Suppurative Pneumonia With Necrosis and Abscess Formation

Three varieties of suppurative pneumonia have occurred in association with influenza.

A. Necrosis and suppuration with formation of one or several abscesses usually below the pleura and almost invariably caused by hemolytic streptococci.

B. Interstitial suppurative pneumonia caused by hemolytic streptococcus.

C. Multiple abscesses in clusters caused by staphylococci.

Suppurative pneumonia with necrosis and abscess formation will be discussed in this section. Pulmonary abscesses which occurred in 43 autopsies may be included in this group; in 4 of these autopsies abscess and interstitial suppurative pneumonia occurred in the same individual. These abscesses were much more frequently situated in the lower than in the upper lobes and more often in the right than in the left lung. In most instances there was one or several abscesses situated below the pleura of one lobe; occasionally abscesses occurred in two lobes of the same lung or in both lungs. The distribution was as follows: Abscess in only one lung occurred in right upper lobe in 6 autopsies; middle lobe, 3; lower lobe, 15; left upper lobe, 2; lower lobe, 16. Abscesses occurred in both right and left lower lobes, twice. The usual situation was at the lower and posterior part of the lower lobe at or near the basal edge, less frequently below the posterior border or upon the basal surface of the lobe. These abscesses in almost every instance were found immediately below the pleural surface, so that they appeared upon the pleura as opaque yellow spots usually surrounded by narrow zones of hemorrhage. In one instance (Autopsy 376) the abscess cavity was separated from the pleural cavity by remains of the pleura which was as thin as tissue paper and in other instances perforation had occurred (Fig. 9). In Autopsy 480 the abscess cavity which had perforated the pleura was in free communication with a bronchus of medium size.

In most instances of suppurative pneumonia there have been associated lesions of bronchopneumonia which have been peribronchiolar, hemorrhagic or lobular and have exhibited no unusual characters. The abscess or abscesses are situated within an area of pneumonic consolidation which is not limited by lobule boundaries and has not the characters of bronchopneumonic consolidation. In some instances this consolidation is limited to a zone immediately about the abscess, but often it involves the greater part of a lobe. The tissue is laxly consolidated and flabby; on section it has a dull, conspicuously cloudy appearance and is grayish red, pinkish gray or gray; it is homogeneous or very finely granular. Turbid gray fluid, which sometimes resembles thin pus, oozes from the cut surface.

Widespread necrosis of tissue is not infrequently a conspicuous feature of this pyogenic pneumonia (Fig. 8). Upon a cloudy gray background of consolidation are numerous opaque yellowish gray or yellow patches, occasionally 2 or 3 cm. across, giving a mottled character to the cut surface. Upon the pleura these necrotic patches appear as dull opaque yellow spots. They may be surrounded by a zone of hemorrhage. The opaque material is at first firm but may undergo softening, becoming semisolid and finally purulent. Necrotic patches may be scattered throughout a lobe, but fully formed abscesses are with few exceptions immediately below the pleura (Fig. 9).

Fig. 8.—Streptococcus pneumonia with massive necrosis. Autopsy 354.

Fig. 9.—Abscess below pleura with perforation caused by hemolytic streptococci. Healing suppurative interstitial pneumonia indicated by yellowish gray lines marking interlobular septa at base of lower lobe. Autopsy 474; right lung. (See left lung, Fig. 10.)

The duration of illness in cases of pneumonia with abscess varied from a week or less (11 instances) to more than four weeks. The duration of the greater number of cases (17 instances) was between one and two weeks. In one instance onset occurred with symptoms of influenza, pneumonia was recognized two days later, and death occurred only four days after the onset of illness. When the duration of the illness was less than a week the symptoms of onset were in some instances those of pneumonia.

Table XLV shows the incidence of pneumococcus, S. hemolyticus, staphylococcus and B. influenzæ in instances of suppurative pneumonia with abscess formation, 4 instances of abscess with interstitial suppurative pneumonia being excluded:

Table XLV
NO. OF CULTURESPNEUMOCOCCIHEMOLYTIC STREPTOCOCCISTAPHYLOCOCCIB. INFLUENZÆ
NO. POSITIVEPER CENT POSITIVENO. POSITIVEPER CENT POSITIVENO. POSITIVEPER CENT POSITIVENO. POSITIVEPER CENT POSITIVE
Bronchus24520.82291.61250.01875.0
Lung36925.03083.31435.6822.2
Blood37616.23183.8

In over 80 per cent of instances of pulmonary abscess hemolytic streptococcus has been found in blood, lungs and bronchus and, when cultures have been made, in the inflamed pleural cavity as well. Streptococci have been found in immense number in sections from the necrotic lung tissue and the abscesses which have been formed. It is evident that hemolytic streptococci have caused suppurative pneumonia and death, being found in the blood of the heart just as frequently as in the lungs (83 per cent). The relative unimportance of pneumococci is indicated by their low incidence in the blood (16.2 per cent) when compared with that of lobar pneumonia (65.5 per cent) or of bronchopneumonia (31.4 per cent). B. influenzæ has been found in three-fourths of these autopsies in the bronchus, but its incidence in the lungs has been much smaller.

In 3 instances of suppurative pneumonia with abscess formation no hemolytic streptococci were found; they are as follows:

Autopsy 380.—Bronchopneumonia with gray and red lobular consolidation in right upper and lower lobes; peribronchiolar nodules of consolidation in left lower lobe; abscess, 1.5 cm. across, below the pleura of the posterior border of the left lower lobe near its base; fibrinopurulent pleurisy (300 c.c.) on right side; serous pleurisy (200 c.c.) on left. Pneumococcus III was found in cultures from the blood of the heart from the right lung and with B. influenzæ from the right pleural cavity. No culture was made from the left lung which contained the abscess. In sections of the abscess gram-positive streptococci in chains of 4 to 8 cocci were numerous.

Autopsy 406.—Acute lobar pneumonia with red hepatization of greater part of right lung; patch of consolidation in lower lobe of left lung containing an abscess cavity 2.5 x 1.5 cm.; localized seropurulent pleurisy (375 c.c.) on left side. Pneumococcus IV was obtained from the blood of the heart; a culture from the lung was contaminated. Tissue from the abscess was not saved for histologic examination.

Autopsy 416.—Suppurative pneumonia with necrosis and abscess formation in right lower lobe; fibrinous pleurisy on right side. Pneumococcus IV was obtained from the blood, right lung and right main bronchus. No streptococci were found in sections from the abscess in the right lung.

The foregoing observations demonstrate that suppurative pneumonia with abscess formation following influenza is with few exceptions caused by S. hemolyticus.

The autopsies (Table XLVI) in which pneumococci have been found in association with hemolytic streptococci in the blood or lungs indicate that pneumococci have had a part in the production of fatal pneumonia.

Table XLVI
AUTOPSYCULTURE FROM BLOODCULTURE FROM LUNGSCULTURE FROM BRONCHUS
258S. hem.S. hem., Pneum. IV B. inf.
282S. hem., Pneum. IIS. hem., Pneum. IIS. hem., B. inf. Pneum. II, staph.
345 S. hem., Pneum. II, staph.
378Pneum. atyp. IIS. hem., Pneum. atyp. IIS. hem., B. inf., Pneum. atyp. II
381S. hem.S. hem., Pneum. II Pneum. IV, staph.
383Pneum. IIIS. hem., Pneum. III B. inf.
387S. hem.Pneum. II, staph., B. inf.S. hem., pneum., staph., B. inf.

These autopsies, notably those in which pneumococci have been found in the blood, suggest that infection with pneumococci has preceded suppurative pneumonia caused by hemolytic streptococci. In a small number of instances the sputum was examined in life after onset of pneumonia.

Table XLVII
AUTOPSYSPUTUMCULTURES FROM BLOOD, LUNGS AND BRONCHUS
282Pneum. IV. B. inf.S. hem., Pneum. II, staph., B. inf.
288S. hem., B. inf.S. hem., B. inf.
376(No S. hem., Oct. 8)S. hem., staph., B. inf. (Oct. 11)

In 2 of these 3 cases infection with hemolytic streptococcus occurred subsequent to the onset of pneumonia.

Several observations help to explain the occurrence of abscess in association with the pneumonia of influenza. The fissures which will be described in association with bronchiectasis represent traumatic ruptures of the bronchial wall consequent upon weakening by necrosis and over distention. They expose the injured bronchial wall and the alveolar tissue adjacent to it to infection by the microorganisms contained within the lumen of the inflamed bronchus. Occasionally a favorable microscopic section demonstrates the relation of pulmonary necrosis and consequent suppuration to injuries of the bronchial wall. Peribronchial fibrinous pneumonia occurs about the bronchi of which the epithelial lining has been destroyed, and when a fissure penetrates the bronchial wall fibrinous pneumonia is almost invariably found in a zone about the tear; it doubtless tends to limit the extension of the process. Occasionally, wide areas of necrosis occur within consolidated tissue near the site of the fissure (Autopsy 312 with S. hemolyticus and B. influenzæ, p. [254]). Accumulation of polynuclear leucocytes between living and dead tissue may form a line of demarcation (Autopsy 387); finally, fairly large, irregularly formed, abscess cavities are found.

Necrosis and beginning suppuration in contact with the lumen of the bronchus will be described in association with bronchiectasis (Autopsies 312, Fig. 24, and 423, p. [256]). In the following autopsies upon individuals who have died with pulmonary abscesses, favorable microscopic sections have demonstrated abscess formation in contact with lesions which have penetrated the walls of small bronchi. They help to explain the pathogenesis of abscess in association with influenza.

Autopsy 376.—H. M., white, aged twenty-four, a fireman, resident of Oklahoma, had been in military service one month. Onset of illness occurred October 1, ten days before his death; he was admitted to the base hospital on the fourth day of his illness with the diagnosis of bronchopneumonia.

Anatomic Diagnosis.—Acute bronchopneumonia with patches of lobular and confluent lobular consolidation in both lungs and hemorrhagic peribronchiolar consolidation in right upper lobe; abscess in right upper lobe below pleura; fibrinopurulent pleurisy on right side; purulent bronchitis; bronchiectasis at base of left lobe.

An irregular abscess, 2 x 1 cm., filled with creamy purulent fluid is separated from the interlobular surface of the right upper lobe by a thin membrane representing the pleura. The right pleural cavity contains 200 c.c. of turbid yellow fluid in which is soft fibrin. The bronchi contain purulent fluid in great abundance. The bronchi at the base of the left lower lobe are widely dilated, so that many small bronchi with no cartilage in their wall measure from 3 to 5 mm. in diameter.

Cultures show the presence of hemolytic streptococci in the blood of the heart and in three plates from the lung; B. influenzæ and S. aureus were found in the left bronchus.

The bronchi have wholly or partially lost their epithelium and there is deep erosion of the walls. Cavities containing polynuclear leucocytes occur within the alveolar tissue; in some instances pus containing cavities are surrounded by alveolar tissue, but in other places it is evident, that they have had their origin in bronchi. In a short segment of the circumference the wall of the preexisting bronchus is preserved and consists of squamous epithelium, vascular connective tissue and smooth muscle. The remainder of the bronchus has disappeared and a cavity is produced. The very irregular wall of the cavity is formed by partially destroyed alveoli filled with fibrin and leucocytes.

Autopsy 387.—C. M., white, aged twenty-one, laborer, resident of Mississippi, had been in military service twenty-one days. Illness began on September 22, nineteen days before death, and the patient was admitted to the hospital on the same day with a diagnosis of bronchitis; a diagnosis of bronchopneumonia was made on October 2, nine days before death. The leucocytes on October 3 numbered 8000 (small mononuclear, 36 per cent; large mononuclear, 5 per cent; polynuclear, 59 per cent).

Anatomic Diagnosis.—Acute bronchopneumonia with consolidation in right upper lobe and hemorrhagic peribronchiolar consolidation in left lower lobe; abscess below pleura in left lower lobe; purulent pleurisy on both sides; edema of mediastinum; purulent bronchitis; bronchiectasis.

There is advanced bronchiectasis, and bronchi with no visible cartilage are dilated to from 4 to 8 mm. in diameter; they contain purulent fluid which wells up from the cut surface. About dilated bronchi there is in places dull red or grayish red consolidation forming an encircling zone. Situated below the pleural surface within an area of consolidation at the posterior border of the left lower lobe there is a spot 3 cm. across where the tissue is yellow and has in places undergone purulent softening. Several smaller abscesses occur nearby.

Cultures from the blood of the heart and from the edematous mediastinum contain hemolytic streptococci. From the abscess are grown S. albus, Pneumococcus II and B. influenzæ. The purulent contents of a small bronchus contains S. hemolyticus, B. influenzæ, S. aureus and a few pneumococci.

Microscopic examination shows that the epithelium of dilated bronchi has disappeared and the denuded surface is covered by fibrin and polynuclear leucocytes; fissures extend from the lumen through the bronchial wall into the surrounding alveolar tissue. A zone of fibrinous pneumonia surrounds these bronchi and fissures in the bronchial wall penetrate into this zone. One dilated bronchus 2.4 mm. in diameter with no cartilage in its wall has vascular connective tissue covered by epithelium on one side, whereas the remainder of the circumference is formed by exposed alveoli filled with fibrin, the bronchial wall having disappeared. A section through a part of the abscess which has been mentioned shows a very irregularly formed cavity approximately 1 x 0.7 cm. Remains of bronchial wall, consisting of very vascular tissue covered by flat epithelium in several layers, indicate the origin of the cavity. Between these remnants of bronchi deep pockets extend into the pulmonary tissue which in the margin of the cavity is the site of fibrinous pneumonia. In one place, in contact with the cavity, a wide area of consolidated tissue has undergone necrosis and both alveolar walls and their contents have lost their nuclei. Leucocytes which are accumulating at the margin of the necrotic patch form a line of demarcation between living and dead tissue.

Abscess may be the result of the profound changes which occur in the bronchi as the result of influenza. Necrosis caused by bacteria within the bronchi weakens and in places destroys the wall. Bacteria penetrate into the surrounding tissue and hemolytic streptococci (or staphylococci) may produce localized abscesses. These abscesses are usually situated near the pleural surface of the lung, because destructive changes causing rupture of the bronchial wall occur more frequently in the smaller peripheral bronchi than in the larger bronchi containing cartilage. Abscesses occur more frequently at the bases of the lungs, because the most severe changes in the bronchi occur in the dependent part. (See “Bronchiectasis,” p. [240].)

Healing of Abscess.—The following autopsy is of interest in relation to the treatment of pulmonary abscess and associated empyema.

Autopsy 467.—P. C., white, aged twenty-five, a farmer from Missouri, had been in military service three months. Illness began September 27, thirty days before death, and the patient was admitted the day following onset with headache, backache and cough. Pneumonia with consolidation in the right lower lobe was recognized on the sixth day of illness. On the ninth day 500 c.c. of fluid were withdrawn from the right pleural cavity; there were cyanosis and dyspnea. On the eleventh day 700 c.c. of fluid were withdrawn. On the twelfth day thoracotomy was performed and 100 c.c. of greenish fluid were removed. The patient’s condition improved for a time, but on the twenty-sixth day 1,000 c.c. of straw colored fluid were aspirated from the left pleural cavity and on the twenty-eighth day the same amount of seropurulent fluid was withdrawn.

Anatomic Diagnosis.—Healing abscess of right lower lobe communicating with the pleural cavity; acute purulent pleurisy with closed thoracotomy wound on the right side; purulent pleurisy on the left side; acute bronchopneumonia with lobular consolidation in the left lung; purulent bronchitis; bronchiectasis with formation of spherical bronchiectatic cavities; acute splenic tumor.

At the base of the right chest is a closed thoracotomy wound 2 cm. in length; the right pleural cavity contains 200 c.c. of thick creamy pus and the cavity is lined by a thick tough membrane. The left pleural cavity contains 800 c.c. of white purulent fluid thinner than that on the right side. The right lung is compressed into the posterior and inner part of the chest. The upper lobe is pink and air containing; the posterior and lower part of the lower lobe is red and atelectatic, and fibrous septa are more conspicuous than elsewhere. The pleura of the external surface near the basal edge, in an area 2 cm. across, is depressed and yellowish gray in color. In the center of this area is a small opening communicating with a pocket 0.5 cm. across within the substance of the lung.

In the lower lobe beneath the interlobular surface are two spherical bronchiectatic cavities, each about 1.5 cm. across, with smooth lining in continuity with two branches of the same bronchus of medium size.

Bacteriologic examination showed the presence of S. hemolyticus in the blood of the heart. No growth was obtained from the left lung; the left pleural cavity contained hemolytic streptococci and S. aureus, the latter in small number. S. hemolyticus and B. influenzæ were grown from the left main bronchus.

A microscopic section through the abscess and its communication with the pleura shows that its cavity contains polynuclear leucocytes and the wall is formed by granulation tissue covered by fibrin. Some alveoli outside the abscess contain compact balls of fibrin containing a few fibroblasts; this fibrin stains deeply with hematoxylin as if it contained calcium. The surface of the lung is covered by fibrin in process of organization.

In the foregoing instance a pulmonary abscess on the right side has ruptured into the pleura and, completely separated from the adjacent lung by a wall of newly formed tissue, is in process of healing. It shows that these pulmonary abscesses below the pleura may heal provided drainage is established by rupture into the pleural cavity and subsequent evacuation of pleural exudate. It is noteworthy that in this instance empyema extended from the right to the left pleural cavity, both S. hemolyticus and S. aureus were found at autopsy. The thoracotomy wound on the right side was closed at autopsy.