THE EFFECT OF ARTIFICIAL PNEUMOTHORAXUPONTHEANOXEMIAOF PNEUMONIA1

By DAVID GOLDSTEIN, MORRIS BLOCK, AND MILTON ROSENBLUTH(From the Departments of Medicine and Physiology of the New York University College of

Medicine and the Third (New York University) Medical Division of BellevueHospital, New York City)

(Received for publication May 26, 1938)

Statements concerning the usefulness of pneu-mothorax in alleviating the anoxemia of lobarpneumonia are few and conflicting, and are limitedto estimates based upon the degree of cyanosis,the severity of dyspnea, and other criteria whichare only roughly quantitative. It seemed that anexamination of the effect of pneumothorax uponthe degree of oxygen saturation of the arterialblood would afford more reliable information onthe therapeutic value of this measure.

The following is a report on the oxygenationof blood in six cases of unilateral pneumococcuslobar pneumonia treated with pneumothorax.Diagnosis was based upon the usual clinical cri-teria and verified by x-ray. Only cases in whompneumothorax could be instituted within 72 hoursof the onset of the disease were selected for study.These were chosen irrespective of the type ofpneumococcus. Pneumococcus serum was givenin only one instance. In establishing pneumo-thorax the technique of Blake (1) was employed,except that air was introduced at a rate of about40 cc. per minute, and collapse of the lung wascarried out as completely and rapidly as was con-sistent with the comfort and safety of the patient.In certain cases mediastinal shift, adhesions, andmassive consolidation limited the extent of col-lapse. Pneumothorax was performed in the lat-eral recumbent position, and inspiratory, expira-tory, and mean intrapleural pressures were re-corded before and after the introduction of air.

Arterial oxygen saturation was determined be-fore the institution of pneumothorax, about twohours after separation of the pleura, during sev-eral stages of collapse, and then throughout thedisease and at less frequent intervals during con-valescence. Serial roentgenograms were takenduring the observation of each case by means ofa 10 milliampere portable bedside unit. Arterial

1 This study was supported in part by a gift from Mr.Bernard Baruch.

blood was collected by puncture of the radial ar-tery without novocaine.

METHOD

Ten cc. of blood were drawn into an oiled syringecontaining sufficient powdered oxalate to make a 0.2per cent solution. The blood was transferred withoutexposure to air and without negative pressure to a storageflask filled with mercury by means of a close-fittingrubber junction. Samples for analysis were transferredin a similar manner to a Van Slyke-Ostwald pipette.Equilibration with air was carried out in a mechanicallyrotated tonometer at room temperature. All analyseswere made in duplicate by means of a Van Slyke mano-metric apparatus and according to the method of VanSlyke and Neill (2). The average deviation observedin duplicate oxygen determination was + 0.25 per cent;the precision of the saturation figures may therefore betaken as + 0.5 per cent. We obtained 93.0 per cent(range 90 to 96 per cent) as the mean value for the ar-terial saturation in six normal subjects, a figure in closeagreement with the data recently published by Looneyand Jellinek (3). Careful examination of the techniqueleads us to agree with these authors that the often quotedfigure of 95 per cent for the saturation of normal ar-terial blood is erroneously high because of the practiceof allowing the blood to stand in contact with oil. Wefind that the oxygen content of blood remains constantfor a period of five hours when it is chilled immediatelyafter collection and preserved over mercury, whereasthere is continuous diffusion of oxygen into the bloodwhen it is preserved under oil at the same temperature,particularly when samples are being removed and theblood must be agitated. All blood gas analyses reportedhere were made within five hours of the time the bloodwas drawn.

RESULTS

A summary of the significant data in the sixcases studied is presented in Table I. Separationof the pleura was associated with a small rise inarterial saturation in two patients (T. C. andW. T.), with no change in two (W. D. andF. J.) and with a slight fall in two (J. J. andB. T.).

659

DAVID GOLDSTEIN, MORRIS BLOCK AND MILTON ROSENBLUTH

TABLE I

Summary of data

Duration Oxygen saturationOf ______-___Effect on

Blood disease Involve- Degree of respira- Effect on Effect onName Age Sex Type culture before ment* Before Sepa- collapse tory pain temperature

pneumo- pramo tion After ratetheourax- pne-lthor ira collapse

years per cet per cent per centJ. J.. 48 M XIV Nega- 40 hours RLL- 91.0 87.2 85 Complete None Mild None

tive RUJL pleural

lieved bypneumo-thorax

B. T... 35 M Uncl. Nega- 54 hours LLL 89.0 86.0 86 20 per cent None Mild Nonetive with apical pleural

adherence painwithrelief

F. J ........ 46 F I Nega- 3 days RLL 82.0 82.0 69 40 per cent None None Questionabletive

T. C... 40 M II Nega- Less RLL 83.0 88.0 83 20 per cent None Severe Questionabletive than consol. pain- depression

3 days 80 per cent relievednormal

W.D. 29 M Uncl. Nega- 14 hours RLL 88.5 88.7 87 90 per cent Fell: Slight Suggeststive 89.7 40 to 30 relief fall

to 22

W. T........ 46 M I Nega- 3 days RUL - 85.2 88.2 77 50 per cent De- Notable Nonetive LUL adherent pressed on sepa-

LLL rate for ration ofone day pleura,but

tempo-rary

* RLL-Right lower lobe. RUL-Right upper lobe. LLL-Left lower lobe. LUL-Left upper lobe.

Further collapse of the lung was accompaniedby no significant change in arterial saturation intwo patients, and by reduction in saturation infour. In two of the latter the oxygen content ofthe arterial blood was reduced to critically lowlevels-69 per cent and 77 per cent.

Our discussion of the rationale of the use ofpneumothorax in lobar pneumonia will be con-fined to its influence upon anoxemia. The anox-emia of pneumonia patients is of the anoxic type.There are varied opinions concerning the mecha-nism by which this anoxemia is produced. Thatshallow breathing is not a major factor has beendemonstrated by Binger and Davis (4). Alteredvital capacity, acceleration of blood flow throughnormal lung tissue, and altered alveolar permea-bility have been suggested as causal factors byBinger and Brow (5), Binger, Brow, and Branch(6), and others. It appears that the most per-tinent and at the same time most debated ques-tion concerns the extent to which the circulationin the consolidated involved lung tissue is im-paired.

Since human autopsy and experimental mate-rial indicate that capillary patency is rarely com-pletely lost, it is frequently argued that the benefitof oxygen therapy in pneumonia is due to in-creasing the availability of oxygen in alveoli whichare relatively unaerated because of the mechanicalbarrier of alveolar and bronchial exudates (7, 8).In this view the major factor leading to anoxemiais the presence of inadequately aerated channelsin the consolidated lobe. If this is the case, theinduction of pneumothorax in lobar pneumoniacan alleviate anoxemia only if blood is deflectedfrom the collapsed to the intact lobes, as appar-ently happens in the normal or tuberculous indi-vidual. But it appears unwarranted to argue thevalue of pneumothorax in lobar pneumonia byanalogy with the normal or tuberculous subjectin whompneumothorax rarely lowers arterial sat-uration, and where, if saturation is lowered byunilateral lesions, pneumothorax may increase it(9). It is possible that because of consolidationof the lung, pneumothorax in lobar pneumoniadoes not effectively close the capillary circulation

660

ARTIFICIAL PNEUMOTHORAXIN PNEUMONIA

in unaerated tissue despite convincing evidence ofadequate collapse by x-ray. It is also possiblethat collapse of an uninvolved lobe may actuallyincrease the blood flow through consolidated tis-sue on the same side. But even if deflection tonormal tissue occurs, the rate of blood flow maybe too great to permit gaseous equilibration whenit is recognized that the rate of metabolism andcardiac output in the febrile pneumonia patientis considerably increased. It is thus evident thatthe cause of anoxemia in lobar pneumonia cannotbe ascertained with any certainty until informa-tion concerning the circulation in consolidatedand unconsolidated lung tissue is available.

In two of our patients the oxygen saturationrose after separation of the pleura, but thesepatients were suffering severe pleural pain priorto induction of pneumothorax, and there wasmarked relief from this pain following the treat-ment. Webelieve that the rise in saturation inthese patients was caused by increased ventilationassociated with relief from pain. The fact thatoxygen saturation after maximal collapse was

unchanged in two of our patients and decreasedin four others argues against the supposition, asstated above, that pneumothorax deflects bloodfrom unaerated to aerated capillary beds; cer-tainly if this occurs, then the latter are inadequateto afford full oxygenation to the increased cir-culation. But regardless of the physiological in-terpretation, in the six cases studied, pneumo-thorax was without value for the relief of anox-emia.

The carbon dioxide content of each blood sam-ple collected was determined. Since the figuresfall roughly within the normal range of 45 to 55volumes per cent, in agreement with previousinvestigations in lobar pneumonia, they are notreported.

CONCLUSIONS

1. Six cases of early pneumococcus pneumoniaof various types were given pneumothorax. Fivecases showed diminished oxygen saturation ofthe arterial blood at the outset (range, 82 to 89

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FIG. 1. J. J., NUMBER26243, MALE 48. R.L.L. PNEUMONIA. PNEUMOCOCCUSTYPE XIV. BLOOD CULTURENEGATIVE THROUGHOUT. INITIAL PNEUMOTHORAX40 HOURSAFTER ONSET

661

DAVID GOLDSTEIN, MORRIS BLOCK AND MILTON ROSENBLUTH

per cent). The extent of final collapse estimatedby x-ray varied from 30 to 90 per cent.

2. Separation of the pleura (initial pneumo-thorax) was followed by (a) no change in oxy-gen saturation in two cases, (b) a fall in oxygensaturation in two cases, (c) a rise in oxygen sat-uration in two cases. This group exhibited themost severe pleural pain, and the greatest reliefafter pneumothorax.

3. Further collapse of the lung in no case wasattended by an increase in oxygen saturation abovethe initial level. In four cases, the oxygen sat-uration fell, after establishing collapse of theinvolved lung.

PROTOCOLS

Case J. J., Number 26243 (Figure 1). A 48-year oldnegro porter was admitted January 22, 1937, two daysafter onset with chilliness and generalized aches andpains. There was no history of previous pulmonarydisease. On physical examination, there was dullnessover the right lower lobe, bronchial breathing, and show-ers of crepitant riles. Sputum examination showed Type

XIV pneumococcus. In addition to the diagnosis ofpneumococcus pnieumonia, right lower lobe, the addi-tional diagnoses of hypertensive and luetic heart diseasewith enlarged heart and dilated aorta were made.

Laboratory. Blood cultures taken January 23 and 27were sterile. Leukocytes ranged between 20,000 and30,000, granulocytes 90 to 94 per cent. Electrocardio-gram showed left deviation of the electrical axis, andregular sinus rhythm.

There was a fall in the arterial oxygen saturation inthe presence of good collapse: in the latter stages thismay have been attributable to the development of aspread to the upper lobe. During the first days of fall,there was neither x-ray nor clinical evidence of newinvolvement. There was mild relief of pleural pain, withno associated rise in saturation on pleural separation.Pneumothorax did not prevent a fall in saturation inthis patient.

The patient died on February 1, 1937, the 13th dayafter onset.

At postmortem right lower lobe and more recent rightupper lobe consolidations were found. Additional find-ings were fibrinous pleuritis with effusion on the right,hypertensive and arteriosclerotic heart disease. Theblood culture was negative.

Case B. T., Number 26023 (Figure 2). A 35-year

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FIG. 2. B. T., NUMBER26023, MALE 35. L.L.L. PNEUMONIA. UNCLASSIFIED PNEUMOCOCCUS.BLOODCULTURIE NEGATIVE. INIIIAL PNEUMOTHRAEX54 HOURSAFTrm ONSET

662

ARTIFICIAL PNEUMOTHORAXIN PNEUMONIA

old handyman had the onset of his disease with chill,thoracic pain, fever, cough, and scanty yellow expectora-tion at 7:30 a.m. on October 31, 1936. There was no

history of previous pulmonary disease. Physical signsin the lung were dullness over the lower half of theposterior left chest, and showers of inspiratory rales.

Laboratory. Blood culture taken November 1, 1936was sterile, leukocytes 13,950, granulocytes 83 per cent.Sputum unclassified Pneumococcus Types I through XIV.

Diagnosis. Pneumococcus pneumonia of left lowerlobe.

A very partial collapse was obtained. Crisis occurredon the fifth day. Arterial oxygen saturation seemedrelatively unaffected by pneumothorax. There was a

persistence of unsaturation throughout the six daysfollowing crisis, despite good re-expansion. During thisperiod, chest signs were minimal.

Case F. J., Number 26281 (Figure 3). A white Polishhousewife, 46 years of age, was admitted on January 6,1937. Two weeks preceding admission she had had a

head cold and cough. On January 5, she expectorateda cupful of bloody sputum. She had generalized chestpain and- several chills. It was estimated that at thetime of admission the pneumonia was of three days'duration. In the past history, the patient was a knowndiabetic, taking insulin 15-00 without a well-regulateddiet. On physical examination there was dullness over

the right lower lobe, without alteration in breath or

voice sounds. The abdomen was not distended.Laboratory. Sputum was thick and tenacious and Type

I pneumococcus was found in the sputum. Leukocytecount was 15,850, with 74 per cent granular cells ofwhich 23 per cent were stab forms, hemoglobin 12.6grams (87 per cent), R.B.C. 3.47 million. The diag-nosis of Type I pneumococcus pneumonia, right lowerlobe, was made. Blood culture was negative throughout.The diabetes was controlled on a diet of, carbohydrate150, protein 65, fat 85: insulin 20-10-20, the latter beingreduced to 5-0 before discharge. No serum was given.

There was progressive fall in arterial oxygen satura-tion within increasing collapse despite the absence ofclinical evidence of mediastinal shift or pneumonia spread.On the third day of collapse, acute respiratory distresssupervened. At this time, the oxygen saturation was

69 per cent and the mean intrapleural pressure was + 2,respirations were 30 per minute, and cyanosis was in-tense. On removal of 600 cc. of air, mean intrapleuralpressure was minus one cm. of water. Twelve hourslater, saturation in an oxygen tent was 80 per cent:when the patient was removed from the tent, the satura-tion fell to 62 per cent. This episode was associatedwith a fall in temperature, which shortly after returnedto normal.

Case T. C., Number 26124 (Figure 4). A 40-year

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FIG. 3. F. J., NUMBER26281, FEMALE46. R.L.L. PNEUMONIA. PNEUMOCOcCUSTYPE I. BLOODCULTURENEGATIVETHROUGHOUT. INITIAL PNEUMOTHORAX72 HOURs Arm ONSET

663

DAVID GOLDSTEIN, MORRIS BLOCK AND MILTON ROSENBLUTH

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FIG. 5. W. D., NumBER26442, MALE 29. R.L.L. PNEUMONIA. UNCLASSIFIED PNEUMOCOCCUS.IBLooD CULTURENEGATIV THROUGHOUT. INITIAL PNEUMO'rHORAX14 HouRs AFTER ONSET

664

ARTIFICIAL PNEUMOTHORAXIN PNEUMONIA

old truck driver complained of malaise and mild painover lower right axilla beginning December 13, 1936and lasting to the time of admission December 15,1936. Chills, cough, and marked pleural pain appearedon December 14, 1936. A convulsion on the morningof December 15, 1936 prompted hospitalization.

Past history was negative for previous pulmonarydisease. Patient had experienced convulsive seizures forthe past five years. Physical examination of the lungsrevealed no abnormal findings. Fluoroscopy and x-rayrevealed a definite shadow over the right lower lobe.

Laboratory. Sputum tenacious and rusty, in which aType II pneumococcus was found. Blood cultures De-cember 15, 20, and 22 were sterile. Leukocytes rangedbetween 26,000 and 50,000, granulocytes 90 to 91 per cent.

Course. 200,000 units Type II antipneumococcus serumwere given.

Diagnosis. Pneumococcus pneumonia. Patient diedon the 9th day of his illness.

Associated with the relief of pleural pain followingseparation of the pleura, the oxygen saturation rose from83 to 88 per cent. With subsequent refills, however, thesaturation fell. There was 20 per cent collapse of theright lower lobe, and 80 per cent collapse of the un-involved lobes. Pneumothorax was discontinued becauseit was felt that consolidation interfered with furthercollapse. The final mean intrapleural pressure reading

was + 2 cm. of water. The patient died. Permissionfor autopsy was not obtained.

Case W. D., Number 26442 (Figure 5). A 29-yearold waiter awoke with a chill at 1 a.m. on February 11,1937 followed by posterior right chest pain several hourslater. Slight cough was present, with no expectoration.Past history revealed nothing but " grippe " in 1935.Physical examination of the chest showed marked dull-ness over right base posteriorly, absent breath sounds,and no riles. X-ray showed a small shadow in the rightlower lung field adjacent to the hilum.

Laboratory. Unclassified pneumococcus, Types I toVIII and XIV were found in the sputum, leukocytes13,000 to 27,000, 82 to 88 per cent granular cells. Bloodculture taken February 11th was sterile.

Diagnosis. Pneumococcus pneumonia of right lowerlobe.

Despite complete collapse (90 per cent) unassociatedwith mediastinal shift, unsaturation continued for twelvedays following fall in temperature.

Case W. T., Number 26348 (Figure 6). A 46-yearold steel worker complained of chill, chest pain, cough,fever, and diarrhea of three days' duration. There wasno expectoration. Headache and chest pain were verysevere on admission. Past history was negative exceptfor a chancre in 1905 inadequately treated.

Physical findings revealed dullness, diminished breath

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FIG. 6. W. T., NUMBER26348, MALE46. R.U.L. PNEUMONIA. PNEU-Mococcus TYPE I. BLODo CULTURE NEGATIVE THROUGHOUT. INITIALPNEUMOTHORAXLESS THAN 72 HOURSAFIR ONSET.

665

DAVID GOLDSTEIN, MORRIS BLOCK AND MILTON ROSENBLUTH

sounds, and a friction rub high in the right axilla.Heart: Position of maximal impulse was not felt.Sounds were of good quality. A, was greater than P,.There were no murmurs and the rhythm was regular.X-ray showed a dilated aorta.

Laboratory. Blood cultures taken February 20 and22 were sterile. Leukocytes ranged from 19,950 to 39,-000; granulocytes 93 to 95 per cent. Wassermann ±,

sputum Type I pneumococcus.Diagnosis. Pneumococcus pneumonia Type I of right

upper lobe, luetic aortitis.Only 50 per cent collapse was obtained because of an

apical adhesion (confirmed at postmortem examination).A transient slight rise in arterial oxygen saturation was

obtained on separation of pleura, seemingly associatedwith definite relief of pleural pain. Following the firstrefill on the second hospital day, saturation fell from88 per cent to 77 per cent. There was no x-ray evidenceof spread at this time, and no shift of the mediastinum.Death occurred on the sixth hospital day. At post-mortem examination there was an empyema on the rightside, with spread of the pneumonia to the left upper lobeand left lower lobe. Syphilitic aortitis and aortic in-sufficiency also were found.

BIBLIOGRAPHY

1. Blake, Francis G., Howard, Marion E., and Hull,Winifred S., Artificial pneumothorax in lobarpneumonia. Medicine, 1936, 15, 1.

2. Van Slyke, D. D., and Neill, J. M., The determinationof gases in blood and other solutions by vacuumextraction and manometric measurement. I. J.Biol. Chem., 1924, 61, 523.

3. Looney, J. M., and Jellinek, E. M., The oxygen andcarbon dioxide content of the arterial and venousblood of normal subjects. Am. J. Physiol., 1937,118, 225.

4. Binger, C. A. L., and Davis, J. S., Jr., The relationof anoxemia to the type of breathing in pneu-monia. A study of respiration by means of abody plethysmograph. J. Clin. Invest., 1928, 6,171.

5. Binger, C. A. L., and Brow, G. R., Studies on therespiratory mechanism in lobar pneumonia; a studyof lung volume in relation to the clinical courseof the disease. J. Exper. Med., 1924, 39, 677.

6. Binger, C. A. L., Brow, G. R., and Branch, A., Ex-perimental studies on rapid breathing. II. Tachyp-nea, dependent upon anoxemia, resulting from mul-tiple emboli in the larger branches of the pulmonaryartery. J. Clin. Invest., 1924, 1, 155.

7. Peters, J. P., and Van Slyke, D. D., Quantitative Clini-cal Chemistry. Vol. I. Interpretations. Williamsand Wilkins Co., Baltimore, 1932, p. 601.

8. Binger, C. A. L., Anoxemia in pneumonia and itsrelief by oxygen inhalation. J. Clin. Invest., 1928,6, 203.

9. Meakins, J. C., and Davies, H. W., Respiratory Func-tion in Disease. Oliver, Edinburgh, 1925.

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