CHAPTER V
Wet Lung
Thomas H. Burford, M.D.
CONCEPT AND GENERAL CONSIDERATIONS
During the first year of fighting in the North African Theater of Operations,U.S. Army, it gradually became apparent that casualties with fluid in the lungs,in contrast to those whose lungs were dry, presented many difficulties ofmanagement. They required strenuous efforts at resuscitation if they were inshock, and they did not respond well to them. They presented poor surgical riskswhen emergency surgery was necessary. They were prone to develop postoperativepulmonary complications, especially if they had coughed up large amounts ofblood before operation. Fatalities were proportionately more frequent among themthan among casualties with similar wounds whose lungs did not contain fluid.When these patients came to autopsy in forward hospitals, pulmonary edema wasthe most prominent finding.
Although most surgeons in the theater were aware of thephenomena just described, the extreme seriousness of the problem was notimmediately realized. There was nothing in the civilian experience to callattention to pulmonary edema as an immediate consequence of thoracic injuries.1As a result, more than a year was to pass after the onset of fighting in NorthAfrica before the concept of what came to be known as wet lung was developed andappropriate methods of treatment were devised.
The term "wet lung" and the concept which underlay it were firstpresented by Maj. Thomas H. Burford, MC, and Maj. Benjamin Burbank, MC, at ameeting of Fifth U.S. Army surgeons at the 38th Evacuation Hospital at Riardo inFebruary 1944. At the same time, they discussed its etiology and outlined theprinciples of prevention and correction.
In their first presentation on this condition, Major Burford and MajorBurbank described wet lung as a more or less specific response of the lung andchest wall to trauma. They postulated the operation of a somatovisceral reflexoriginating in the chest wall and mediating alveolar and bronchiolar
1In 1937, Betts and Overholt (1) described a syndrome which sometimes occurred from 24 to 48 hours after thoracic surgery, usually at night, and which consisted of slight cyanosis, noisy respirations, depression of the cough reflex, and a shocklike state. No matter how hard the patient tried, he could not raise the secretions whose retention was producing anoxia and anoxemia. The only way to break the cycle was to remove the retained secretions, for which bronchoscopic aspiration was necessary. In a number of respects, this syndrome seems to resemble the wet lung encountered in combat-incurred injuries.
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responses. They particularly emphasized the part played bythe painful chest wall in the pathogenesis of wet lung. It was the chiefexplanation of the patient's inability to raise the secretions formed in excessas the result of trauma. The immobilization of the chest wall made effectualcoughing impossible, and the result was the saturation of the tracheobronchialtree with secretions which, under normal circumstances, would have been coughedup.
Major Burford and Major Burbank further suggested that a definite one-tworelation probably existed between the wet lung of trauma and the massivepulmonary collapse which was so common in World War I. Their theory was that thewet phase, which was not recognized, precipitated the second phase, in whichmassive collapse occurred (p. 210).
The concept of wet lung, as presented by Major Burford and Major Burbank, wasprecise and specific. Later, Maj. Lyman A. Brewer III, MC, and other chestsurgeons in the Mediterranean Theater of Operations, U.S. Army, expanded theoriginal concept into a looser, broader concept of traumatic wet lung. In thislater concept, the term "wet lung" was used for all forms of retainedtracheobronchial fluid resulting directly or indirectly from trauma.
Recognition of the importance of wet lung in no wise detracted from theimportance of the primary lesion or of associated injuries. On the contrary, itpermitted a more rational approach to the entire problem of combat-incurredchest injuries. The important considerations stressed by Major Burford and MajorBurbank were as follows:
l. The chest reacts to trauma in a way peculiar to itself, whether the injuryis a slight contusion of the chest wall or a severe penetrating or perforatinginjury.
2. The reaction caused by trauma profoundly influences the whole pathologicprocess, the therapy applied, and the prognosis.
PATHOGENESIS AND PATHOPHYSIOLOGY
The pathogenesis of wet lung can be understood only if the normal physiologyof the respiratory tract is borne in mind. In addition to its function as anairway, the tracheobronchial tree has a definite secretory function, combinedwith the capacity to rid itself of its own secretions and of aspirated materialor other fluid substances which do not normally belong within its lumen.Evacuation of the tracheobronchial tree is accomplished (1) involuntarily, byaction of the cilia and movement of the bronchial musculature, and (2)voluntarily, by coughing.
In spite of the extensive experience of World War II, littleis yet understood concerning the effect of trauma to the chest on the functionof the bronchial cilia and on other factors influencing the passage ofsecretions through the tracheobronchial tree. The presumption seemed warrantedthat after trauma, these functions became depressed or were perhaps entirelyinterrupted. Clinically, it was clear that the normal cough mechanism was
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seriously impaired in the presence of moderate and severe trauma, andsometimes of slight trauma.
The lung, which is a specialized organ, reacts to trauma in just asspecialized a manner as does the brain or any other specialized organ. In combatcasualties with chest injuries, the pulmonary reaction took two forms:
1. The production of an excess of secretions or, in the broader concept ofMajor Brewer and his associates, of transudates and extravasated blood also.
2. The development of conditions which prevented the normal and adequateelimination of these fluids.
At present, there is insufficient evidence to permit formulation of a preciseexplanation for this dual process. Experimentally, de Takats and his associates(2) demonstrated that any appreciable trauma to the chest wall wasfollowed almost immediately, in 60 percent of the animals, by widespreadbronchial spasm and increased bronchial secretions. Bronchial spasm of the samedegree could also be produced by stimuli applied within the abdomen, such astraction on the cystic duct or the mesentery.
It would be tempting to apply these experimental results to combat casualtiesand to postulate the existence of reflex bronchial and bronchiolar spasmoriginating after trauma as the result of a painful chest wall or pleura, butthere are two reasons why the transfer would not be justified:
1. The whole case for bronchospasm rests on evidence that is still far fromacceptable.
2. The hypothesis of bronchial spasm would explain only part of the phenomenaobserved in traumatic wet lung.
Even though it was not possible to explain the initial effect of thoracictrauma on the function of the tracheobronchial tree, the course of eventsafterward was quite clear:
1. The presence in the tracheobronchial tree of mucoid secretions in far morethan normal amounts, as well as of transudates, blood, and aspirated materialcaused a mechanical obstruction and prevented adequate oxygenation of thealveoli.
2. With the suppression of the normal cough reflex, the tracheobronchial treebecame increasingly less capable of eliminating secretions, and more fluidaccumulated in it.
3. As these conditions continued, less oxygen became available to thepulmonary capillaries. It could be assumed from the work of Drinker and Warren (3)that anoxia increased capillary permeability and permitted more plasma to belost into the tissues. Increased amounts of fluid extravasated from thepulmonary capillaries into the alveoli further decreased the oxygen availablefor the bloodstream.
4. The plugging of branch bronchi with secretions preventedthe exchange of gases in the lobules supplied by these bronchial divisions, andlobular atelectasis resulted.
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5. Plugging of a branch bronchus to a lobe or of a stem bronchus to a lungincreased the anoxic anoxia that was the result of partial obstruction, for tworeasons: (1) The alveolar bed available for the absorption of oxygen was farsmaller than normal, and (2) sooner or later, a mediastinal shift resulted.
When blood was present in the tracheobronchial tree as the result of trauma,it could, in itself, cause bronchial obstruction. It also had another effect,that the irritation of the bronchial mucosa that it caused was responsible, inturn, for an increase of tracheobronchial secretions.
When wet lung appeared soon after wounding, its most potent effect was thepromotion of anoxia. When it persisted or was allowed to progress withouttreatment to the point just described, it paved the way for subsequent pulmonarycomplications. A patient who was not too severely wounded and in whom otherconditions were favorable might recover from his initial shock without completeremoval of the fluid that was producing obstruction of the tracheobronchialtree. In such an instance, however, the causative factors were unchanged, andthe stage was set for the development of tracheobronchitis, atelectasis,pneumonitis, and pneumonia. Wet lung sometimes seemed to be the chief factorupon which the outcome of an injury hinged. Failure to take active measures tocombat it could lead to chronic pulmonary invalidism, and, before thiscomplication was clearly understood, more than one patient with an uncontrolledwet lung died from this cause alone.
It was of the greatest importance that anoxia be relievedpromptly. If it was not, serious changes occurred in other organs, particularlyin the central nervous system, which is highly sensitive to an oxygen deficit.Severe cerebral anoxia, even if it persisted for only a short time, could resultin serious cortical impairment. The psychotic manifestations and coma observedin some patients with chest injuries could reasonably be attributed to thiscause.
There was clear clinical evidence of the relation of the pathophysiologicdisturbances produced by wet lung to the patient's general status. In numerousinstances, shock which had not responded to standard replacement therapy andother resuscitative measures, or which had become deeper as they were inprogress, cleared up quickly, and even dramatically, when appropriate measuresfor the relief of wet lung were instituted.
As clinical experience accumulated, the theory seemed reasonable that adefinite relation might exist between the wet lung of trauma as it wasrecognized in World War II and the massive pulmonary collapse described byPasteur (4) in 1914 and described later, under the name of acute massiveatelectasis, by Churchill (5). It was an attractive hypothesis toconceive of wet lung as the antecedent stage, and in a sense the precipitatingcause, of silent massive pulmonary collapse.
Such an assumption would explain the extreme rarity ofmassive pulmonary collapse in the Mediterranean theater, where surgeons becameincreasingly alert to the recognition of wet lung and increasingly vigorous inits
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treatment. Minor degrees of atelectasis were frequently observed in cases ofwet lung which were inadequately treated.
ETIOLOGIC FACTORS
The events just described were most often observed afterchest injuries. Wet lung, however, was a possibility in other injuries,including thoracoabdominal injuries, abdominal injuries, and head injuries,particularly those that were associated with coma and unconsciousness.
Usually, though by no means always, the degree of wetnessdepended upon the type and severity of the primary lesion, the size and velocityof the missile, and whether or not the missile had struck a portion of the bonycage or only the soft tissues. The size of the intrapulmonary vessels that weredamaged had a bearing on the amount of blood extravasated. Wet lung was presentto some degree in practically all cases of thoracic trauma, though it might betransitory or so slight as to be almost unrecognizable clinically even when itwas carefully searched for. Sometimes, too, the primary thoracic lesion was ofsuch severity that it masked the underlying physiopathologic substratum. In manycases, on the other hand, wet lung was present to a far more severe degree thanmight have been expected from the relative mildness of the initial wounds.
A number of other factors played a part in the causation of wet lung:
Pain
Pain was an almost invariable component of chest trauma. Itsexact influence in the production of wet lung was never fully clarified, butthere was no doubt that it played an important part in both its inception andits progress. It had at least three harmful effects:
1. It induced a shallow type of respiration, for protective reasons.
2. The natural reaction to pain was voluntary splinting of the affected area.
3. The affected hemithorax therefore moved less than the unaffected side,with a resultant decrease in the movement of air back and forth in the bronchi.A decrease in the tidal respiration was probably of more importance than was atfirst recognized, as it lessened the amount of secretion that might be disposedof by evaporation.
Suppression of the Cough Reflex
The normal voluntary cough mechanism consists of four steps:
1. The air is drawn voluntarily into the lungs by raising the ribs andlowering the diaphragm.
2. The breath is held momentarily by closing the glottis.
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3. The abdominal muscles are tensed, the intercostal spaces are narrowed, andthe diaphragm is relaxed to provide explosive force.
4. The glottis is then suddenly opened, and the bechic blast required toraise the sputum is thus released.
A number of conditions present in chest trauma prevented the succession ofsteps just listed, all of which are necessary for effective coughing. Painarising in either the chest wall or the pleura prevented both expansion andforceful contraction of the thorax. Rib fractures were frequently associatedwith severe pain when either coughing or deep breathing was attempted. If therewere multiple fractures of the ribs or of the sternum, with a resulting flailchest, the paradoxical movement of the chest wall made effective coughingimpossible. On inspiration, it moved outward. Attempts at coughing simplyaggravated these paradoxical movements.
Wounds that caused abdominal pain, whether they were locatedin the abdomen or in the chest, prevented the tensing of the abdominal musclesnecessary for an effective cough. The pistonlike action of the diaphragm, whichis a part of the act of coughing, was impossible in a diaphragmatic injury.Ileus, acute dilatation of the stomach, and the presence of free fluid in theperitoneal cavity also had a more or less inhibitory action on the coughmechanism.
Sedation and Anesthesia
Oversedation from the too-liberal use of morphine was a fairlyfrequent contributing cause of wet lung. As their experience increased, shockofficers in field and evacuation hospitals learned to be constantly on theirguard against giving morphine to freshly wounded casualties. Often the patientsdid not need it at all. They were simply apprehensive as the result of anoxiaand disturbed and uncomfortable from the ambulance ride. When morphine wasreally needed, it was given intravenously, not subcutaneously, in ?-gr. or atmost ?-gr. doses.
Early in the war, as pointed out elsewhere (vol. I), and muchless often later in the war, casualties with fractured ribs, flail chests, andother painful thoracic and abdominal wounds often arrived in the shock wards offield and evacuation hospitals with overdosages of morphine compounding theiroriginal difficulties. For a variety of reasons they had received too muchmedication. Respiratory distress was sometimes as inherently frightening to theinexperienced medical officer as to the casualty, and efforts made by theseofficers to relieve the patient were sometimes as frantic and ineffectual as thepatient's own efforts to get his breath.
Whatever the background, oversedation invariably led to an increase in theaccumulation of secretions in the tracheobronchial tree and a decrease in thecough reflex. As a result, shock was increased, and preparation of the casualtyfor emergency surgery or for further evacuation became more difficult.
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Prolonged administration of an inhalation anesthetic to apatient in poor condition, whose reaction was delayed after operation, often ledto the retention of bronchial secretions and to later pulmonary complications.This was particularly true if the airway had not been kept clear by cathetersuction during the operation and if bronchoscopy had not been performed at theconclusion of the procedure when there was any doubt at all about the efficacyof suction.
Preexistent Respiratory Infection
It was not unusual for secretions to be present in thebronchial tree before injury. Soldiers who had undergone exposure during combat,particularly during the cold, wet months of winter, frequently had upperrespiratory infections or frank bronchitis, associated with mucopurulentsecretions. In the Mediterranean theater, preexistent respiratory infectionswere often aggravated by the circumstances of evacuation. During the mountainfighting in the winter of 1943-44, casualties had to be brought down themountain by litter carry. Often as many as 8 to 12 relays were required betweenthe battalion aid station and the collecting station. As a result, exposures of12 hours or more after wounding were not unusual.
Overhydration
No matter how urgently replacement therapy might be needed, ithad to be instituted judiciously in patients whose cardiorespiratory physiologywas disturbed after wounding (vol. I). The administration of too much plasma inbattalion aid and clearing stations, or even of too much blood in field andevacuation hospitals, might place such an extra load on the circulatory systemthat pulmonary edema might develop and contribute to the etiology of wet lungarising directly from the wound.
CLINICAL PICTURE
Wet lung usually appeared shortly after wounding, sometimes within a fewhours. Less often, it did not develop for as long as 5 or 6 days after injury.
The presence of abnormal amounts of fluid in the tracheobronchial tree inthoracic injuries was manifested by certain cardinal symptoms and signs, theearly recognition of which prevented the development of graver complications.Cough and dyspnea were the chief symptoms, and rales were the predominantphysical finding.
Symptoms-The cough associated with wet lung was usuallydescribed as a wet cough because of the rattling or gurgling element alwayspresent in it. It might be hacking, harassing, continuous, or paroxysmal. Smallamounts of sputum were often raised by constant coughing, but the cough remainedmoist; because there was little expulsive force behind it, it was never fullyproductive.
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Inexperienced medical officers might receive the impressionthat, because some sputum was raised, tracheobronchial drainage was good, butthe persistence of wheezes and rattles in the chest proved that it was stillpoor. As a matter of fact, only the most superficial secretions were raised,just as small amounts of fluid are splashed out from the top of a full cup thatis continuously replenished.
The dyspnea characteristic of wet lung could be explained in a number ofways. It might be the result of painful, jerky, shallow respirations, eachinspiratory effort being limited by the pain that the preceding effort hadcaused. When trauma had been considerable, the explanation might be hemothoraxor mediastinal shift. When damage had been minimal, the most reasonableexplanation was partial bronchial obstruction with resulting anoxia. Somepatients seemed to be having typical asthma. Apprehension was an occasionalcause of dyspnea.
When dyspnea was extreme, orthopnea, restlessness, excitement, anddisorientation were present as the result of cerebral anoxia.
Signs-The patient's appearance varied according to the severityof his injury and whether or not he was in shock. Fever and evidences oftoxicity were constantly present in late cases.
Respirations were frequently grunting because they were painful. Motion wasusually restricted over the involved area of the chest. Breath sounds werereduced in intensity, but if hemothorax, pulmonary hematoma, or some similarcomplication were not associated with the injury, the percussion note and thetactile fremitus were unlikely to be materially altered.
The most characteristic physical finding in wet lung was the presence ofrales, bronchial in character. They were sometimes heard on both sides of thechest; their bilateral presence was a valuable diagnostic sign. More often, theywere more intense on the injured side. They ranged from high-pitched wheezes,which some surgeons considered indicative of associated bronchospasm, to mediumor coarse bubbling rales or rhonchi. Rales that were wheezing and high-pitchedsometimes had a dry quality. Sometimes fine rales that were predominantly moistor bubbling were so numerous as to suggest the type heard in simple,nontraumatic pulmonary edema or in bronchial asthma. These rales were frequentlybilateral. Bubbling, sonorous rales were sometimes heard in combination with aclassical tracheal rattle; in such cases, the sputum was predominantly liquid.
Rales were often so loud that the stethoscope was not needed to identifythem. They could be heard at the bedside, or even at some distance from thepatient, just as in typical bronchial asthma. While all varieties and gradationsof rales might be present in any single chest, diffuse moist rales wereespecially characteristic of the primary phase of traumatic wet lung.
Rales were sometimes not demonstrable unless the examinationwas made immediately after the patient had coughed. They might not be heard atall if sticky mucus was attached to the tracheal or bronchial wall or if abranch
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bronchus was completely blocked. In such cases, fine crackling sounds couldusually be heard if the stethoscope was placed over the patient's mouth.
As already indicated, a coexistent hemothorax, pneumothorax, or some otherfinding might so alter or mask the typical clinical symptoms and signs of wetlung that its existence would not be suspected unless the medical officer borethe possibility in mind.
DIAGNOSIS
Clinical observations-In early stages of traumatic wet lung,the evidence of moisture obtained by auscultation was the most importantdiagnostic sign. The presence of rales anywhere in the chest, even over portionsnot involved in the trauma, was a valuable clue, indicating as it did that wetlung was either present or in process of development.
In advanced cases, the diagnosis, as already stated, couldsometimes be made without the use of the stethoscope because dyspnea was soobvious and rales were audible even at a distance from the bed. The physicalfindings in late cases were those ordinarily observed in atelectasis andpneumonia. Distant bronchial breathing was often heard over small areas of thechest and might represent either patchy lobular atelectasis or a pneumonicprocess. The diagnosis of wet lung was established if the intensity or locationof bronchial breathing changed with forced coughing.
The character of the secretions raised was also of diagnosticsignificance. Hemoptysis usually denoted pulmonary injury; the blood wasfresh-looking when hemorrhage was recent and was clotted and mixed with mucuswhen it was not. If the secretions were the result of reflex stimuli from traumato the chest or irritation from aspirated material, or were part of a very earlyinfection, they were likely to be mucoid. As infection developed in thebronchial tree, they became increasingly purulent. The presence of purulentsputum could sometimes be explained on the basis of a preexisting respiratoryinfection and sometimes by the development of a new infection in the stagnatedbronchial secretions. Thin, yellow, pink or colorless fluid, often frothybecause of the admixture of air, indicated the pulmonary transudation andexudation (edema) typical of more advanced wet lung. Then, serosanguineous fluidsuggested hemothorax with bronchopleural fistula. Similarly, thin, seropurulentfluid suggested early empyema with bronchopleural fistula. Most often, thesputum represented a combination of the types described rather than a single,clear-cut type.
Roentgenologic examination-While roentgenologicexamination was highly desirable in all instances of chest trauma, it was alwaysdeferred until the patient was brought out of shock and steps had been taken todry out the tracheobronchial tree.
The roentgenograms, which were taken, whenever possible, in at least twoplanes, were frequently difficult to interpret and were not always useful. Inthe initial stages of wet lung, roentgenologic changes were minimal, even when
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there was clinical and auscultatory evidence of aconsiderable degree of obstruction and moisture. Patchy lobular atelectasis inthe early stages might be indistinguishable from the shadows cast by a pulmonaryhematoma (p. 165) or the pathologic process present in pulmonary contusion (p.4). When intrapulmonary bleeding had occurred, the shadows were likely to beround or oval. When a hematoma was present, there might be evidence of small,loculated air pockets. Later, when lobular or total pulmonary atelectasis hadoccurred, the collapse of the affected parts of the lung produced the classicalsigns of mediastinal shift and narrowing of the intercostal spaces.
On the whole, while roentgenologic examination was sometimesuseful and was never omitted because of the chest injury, the diagnosis of wetlung in the early stages was a clinical matter.
Differential diagnosis-As a practical consideration, thequestion of differential diagnosis seldom arose in connection with traumatic wetlung. Theoretically, the condition had to be distinguished from bronchialasthma, pulmonary edema of cardiac origin, and pulmonary edema associated withperipheral vascular failure.
The differentiation was not difficult. The history of traumaand the absence of any history of previous asthmatic attacks promptly ruled outbronchial asthma. Since the young soldier was almost never a cardiac subject,the necessity of differentiating traumatic wet lung from pulmonary edema ofcardiac origin almost never arose. Occasionally, however, patients with thoracicinjuries had had such vigorous intravenous fluid therapy that the blood volumehad become too much for an already embarrassed respiratory mechanism and rightheart failure had supervened. In such cases, the manifestations of wet lung wereinterwoven with, and intensified by, those of right heart failure.
Pulmonary edema associated with peripheral vascular failureeither from shock due to severe trauma or from an overwhelming toxemia wassometimes difficult to differentiate from wet lung, particularly when shock wasassociated with the latter. The nature of the exciting lesion, the pallor, lowblood pressure, tachycardia, and weak, thready pulse had to be evaluated, aswell as the response to attempts to clear the tracheobronchial tree. In wetlung, the response was usually rapid. If the pulmonary edema was associated withperipheral vascular failure, it would not respond to the therapy indicated forwet lung because its etiology was different.
PROPHYLAXIS
As their experience accumulated, medical officers came torealize that it was the part of wisdom to regard as a potential candidate forwet lung every casualty with a chest wound, a thoracoabdominal wound, a severeabdominal injury, or a head injury. On their admission to forward hospitals, allpatients in these categories, particularly those who complained of thoracic painor who presented dyspnea, wheezing, hemoptysis, and a cough, were carefullyexamined
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for evidences of fluid in the pulmonary tree. The following routine wascarried out:
1. Unless the patient was in shock or unconscious, he wasplaced in Fowler's position, so that the abdominal contents would gravitate intothe pelvis. The diaphragm could thus act more effectively, with correspondingimprovement in respiration and in the efficacy of the cough. The position waschanged frequently if the patient could not turn himself. This measure was notalways stressed as it should have been.
2. If the patient was dyspneic or cyanotic, oxygen was administered by nasalcatheter or by the Boothby-Lovelace-Bulbulian mask.
3. If his breathing was at all wet, the patient wasencouraged to cough (fig. 67A), the chest being supported manually wheneverpersonnel could be spared for this purpose. The physical support of a painfulchest was helpful, and the psychic effect was excellent; the patient wasimpressed with the importance of coughing because someone took the time andtrouble to help him to do so. If he was sufficiently alert to comprehend, asalready mentioned, the importance and rationale of coughing were explained tohim, which made him much more willing thereafter to cough, in spite of anyassociated discomfort.
4. If the patient was conscious, complained of pain, and hadevidently had no previous sedation, a small dose of morphine sulfate, preferablynot more than gr. 1/8, was given byvein, so that it would act promptly and its effect on the painful chest could bemore accurately evaluated.
5. The usual measures employed in all chest wounds were carried out. If thedressing covering a sucking wound was not already airtight, it was rearranged.The indicated resuscitative measures were instituted, with great care not tooverload the circulation with fluids. The gastric tube was inserted if there wasevidence of ileus or gastric distention (fig. 67B). If a hemothorax or tensionpneumothorax was present, aspiration was employed to increase the vitalcapacity.
If wet lung had not yet become established but was merelyimpending or incipient, these measures were usually effective and the patientrapidly became a fit candidate for surgery in a forward hospital or could besafely evacuated to a fixed hospital.
MANAGEMENT
Principles
As already pointed out, the various factors responsible for wet lungconstituted a vicious circle. They included accumulation of secretions in thesmaller bronchi; limitation of normal respiratory motion because of pain; thesuppression of the cough reflex, as well as of the desire to cough, because ofpain; and the resultant effect of the wet lung on the oxygenation of the blood.
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Breaking this vicious circle by attacking its variouscomponents was the basis of the active therapy of established wet lung. In itsactive management, as well as in its prophylaxis, the principal aims of therapywere:
1. The maintenance of an open airway, so that inspired oxygen could reach thealveolar capillaries.
2. The prompt correction of conditions that were contributing to dyspnea,anoxia, and shock.
To achieve these aims, it was necessary to control the production of fluid inthe lungs and to promote adequate bronchial drainage, as well as to institutesuch other measures as were necessary to correct the disturbed cardiorespiratoryphysiology.
Relief of Pain
Relief of pain and physiologic remobilization of the chest wall afterthoracic injury were the sine qua non of a successful therapeutic effort in wetlung. In prewar civilian practice, the desired results had been achieved byadhesive strapping and the administration of morphine. These measures had neverbeen physiologically sound. In combat-incurred injuries, both were ineffective,and even in stove-in chest, they were not necessary.
In severe flail chest with extreme paradoxical respiration, strapping of thechest or the use of a firm binder was occasionally necessary to preventballooning out of the chest wall (fig. 67C). The method was never officiallyforbidden, but with these very occasional exceptions, its use was avoided.
The administration of morphine was equally undesirable. It made the patientless aware of his discomfort, it is true, but it did not make the coughmechanism painless, and it diminished the cough reflex. Furthermore, by dullingthe sensorium, it made the patient less aware of his own responsibility forovercoming his respiratory difficulties.
Intercostal Nerve Block
The most effective method of relieving chest pain and making it possible fora casualty with a chest wound to evacuate the tracheobronchial tree by coughingwas intercostal nerve block at the site of injury (fig. 67D), or, alternatively, paravertebral sympathetic nerve block. One reason that it wasnecessary to employ both the intercostal and the paravertebral techniques ofnerve block was that certain wounds were so situated that simple intercostalblock was not always feasible.
Whether intercostal nerve block did more than abolish pain and effect aninterruption of the reflex are was a matter of speculation. It was, however, alogical procedure. According to Lewis (6), afferent pain impulses fromthe thoracic abdominal wall are transmitted by way of the sympathetic nerves,whose fibers accompany the intercostal nerves as far as the intervertebralforamina, whence they depart as rami communicantes to form part of theparavertebral sympathetic chain. There seemed little difference, therefore,between
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interrupting the pain pathway by blocking the intercostal nerves or blockingthe paravertebral chain through which pain impulses pass.
The nerves could be anesthetized at any point posterior to the lesion. Atleast three nerves were always injected, to provide a generous margin ofanesthesia around the traumatized area. As many as 10 intercostal nerves orparavertebral ganglia could be blocked with safety, but when more than 4 or 5nerves were to be injected, it was the policy to give a small preliminary doseof some barbiturate, to lessen the risk of a procaine hydrochloride reaction.
Local infiltration, which produced its effects by blocking the sensory endorgans, was effective in simple, uncomplicated rib fractures with contusion ofthe chest wall, but it was contraindicated in casualties with open wounds,because all such wounds were potentially if not actually contaminated.Furthermore, the involved area in casualties with open wounds was frequently tooextensive for local infiltration to be practical. This was sometimes, however, avaluable supplement to an extensive blocking procedure after which a smalllocalized area of pain occasionally persisted, though an otherwise effectiveblock had been obtained.
If the site of injury were so located posteriorly that even paravertebralblock would require injection through contaminated tissue, paravertebral blockincorporating at least two nerve segments above the superior margin of theinjury was useful, for it blocked an appreciable number of the pain impulseswhich travel cephalad in the paravertebral sympathetic chain.
Technique of nerve block-The needles used for intercostal nerveblock were ordinary intravenous needles, 1? inches long. A 1-percentsolution of procaine hydrochloride was usually used, though an occasionalsurgeon preferred a 2-percent solution. An intradermal wheal was raised over thechosen rib at its angle over the inferior border of the rib between the costalangle and the wound or fracture site (fig. 68). Then the needle, without thesyringe attached, was introduced through the wheal until the point had impingedlightly upon the inferior margin of the rib. From this point, with the beveldirected inferiorly, the needle was moved until the tip just cleared theinferior edge of the same rib. After the needle had been advanced about 0.5 cm.,aspiration was carried out in two planes, to exclude the possibility that itmight have entered a blood vessel. When this point had been settled, from 4 to 6cc. of 1-percent procaine hydrochloride solution was introduced into thetissues. The total number of thoracic segments injected was determined by thenumber of ribs fractured or, if the lesion was a simple contusion, by the areainvolved.
Needles 3 or 3? inches long were preferred for paravertebral nerve block. Asmall piece of loose rubber on the shaft indicated the depth to which the needlewas to be inserted.
Paravertebral injection of the thoracic sympathetic ganglia was bestperformed with the patient in the lateral recumbent or the prone position. Thesites for injection were marked on the skin, opposite the spinous processes andabout 4 cm. lateral to the midline on the affected side. These points liedirectly
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over the transverse processes. The best results were achieved when one or twoganglia cephalad to the area of involvement were also incorporated in the block.
The needle, without the syringe, was introduced perpendicularly through theskin until contact was made with the dorsal surface of the transverse process;it was seldom necessary to introduce it more than 4 centimeters. The rubbermarking was readjusted on the shaft from 3 to 4 cm. from the skin surface beforethe needle was withdrawn slightly. Then, with its bevel directed medially, theneedle was redirected anteromedially and passed just inferior or just superiorto the transverse process. It was slid along the body of the vertebra to thedepth indicated by the marker. At this location, the tip of the needle lay inthe immediate vicinity of the sympathetic chain.
If, during its insertion, blood or spinal fluid appeared, the needle waswithdrawn and was reinserted in a slightly different direction. If blood orspinal fluid did not appear, the syringe was attached to the needle, andaspiration was carried out in two planes, to be sure that the needle did not liein a blood vessel, in a prolongation of the subarachnoid space, or in thepleural cavity.
If aspiration was negative, 6 cc. of 1-percent procaine hydrochloridesolution was injected into the tissues. If the needle had been introducedcorrectly, relief from pain was almost immediate, only just enough time beingrequired for infiltration of the solution through the tissues surrounding thesympathetic chain.
As soon as either intercostal or paravertebral nerve block had beenaccomplished, an attendant forced the patient to cough.
If open thoracotomy was necessary in a patient who had not previously beensubmitted to nerve block, advantage was taken of the opportunity to block thenerves under direct vision by injecting procaine hydrochloride solution.Crushing the nerves with a fine hemostat was a much less desirable procedure.
Results of nerve block-Blocking out of the pain stimuli byinjection of the intercostal nerves or by paravertebral block produced promptand often dramatic results. Pain and discomfort almost invariably disappeared.The patient was willing to cough because it was no longer painful to do so, andevacuation of the fluids in the tracheobronchial tree was effected.
It was impossible to overlook the possible influence of nerveblock on constriction of the bronchial tree and secretion of mucus. Clinicalevidence supported the hypothesis of its role. Frequently, casualties were seenwith respiratory distress that could not be accounted for by the severity of thethoracic injury, pain in the chest wall, shock, the presence of blood or otherfluid in the bronchial tree, aspiration of gastric contents, infection, orexposure to noxious gases. Coughing was apparently free and forceful, butwheezing persisted, and sputum was not raised. Once the intercostal nerves wereblocked, however, the picture changed. Wheezing disappeared promptly, sandsputum was raised freely. The assumption in such cases was that reflex bronchialspasm probably played some role in the previous symptoms and signs.
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Relief of pain and discomfort after intercostal nerve block lasted forvarying periods of time but almost never for less than 24 hours. The block couldbe repeated as necessary, but frequently a single injection gave permanentrelief. Why relief of pain extended beyond the period of the pharmacologicaction of the drug is difficult to explain. Possibly relaxation of muscle spasmand improvement of the blood supply to the traumatized area played some part inthe results.
The beneficial effect of paravertebral block usually lasted from 2 to 4hours. One injection frequently gave permanent relief, and more than three werealmost never necessary.
An effective nerve block, in addition to rendering anesthetic the areainnervated by the somatic nerves blocked, sometimes also provided immediaterelief of pain in a referred area, occasionally on the side opposite the trauma.
When the nerves were blocked at thoracotomy, the stimuli arising from thechest wall and parietal pleura were diminished, and the patient was usually freefrom pain during the most important part of the postoperative period. Nerveblock at operation also eliminated the necessity for later intercostal nerveblock.
Catheter Aspiration
If, after a reasonable period of time, a patient with traumaticwet lung did not improve under the measures just outlined, combined with theusual regimen of resuscitation, mechanical measures had to be employed. Thecircumstances of the individual case determined whether catheter aspiration(fig. 67E) should be tried or bronchoscopy (fig. 67F) resorted to at once. Thelength of the trial period, which might be as short as 5 or 6 hours or as longas 20 to 24 hours, depended upon the patient's original injury, his clinicalstatus, the roentgenologic findings, and his progress under treatment. Somepatients were too exhausted to cough effectively without aid, and some wereuncooperative for other reasons.
Whether catheterization or bronchoscopy was used, the aims were the same:
1. To remove excess fluid in the lower airway.
2. To loosen deeper secretions by local manipulation.
3. To promote more efficient cough.
A long delay was not justified if the situation was complicated by acommunication between the tracheobronchial tree and a pleural cavity containingfluid.
Catheter aspiration of the tracheobronchial tree had so many advantages thatit was employed in all cases in which bronchoscopy was not clearly indicated (p.227):
1. It was preferable to bronchoscopy in patients who were desperately ill butconscious. Experience showed that in such cases the manipulations required inbronchoscopy might be extremely dangerous.
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2. Catheter aspiration was particularly valuable in acute emergencies whichpermitted no delay.
3. The equipment was almost always readily available from standard hospitalsupplies.
4. The technique was so simple that it could be readily mastered, in contrastto the elaborate training necessary in bronchoscopy.
5. Catheter suction could be repeated as often as necessary.
Technique-The technique generally employed forcatheterization (fig. 69) was a modification of the method described by Haight (7)in 1938. Suction was usually provided by ordinary ear, nose, and throat suctionmachines, which delivered from 15 to 20 pounds of negative pressure. Connectingtubing and a Robinson ureteral catheter or a similar catheter, size No. 16 orNo. 18, with one or two openings, constituted all the equipment necessary. Ifelectricity was not available, as it sometimes was not in combat areas, anattachment to the windshield wiper or gas intake manifold of a motor vehicleserved as an emergency source of power. The portable hand suction machinedevised by Major Brewer was often used in forward installations in whichelectrical suction machines were not always at hand.
Anesthesia was not required unless the gag reflex washyperirritable. Then 2 percent Pontocaine hydrochloride (tetracainehydrochloride) or 5 percent cocaine was sprayed onto the pharynx and paintedonto the hypopharynx with a curved swab or applicator. When local analgesia wasnecessary, a small dose of some barbiturate was given before it was applied, andfluids were withheld until the gag reflex had returned.
The patient was placed in the semi-Fowler position, with theneck flexed. If he was unconscious, the neck was fixed by supporting the raisedhead on a pillow or a folded blanket. If he was conscious, the tongue was pulledrather sharply forward, to anchor the larynx. Occasionally an epiglottis thatwas unusually flaccid so covered the larynx that catheterization was impossiblewithout a laryngoscope to provide direct vision.
The catheter was introduced through the nostril and advanced until the larynxwas reached. If the patient was unconscious, the index finger of the
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left hand engaged the tip of the epiglottis, so that the catheter could bepassed through the larynx without difficulty.
When the catheter had entered the larynx, it was withdrawn for about 1centimeter. If the patient was conscious, he was asked to take a rapid, deepbreath. During the inspiration, the catheter was quickly advanced into thetrachea. In an occasional case, it was easier to introduce it during theexpiratory phase of a cough. The successful entrance of the catheter into thetrachea was signified by involuntary coughing, passage of air through thetrachea, or sudden hoarseness. The irritation caused by the catheter was likelyto stimulate all but moribund patients to cough, but hoarseness was the mostcertain indication that the catheter was in the trachea. Occasionally, when thetube had been accidentally introduced into the esophagus, a free flow of airabout it simulated respiration. If the accident was not recognized and oxygentherapy was used, gastric dilatation of serious proportions might occur.
Suction was not applied until the catheter had been advanced into the tracheafor several centimeters. When the manipulations were discontinued, the patientwas urged to cough. This he usually did forcibly-in fact, he found it impossiblenot to-because of the stimulation of the tracheal mucosa by the catheter. Oftenmore sputum was coughed up around the tube than was aspirated through it.Suction, coughing, and manipulation of the catheter were alternated until allportions of the tracheobronchial tree were apparently free of fluid. Continuousperiods of suction never exceeded 5 seconds, and they were briefer if thepatient seemed exhausted by them or if he became cyanotic.
It was simple to introduce the catheter into the right stem bronchus; thepatient's head was merely turned well to the left. To enter the left stembronchus was somewhat more difficult (vol. I). The head had to be turned far tothe right and the chin elevated. The tube was advanced as far as possible intoeach stem bronchus. After aspiration, the patient was rolled on his side, withthe more involved lung uppermost, to permit drainage of the small bronchi bygravity.
After catheter aspiration, most patients coughed with greaterefficiency because of the improved ventilation of the pulmonary tree. Because ofthe absence of appreciable trauma to the larynx or bronchi, the procedure couldbe repeated as often as every 2 to 3 hours if this was necessary. In theoccasional case, bronchial secretions and pulmonary transudates formed with suchrapidity that aspiration was necessary at 30-minute intervals. In such cases,the catheter was left in the trachea, sometimes from 8 to 12 hours. When thiswas necessary, 100 percent oxygen was administered continuously through thecatheter between aspirations, at the rate of 1 to 2 liters per minute.
Bronchoscopy
Bronchoscopy played a valuable role in the management of warwounds of the chest. At no time was its use routine. It was properly considereda highly technical procedure, requiring skill and experience for its safe useand
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to be used only on definite indications. It was made morewidely available as the war progressed, however, because thoracic surgeonsalready trained in its use taught the technique to selected general surgeons andqualified anesthesiologists.
The decision to employ bronchoscopy rather than catheter aspiration was madeon the indications of the individual case. It was sometimes preceded by a trialof catheter aspiration but in other instances was resorted to immediately. Itschief advantage over catheter suction was that it was more thorough. Becauseboth stem bronchi were visualized, aspiration could be carried out with moreassurance that all secretions and obstructing mucous plugs had been removed.When it was indicated, bronchoscopy also permitted the direct application ofprocaine hydrochloride, cocaine, or epinephrine solutions to the swollenbronchial mucosa. The resulting shrinkage of the mucosa further increased thelumen of the airway.
Indications-No hard-and-fast rules were formulated, but ingeneral, bronchoscopy was regarded as the procedure of choice in wet lung underthe following circumstances:
1. When tracheobronchial aspiration by catheter had been ineffective becauseof failure of the lung or segments of the lung to reexpand with positivepressure, and moisture persisted in the chest.
2. When mucous plugs or blood clots were thought to be present in the branchbronchi.
3. When obstruction of the trachea or bronchi had been present for aconsiderable time. Under these circumstances, sudden loosening of large amountsof secretion from the obstructed bronchus might flood a normal bronchus, withgrave consequences.
4. When the cough was weak and ineffectual and there was danger of floodingthe contralateral bronchus by sudden release of large amounts of secretion.
5. When a patient was admitted to the hospital completely exhausted, with thetracheobronchial lumen brimming with secretions that he did not have thestrength to cough up. In this type of patient, bronchoscopy was mandatory. Infact, the more critical his condition, the more urgent was the indication.
6. When lobar or total pulmonary atelectasis had occurred, because of thedangerous reduction in the vital capacity.
7. When bronchial obstruction recurred in spite of repeated tracheobronchialcatheter aspirations. The cause of the obstruction was usually incompleteremoval of obstructing material by catheter suction.
8. When vomitus had been aspirated, or was thought to have been aspirated,into the lungs. This was an imperative indication, because of the highlydeleterious effect of gastric secretions on bronchial and pulmonary tissue.
9. When emergency thoracotomy was necessary. Bronchoscopy immediately beforeoperation, in addition to emptying the tracheobronchial tree and
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improving the cardiorespiratory status, made the administration of theanesthetic simpler and safer.
Techniques-The standard technique of bronchoscopy was employed.The procedure was usually carried out in the operating room but could beperformed by a skilled bronchoscopist without moving the patient from thestretcher or bed.
General anesthesia was contraindicated if there was an unusual amount offluid in the tracheobronchial tree. Topical analgesia was employed in mostcases, but in numerous semicomatose or apparently moribund patients, noanesthesia was used. Oxygen (100 percent) was administered continuously to allpatients who showed any evidence of anoxia.
The operation was performed as rapidly as possible, so that a severelywounded patient, in shock, would not be exposed to the fatiguing effects ofprolonged coughing.
Some surgeons, after the trachea and main bronchi were cleared, palpated thechest carefully, in an endeavor to find secretions still in situ in spite ofapparently successful aspiration. When such areas were found, the tip of theaspirator was applied directly to the orifice of the affected lobe, to excitecoughing and raise the remaining secretions.
Oxygen Administration
Oxygen inhalations by means of the nasal catheter or theBoothby-Lovelace-Bulbulian mask were used promptly whenever cyanosis accompaniedwet lung or dyspnea was severe. Some patients were disturbed at first by theface mask, but with sufficient encouragement, they all became reconciled to itsuse.
If moisture persisted in the lungs after intercostal nerve block and catheteraspiration or bronchoscopy, the oxygen was delivered under positive pressure(figs. 67G and 70). This was a technique described by Barach and his associates(8) shortly before the war, to relieve the pulmonary edema associatedwith pneumonia, gas poisoning, and cardiac disease. When the technique was firstapplied to combat-incurred wounds in the winter of 1943-44, considerabledifficulty was encountered. A simple and effective solution of the problem wasthe use of a to-and-fro anesthetic system, with a soda-lime canister andrebreathing bag. Positive pressure was maintained manually on the bag, carebeing taken to avoid pressures higher than from 2 to 6 cm. H2O.Pressures as high as 10 cm. H2O or more weredangerous; they could cause a considerable rise in venous pressure; a fall insystolic, diastolic, and mean blood pressures; and a decreased blood flow.
Fluid that was constantly forming in the alveoli andbronchioles could not be completely removed by suction, but suction, with nerveblock and the other measures described, removed enough fluid for oxygen underpositive pressure to keep the bronchioles patent. The use of oxygen underpressure also opposed the hydrostatic pressure of the blood in the capillariesand increased the vital capacity. If the lungs were not too severely damaged andif shock, tension
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pneumothorax, and other adverse factors could be controlled, this method waspractically always successful in drying up wet lung caused by tracheobronchialtransudation and exudation. It was of particular value when an excessive andinjudicious use of blood and plasma was a contributory factor in the edema andwhen ventricular failure was impending.
Oxygen was sometimes administered under positive pressure in the early stagesof traumatic wet lung. Its prophylactic value was thought to be consid-
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erable, but the indications for its employment on thisindication did not become fully established during the war.
Other Measures
Atropine administration-If moisture continuedto be present in the lungs and vigorous measures to empty the tracheobronchialtree proved ineffective, atropine was sometimes given intravenously, in 1/100-gr.doses. If reflex- spasm of the bronchus were initiated by thoracic injury, asthe experimental work of de Takats and his associates (2) had suggested,one might expect atropine to abolish vagal reflexes and reduce tracheobronchialsecretions. De Takats himself, however, found that this method preventedbronchospasm in less than half of his experimental animals, even when amounts upto gr. 1/8 were employed. Atropinewas not widely used during the war, and the clinical experience with it was tooconflicting to permit any definitive statements concerning its value except thatwhen wet lung was fully developed, this drug was not effective.
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Carbon dioxide inhalations-Carbon dioxideinhalation was another controversial measure occasionally employed in wet lung.This gas is a true expectorant, and hyperventilation with it had the mechanicaleffect of loosening viscid secretions and propelling them upward along thetracheobronchial lumen. If hypoxia was present, most observers regarded themethod as equivalent to whipping a tired horse.
The preferred method was to use 100 percent carbon dioxideand to administer it by means of a catheter and small funnel as the patient tooktwo or three deep breaths. Forced coughing during and following the brief periodof hyperpnea thus produced was of the greatest importance and was not alwayssufficiently stressed. Unless the patient coughed, the method lost much of itseffectiveness. If carbon dioxide was not available, rebreathing into a paper bagwas often employed as a substitute, usually very effectively.
RESULTS OF THERAPY
Once proper measures had been instituted to relieve pain in thechest wall, clear the airway, and permit effective coughing, the entire pictureof a patient with wet lung usually changed promptly. Results were oftendramatic. A cyanotic, comatose patient, with wet, rattling respirations, oftenbecame alert and oriented, with good color and almost normal respirations,within a matter of minutes.
Once the wet lung was controlled, it was possible to evaluate the primaryinjury. Hemothorax, shattered ribs, and the shell fragment in the lung lookedless ominous and often seemed less urgent. The lung had been restored to normal,or almost normal, capacity to cope with the injury or with the surgery requiredto correct the injury. Evaluation of the total patient was possible, in short,under circumstances which permitted a deliberate rather than a frantic approachto the problem.
An undoubted result of the recognition and vigorousmanagement of wet lung was apparent in the Mediterranean theater in a number ofrespects, including (1) the low case fatality rate and low morbidity of chestinjuries, (2) the infrequency of lung abscess after injury, and (3) the almostcomplete absence of massive atelectasis.
CASE HISTORIES
The following case histories illustrate a number of the points in theforegoing discussion of traumatic wet lung:
Case 1-A 23-year-oldsergeant was received in an evacuation hospital 3 hours after he had sustainedpenetrating wounds of the chest and buttocks from a high explosive shellfragment. The pulse was 110, the respiration 30 and noisy, and the bloodpressure 110/80 mm. Hg. The patient was extremely dyspneic and complained ofsevere pain in the chest and abdomen.
Evidence of a large amount of fluid in theleft chest almost obliterated all other physical findings. Loud musical wheezeswere heard over the right chest anteriorly and posteriorly. Roentgenologicexamination confirmed the presence of fluid in the left chest. The
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left eighth rib was fractured, and a small foreign body wasseen above the left diaphragm behind the heart.
Morphine (gr. ?) and atropine (gr. 1/100)were given by vein. The pain was somewhat relieved, but not enough to permiteffective coughing. Complete relief followed blocking of the fifth through thetenth left intercostal nerves. The patient immediately coughed up a large amountof mucus mixed with fresh and old blood, after which he was able to breathedeeply and without discomfort. The lungs were dry on auscultation. Debridementof the chest wall was then carried out without difficulty under Pentothal sodium(thiopental sodium) anesthesia.
The patient continued to raise bloody sputum for a week, butthere was no reaccumulation of fluid in the tracheobronchial tree and norecurrence of chest pain. After a total of 2,730 cc. of bloody fluid had beenremoved from the left chest by repeated thoracenteses, the left lung was almostcompletely reexpanded, and the remainder of the patient's convalescence wasuneventful.
Comment.-In thiscase, retention of blood in the bronchial tree as the result of intrapulmonaryhemorrhage was chiefly responsible for the wet lung, though an excess of mucuswas also a factor. Severe chest pain, which prevented effective coughing, wasnot relieved by a large dose of morphine but was promptly relieved by blockingthe appropriate intercostal nerves. Immediately thereafter, the patient, by hisown efforts, raised the blood and mucus that had accumulated in thetracheobronchial tree, and recovery was without further complications.
Case 2-A 21-year-oldsergeant was received in a field hospital in severe shock 3 hours after he hadsustained a sucking wound of the left chest and penetrating wounds of the rightchest, thigh, forearm, hand, and cheek. The pulse was 140, and the bloodpressure could not be obtained. Breath sounds were diminished on the right sideof the chest, and signs of fluid were elicited on the left side.
The patient had had no medication since he wasinjured and was in severe pain. He was therefore given morphine gr. 1/8by vein after an occlusive dressing had been placed over the sucking wound. Painwas completely relieved after a second injection of morphine, in the same amountand also by vein, but only small quantities of bloody sputum were raised. Afterthe administration of two units of plasma and 500 cc. of blood, the pulse fellto 132 and the blood pressure was 104/80.
Two hours later, the patient's condition suddenly becamecritical. He was comatose and cyanotic. The pulse was weak and thready. Raleswere audible in the trachea. Catheter suction was instituted at once, and largeamounts of frothy yellow sputum were aspirated. The response to this measure wasdramatic. The patient immediately regained consciousness, and his color andpulse improved. The catheter was kept in place for 8 hours, and suction wasrepeated every 20 to 30 minutes. Between aspirations, 100 percent oxygen wasadministered through the catheter.
At the end of 8 hours, during which time thepatient's condition steadily improved, roentgenograms of the chest showed fluidin the left chest and foreign bodies in both lung fields. Since thetracheobronchial tree was now apparently dry, the catheter, which meantime hadslipped into the right main bronchus, was removed. After a transfusion of 500cc. of blood and a unit of plasma, 100 cc. of air and 200 cc. of bloody fluidwere aspirated from the left chest.
Seventeen hours after admission, when theblood pressure had reached 108/74 mm. Hg, bronchoscopy produced a considerableamount of bloody fluid from both main bronchi. Careful inspection showed thatthe prolonged intubation had apparently caused no trauma to the larynx or thetrachea.
Immediately after bronchoscopy, operation was done underintratracheal ether-oxygen-anesthesia. It included debridement of the suckingwound of the chest wall; ligation of the internal mammary vessels, which werelacerated though not actively bleeding; suture of the laceration of the upperlobe of the left lung; removal of several small metallic foreign
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bodies from the pericardium and another fromthe right chest wall; and intercostal drainage. A foreign body in the lower lobeof the left lung and another in the right lung were left in situ. While thechest operation was in progress, another surgical team debrided the otherwounds. At the conclusion of the operation, bronchoscopy was repeated, and amoderate amount of bloody mucus was aspirated from both stem bronchi. Thepatient received a unit of plasma and 500 cc. of blood during the operation.
The immediate postoperative status was satisfactory. Thefollowing day, the patient became disoriented, presumably as the result ofcerebral anoxia, though he had been receiving oxygen continuously, by nasalcatheter, since operation. The temperature was 99.4? F., the pulse 150, and therespiration 48. Coughing produced thin yellow fluid, but the pulmonary treeappeared to be filling up with moisture.
Tracheobronchial aspiration by catheter somewhat improved thepatient's critical condition. Tracheal rhonchi and coarse bronchial ralesdisappeared, but medium and fine rales could still be heard diffusely over alllobes of both lungs. Fluid was apparently being formed more rapidly in theperipheral portions of the pulmonary tree than it could be removed by naturalprocesses. Since the clinical picture resembled that seen in pulmonary edemaaccompanying heart disease and gas poisoning, positive pressure oxygen wasbegun. Within 15 minutes, a notable improvement occurred. The pulse fell to 120.The respirations fell to 32 and became considerably less labored. Only a fewfine rales could be heard at the bases of both lungs. At this point, positivepressure oxygen was discontinued, and administration by theBoothby-Lovelace-Bulbulian mask was resumed.
During the next 24 hours, the patient had two additionalattacks of pulmonary edema, each one resembling the acute attack just described.In each one, the effect of oxygen administration under mild positive pressurewas as striking as in the first attack. Recovery thereafter was uneventful.
Comment-This caseis a striking example of the therapeutic problems presented by traumatic wetlung in a patient with multiple chest and other wounds. Immediatetracheobronchial catheter aspiration, intratracheal oxygen administration, andcautious fluid replacement over an 8-hour period made this soldier a suitablecandidate for surgical closure of a sucking chest wound and the intrathoracicsurgery required. Bronchoscopy just before operation aided in the maintenance ofa patent airway during operation, and its repetition at the conclusion of theprocedure simplified the first 24 hours of the postoperative course. Threeattacks of apparently true pulmonary edema over the next 48 hours werecontrolled by the administration of oxygen under mild positive pressure. Whyedema developed in this case after operation is not clear, but anoxia caused bysevere trauma to both lungs was probably an important factor, as was trachealobstruction from mucus and blood.
There seems little doubt that this patient survived because ofthe therapy instituted for the control of the wet lung that followed hiscombat-incurred injuries, one of which was a sucking wound of the chest.
Case 3-A27-year-old lieutenant sustained a sucking wound of the chest that was treatedimmediately by an occlusive dressing and 24 hours later by suture; the skin wasleft open. For the next 3 days, small amounts of pure blood were expectorated.
When the patient was admitted to a thoracic surgery center 5days after wounding, he was comfortable while at rest but moderately dyspneic onexertion. The cough was wet but was productive of only small amounts ofblood-tinged mucoid sputum. A few coarse rales were heard parasternally on theright. Roentgenograms taken the following day showed a right-sidedhydropneumothorax without cardiac shift. Aspiration of the chest on the secondand third days after admission produced 360 cc. and 390 cc., respectively, ofold blood and air from the right pleural cavity. On each occasion, highlynegative intrapleural pressure prevented further aspiration.
The patient's wet cough continued in spite of thesethoracenteses, frequent changes of position, and the administration of carbondioxide. On the third day after admission,
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roentgenograms of the chest showed a minimal residualhemopneumothorax, an expanded upper lobe, and atelectasis of the middle andlower lobes on the right side. Bronchoscopic aspiration, instituted immediately,produced large amounts of blood clots and mucus, amid which partly formedbronchial and bronchiolar casts were discernible. Roentgenologic examination 18hours later showed almost complete reaeration of the atelectatic lobes. Thecough became loose and remained productive for 4 days after bronchoscopy, thenceased altogether. On the 12th day after wounding, roentgenograms showed theright lung to be completely expanded and almost normal in appearance.
Comment-In thiscase, although roentgenologic evidence of atelectasis was obscured in the firstroentgenograms by the overlying hemothorax, certain points in the history andphysical findings pointed to the diagnosis. They included continued wet coughwith inadequate expectoration, extensive pneumothorax without cardiac shift,and the development of pronounced evidence of negative pressure after aspirationof relatively small amounts of fluid from the pleural cavity. The aspiration ofold blood clots and mucus by bronchoscopy resulted in the prompt reestablishmentof a patent airway and prompt reexpansion of the lung.
Earlier attention to the wet lung in this case would havepermitted the use of simpler methods of management and might have prevented thedevelopment of the complicating atelectasis.
Case 4.-When thispatient was seen 2 hours after he had fallen off a motorcycle, he wascomplaining of severe pain in the left chest and dyspnea. He had a paroxysmal,ineffectual wet cough. There was extreme tenderness over the left fifth andsixth ribs, and a flail segment in this area was undergoing paradoxicaloscillations. Numerous wheezes and rhonchi were present bilaterally.Roentgenologic examination revealed anterior and posterior fractures of the leftfifth and sixth ribs.
Intercostal block of the third through the ninth ribs, whichresulted in only partial relief of pain, was supplemented by paravertebral blockof the sympathetic ganglia of the same segment. Pain was promptly relieved, andparadoxical oscillations of the flail segment ceased. There was still somemoisture in the lung, but the remaining wheezes and rhonchi disappeared, andrespirations became entirely normal, within 5 minutes after the intravenousadministration of 1/150 gr. of atropine sulfate.
On the third day after wounding, a moderate recurrence of painand wetness was immediately controlled by repetition of the paravertebral block.
Comment-This casewell illustrates the effectiveness of nerve block in the management of flailchest of limited extent, as well as the (occasional) effectiveness of atropineas an adjuvant measure in the control of wet lung.
Case 5-This patient wasseen in a shock tent on 4 February 1944, 43? hours after wounding. He hadsustained a penetrating wound of the left anterior chest and was complaining ofhemoptysis; dyspnea; a painful wet cough; and pain in the left shoulder, leftchest, and hepatic area. He was in critical condition, extremely dyspneic andcyanotic, and showers of moist rales were heard throughout both lungs.Examination also revealed tenderness and rigidity in the left upper quadrant ofthe abdomen. Roentgenologic examination revealed a retained missile in theregion of the left diaphragm and an extensive pathologic process in the leftlung and left pleural cavity.
An hour after the patient had been received inthe shock tent, intercostal block of the left fourth and fifth intercostalnerves was carried out, and 200 cc. of air and blood were aspirated from theleft pleural cavity. There was immediate improvement in the pain, dyspnea, andcyanosis originally present. The left upper quadrant of the abdomen was nolonger rigid. There was also an improvement in the wet lung. Two hours later,the patient again complained of pain, and there was a recurrence of thepulmonary difficulties. A paravertebral sympathetic block (D4-9) was immediatelyperformed, and a large amount of blood and mucopurulent sputum was aspiratedthrough a tracheal
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catheter. Pain was promptly relieved, and pulmonary moisturewas greatly reduced. Shortly afterward, the wound was debrided.
Recovery was smooth except for slight pain and moderatedyspnea the day after operation. Both symptoms were promptly relieved byintercostal block of the fifth through the ninth intercostal nerves. A weekafter his admission, the patient was so much improved that he could beevacuated.
Comment-When thispatient was first seen, his condition was so critical that it did not seem thathe could possibly survive. Nerve block effected considerable improvement, butwhen his pulmonary difficulties recurred, he seemed so exhausted that mechanicalaspiration of the tracheobronchial tree was resorted to at once. In this case,the correction of wet lung was clearly lifesaving.
Case 6.-A 21-year-oldsoldier, injured in an automobile accident, complained of hemoptysis, persistentpain on coughing, and pain on deep breathing. When he was admitted to a thoracicsurgery service 48 hours after the accident, he was dyspneic and complained ofdiscomfort and pain in the left lower chest. There was no external evidence ofinjury. The percussion note was resonant bilaterally, but there were diffusewheezes and rhonchi throughout both lungs. Pain was so severe that coughing wasimpossible, in spite of urging. Pressure over the seventh, eighth, and ninthribs in the left anterior axillary line elicited exquisite tenderness, but rontgenograms of the chest revealed no abnormalities.
In spite of failure to demonstrate any rib fractures, anintercostal block of the area of tenderness completely relieved the pain.Shortly afterward, the patient coughed up several tablespoonsful of thick,white, tenacious mucus. Two hours later, physical examination revealed entirelynormal findings in both lungs. Recovery was uneventful thereafter.
Comment-In thiscase, nerve block permitted effectual coughing by relieving the pain that hadprevented it previously. There was only mucus in the tracheobronchial tree, andit may be that this is an instance of an abnormally large secretion of mucusbecause of reflex stimulation via the intercostal nerves. If this reasoning iscorrect, one effect of the nerve block may have been to reduce the secretion ofmucus.2
References
1. Betts, R. H., and Overholt, R. H.: ThePrevention and Treatment of Postoperative Pulmonary Complications byBronchoscopic Aspiration. S. Clin. North America 17: 885-893, June 1937.
2. De Takats, G., Beck, W. C., and Fenn, G. K.: PulmonaryEmbolism. An Experimental and Clinical Study. Surgery 6: 339-367, September1939.
3. Drinker, C. K., and Warren, M. F.: The Genesis andResolution of Pulmonary Transudates and Exudates. J.A.M.A. 122: 269-273, 29 May1943.
4. Pasteur, W.: Massive Collapse of the Lung (Syn. ActiveLobar Collapse). Brit. J. Surg. 1: 587-601, April 1914.
5. Churchill, E. D.: Pulmonary Atelectasis, With EspecialReference to Massive Collapse of the Lung. Arch. Surg. 11: 489-518, October1925.
6. Lewis, Thomas: Pain. New York: The Macmillan Co., 1942.
7. Haight, C.: Intratracheal Suction in the Management ofPostoperative Pulmonary Complications. Ann. Surg. 107: 218-228, February 1938.
8. Barach, A. L., Martin, J., and Eckman, M.:Positive Pressure Respiration and Its Application to the Treatment of AcutePulmonary Edema. Ann. Int. Med. 12: 754-795, December 1938.
2The reader is referred to chapter XI (p. 441) for long-term followup studies on casualties whose chest wounds were complicated by the wet lung syndrome.
