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ilateral massive pulmonary embolism secondaryo decompression sickness: A case reportlubay Gaye, MD,a Sarınc Ulaslı Sevinc, MD,a Karacan Ozgur, MD,a Gumus Tuna, MD,b

nd Eyuboglu Oner Fusun, MDa

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This case report describes massive pulmonary embolism in a patient as a complication of decompressionillness. 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 thatRESULTS in formation of bubbles of inert gas is a risk for both aviators and divers. The present casestrongly suggests that micro-bubbles may cause life-threatening massive pulmonary embolism. (HeartLung® 2007;36:450–453.)

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50-year-old man was admitted to the hospitalwith generalized weakness and dyspnea afterhaving made a 50-meter scuba dive 24 hours

arlier. After diving, he developed hemoptysis,eadache, and neck pain. He had a 20-year historyf smoking history. On admission, the patient wasyspneic. His physical examination was unremark-ble except for peripheral cyanosis. His blood pres-ure was 120/80 mm Hg, and his heart rate was 80pm. Results of a chest radiograph (Fig 1), as well asalues for complete blood count, C-reactive protein,rythrocyte sedimentation rate, blood chemistry,erum D-dimer (0.3 �g/mL by way of turbidimetricethod), Creatine Kinase-MB and troponin-I, were

ll within normal limits. Arterial blood gases atoom air showed moderate hypoxemia (pH 7.45;O2 45 mm Hg; PcO2 35 mm Hg; HcO3 22.9 mmol/L,pO2: 83%), and his P(A-a) ScO2 was 64 mm Hg.esults of thoracic and cranial computed tomogra-hy scans were normal; however, echocardiographyhowed increased pulmonary arterial systolic pres-ure of 47 mm Hg and enlargement of the right

rom aDepartment of Pulmonary Disease, Baskent Universityaculty of Medicine, and bDepartment of Hyperbaric and Under-ea Medicine, Gulhane Military Medical Academy, Ankara, Tur-ey.

eprint requests: Gaye Ulubay, MD, Department of Pulmonaryiseases, Baskent University, Fevzi Cakmak Cad, 5 sok, No 48,ostal Code 06490 Besevler, Ankara, Turkey.

147-9563/$ – see front matteropyright © 2007 by Mosby, Inc.

s10.1016/j.hrtlng.2007.02.007

www.heartandlung.org

trium and ventricle. He was diagnosed with de-ompression illness, acute respiratory failure, andorpulmonale preceded by recent scuba diving, sug-esting an arterial air embolism. The patient wasiven hyperbaric oxygen therapy (8 hours/d) andubcutaneous heparin as enoxaparine. He was notlaced on leg compression. Hypoxemia improvedfter hyperbaric oxygen therapy.

On day 6 of hospitalization, substernal pain andyspnea developed. While breathing nasal oxygent 10 L/min, arterial blood gas analysis showed

ig 1 Chest x-ray on admission to our hospital. Noathology was noted.

evere hypoxemia and hypocapnia (pH 7.25; PO2

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1 mm Hg; PcO2 26 mm Hg; HcO3 11.4 mmol/L. Anncreased serum D-dimer level (9.3 �g/mL by way ofurbidimetric method) led us to take him to thentensive care unit. Bilateral lower-extremity ultra-onography showed an acute thrombus in the leftopliteal vein, and thoracic computed tomographycan (Fig 2) showed bilateral massive pulmonarymboli in the main pulmonary arteries. Fibrinolyticherapy was given with recombinant tissue plasmin-gen activators (r-TPA) (Alteplase 100 mg intrave-ous infusion during 2 hours).1

The patient’s symptoms and arterial blood gasnalysis in room air (pH 7.44; PO2 63 mm Hg; PcO2

6 mm Hg; SpO2 93%) improved after 2 hours ofhrombolytic therapy. Arterial bleeding from the leftemoral vein, which was used for coronary angiog-aphy, was seen as a complication of thrombolytic

Fig 2 Thorax Computed Tomography Thrombmain pulmonary artery supplying upper andlower lobe caused by thromboemboli.

Fig 3 Control thorax computed axial tomograpartial thrombi in left main pulmonary arter

herapy. A control thoracic computed tomography a

EART & LUNG VOL. 36, NO. 6

can (Fig 3) and echocardiography (pulmonary arte-ial systolic pressure was 30 mm Hg; there were nother pathologic findings) were normal at day 7 ofhrombolytic therapy.

The patient was discharged with oral anticoagu-ant therapy (warfarin dosage regulated to Interna-ional Normalization Ratio levels of 2 to 2.5).

ISCUSSIONPatients with decompression illness present withwide range of symptoms occurring alone or in

ombination, including dermatologic symptoms,oint pain, neurologic injury, and respiratory or con-titutional symptoms.1-4 Although its most com-only involved systems are the musculoskeletal

nd neurological systems; arterial gas embolism

t main pulmonary artery and branches of leftlobes. Infarct areas and atelectasias on right

o thrombus in right main pulmonary artery;farct areas.

i in righlower

phy. N

lso may be seen.2,3,5

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A rare cause of pulmonary embolism Gaye et al

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Decompression illness is divided into type I, type II,nd pulmonary barotrauma with arterial gas embo-ism depending on its clinical presentation. Our pa-ient was diagnosed with pulmonary barotrauma withrterial gas embolism because of the presence ofough, hemoptysis, dyspnea, headache, myalgia, andatigue.4 The clinical symptoms were typical of decom-ression illness presentation 24 hours after diving.

Increased intraalveolar pressure either forces airubbles across the alveolar capillary membrane orauses rupture of the alveolar wall. This can result inneumothorax pneumomediastinum, subcutaneousmphysema, and alveolar hemorrhage, also calledpulmonary overinflation.”6 In our patient, anotherrobable diagnosis might have been pulmonaryverinflation syndrome because of evidence of he-optysis and dyspnea; however, this was ruled out

y thoracic computed tomography because thereas no pneumothorax pneumomediastinum, sub-utaneous emphysema, or alveolar hemorrhage.

Micro-bubbles obstruct blood flow in the capil-ary system, causing tissue ischemia, which resultsn inflammation and complement activation. Aggre-ation of platelets and clot formation also occur,eading to obstruction of microcirculation and dam-ge, although micro-bubbles in the capillary vascu-ar bed are a rare complication.1,7

Studies to explain the relation between N2 micro-ubbles and thrombus formation are rare. In an earlytudy, Thorsen et al demonstrated that N2 micro-bub-les activated human platelets, which adhere to theurface of the N2 micro-bubbles in vitro.8 They re-orted that this adhesion induces ultrastructuralhanges that are similar to classical agonists, such asdenine diphosphate, collagen, and thrombin.

Another study to reveal the relation between de-ompression illness and thrombus formation wasade by Lehtosalo et al.9 They demonstrated platelet

ggregates at both the electron-dense layer of thelood–bubble interface and in pial veins in decom-ressed rats. They concluded that during decompres-ion sickness, bubbles and both activation and aggre-ation of platelets occur in intracranial veins.

No data currently exist about the occurrence ratef pulmonary embolism (PE) secondary to decom-ression illness in the literature. This is the firsteport of massive PE in a patient with decompres-ion illness. We describe a rare case of massiveulmonary embolism in a 50-year-old man with de-ompression illness.

It is known that plasma fibrinogen levels are in-reased in persons who smoke. Factor XIII, which sta-ilizes fibrin clots, is increased in persons who smoke.

uantitative exposure to passive smoke has been pos-

52 www.heartandlung.org

tively correlated with blood coagulation activity.10 An-ther possible risk factor for our patient was pro-

onged bed rest. No other risk factors, such asedentary lifestyle, drug use, obesity, and history ofurgical operation, trauma, or concomitant malignan-ies, were present. It could be argued why our patientxperienced PE: Although venous bubbles can be ob-erved in a high proportion of recreational divers, PE isxtremely uncommon. We suggest that a history ofmoking and prolonged bed rest during 6 days maylay an important role in contributing to PE in pa-ients with decompression illness.

Massive PE and decompression illness are life-hreatening conditions that can cause suddeneath.11 Current therapeutic strategies have noteen elucidated for massive PE secondary to de-ompression illness. The 2004 ACCP guideline rec-mmends r-TPA therapy in patients with PE who areemodynamically unstable.12,13 Some authoritiesecommend the use of nonsteroidal antiinflamma-ory agents, whereas others believe the risk of hem-rrhage is too great to use these agents.14 Hyper-aric oxygen is given to increase the gradient ofitrogen from tissues to blood and hyperoxygen-tion of ischemic tissue and to decrease tissuedema by inducing vasoconstriction in such pa-ients.1,11 Based on this, we administered hyper-aric oxygen and r-TPA subsequently because aassive PE was verified.In conclusion, PE secondary to decompression

llness is a rare life-threatening situation. Physicianshould be aware of its presentation and immediateeed for treatment with hyperbaric oxygen andhrombolytics. In our opinion, when severe hypox-mia and dyspnea develop in patients with decom-ression sickness, the presence of massive PEhould be considered for early diagnosis and treat-ent in this situation.

EFERENCES

1. Barak M, Katz Y. Microbubbles: pathophysiology and clinicalimplications. 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 Med1977;48(8):722-30.

3. Bason R, Yacavone D. Decompression sickness: UnitedStates Navy altitude chamber experience 1 October 1981 to30 September 1988. Aviat Space Environ Med 1991;62(12):1180-4.

4. Wirjosemito SA, Touhey JE, Workman WT. Type II altitudedecompression 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;

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6. Neuman T. Pulmonary barotrauma. In: Bove AA, editor. Divingmedicine. 3rd ed. Philadelphia, PA: Saunders; 1997. p. 176-183.

7. Malik AB, Johnson A, Tahamont MW. Mechanisms of lungvascular injury after intravascular coagulation. Ann N Y AcadSci 1982;100:77-84.

8. Thorsen T, Dalen H, Bjerkvig R, et al. Transmission and scanningelectron 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 hematologicalterations in intracranial veins during experimental decom-pression sickness. Acta Neuropathol 1983;59(2):139-44.

0. Tapson VF. The role of smoking in coagulation and throm-

boembolism in chronic obstructive pulmonary disease. ProcAm Thorac Soc 2005;2(1):71-7.

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1. Task Force on Pulmonary Embolism, European Society ofCardiology. Guidelines on diagnosis and management ofacute pulmonary embolism. Eur Heart J 2000;21(16):1301-36.

2. Buller HR, Agnelli G, Hull RD, Hyers TM, Prins MH, RaskobGE. Antithrombotic therapy for venous thromboembolic dis-ease: the Seventh ACCP Conference on Antithrombotic andThrombolytic Therapy. Chest 2004;126(suppl 3):401S-428S.

3. 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 hearthaemodynamics and pulmonary vascular obstruction. EurHeart J 1997;18(7):1141-8.

4. Neuman TS. Arterial gas embolism and decompression sick-ness. News Physiol Sci 2002;17:77-81.

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