CASE REPORT
pneumothorax
thoracostomy
From the EmergencyDepartment,
Depaitment of Medicine, University
of Pennsylvania, Philadelphia.
Receivedfor publication
September9, 1992. Acceptedfor
publication November 16, 1992.
MAY 1993 22:5 ANNALS OF EMERGENCY MEDICINE
N e e d l e Thoracostomy Fails to Detect a Fatal
Tension Pneumothorax
Daniel Mines, MD
Stephanie Abbuhl, MD, FACEP
Needle thoracostomy is an emergency procedure used to beth
diagnose and initially treat a tension pneumothorax. We report a
case of fatal tension pneumothorax in an intubated patient with
chronic obstructive pulmonary disease that was missed by this
technique. A tension pneumothorax involving only the right
middle and lower lobes was found at autopsy.The autopsy also
suggested that needle thoracostomy was misleading because it
sampled air from a noncommunicating bulla in the right upper
lobe rather than from the pleural space. Tension physiology
can exist with only localized collapse of a lung, and diagnostic
needle thoracostomy can be falsely negative. When tension
pneumothorax is strongly suspected, if empiric thoracentesis
does not vent air under pressure, subsequenttube thoracostomy
is indicated.
[Mines D, Abbuhl S: Needle thoracostomy fails to detect a fatal
tension pneumothorax. Ann EmergMed May 1993;22:863-866.]
INTRODUCTION
Tension pneumothorax, which can be rapidly fatal, often
is diagnosed on clinical grounds because time may not
permit radiographic confirmation. Needle thoracostomy--
also known as thoracentesis and needle decompression of
the chest--can quickly diagnose and temporarily treat a
tension pneumothorax by venting intrapleural air under
pressure to the atmosphere. 1-3 Although it is used
commonly in this setting, this technique has limitations
that may not be widely recognized, as the following case
illustrates.
CASE REPORT
A 68-year-old man with a history of chronic obstructive
pulmonary disease and hypertension presented to the
emergency department because of difficulty breathing.
During the course of the daB the patient became short
of breath, and after the onset of left-sided chest pain that
radiated to his back, the dyspnea intensified. There was
863/ 133
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Mines & Abbuhl
no recent change in sputum, fever, or chills, nor history of
coronary artery disease. Medications included an albuterol
inhaler, sustained-release theophylline, and prednisone.
The patient was cyanotic, unresponsive, and in marked
respiratory distress. Blood pressure was 190/110 mm Hg
in both arms; pulse, 140; rectal temperature, 37.4 C; and
respirations, 40. The jugular veins were not distended. On
auscultation, breath sounds were markedly diminished
bilaterally, and there were scattered rhonchi. Heart sounds
were distant and regular; no murmur, rub, or gallop was
heard. The abdomen was soft and not distended. The
extremities were not edematous.
The patient was intubated because of his impending
respiratory failure, using an orotracheal approach and
topical anesthesia. A chest radiograph showed the endo-
tracheal tube in satisfactory position, a normal mediastinal
contour, a left perihilar infiltrate, and bullous changes in
both upper lung fields. An ECG revealed sinus tachycar-
dia without ischemic changes. An arterial blood gas,
drawn before intubation when the patient was breathing
100% oxygen, returned with a pH of 7.04; CO 2, 105 mm
Hg; oxygen, 95 mm Hg; and HCO3,26 mEq/L.
After intubation, the patient became more alert and
was able to follow commands. However, ten minutes later
he suddenly became unresponsive, profoundly hypoten-
sire, and, within seconds, pulseless. The rhythm on the
monitor remained sinus tachycardia.
CPR and volume resuscitation were begun. IV epine-
phrine and bicarbonate were administered as empiric
treatment for electromechanical dissociation. The endo-
tracheal tube position was verified. Distant breath sounds
still were heard symmetrically over both lung fields, and
the trachea was midline. When the patient did not
respond to these initial measures, a 1&gauge over-the-
needle catheter connected to water seal was inserted into
the left chest in the second intercostal space, midclavicu-
lar line. Air bubbled continuously through the water seal,
and a spontaneous pulse returned. A 28F thoracostomy
tube was inserted in the midaxillary line, fifth intercostal
space. As the tube was being secured, the patient again
became tachycardic and then pulseless. CPR was restarted.
Patency of the chest tube was confirmed by a persistent
air leak.
Because there was now a strong suspicion for a contra-
lateral tensio n pneumothorax, thoracentesis of the right
chest was attempted, in the same high anterior position
as had been used on the left. There was no efflux of air
through the needle. Pericardiocentesis was performed
using a left subxiphoid approach, yielding 2 mL of yellow
fluid, without clinical improvement. Shortly afterward,
1 3 4/864
the patient went into ventricular fibrillation and could
not be resuscitated.
At autopsy, air under pressure escaped when the right
hemothorax was opened. The right middle and lower
lobes of the lung were collapsed completely, and the
mediastinum was deviated leftward. There was no evidence
of myocardial infarction, cardiac tamponade, thoracic
aortic dissection, or pulmonary embolism. These findings
suggest that the patient died from a right-sided tension
pneumothorax.
Unexpectedly, the right upper lobe remained inflated
when the anterior chest wall was removed (Figure). No
obstructing endobronchial lesion or pleural scarring was
found to account for this finding. Air trapped in large,
noncommunicating buflae was responsible for the persis-
tent expansion of the right upper lobe.
DISCUSSION
The classic findings of tension pneumothorax--tracheal
deviation, hyperresonant hemithorax, and unilaterally
decreased breath sounds--are useful to suggest the diag-
nosis, but they are not always present.l,2, 4 In patients
with chronic obstructive pulmonary disease, the diagnosis
of tension pneumothorax can be especially subtle.
Physical signs are often absent or overlooked because
their underlying disease already may have produced
diminished chest wall motion, decreased breath sounds,
and hyperresonance to percussion. 2 Similarly, distended
neck veins, which are suggestive of tension pneumothorax
in patients without underlying cardiopulmonary disease,
are nonspecific in this population because they are
observed frequently during an exacerbation of chronic
obstructive pulmonary disease.
Figure.
Autopsy photograph of the
thoracic structures after the
anterior chest wall was
removed. Although the right
middle and lower lobes
(arrow 1) are collapsed as
expected, the right upper
lobe (arrow 2) is still
inflated because of air
trapped in bullae. A chest
tube is present in the left
hemithorax.
ANNALS OF EMERGENCY MEDICINE 22:5 MAY 1993
TENSION PNEUMOTHORAX
Mines & Abbuhl
Besides physical findings, the clinical setting may suggest
the diagnosis of tension pneumothorax. Positive-pressure
ventilation, through a bag-valve system or a mechanical
ventilator, increases the risk of tension pneumothorax,
particularly when there is coexistent pulmonary disease. 1-3,5
Both risk factors were present in the index case.
When a tension pneumothorax is suspected clinically
and the patient is unstable, time does not permit a radio-
graphic diagnosis. Instead, empiric needle or catheter
thoracentesis is indicated. 1-3 If a tension pneumothorax
is present, one expects to see the "the rapid efflux of air
through the needle during both inspiration and expiration"
along with clinical improvement. 1 Needle thoracostomy is
thus a quick diagnostic and therapeutic maneuver, which
needs to be followed by a more definitive tube thoracostomy
Most authorities1,6, r recommend needle decompres-
sion using a high anterior approach in the second or
third intercostal space at the midclavicular line. McEwen 2
favored empiric placement of the needle in the fourth or
fifth intercostal space, anterior axillary line, but Ross 1
believed that the lateral approach is less safe. He argued
that because free air in the pleural space theoretically rises
to the high anterior chest, the lateral approach presents a
greater risk of lung injury if a large pneumothorax is not
present. Also, one is more likely to encounter pleural
adhesions using the lateral approach because they are
more prevalent in dependent areas of the thorax.
Empiric needle decompression of the chest is not with-
out risks. At best, if a tension pneumothorax is present,
thoracentesis converts the injury to a simple pneumotho-
tax. On the other hand, if the diagnosis is wrong and the
lung is inflated normally, thoracentesis actually can pro-
duce a pneumothorax. This outcome can be minimized
by attaching the needle to a water seal or syringe. Even if
it does not create a simple pneumothorax, thoracentesis
produces a tiny pleural puncture wound that, in concert
with positive-pressure ventilation, can result in a tension
pneumothorax. For this reason, in intubated patients,
tube thoracostomy is the preferred technique to empiri-
cally exclude tension pneumothorax when time permits, t
The case described here also shows that needle thora-
costomy is not a perfectly sensitive test to detect tension
pneumothorax. Moreover, it illustrates an important point
about clinical reasoning. A single negative diagnostic test
result that does not concur with a strong clinical suspicion
should make the physician question whether this is a false-
negative result> In retrospect, it would have been reason-
able for the physicians here to proceed with a right-sided
tube thoracostomy despite the negative thoracentesis.
MAY 1993 22:5 ANNALS OF EMERGENCY MEDICINE
Reviewing the medical literature since 1966, we could
identify no study that quantitated the sensitivity of needle
thoracostomy in diagnosing tension pneumothorax. Several
authorities2,5, 6 who advocate needle thoracostomy to
empirically diagnose this condition do not mention its
limitations, implying that it is virtually 100% sensitive.
Ross 1 mentioned that in performing thoracentesis using
the anterior approach, a loculated simple pneumothorax
can be missed. To our knowledge, this case report is the
first description of a false-negative result of needle thora-
costomy in a tension pneumothorax that was confirmed
at autopsy
Our case also shows that an entire lung need not be
collapsed for tension physiology to exist. This observation
is consistent with results of a controlled study of tension
pneumothorax in animals. 9 In this experiment, air was
introduced into the pleural cavities of mechanically venti-
lated sheep. Cardiac output decreased as the degree of
pneumothorax increased, even before the entire lung was
collapsed and before mediastinal shift was seen on chest
radiograph. In another report, radiographically small pneu-
mothoraces resulted in severe cardiopulmonary compro-
mise in mechanically ventilated patients with adult respira-
tory distress syndrome, lo Tension physiology developed in
some of these patients despite a functioning ipsilateral chest
tube because the pneumothoraces were loculated.
SUMMARY
A patient with chronic obstructive pulmonary disease was
intubated because of acute respiratory failure and soon suf-
fered cardiovascular collapse. A left-sided tension pneu-
mothorax was diagnosed and treated quickly, but a subse-
quent right-sided tension pneumothorax was missed
because needle thoracostomy did not vent air under pres-
sure. An autopsy suggested that the needle thoracostomy
was falsely negative because it sampled air from a noncom-
municating bulla rather than from the pleural space.
In intubated patients, tension physiology can exist with
only localized collapse of a lung, and diagnostic needle
thoracostomy can be falsely negative. When a high index
of suspicion for tension pneumothorax is present in very
unstable patients, empiric tube thoracostomy is a reason-
able first step and a mandatory second step if initial
thoracentesis does not yield expected results.
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Clinical Practice, ed 3. Philadelphia, MosbyYear Book,1992, p 1121-1131.
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M~nes & Abbuhl

I II

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