I'obstruction d'une bronche souche.
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