Pulmonary Interstitial Fibrosis following Near-Drowning and Exposure to Short-term High Oxygen Concentrations

successful cases, 20 and 40 minutes respectively had elapsed prior to resuscitation attempts. One of the successfully treated cases of Cobbs et aP had only minor nonspecific ST segment and T wave changes on the electrocardiogram prior to the rupture and they emphasized the importance of remembering that electrocardiographic evidence of acute myocardial infarction may be absent. Their success and this case demonstrate that a normal or only slightly abnormal electrocardiogram should not deter immediate surgery if the characteristic syndrome of cardiac rupture should develop. REFERENCES

1 London RE, London SB: Rupture of the heart : A critical analysis of 47 consecutive autopsy cases. Circulation 31: 202-208, 1965 2 Friedman HS, Kuhn LA, Katz AM : Clinical and electrocardiographic features of cardiac rupture following acute myocardial infarction. Am J Med 50:709-720, 1971 3 Cobbs BW, Hatcher CR, Robinson PH : Cardiac rupture: Three operations with two long-term survivals. JAMA 223 :532-535, 1973 4 Biiirck C , Mogensen L, Nyquist 0, et al: Studies of myocardial rupture with cardiac tamponade in acute myocardial infarction. l. Clinical features. Chest 61 :4-6, 1972 5 Hammer J, Fabian J, Pavlovic J, et al: Myocardial rupture in acute myocardial infarction. Cor Vasa 14 :180-187, 1972 6 Mogensen L, Nyquist 0 , Orinius E, et al : Studies of myocardial rupture with cardiac tamponade in acute myocardial infarction . 11. Electrocardiographic changes. Chest 61 :6-10, 1972 7 London RE, London SB: The electrocardiographic sign of acute hemopericardimn. Circulation 25 :780-786, 1962 8 Naeim F, de Ia Maza LM, Robbins SL: Cardiac rupture during myocardial infarction : A review of 44 cases. Circulation 45:1231-1239, 1972

26th hospital day showed interstitial fibrosis. Over the ensuing two months, the che!u .adiograph and pulmonary function tests returned towards normal. We attribute the pulmonary fibrosis to incomplete resolution of the alveolar interstitial pathology secondary to the near-drowning and exposure to high oxygen mixtures.

T

he acute clinical ~nd physiologic se.quela~ attendant upon near-drowmng are well descnbed.'-.. Most abnormalities reverse rapidly with appropriate therapy; the majority of patients are discharged from the hospital within one week. It has been assumed that the pulmonary pathology, consisting of alveolar and interstitial edema with varying degrees of alveolar and capillary cellular damage, 6 reverses rapidly and leaves the patient with normal lung architecture and function. That this may not always be true is pointed out in this report, in which fresh water near-drowning and short-term high dose oxygen exposure led to pulmonary fibrosis as evidenced by pulmonary function tests and lung biopsy. CASE REPORT

A 19-year-old caucasian man was discovered face down in a swimming pool on ~1ay 26, 1974. He was taken to a local hospital where an oropharynageal airway was placed. On subsequent traf\sfer to the Orange County Hospital, he was intubated with an oral endotracheal ( ET) tube and placed on 100 percent oxygen by volume ventilator. The patient had never had any pulmonary problems and had a nom1al preemployment chest radiograph two months prior to admission. Physical Examination The blood pressure was 110/60 mm Hg, pulse 160/minute and regular, rectal temperature 39.9 ° C. The patient was in severe respiratory distress with pink frothy fluid exuding from the ET tube. Auscultation of the chest revealed multiple fine and coarse inspiratory rales bilaterally.

Pulmonary Interstitial Fibrosis following Near-Drowning and Exposure to Short-term High Oxygen Concentrations* Frederick L . Glauser, M.D. and William Richard Smith, M.D.

Following near-drowning in fresh water, a 19-year-o~d man experienced severe adult respiratory distress syndrome, necessitating ventilatory support with positive end-expiratory pressure and high oxygen concentrations. Post-extubation, his course was highlighted by persistent hypoxemia and interrupted by a lung abscess which responded promptly to antibiotics. Pulmonary function tests were consistent with severe restrictive disease and chest radiograph revealed persistent bilateral alveolar and interstitial infiltrates. An open lung biopsy on the °From the Department of Medicine, University of California, Irvine.

CHEST, 68: 3, SEPTEMBER, 1975

FIGURE l. Admission chest x-ray film . Bilateral alveolar and interstitial infiltrates are present.

PULMONARY INTERSTITIAL FIBROSIS 373

Table 1-Serial Pulmonary Function Tests Da~· Po~t ~(·:tr-Drownin~

12

Hl

22

:l8

47

62

103

vc•

-10 3-1 50 8.'i 66 27 62 33

28 2-1 3!1 83 61 20 54 36

33 28 -15 74 5!l 26 7-1 31

.')I .')0 56 8.') !lO 3!l 77 3-1

.')8 50 65 85 80 38 81 35

71 72 73 100 !l1 50 81 35

82 78 83 100 87 62 88 35

FEV,* TLC* RV* FHC* DLCO~
Pao,••

PaCo,••

*Expr('~s(•d in ~·;~ of prPdictPd • *ExprP~s('(l in torr

Lahoratory Data Chest roentgenogram was compatible with bilateral diffuse pulmonary edema (Fig 1). Arterial blood gases were pH 7 .20, Po~ 39 torr (Flo~ 1.0), Pco~ 30 torr. Serum electrolytes were sodium 130 mEq/L, chloride 96 mEq/L, bicarbonate I3 mEq / L, potassium 4.2 mEq/L.

Hos]Jital Course Adequatt• oxygenation could not be maintained with 100 pere('nt oxygen by volume ventilator alone. The addition of positive end-t>xpiratory pressure ( PEEP) optimized at II cmii:!O, inen•ased his Po:! to only 51 torr. Mediastinal and subcutaneous emphysema developed eight hours following hospitalization. On the second hospital day, 5 percent right pneumothorax devdoped; this was treated without a chest tube. During this t•ntire time his blood pressure, peripheral perfusion and urinary output remained stable although his hemoglobin dPcreased from 18.7 to 10.1 grams percent as a result of an increased vascular volume and hemolysis. By till' 48th hospital hour, PEEP had been decreased to zero and Flo~ reduced to 0 .50; arterial Po~ was 55 torr. The chest x-ray picture showed improven;ent, but infiltrates renminl'
Fl(;um-: 2. Lingula biopsy specimen obtained on 42nd hospi-

tal day. Areas of interstitial fibrosis evident. No inflammatory et>lls noted.

374 GLAUSER, SMITH

he was given supplemental na~al oxygen (Flo:! 0.30); the resulting PaO:! was 65 torr. Chest x-ray film findings and arterial blood gases slowly improved. On the 12th hospital day puLnonary function tests were consistent with severe restrictive disease (Table 1 ) . Over the next week these tests showed an increasing restrictive pattern (Table 1). By the 19th hospital day, right lower lobe abscess cavity and right pleural effusion were evident by chest x-ray film. Thoracentesis produced sterile exudate. High dose intravenous penicillin was begun with subsequent slow clinical improvement. :\'evertheless, persisting generalized infiltrates were evident on the chest radiogram so an open biopsy was done on the 26th hospital day (Fig 2). Inspection and palpation of the left lung at surgery revealed diffuse involvement of all lobes. Microscopic examination of the lingula was consistent with pulmonary fibrosis . A few foreign body giant cells were present. No significant inflammatory cells were seen and there were no significant increases in desquamated pneumonocytes. Focal accumulations of proteinaceous eosinophilic edema fluid were identified in occasional alveoli. Cultures produced no growths. Over the ensuing 27 days, the patient's chest film and pulmonary function tests slowly improved. By discharge, his vital capacity ( VC), total lung capacity ( TLC), and DL,. 0 were increased 40-100 percent above their lowest levels (Table 1) . Follow-up 50 days after discharge ( 103 days post near-drowning) showed marked improvement in all parruneters of PFTs. VC and TLC had returned to 82 percent of predicted. DL.. 0 , although markedly improved, remained low ( 62 percent of predicted) (Table 1). Chest film showed minimal interstitial infiltrates in both bases and the lingulae (Fig3). DISCUSSION

Pulmonary edema following near-drowning has been considered a form of the adult respiratory distress syndrome.;·' The pathophysiology has been attributed to several mechanisms: 1) direct damage to surfactant and the alveolo-capillary membrane by fresh water; 2) osmotic movement of intravascular fluid from the capil-

FIGURE 3. Chest x-ray film 103 days after near-drowning. Previously noted alveolar and interstitial infiltrates have cleared as has the abscess cavitv. Note some residual infiltrate in right and left lower lobes and lingulae.

CHEST, 68: 3, SEPTEMBER, 1975

!aries into the alveolus secondary to hypertonic salt water; 3) washing out of surfactant resulting in atelectasis and alveolar fluid accumulation; 4) cerebral hypoxemia with a secondary alveolo-capillary leak. 9 Depending upon the extent of loss of integrity of the alveolocapillary membrane, plasma and formed elements move into the interstitium and alveolus to a variable degree. In most reported series these events do not progress. Our patient's early hospital course was typical for severe near-drowning, eg, pulmonary edema with marked hypoxemia necessitating ventilatory support with PEEP. Even pneumomediastinum, recurrent pneumothoraces and pulmonary infection with abscess formation would not be unexpected in this patient. Unique in this case is the biopsy evidence of pulmonary fibrosis (Fig .3 ), and documented slow improvement of restrictive pulmonary disease (Table I) over several months. It is possible that the interstitial fibrosis was secondary to infection and / or supplemental oxygen. However, the former seems unlikely since: I) the lung biopsy was obtained from the side contralateral to the abscess; 2) histologic examination of the lung tissue revealed no significant inflammatory cells or bacteria; 3) no organisms were cultured from the biopsy specimen; and 4) other entities which mimic "drown lung" reportedly terminate in some degree of interstitial fibrosis. 10 Whether these cases are comparable to our own is not apparent for the report 10 does not indicate how the diagnosis of pulmonary fibrosis was made. Neither does it state how many cases have been observed, or the extent of disease in any case. The role of the supplemental oxygen in the genesis of the interstitial fibrosis in this case is unclear. The patient received oxygen in excess of 50 percent for only 48 hours and by the 6th hospital day his Flo" was 0.28. We would consider this duration and amount of oxygen inadequate to cause fibrosis . On the other hand, Pratt" has evidence that pulmonary fibrosis can follow this duration and amount of oxygen. Thus, we cannot exclude excess oxygen as an additional contributor in the pathogenesis of our case of pulmonary fibrosis. Our patient differs from those of Butt et al. 12 They investigated I3 patients and performed pulmonary function tests from two weeks to two years following neardrowning. None of their patients (excluding those with preexisting pulmonary diseases) manifested abnormalities in lung volumes, DL,.,, and arterial blood gases. Whether any of their patients had severe near-drowning necessitating PEEP and high oxygen exposure is not stated. There are several other reports of pulmonary dysfunction or pulmonary infiltrates on chest radiograms following near-drowning.8 • 13 Biopsy evidence of pulmonary fibrosis was not obtained in these cases. The etiology of the pulmonary fibrosis secondary to the many causes of acute respiratory distress syndrome in the adult is unknown. Most investigators feel that the fibrin, plasma proteins, and leukocytes (with their disrupted lysozyme packages) in association with brady-

CHEST, 68: 3, SEPTEMBER, 1975

kinin , histamine, serotonin and other humoral agents cause a fibrogenic reaction. H \Vhether an individual patient's lung will undergo fibrosis and to what degree might depend on several factors : 1) the quantity, quality and duration of noxious agent exposure, and 2) the reparative capabilities of the lung. Although our patient was lost to follow-up during the fourth month after near-drowning, his chest roentgenograms and pulmonary function tests revealed marked improvement by this time. His final chest x-ray film (Fig 3) showed some nonspecific densities in both lungs but no changes suggesting diffuse pulmonary fibrosis. His pulmonary function tests (Table I) had all returned to the normal or low range. Interestingly, his DL,·o (corrected for persisting anemia) was only 62 percent of predicted. His arterial Po" of 88 torr, with a Pco" of 35 torr probably represents continued mild hypoxemia, especially for a I9-year-old. 15 Whether these parameters will stabilize or continue to improve is speculative. REFERENCES

2 3

4

5 6 7 8

9 10

11 12

13

14

15

Hasan S, Avery WG, Fabian C, et al : !\'ear-drowning in humans. A report of 36 patients. Chest 59 : 191-197, 1971 Modell JH, Davis DH: Electrolyte changes in human drowning victims. Anesthesiology, 30 :414-420, 1969 Modell JH, Davis DH, Giammona ST, et al : Blood gas and electrolyte changes in human near-drowning victims. JAMA 203 :337-343, 1968 Modell JH, Moya F, Newby EJ, et al : The effects of fluid volume in seawater drowning. Ann Intern Med 67:68, 1967 Rivers JF, Orr G, Lee HA : Drowning. Its clinical sequelae and management. Br Med J, 2:157-161 , 1970 Fuller RH : The clinical pathology of hwnan near-drowning. Roy Soc Med Proc 56:33-38, 1963 Petty TL, Ashbaugh DC: The adult respiratory distress syndrome. Chest 60 :233-239, 1971 Fine NL, Myerson DA, Myerson PJ, et al: Near-drowning presenting as the adult respiratory distress syndrome. Chest 65 :347-349, 1974 Moss G: Shock lung : A disorder of the central nervous system . Hosp Practice 9:77-86, 1974 Respiratory diseases. Task force report on problems, research approaches, needs. Respiratory distress syndrome, 167-180, Dept. of HEW publication No. (1\'IH) 73-432, October, 1972 Pratt PC: Pathology of pulmonary oxygen toxicity. Am Rev Resp Dis 110:51, 1974 Butt M, Jalowayski A, Modell JH, et al : Pulmonary function after resuscitation from near-drowning. Anesthesiology 32:275-277, 1970 Modell JH: The Pathophysiology and Treatment of Drowning and Near-Drowning. Springfield, Illinois, CC Thomas, 1971, p 1 Wilson JW, Ratliff NB, Hackel DB, et al: Inflammatory response in reaction of lung to acute hemodynamic injury. In Immunopathology of Inflammation, Forsher BK, Rouch JC, eds. Amsterdam, Excerpta, 1971, p. 183 Marshall BE, Millar RA : Some factors influencing postoperative hypoxemia. Anaesthesia, 20 :408-411, 1965

PULMONARY INTERSTITIAL FIBROSIS 375