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The Importance of Early Detection and Therapy of Reexpansion Pulmonary Edema F. M. Smoll e-Jueuner' , G. Prause', B. Ratzenhofe r' , M. Pongratz', G. Priehs', W F. List Dep artm en t of Th oracic a nd Hyperba ric Su rgery Departm ent of Anesthesiology 3 Division of Pneum ology Unive rs ity ofG raz , Med ical Sch ool, Graz , Aus t ria 1
Sum mar)'
Three cases are repo rte d of un ilate ral pulmonary edema, two followi ng rapid reexpan sicn a fter prolonged ten sion pneumothorax, with tota l collapse or the right lung a nd one afte r re expanded at electas is followi ng left intrabron chial obst ruction . In all cases decr ease of blood pressure and ta chycardia not responding to intraveno us fluid subst itu tion were alrea dy present within th e first 15 m in after chest drainage Of after rem oval of the intra bronch ial obst ruc tion . The pre existent dyspnea failed to improve. A cloudy opaci ty of the re expa nded lung was found imme diately after drainage in 2 cases. After immediate application of a conti nous positive airway pressur e mask no more exte ns ive thera py was necessary in one pati ent. The two other s in whom tr eatm ent was begun with more tha n 1 hour delay required a rt ificia l ventilation a nd adre ne rgics for 2 an d 4 days, respectively. Dte Bed eutung der fr uh en Er ke nnung und T he rapie des He exp ansionsddem s der Lunge Drei Faile unilaterale n l.ungeno dems wur de n beobachtet: Zwei entsta nden na ch rascher Reexpan sion total kollab iert er Lungen bei langer bestehend em rechtsse itigen Pneumothorax. eines na ch Wiederbeluftung eine r Atelektas e infolge ku rzzeitiger Ha uptb ronchusobstruk tion links . Bei allen Patient en fanden sich bereits innerhalb der crste n 15 Minuten nach Thoraxd rainage bzw. Entfer nung der Obstruk tion ein durc h intra ven6se
Fltlssigkeitsga be un beeinfluBbarer Blutdruckabfall sowi e eine Tachykardie. Zude m blieb eine Besseru ng der vorbes tehende n Dysp noe aus. Bei allen 3 Patient en zeigte stch ber eits unmittelba r nach Drainage bzw. nach Entfernung der Obst rukt ion eine wolkige Verschattung der reexpandiert en Lunge. Durch sofort initiierte Cr'Ar -Maskenaun ung und kontrollierte v olumensub stitution konnt en bei eine m Pati ent en eingre ifende re Mafln ahmen vermi ed en werd en. Bei den beiden a nde re n wurde die Behandlung mit einer v er zogerun g von mehr als cine r Stunde eingeleitet und erford erte zu erst kc nirolllen e. da nn assistierte Respiratortherapie , Katechola mine und Volumensubstituti on fur 2 bzw. 4 Tage. Bel allen Patien ten er folgte eine Rest itutio ad integrum . Die Literat ur zelgt. daB a nam nes tische Daten keine sicheren Hinweis e auf die Moglic hkeit der Entwic klung eines Reexpan sionsodem s gebcn. und daB dessen Auftre ten durc h lan gsa me bzv..·. schrittweise Reexpansion der Lunge n icht verhi ndert werden kann . Es sche int dah er in Anbet racht de r inte rna tion al bertchteten . hoh en Letalitat von 20 % sinnvoll, na ch jede r Drainage bzw. anderwe itig erzielten Wide ra usde hnung eine r kollabierte n Lunge au f die Frtihsymp tome eines Heexpansionsodcm s zu achten, daf in diesc r Phase mdgliche rw eise le ichter rever sibel ist, als im voll en twickelt en Stad ium. Key wo rd s
Unilateral pulmon ary edema - Pneum otho rax - Atelectas is Earl y diagno sis - Treatment
Introdu ction
Case 1
Unilateral pulm onary edema following reexpan sion (RPE) of one lung after a prolonged period of total collapse is a well known phenomen on (9). In most cases . rapid evacuation of the pleural cavity after long-standing pneu mothorax or pleural effusion trigger s the process, but a variety of other conste llations have also been reported to cause acute unilat eral edema (3, 8. 9). The clinical course is usually dramatic and in most cas es reported in the liter ature intubati on and artificial ventilation had to be perform ed (9). We pre sent three person al observations which point to the possibility of an early, effective. an d unspectaculartreatment. provided the first signs of the complication are interpreted correctly.
A zl -years-old mal e. nonsmok er witho ut a ny noticeable diseases in his history, wa s admitted for right-sided chest pain , intermittent cough. an d dysp nea on exert ion th at had peristed for a bout 4 week s. The a rterial blood pre ssur e was 115/ 80 mmHg. With the exception of a slight hypocapn ia and hypoxia th e laborator y par a meter s wer e norm al. Th chest rad iograp h showed a right ten sion pneum othorax with a tota l collapse of the right lung (Fig. 1). After int ravenou s premed ica tion with atro pine a chest tube for intercosta l suction dr a inage (12 cmHzO) was insert ed under local a nes thes ia. Five minutes late r, whe n the postoperat ive ra diogra ph wa s being taken, the pati ent complained about dizziness and na usea . Tachypn ea developed a nd the arterial blood pressure was 80/ (diastolic pressure not measur able) at a pulse rate of 140/mi n. The
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2
Fig.!
Case 1: Right tension pneumothorax with total collapse of the lung
Fig. 2 Case 1: Five minutes afterdrainage:Ooacuenssof the right lung, predominantly in the upperfield, hyperinflation of the left side
radi ograp h showed the right lung fully reexpanded but diffusely opaq ue, especia lly in the upper lung field (Fig. 2). The dyspnea failed to improve inspite of breat hing 100 % oxygen. The patient did not com plain of pa in at the dr a inage area . Moist rales cou ld be auscultated over the right lung. A reexpa nsion edema was suspected . 800 ml of cristallc id was adm inister ed with in 15 min afte r drainage a nd contin uous-positive-a irway-pressure br eathi ng (CPAP) was initiat ed but the blood pressure drop ped furt he r to 65/mmHg wit h all signs of shock develop ing. The arteria l blood gas a nalysis yielded acidos is an d hypoxemia {pi I: 7.35, Pa0 2: 60 ).
Thome. cardioca sc. SIlrgeon39 (1991)
Fig.3 Case 1: Onehour afterdrainage:Intensification of theopacity.now predominantly in the lower lung field
Fig.4 Case 1:Eighteenhoursafter drainage:Therightlunghasalmost cleared, but there is still a hazyopacity in the upper and middle lung field
While the acidosis even increased during the first hour (pH: 7.30 , PaDz: 8 11a nd the opacit y on the radiog ra ph intens ified (Fig. 3),
the blood press ure stabilized at 95/ 60 mmHg. The patien t felt well and the dyspn ea imp roved. After 5 hour s , the rad iograph showed first signs of clear ing. CPAP-mask vent ilation at 10 crnll -O was continued togethe r with a further su bstitution of cr lstalloids a nd sodium-bica rbonate during the following 18 hours up to a positive fluid bala nce of 2 500 ml . After 18 hours the blood pressure was sta ble at 120/7 5 mm Hg and the patient did not requir e an y more intraven ous substitution of fluids. Acidosis was still presen t. however (pll : 7.33 . PaOz: 871. a nd
163
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The Importan ce of Early Detection ana Therapu ofHeexpansion Pulmonary Edema
Thorae. eardiouasc. Su rgeon 39 (199 1)
F. M. Smo lte-Jue ttne r. G. Prause . B. Ratzenhofe r. M. Pongra tz. G. Friehs. W. F. List
the rad iograph was still path ological (Fig. 4). The loss of serous fluid over the chest tube was 1050 ml on the first. 250 on the second and 50 on the third day. The protein content of this fluid was 4.8 mg/ ml Ialbumin: 1.8 mg/rnll, Both protein and albumi n in the se rum were within norm al range. CPAP was continued th roughout the next 36 hours. whereup on all findings returned to normal. After an uneventful recovery and removal of the chest tube on day 9 the patient was discharged. Case 2
Four weeks after her third child had been deliver ed by cesarean section a 40-years-old woma n, nonsmoker. without any noticea ble diseases in her history. was admitted for severe dyspnea and rightsided chest pain. The arterial blood pressur e was 120/ 60 mmHg at a hear t ra te of 84 . The art erial blood gas check showed acidosis and hypoxemia lpH, 7.34. p. o,' 63). The routine chest radiograph revealed a right tension pneumo thorax with total collapse of the lung. An emergency intercostal suction drainage (12 emH20 ) was performed under local anesthesia after premedication with atropi ne. The lung reexpa nded immediately. but the dyspn oe did not improve. 25 min after the drainage the arterial blood pressure dro pped to 50/ - mmHg and the heart rate increased up to 156/ m in . A central venous cat heter was positioned and revealed a central venous pressure of 2 cmH20 . The arterial blood gas check under continuous breat hing of 311min 100 % oxygen did not improve ma rkedly lpH, 7.35. p. o,' 85). The blood pressu re did not increase inspite the administration of 1000 ml cristalloid and 10 00 ml of 5 % albumin. Under 100 % oxygen breathing with a tachypnea of 28 per min P.02 two hours after drainage was 43. Distinct rales over the right lung were misinterpreted as a "silent as pira tion" and emergency bronchoscopy was done. A constant flow of edema fluid from the right segmental ostia was see n. otherwise the findings were norm al. The diagnosis of reexpansion edema was established. Thr ee hours after dr ainage the patient was intu bated and controlled inverse ratio ventilation with a positive end-expiratory pressur e (PEEP) of9 cml l-Owas initiated but had to be redu ced to 5 du e to persistent arterial hypotension. Dopa min an d dobutamin were administered by continuous infusion. Sedation was achieved with Midazolam . Durin g the following 12 hours the patient was given 3000 ml crtstalloids. 1000 ml colloids and 250 ml mannitol. A fluid balance of plus 2200ml during the first 12 hours was necessary to stabiliz e the arterial pressure at 115175 mmHg. The fluid loss over the chest tub e dur ing this time was 350 011. The analysis of the fluid yielded the same protein and albumin content as found in the serum of the patient (4.3 mg/dl protein. 2.8 mg/dl albumin). Four hours after intubation the P, » was 65 under 60 % F10 2 with a pers istent acidosis of - 6 BE. Only after 24 hours F10 2 and the dose of the adren ergic substances could be gradu ally reduced. Intermittent mandatory ventilation (IMV) was initiated . The chest radi ograph showed a slight improvemen t. After 36 hours IMVwas changed to CPAP breat hing over the tub e. Four days after the initial event the chest ra diograph showed norma l findings an d the patient was extubate d. The chest tube could not be removed for 25 days due to two recur rent collapses of the lung which occurred when the drainage was clamp ed tentatively. Otherwise the course was uneventful. Cas e 3
A 73-years -old female patient who had a history of cerebrovascular and ca rdiac insufficiency developed acute respiratory insufficiency following as pira tion of chunks of an unpeeled ora nge. After the glottis had been cleared by the emergency doctor. there were still no breathing sounds over the left lung and the patient remained dyspnolo inspite of 3 U min oxygen adm inistered by mask. Because of a cicatrised deviation of the epiglottis and the right arye piglottic fold the emergency doctor did not succeed in intu bating the patient. During trans port to the hospital, 30 min later. she coughed up another piece of oran ge peel and ventilation was reestab lished on
Fig. 5 Case 3: Roentgenogram at thetimeofadmission: Patchyopacity ofthe left lungwhich isnot fullyexpanded (2em borderbetween upperlobeandchest wall)
Fig. 6 case3:Eighteenhoursafter intubation the left lung hasmarkedly cleared. is reexpanded, but still shows a hazy opacity
the left side but without improvemen t of the ca rdiores piratory situation. however . Another 45 min later she entered the emergency room in a severely dyspn eic and cyanotic condition. The art erial pressure was 60/- mmllg at a hean rate of 178/min . The arterial blood gas analysis yielded pH: 7.32 and P.~: 37. Intubation and controlled ventilation were immediat ely performed. 1000 mV30 min cristalloids and dopamine were admini ste red. The chest radiograph show ed the left lung opaque and not totally expanded (Fig. 5). Moist rales were prese nt over the left lung. As a residual. part ially obstructing foreign body was suspected. bronc hoscopy was done. The trachea and both bronchial trees were free, a consta nt flow of a frothy fluid from the periphe ry oft he left lung into the left lobar bronchi was found . The wall of the left
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main stem bronchus show ed a se m icircular hemorr hagic imbibition of th e mucosa. probably co rresponding to the former site of th e foreign body . Again . the diagnosis of reexpansion ede ma was es tablishe d by bronchos copy. For 48 hours controlled ventil ation with a PEEP of 5 cmHzQ wa s do ne. Prophylactic treatmen t with cephalosporine and amin oglycoside antibi otics was initiated . Continuous drip infus ions of cristalloids . dopamine and dobutam ine were given during 18 hours. A fluid balan ce of plus 1050 was achieved. Then the catecholamine dosag e was gradually reduced and controlled vent ilatio n was changed to intermitten t mandatory ventilation(lMV)breathi ng. At that time the left lung had markedly cleared on the contro l rad iograp h (Fig. 6). After 48 hours the patient was extubated . One we ek late r she was dis charged w ith a normal chest radiog raph.
Discussion Many cases of se vere unilateral reexpansion pulmonary edema (RPE) have been repon ed in the liter ature (3). It seems to occur seldomly, following intercostal suction drainage in the treatme nt of pneumo-, or sero tho rax . The actual incidence is probably unknown because many cases do not become clinically mani fest inspite of radiographi c signs of edema (9). A relative lack of surfactant has been suggeste d as causa tive factor. This was supported by the fact that most RPE occurred a fter long-standing total collapse of the lung, which might have impinged the surfactant production (13). On the other hand , however , RPE also does develop after very sho rt int ervals of pulmonar y collapse (9). A high speed of reexpan sion following insertion of the inter costal tub e has also been accused to be causative for the formation of RPE. Minimal capillary leakage together with lack of surfactant and negative pressure forming suddenly in the alveoli might enha nce the inflow of fluid from the ca pillaries (12). This theory is opposed by the fact that RPE has been observed as well in lungs reexpanded without suction at the intercostal tube and in atelectases reexpanding "spontaneously" after rem oval of an intrabronchial obst ru ction (8, 9, 14, 15). Undoubtedly, howe ver. Iung capilla ry permea bility is increas ed in the lung tiss ue and in the pleura l surface, the laller accounting for the high amount of protein in the pleur al fluid recover ed from the patients. Though the abovem entioned factors may play a certa in role, RPE pr obably is a reoxygenati on injury with the lung tissue pr oducing excess superoxide and other toxic metabolites (7). These metabolites might enhance the formation of leucotriens and kinins and ther eby trigger the complement cascade (5, 6). The reduced degradati on of kinins in hypoxic alveolar compart ments contributes to the inju ry (11). Other causes of un ilatera l pulmonary edema such as hypostasis in the depend ent lung following lateral decubitus position (1, 16), contralateral bronchial obstruction redirecting blood flow to the "healthy" side which subsequently develo ps edema (17), as well as vas cular caus es such as contralateral pulmona ry a rtery stenos is (10, 18) an d ipsilateral postlobectomy pulmonary vein th rombosis (4) have also bee n reponed . From the clinical point of view, seve re RPE is a serious complication, as 20 % have a lethal outcome (9). This is main ly due to pitfalls in the diagnosis: asp irat ion, residu al intrapleural fluid, and pneumoni c inflltrate are the most common radiological misint er pretations of the homogeneous opacity forming in the reexpand ed lung (9, 15). Clinically, and "unexplained" hypovolemic shock is the first
Thom e. cardiovasc. S urgeon 39 (99 1)
striking feature. Subsequently, all signs of an adult respira tory distr ess synd rome (ARDS) develop inspite of the unllaterality of the process (7). If RPE is not diagnosed early enough, the resulting hypoxemia increases the damage to the edematous lung and may even result in irreve rsib le bilateral ARDSand multiorgan failure. Therapy basically comprises an increase of the intraalveolar pressure thus redirecting the fluid into the interstitium and into the capillaries. Inverse ratio ventilation (7) or even independ ent art ificial ventilation by using two respirators might be indicated in desper ate situa tions (16). The initial fluid loss into the inter stitium ha s to be balan ced by infusions. Even in the presence of a low serum albumin the use of colloids may be dan gerous as long as ther e is capillary leakage, because the lar ge molecules are lost into the pulmonary inter stit ium further increasing the oncotic press ure there. If a severe form develops, catecholamines become indispensable. Our case NO.1 illustrat es the rapid reversibility of the process if therapy is begun immediately: only CPAP-mask breathi ng and substitution of cristalloid fluid was needed . Diagnosis was based upon the radiologica l cha nges and the rapid deterioration of the cardio res piratory function. Anothe r diagnostic clue was the high amount of serum -like fluid lost over the chest tube. During the long interva l un til therapy was initiated RPE developed into a more severe form in the two other patients. Though basically the therapeutical strategy was the same as in case no. 1, catecholamines and controlled ventilation with inver se rati o in case no. 2 were needed to sta bilize the cardiorespirat ory function. Bronchoscopy has been the mea ns of diagn osis in these two patients, but a more thorough clinical examina tion would have obviated the necessity for this invasive investigation. Any physician who rout inely performs a large quantity of intercostal suction drainages or who does emergency bronchoscopies ough t to be familiar with ea rly diagnosis and therapy of RPE, the occurrence of which is unp red ictable and the incidence of which cannot be prevent ed. References Baraka. A.. R. Moghrabi. and A. Yazigi : Unilateral pulmonary edema/atelectasis in lateral decubitus position. Anaesthesia 42 (1987) 171- 174 a Bows er. B.. 1. M. Stinso n: Spontaneous unilateral pulmonary edema. J. Natl. Med. Assoc. 78 (1986) 88 2-88 3 3 Fanning. 1.. L. Lettieri. andM. S. Piver: Fatal recurrent reexpansion pulmonary edema. Obstet. Gyneeol. 74 (1989) 495- 549 4 Gyves- Ray . K. M.. D. L. Spi zarny. B. H. Gross: Unilateral pulmonary edema due to postlobectomy pulmonary vein thrombosis. AJR 148 (19871 t079- 1080 5 Jackson. R. M.. C. R. Veal. C. B. Al exander. A. L. Brannen. and 1. D. Fulmer: Neutrophils in reexpansion pulmonary edema. J. Appl. Physiol. 65 (1988) 228-234 6 Jac kson. R. M.. and C F. Veal: He-expansion. re -oxygenati on and rethinking. Am. J. Med. Sci. 298 0 989144-50 7 Koller. W . N. Mutz. C. Putens en. and G. Putz: Treatment of reexpansion edema r unilateral ARDS·) after rapid pneumothorax drainage. Anaesthesist 36 09871655 -65 8 8 Kramer. M. R.. E. Melz er. and C Sprung: Unilateral pulmonary edema after intubation of the right main stem bronchus. Crit. Care Med,17( 1989) 472- 474 9 Mahfood. S.. W R. Hix, B. L. Aa ron. P. Blaes . and D. C Wat son: Reexpansion pulmonary edema. Ann. Thorae. Surg. 45 (1988) 340-345 10 McTigue. C. 1. P. Scurr y. and M. Silbers tei n: Unilateral pulmonary I
16 5
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The Importance ojEarly Dete ction and Therapy ojRee:rpansion Pulmona ry Edema
Thorae. eardiovase. Surgeon 39 (99 1)
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12
13
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F. M. Smolte-Jueuner. G. Prause. B. Rc tze nhcfer. M. Pongrat z. G. Friehs. W. F. List
ede ma assoc iate d with pu lmonary arte rial comp ression. Australas Radial. 32(1988) 390-3 93 Pett y . T. L.. G. W. S ilve rs. G. W. Paul. and R. E. Stanford: Abnormalities in lung elast ic properties and surfactant function in adult respiratory distress syndrome. Chest 75 (1979 ) 571-575 Pang. L. M.. II. M. O'Brodooich, R. B. Millins, an d S. A. Stalcup: Bradykinin induced increase in pulmo na ry vascu lar per meability in hypoxic sheep. J. Appl. Physiol. 52 09821370-377 Parisi. A.. P. M. Ma rianeschi. G. M. Giustozzi . G. Bef/a vig na. D. Alberti. and F. Sciannameo: Unilateral pulmonary edema due to ra pid reexpansion in pne umoth or ax. Minerva med. 77 ( 986) 2327- 2329 Ravin. C. E.. and N. S . Dahmash: Reexpan sion pulmonary ede ma . Chest 77 (1980) 708 -710 Sautter. R. D.• W. fI. Dreker, and 1. H. Ma cJndoe: Fata l pulmonary ede ma and pneumo nitis after reexpan sion of chro nic pneumothorax. Chest 60 ( 971) 399-401
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Schere r, R.• P. Reinhold, and B. Buchholz: Unilateral lun g ede ma following chest injury: an ind ication for indepen dent ar tificial respira tion. Anast h. lntenstvther. Notfallmed. 18 (1983) 65-6 7 Shikhani. A. H.. S. D. Salman. and R. Melhem : Unilateral pu lmon ar y edema as a complication of contralateral bronchial obst r uction. Laryngoscope 97 ( 987) 748-75 1 Takeda . K.. M. J. Knap p, W. G. Wolfe, and J. D. Crapo: Hypoxia enhances unilater al lung injury by increasing blood now to the injured lung. J. Appl. Physiol. 63 (1987 ) 2516-2523
F. M. Smolie-Juettner
Depar tment Thora cic an d Hyperb ari c Surge ry Univers ity ofGraz. Medical School A·8 036 Graz/Austria
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The Importance of Early Detection and Therapy of Reexpansion Pulmonary Edema F. M. Smoll e-Jueuner' , G. Prause', B. Ratzenhofe r' , M. Pongratz', G. Priehs', W F. List Dep artm en t of Th oracic a nd Hyperba ric Su rgery Departm ent of Anesthesiology 3 Division of Pneum ology Unive rs ity ofG raz , Med ical Sch ool, Graz , Aus t ria 1
Sum mar)'
Three cases are repo rte d of un ilate ral pulmonary edema, two followi ng rapid reexpan sicn a fter prolonged ten sion pneumothorax, with tota l collapse or the right lung a nd one afte r re expanded at electas is followi ng left intrabron chial obst ruction . In all cases decr ease of blood pressure and ta chycardia not responding to intraveno us fluid subst itu tion were alrea dy present within th e first 15 m in after chest drainage Of after rem oval of the intra bronch ial obst ruc tion . The pre existent dyspnea failed to improve. A cloudy opaci ty of the re expa nded lung was found imme diately after drainage in 2 cases. After immediate application of a conti nous positive airway pressur e mask no more exte ns ive thera py was necessary in one pati ent. The two other s in whom tr eatm ent was begun with more tha n 1 hour delay required a rt ificia l ventilation a nd adre ne rgics for 2 an d 4 days, respectively. Dte Bed eutung der fr uh en Er ke nnung und T he rapie des He exp ansionsddem s der Lunge Drei Faile unilaterale n l.ungeno dems wur de n beobachtet: Zwei entsta nden na ch rascher Reexpan sion total kollab iert er Lungen bei langer bestehend em rechtsse itigen Pneumothorax. eines na ch Wiederbeluftung eine r Atelektas e infolge ku rzzeitiger Ha uptb ronchusobstruk tion links . Bei allen Patient en fanden sich bereits innerhalb der crste n 15 Minuten nach Thoraxd rainage bzw. Entfer nung der Obstruk tion ein durc h intra ven6se
Fltlssigkeitsga be un beeinfluBbarer Blutdruckabfall sowi e eine Tachykardie. Zude m blieb eine Besseru ng der vorbes tehende n Dysp noe aus. Bei allen 3 Patient en zeigte stch ber eits unmittelba r nach Drainage bzw. nach Entfernung der Obst rukt ion eine wolkige Verschattung der reexpandiert en Lunge. Durch sofort initiierte Cr'Ar -Maskenaun ung und kontrollierte v olumensub stitution konnt en bei eine m Pati ent en eingre ifende re Mafln ahmen vermi ed en werd en. Bei den beiden a nde re n wurde die Behandlung mit einer v er zogerun g von mehr als cine r Stunde eingeleitet und erford erte zu erst kc nirolllen e. da nn assistierte Respiratortherapie , Katechola mine und Volumensubstituti on fur 2 bzw. 4 Tage. Bel allen Patien ten er folgte eine Rest itutio ad integrum . Die Literat ur zelgt. daB a nam nes tische Daten keine sicheren Hinweis e auf die Moglic hkeit der Entwic klung eines Reexpan sionsodem s gebcn. und daB dessen Auftre ten durc h lan gsa me bzv..·. schrittweise Reexpansion der Lunge n icht verhi ndert werden kann . Es sche int dah er in Anbet racht de r inte rna tion al bertchteten . hoh en Letalitat von 20 % sinnvoll, na ch jede r Drainage bzw. anderwe itig erzielten Wide ra usde hnung eine r kollabierte n Lunge au f die Frtihsymp tome eines Heexpansionsodcm s zu achten, daf in diesc r Phase mdgliche rw eise le ichter rever sibel ist, als im voll en twickelt en Stad ium. Key wo rd s
Unilateral pulmon ary edema - Pneum otho rax - Atelectas is Earl y diagno sis - Treatment
Introdu ction
Case 1
Unilateral pulm onary edema following reexpan sion (RPE) of one lung after a prolonged period of total collapse is a well known phenomen on (9). In most cases . rapid evacuation of the pleural cavity after long-standing pneu mothorax or pleural effusion trigger s the process, but a variety of other conste llations have also been reported to cause acute unilat eral edema (3, 8. 9). The clinical course is usually dramatic and in most cas es reported in the liter ature intubati on and artificial ventilation had to be perform ed (9). We pre sent three person al observations which point to the possibility of an early, effective. an d unspectaculartreatment. provided the first signs of the complication are interpreted correctly.
A zl -years-old mal e. nonsmok er witho ut a ny noticeable diseases in his history, wa s admitted for right-sided chest pain , intermittent cough. an d dysp nea on exert ion th at had peristed for a bout 4 week s. The a rterial blood pre ssur e was 115/ 80 mmHg. With the exception of a slight hypocapn ia and hypoxia th e laborator y par a meter s wer e norm al. Th chest rad iograp h showed a right ten sion pneum othorax with a tota l collapse of the right lung (Fig. 1). After int ravenou s premed ica tion with atro pine a chest tube for intercosta l suction dr a inage (12 cmHzO) was insert ed under local a nes thes ia. Five minutes late r, whe n the postoperat ive ra diogra ph wa s being taken, the pati ent complained about dizziness and na usea . Tachypn ea developed a nd the arterial blood pressure was 80/ (diastolic pressure not measur able) at a pulse rate of 140/mi n. The
Thorac. cardiovasc. Surgeon 39 (1991) 162-1 66 © Georg Thieme Verlag Stuttgart - New York
Received for Publi cation: J anuar 10,1 991
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2
Fig.!
Case 1: Right tension pneumothorax with total collapse of the lung
Fig. 2 Case 1: Five minutes afterdrainage:Ooacuenssof the right lung, predominantly in the upperfield, hyperinflation of the left side
radi ograp h showed the right lung fully reexpanded but diffusely opaq ue, especia lly in the upper lung field (Fig. 2). The dyspnea failed to improve inspite of breat hing 100 % oxygen. The patient did not com plain of pa in at the dr a inage area . Moist rales cou ld be auscultated over the right lung. A reexpa nsion edema was suspected . 800 ml of cristallc id was adm inister ed with in 15 min afte r drainage a nd contin uous-positive-a irway-pressure br eathi ng (CPAP) was initiat ed but the blood pressure drop ped furt he r to 65/mmHg wit h all signs of shock develop ing. The arteria l blood gas a nalysis yielded acidos is an d hypoxemia {pi I: 7.35, Pa0 2: 60 ).
Thome. cardioca sc. SIlrgeon39 (1991)
Fig.3 Case 1: Onehour afterdrainage:Intensification of theopacity.now predominantly in the lower lung field
Fig.4 Case 1:Eighteenhoursafter drainage:Therightlunghasalmost cleared, but there is still a hazyopacity in the upper and middle lung field
While the acidosis even increased during the first hour (pH: 7.30 , PaDz: 8 11a nd the opacit y on the radiog ra ph intens ified (Fig. 3),
the blood press ure stabilized at 95/ 60 mmHg. The patien t felt well and the dyspn ea imp roved. After 5 hour s , the rad iograph showed first signs of clear ing. CPAP-mask vent ilation at 10 crnll -O was continued togethe r with a further su bstitution of cr lstalloids a nd sodium-bica rbonate during the following 18 hours up to a positive fluid bala nce of 2 500 ml . After 18 hours the blood pressure was sta ble at 120/7 5 mm Hg and the patient did not requir e an y more intraven ous substitution of fluids. Acidosis was still presen t. however (pll : 7.33 . PaOz: 871. a nd
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The Importan ce of Early Detection ana Therapu ofHeexpansion Pulmonary Edema
Thorae. eardiouasc. Su rgeon 39 (199 1)
F. M. Smo lte-Jue ttne r. G. Prause . B. Ratzenhofe r. M. Pongra tz. G. Friehs. W. F. List
the rad iograph was still path ological (Fig. 4). The loss of serous fluid over the chest tube was 1050 ml on the first. 250 on the second and 50 on the third day. The protein content of this fluid was 4.8 mg/ ml Ialbumin: 1.8 mg/rnll, Both protein and albumi n in the se rum were within norm al range. CPAP was continued th roughout the next 36 hours. whereup on all findings returned to normal. After an uneventful recovery and removal of the chest tube on day 9 the patient was discharged. Case 2
Four weeks after her third child had been deliver ed by cesarean section a 40-years-old woma n, nonsmoker. without any noticea ble diseases in her history. was admitted for severe dyspnea and rightsided chest pain. The arterial blood pressur e was 120/ 60 mmHg at a hear t ra te of 84 . The art erial blood gas check showed acidosis and hypoxemia lpH, 7.34. p. o,' 63). The routine chest radiograph revealed a right tension pneumo thorax with total collapse of the lung. An emergency intercostal suction drainage (12 emH20 ) was performed under local anesthesia after premedication with atropi ne. The lung reexpa nded immediately. but the dyspn oe did not improve. 25 min after the drainage the arterial blood pressure dro pped to 50/ - mmHg and the heart rate increased up to 156/ m in . A central venous cat heter was positioned and revealed a central venous pressure of 2 cmH20 . The arterial blood gas check under continuous breat hing of 311min 100 % oxygen did not improve ma rkedly lpH, 7.35. p. o,' 85). The blood pressu re did not increase inspite the administration of 1000 ml cristalloid and 10 00 ml of 5 % albumin. Under 100 % oxygen breathing with a tachypnea of 28 per min P.02 two hours after drainage was 43. Distinct rales over the right lung were misinterpreted as a "silent as pira tion" and emergency bronchoscopy was done. A constant flow of edema fluid from the right segmental ostia was see n. otherwise the findings were norm al. The diagnosis of reexpansion edema was established. Thr ee hours after dr ainage the patient was intu bated and controlled inverse ratio ventilation with a positive end-expiratory pressur e (PEEP) of9 cml l-Owas initiated but had to be redu ced to 5 du e to persistent arterial hypotension. Dopa min an d dobutamin were administered by continuous infusion. Sedation was achieved with Midazolam . Durin g the following 12 hours the patient was given 3000 ml crtstalloids. 1000 ml colloids and 250 ml mannitol. A fluid balance of plus 2200ml during the first 12 hours was necessary to stabiliz e the arterial pressure at 115175 mmHg. The fluid loss over the chest tub e dur ing this time was 350 011. The analysis of the fluid yielded the same protein and albumin content as found in the serum of the patient (4.3 mg/dl protein. 2.8 mg/dl albumin). Four hours after intubation the P, » was 65 under 60 % F10 2 with a pers istent acidosis of - 6 BE. Only after 24 hours F10 2 and the dose of the adren ergic substances could be gradu ally reduced. Intermittent mandatory ventilation (IMV) was initiated . The chest radi ograph showed a slight improvemen t. After 36 hours IMVwas changed to CPAP breat hing over the tub e. Four days after the initial event the chest ra diograph showed norma l findings an d the patient was extubate d. The chest tube could not be removed for 25 days due to two recur rent collapses of the lung which occurred when the drainage was clamp ed tentatively. Otherwise the course was uneventful. Cas e 3
A 73-years -old female patient who had a history of cerebrovascular and ca rdiac insufficiency developed acute respiratory insufficiency following as pira tion of chunks of an unpeeled ora nge. After the glottis had been cleared by the emergency doctor. there were still no breathing sounds over the left lung and the patient remained dyspnolo inspite of 3 U min oxygen adm inistered by mask. Because of a cicatrised deviation of the epiglottis and the right arye piglottic fold the emergency doctor did not succeed in intu bating the patient. During trans port to the hospital, 30 min later. she coughed up another piece of oran ge peel and ventilation was reestab lished on
Fig. 5 Case 3: Roentgenogram at thetimeofadmission: Patchyopacity ofthe left lungwhich isnot fullyexpanded (2em borderbetween upperlobeandchest wall)
Fig. 6 case3:Eighteenhoursafter intubation the left lung hasmarkedly cleared. is reexpanded, but still shows a hazy opacity
the left side but without improvemen t of the ca rdiores piratory situation. however . Another 45 min later she entered the emergency room in a severely dyspn eic and cyanotic condition. The art erial pressure was 60/- mmllg at a hean rate of 178/min . The arterial blood gas analysis yielded pH: 7.32 and P.~: 37. Intubation and controlled ventilation were immediat ely performed. 1000 mV30 min cristalloids and dopamine were admini ste red. The chest radiograph show ed the left lung opaque and not totally expanded (Fig. 5). Moist rales were prese nt over the left lung. As a residual. part ially obstructing foreign body was suspected. bronc hoscopy was done. The trachea and both bronchial trees were free, a consta nt flow of a frothy fluid from the periphe ry oft he left lung into the left lobar bronchi was found . The wall of the left
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main stem bronchus show ed a se m icircular hemorr hagic imbibition of th e mucosa. probably co rresponding to the former site of th e foreign body . Again . the diagnosis of reexpansion ede ma was es tablishe d by bronchos copy. For 48 hours controlled ventil ation with a PEEP of 5 cmHzQ wa s do ne. Prophylactic treatmen t with cephalosporine and amin oglycoside antibi otics was initiated . Continuous drip infus ions of cristalloids . dopamine and dobutam ine were given during 18 hours. A fluid balan ce of plus 1050 was achieved. Then the catecholamine dosag e was gradually reduced and controlled vent ilatio n was changed to intermitten t mandatory ventilation(lMV)breathi ng. At that time the left lung had markedly cleared on the contro l rad iograp h (Fig. 6). After 48 hours the patient was extubated . One we ek late r she was dis charged w ith a normal chest radiog raph.
Discussion Many cases of se vere unilateral reexpansion pulmonary edema (RPE) have been repon ed in the liter ature (3). It seems to occur seldomly, following intercostal suction drainage in the treatme nt of pneumo-, or sero tho rax . The actual incidence is probably unknown because many cases do not become clinically mani fest inspite of radiographi c signs of edema (9). A relative lack of surfactant has been suggeste d as causa tive factor. This was supported by the fact that most RPE occurred a fter long-standing total collapse of the lung, which might have impinged the surfactant production (13). On the other hand , however , RPE also does develop after very sho rt int ervals of pulmonar y collapse (9). A high speed of reexpan sion following insertion of the inter costal tub e has also been accused to be causative for the formation of RPE. Minimal capillary leakage together with lack of surfactant and negative pressure forming suddenly in the alveoli might enha nce the inflow of fluid from the ca pillaries (12). This theory is opposed by the fact that RPE has been observed as well in lungs reexpanded without suction at the intercostal tube and in atelectases reexpanding "spontaneously" after rem oval of an intrabronchial obst ru ction (8, 9, 14, 15). Undoubtedly, howe ver. Iung capilla ry permea bility is increas ed in the lung tiss ue and in the pleura l surface, the laller accounting for the high amount of protein in the pleur al fluid recover ed from the patients. Though the abovem entioned factors may play a certa in role, RPE pr obably is a reoxygenati on injury with the lung tissue pr oducing excess superoxide and other toxic metabolites (7). These metabolites might enhance the formation of leucotriens and kinins and ther eby trigger the complement cascade (5, 6). The reduced degradati on of kinins in hypoxic alveolar compart ments contributes to the inju ry (11). Other causes of un ilatera l pulmonary edema such as hypostasis in the depend ent lung following lateral decubitus position (1, 16), contralateral bronchial obstruction redirecting blood flow to the "healthy" side which subsequently develo ps edema (17), as well as vas cular caus es such as contralateral pulmona ry a rtery stenos is (10, 18) an d ipsilateral postlobectomy pulmonary vein th rombosis (4) have also bee n reponed . From the clinical point of view, seve re RPE is a serious complication, as 20 % have a lethal outcome (9). This is main ly due to pitfalls in the diagnosis: asp irat ion, residu al intrapleural fluid, and pneumoni c inflltrate are the most common radiological misint er pretations of the homogeneous opacity forming in the reexpand ed lung (9, 15). Clinically, and "unexplained" hypovolemic shock is the first
Thom e. cardiovasc. S urgeon 39 (99 1)
striking feature. Subsequently, all signs of an adult respira tory distr ess synd rome (ARDS) develop inspite of the unllaterality of the process (7). If RPE is not diagnosed early enough, the resulting hypoxemia increases the damage to the edematous lung and may even result in irreve rsib le bilateral ARDSand multiorgan failure. Therapy basically comprises an increase of the intraalveolar pressure thus redirecting the fluid into the interstitium and into the capillaries. Inverse ratio ventilation (7) or even independ ent art ificial ventilation by using two respirators might be indicated in desper ate situa tions (16). The initial fluid loss into the inter stitium ha s to be balan ced by infusions. Even in the presence of a low serum albumin the use of colloids may be dan gerous as long as ther e is capillary leakage, because the lar ge molecules are lost into the pulmonary inter stit ium further increasing the oncotic press ure there. If a severe form develops, catecholamines become indispensable. Our case NO.1 illustrat es the rapid reversibility of the process if therapy is begun immediately: only CPAP-mask breathi ng and substitution of cristalloid fluid was needed . Diagnosis was based upon the radiologica l cha nges and the rapid deterioration of the cardio res piratory function. Anothe r diagnostic clue was the high amount of serum -like fluid lost over the chest tube. During the long interva l un til therapy was initiated RPE developed into a more severe form in the two other patients. Though basically the therapeutical strategy was the same as in case no. 1, catecholamines and controlled ventilation with inver se rati o in case no. 2 were needed to sta bilize the cardiorespirat ory function. Bronchoscopy has been the mea ns of diagn osis in these two patients, but a more thorough clinical examina tion would have obviated the necessity for this invasive investigation. Any physician who rout inely performs a large quantity of intercostal suction drainages or who does emergency bronchoscopies ough t to be familiar with ea rly diagnosis and therapy of RPE, the occurrence of which is unp red ictable and the incidence of which cannot be prevent ed. References Baraka. A.. R. Moghrabi. and A. Yazigi : Unilateral pulmonary edema/atelectasis in lateral decubitus position. Anaesthesia 42 (1987) 171- 174 a Bows er. B.. 1. M. Stinso n: Spontaneous unilateral pulmonary edema. J. Natl. Med. Assoc. 78 (1986) 88 2-88 3 3 Fanning. 1.. L. Lettieri. andM. S. Piver: Fatal recurrent reexpansion pulmonary edema. Obstet. Gyneeol. 74 (1989) 495- 549 4 Gyves- Ray . K. M.. D. L. Spi zarny. B. H. Gross: Unilateral pulmonary edema due to postlobectomy pulmonary vein thrombosis. AJR 148 (19871 t079- 1080 5 Jackson. R. M.. C. R. Veal. C. B. Al exander. A. L. Brannen. and 1. D. Fulmer: Neutrophils in reexpansion pulmonary edema. J. Appl. Physiol. 65 (1988) 228-234 6 Jac kson. R. M.. and C F. Veal: He-expansion. re -oxygenati on and rethinking. Am. J. Med. Sci. 298 0 989144-50 7 Koller. W . N. Mutz. C. Putens en. and G. Putz: Treatment of reexpansion edema r unilateral ARDS·) after rapid pneumothorax drainage. Anaesthesist 36 09871655 -65 8 8 Kramer. M. R.. E. Melz er. and C Sprung: Unilateral pulmonary edema after intubation of the right main stem bronchus. Crit. Care Med,17( 1989) 472- 474 9 Mahfood. S.. W R. Hix, B. L. Aa ron. P. Blaes . and D. C Wat son: Reexpansion pulmonary edema. Ann. Thorae. Surg. 45 (1988) 340-345 10 McTigue. C. 1. P. Scurr y. and M. Silbers tei n: Unilateral pulmonary I
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The Importance ojEarly Dete ction and Therapy ojRee:rpansion Pulmona ry Edema
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ede ma assoc iate d with pu lmonary arte rial comp ression. Australas Radial. 32(1988) 390-3 93 Pett y . T. L.. G. W. S ilve rs. G. W. Paul. and R. E. Stanford: Abnormalities in lung elast ic properties and surfactant function in adult respiratory distress syndrome. Chest 75 (1979 ) 571-575 Pang. L. M.. II. M. O'Brodooich, R. B. Millins, an d S. A. Stalcup: Bradykinin induced increase in pulmo na ry vascu lar per meability in hypoxic sheep. J. Appl. Physiol. 52 09821370-377 Parisi. A.. P. M. Ma rianeschi. G. M. Giustozzi . G. Bef/a vig na. D. Alberti. and F. Sciannameo: Unilateral pulmonary edema due to ra pid reexpansion in pne umoth or ax. Minerva med. 77 ( 986) 2327- 2329 Ravin. C. E.. and N. S . Dahmash: Reexpan sion pulmonary ede ma . Chest 77 (1980) 708 -710 Sautter. R. D.• W. fI. Dreker, and 1. H. Ma cJndoe: Fata l pulmonary ede ma and pneumo nitis after reexpan sion of chro nic pneumothorax. Chest 60 ( 971) 399-401
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Schere r, R.• P. Reinhold, and B. Buchholz: Unilateral lun g ede ma following chest injury: an ind ication for indepen dent ar tificial respira tion. Anast h. lntenstvther. Notfallmed. 18 (1983) 65-6 7 Shikhani. A. H.. S. D. Salman. and R. Melhem : Unilateral pu lmon ar y edema as a complication of contralateral bronchial obst r uction. Laryngoscope 97 ( 987) 748-75 1 Takeda . K.. M. J. Knap p, W. G. Wolfe, and J. D. Crapo: Hypoxia enhances unilater al lung injury by increasing blood now to the injured lung. J. Appl. Physiol. 63 (1987 ) 2516-2523
F. M. Smolie-Juettner
Depar tment Thora cic an d Hyperb ari c Surge ry Univers ity ofGraz. Medical School A·8 036 Graz/Austria
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