Bilateral massive pulmonary embolism secondary

to decompression sickness: A case report

Ulubay Gaye, MD,
a
Sarnc Ulasl Sevinc, MD,
a
Karacan Ozgur, MD,
a
Gumus Tuna, MD,
b
and Eyuboglu Oner Fusun, MD
a
This case report describes massive pulmonary embolism in a patient as a complication of decompression
illness. Twenty-four hours after a scuba dive, a 50-year-old man developed acute pulmonary hyperten-
sion and decompression sickness that produced bilateral embolism in the lung at day 6 of hospitalization.
He had no risk factor for pulmonary embolism earlier except smoking. Decompression sickness that
RESULTS in formation of bubbles of inert gas is a risk for both aviators and divers. The present case
strongly suggests that micro-bubbles may cause life-threatening massive pulmonary embolism. (Heart
Lung 2007;36:450453.)
A
50-year-old man was admitted to the hospital
with generalized weakness and dyspnea after
having made a 50-meter scuba dive 24 hours
earlier. After diving, he developed hemoptysis,
headache, and neck pain. He had a 20-year history
of smoking history. On admission, the patient was
dyspneic. His physical examination was unremark-
able except for peripheral cyanosis. His blood pres-
sure was 120/80 mm Hg, and his heart rate was 80
bpm. Results of a chest radiograph (Fig 1), as well as
values for complete blood count, C-reactive protein,
erythrocyte sedimentation rate, blood chemistry,
serum D-dimer (0.3 g/mL by way of turbidimetric
method), Creatine Kinase-MB and troponin-I, were
all within normal limits. Arterial blood gases at
room air showed moderate hypoxemia (pH 7.45;
PO
2
45 mm Hg; PcO
2
35 mm Hg; HcO
3
22.9 mmol/L,
SpO
2
: 83%), and his P(A-a) ScO
2
was 64 mm Hg.
Results of thoracic and cranial computed tomogra-
phy scans were normal; however, echocardiography
showed increased pulmonary arterial systolic pres-
sure of 47 mm Hg and enlargement of the right
atrium and ventricle. He was diagnosed with de-
compression illness, acute respiratory failure, and
corpulmonale preceded by recent scuba diving, sug-
gesting an arterial air embolism. The patient was
given hyperbaric oxygen therapy (8 hours/d) and
subcutaneous heparin as enoxaparine. He was not
placed on leg compression. Hypoxemia improved
after hyperbaric oxygen therapy.
On day 6 of hospitalization, substernal pain and
dyspnea developed. While breathing nasal oxygen
at 10 L/min, arterial blood gas analysis showed
severe hypoxemia and hypocapnia (pH 7.25; PO
2
From
a
Department of Pulmonary Disease, Baskent University
Faculty of Medicine, and
b
Department of Hyperbaric and Under-
sea Medicine, Gulhane Military Medical Academy, Ankara, Tur-
key.
Reprint requests: Gaye Ulubay, MD, Department of Pulmonary
Diseases, Baskent University, Fevzi Cakmak Cad, 5 sok, No 48,
Postal Code 06490 Besevler, Ankara, Turkey.
0147-9563/$ see front matter
Copyright 2007 by Mosby, Inc.
doi:10.1016/j.hrtlng.2007.02.007
Fig 1 Chest x-ray on admission to our hospital. No
pathology was noted.
ISSUES IN PULMONARY NURSING
450 www.heartandlung.org NOVEMBER/DECEMBER 2007 HEART & LUNG
61 mm Hg; PcO
2
26 mm Hg; HcO
3
11.4 mmol/L. An
increased serum D-dimer level (9.3 g/mL by way of
turbidimetric method) led us to take him to the
intensive care unit. Bilateral lower-extremity ultra-
sonography showed an acute thrombus in the left
popliteal vein, and thoracic computed tomography
scan (Fig 2) showed bilateral massive pulmonary
emboli in the main pulmonary arteries. Fibrinolytic
therapy was given with recombinant tissue plasmin-
ogen activators (r-TPA) (Alteplase 100 mg intrave-
nous infusion during 2 hours).
1
The patients symptoms and arterial blood gas
analysis in room air (pH 7.44; PO
2
63 mm Hg; PcO
2
36 mm Hg; SpO
2
93%) improved after 2 hours of
thrombolytic therapy. Arterial bleeding from the left
femoral vein, which was used for coronary angiog-
raphy, was seen as a complication of thrombolytic
therapy. A control thoracic computed tomography
scan (Fig 3) and echocardiography (pulmonary arte-
rial systolic pressure was 30 mm Hg; there were no
other pathologic findings) were normal at day 7 of
thrombolytic therapy.
The patient was discharged with oral anticoagu-
lant therapy (warfarin dosage regulated to Interna-
tional Normalization Ratio levels of 2 to 2.5).
DISCUSSION
Patients with decompression illness present with
a wide range of symptoms occurring alone or in
combination, including dermatologic symptoms,
joint pain, neurologic injury, and respiratory or con-
stitutional symptoms.
1-4
Although its most com-
monly involved systems are the musculoskeletal
and neurological systems; arterial gas embolism
also may be seen.
2,3,5
Fig 2 Thorax Computed Tomography Thrombi in right main pulmonary artery and branches of left
main pulmonary artery supplying upper and lower lobes. Infarct areas and atelectasias on right
lower lobe caused by thromboemboli.
Fig 3 Control thorax computed axial tomography. No thrombus in right main pulmonary artery;
partial thrombi in left main pulmonary artery; no infarct areas.
Gaye et al A rare cause of pulmonary embolism
HEART & LUNG VOL. 36, NO. 6 www.heartandlung.org 451
Decompression illness is divided into type I, type II,
and pulmonary barotrauma with arterial gas embo-
lism depending on its clinical presentation. Our pa-
tient was diagnosed with pulmonary barotrauma with
arterial gas embolism because of the presence of
cough, hemoptysis, dyspnea, headache, myalgia, and
fatigue.
4
The clinical symptoms were typical of decom-
pression illness presentation 24 hours after diving.
Increased intraalveolar pressure either forces air
bubbles across the alveolar capillary membrane or
causes rupture of the alveolar wall. This can result in
pneumothorax pneumomediastinum, subcutaneous
emphysema, and alveolar hemorrhage, also called
pulmonary overinflation.
6
In our patient, another
probable diagnosis might have been pulmonary
overinflation syndrome because of evidence of he-
moptysis and dyspnea; however, this was ruled out
by thoracic computed tomography because there
was no pneumothorax pneumomediastinum, sub-
cutaneous emphysema, or alveolar hemorrhage.
Micro-bubbles obstruct blood flow in the capil-
lary system, causing tissue ischemia, which results
in inflammation and complement activation. Aggre-
gation of platelets and clot formation also occur,
leading to obstruction of microcirculation and dam-
age, although micro-bubbles in the capillary vascu-
lar bed are a rare complication.
1,7
Studies to explain the relation between N
2
micro-
bubbles and thrombus formation are rare. In an early
study, Thorsen et al demonstrated that N
2
micro-bub-
bles activated human platelets, which adhere to the
surface of the N
2
micro-bubbles in vitro.
8
They re-
ported that this adhesion induces ultrastructural
changes that are similar to classical agonists, such as
adenine diphosphate, collagen, and thrombin.
Another study to reveal the relation between de-
compression illness and thrombus formation was
made by Lehtosalo et al.
9
They demonstrated platelet
aggregates at both the electron-dense layer of the
bloodbubble interface and in pial veins in decom-
pressed rats. They concluded that during decompres-
sion sickness, bubbles and both activation and aggre-
gation of platelets occur in intracranial veins.
No data currently exist about the occurrence rate
of pulmonary embolism (PE) secondary to decom-
pression illness in the literature. This is the first
report of massive PE in a patient with decompres-
sion illness. We describe a rare case of massive
pulmonary embolism in a 50-year-old man with de-
compression illness.
It is known that plasma fibrinogen levels are in-
creased in persons who smoke. Factor XIII, which sta-
bilizes fibrin clots, is increased in persons who smoke.
Quantitative exposure to passive smoke has been pos-
itively correlated with blood coagulation activity.
10
An-
other possible risk factor for our patient was pro-
longed bed rest. No other risk factors, such as
sedentary lifestyle, drug use, obesity, and history of
surgical operation, trauma, or concomitant malignan-
cies, were present. It could be argued why our patient
experienced PE: Although venous bubbles can be ob-
served in a high proportion of recreational divers, PE is
extremely uncommon. We suggest that a history of
smoking and prolonged bed rest during 6 days may
play an important role in contributing to PE in pa-
tients with decompression illness.
Massive PE and decompression illness are life-
threatening conditions that can cause sudden
death.
11
Current therapeutic strategies have not
been elucidated for massive PE secondary to de-
compression illness. The 2004 ACCP guideline rec-
ommends r-TPA therapy in patients with PE who are
hemodynamically unstable.
12,13
Some authorities
recommend the use of nonsteroidal antiinflamma-
tory agents, whereas others believe the risk of hem-
orrhage is too great to use these agents.
14
Hyper-
baric oxygen is given to increase the gradient of
nitrogen from tissues to blood and hyperoxygen-
ation of ischemic tissue and to decrease tissue
edema by inducing vasoconstriction in such pa-
tients.
1,11
Based on this, we administered hyper-
baric oxygen and r-TPA subsequently because a
massive PE was verified.
In conclusion, PE secondary to decompression
illness is a rare life-threatening situation. Physicians
should be aware of its presentation and immediate
need for treatment with hyperbaric oxygen and
thrombolytics. In our opinion, when severe hypox-
emia and dyspnea develop in patients with decom-
pression sickness, the presence of massive PE
should be considered for early diagnosis and treat-
ment in this situation.
REFERENCES
1. Barak M, Katz Y. Microbubbles: pathophysiology and clinical
implications. Chest 2005;128(4):2918-32.
2. Davis JC, Sheffield PJ, Schuknecht L, Heimbach RD, Dunn JM,
Douglas G, et al. Altitude decompression sickness: hyper-
baric therapy results in 145 cases. Aviat Space Environ Med
1977;48(8):722-30.
3. Bason R, Yacavone D. Decompression sickness: United
States Navy altitude chamber experience 1 October 1981 to
30 September 1988. Aviat Space Environ Med 1991;62(12):
1180-4.
4. Wirjosemito SA, Touhey JE, Workman WT. Type II altitude
decompression sickness (DCS): United States Air Force ex-
perience with 133 cases. Aviat Space Environ Med 1989;60(3):
256-62.
5. Russi EW. Diving and the risk of barotrauma. Thorax 1998;
53(suppl 2):S20-S24.
A rare cause of pulmonary embolism Gaye et al
452 www.heartandlung.org NOVEMBER/DECEMBER 2007 HEART & LUNG
6. Neuman T. Pulmonary barotrauma. In: Bove AA, editor. Diving
medicine. 3rd ed. Philadelphia, PA: Saunders; 1997. p. 176-183.
7. Malik AB, Johnson A, Tahamont MW. Mechanisms of lung
vascular injury after intravascular coagulation. Ann N Y Acad
Sci 1982;100:77-84.
8. Thorsen T, Dalen H, Bjerkvig R, et al. Transmission and scanning
electron microscopy of N2 microbubble activated human plate-
lets in vitro. Undersea Biomed Res 1987;14(1):45-58.
9. Lehtosalo J, Tervo T, Laitinien LA. Bubbles and hematologic
alterations in intracranial veins during experimental decom-
pression sickness. Acta Neuropathol 1983;59(2):139-44.
10. Tapson VF. The role of smoking in coagulation and throm-
boembolism in chronic obstructive pulmonary disease. Proc
Am Thorac Soc 2005;2(1):71-7.
11. Task Force on Pulmonary Embolism, European Society of
Cardiology. Guidelines on diagnosis and management of
acute pulmonary embolism. Eur Heart J 2000;21(16):1301-36.
12. Buller HR, Agnelli G, Hull RD, Hyers TM, Prins MH, Raskob
GE. Antithrombotic therapy for venous thromboembolic dis-
ease: the Seventh ACCP Conference on Antithrombotic and
Thrombolytic Therapy. Chest 2004;126(suppl 3):401S-428S.
13. Meneveau N, Schiele F, Vuillemenot A, Valette B, Grollier G,
Bernard Y, et al. Streptokinase vs. alteplase in massive pul-
monary embolism. A randomized trial assessing right heart
haemodynamics and pulmonary vascular obstruction. Eur
Heart J 1997;18(7):1141-8.
14. Neuman TS. Arterial gas embolism and decompression sick-
ness. News Physiol Sci 2002;17:77-81.
Gaye et al A rare cause of pulmonary embolism
HEART & LUNG VOL. 36, NO. 6 www.heartandlung.org 453