In two instances slight hemorrhages were observed into the conjunctival tissues. In each case they were unilateral and occupied the tissues contiguous to the inner canthus. In one case there was well-marked icterus with yellow coloration of the scleræ and skin. In this case the icterus was associated with degenerative changes in the liver, there being no recognizable obstruction to the bile passages. The icterus had come on quite acutely and without any special clinical manifestations. In the epidemic of 1890 jaundice was present in a considerable number of cases (Medical Record, 1890, xxxvii, 473). Cole made similar observations in the epidemic of influenza amongst the Canadian soldiers. Œdema of the skin was not met with in any of our cases. This point is worthy of comment, inasmuch as some authors have been impressed with the serious damage taking place in the kidney and the resulting incapacity of these organs. Although, as we shall point out later, the kidney tissues in these cases showed a decided toxic degeneration, there was no evidence that a glomerular damage of serious degree ever occurred. The urinary excretion, as is pointed out in a report by Dr. Zeedick, varies considerably with the intensity of the disease. It is unusual to find derangement of kidney function to a degree to reflect seriously upon the general bodily state. At least this has been our experience in the present epidemic. Even where subsequently we were able to demonstrate a considerable tubular degeneration in the cortex of the kidney the change in the kidney function was not of sufficient magnitude to lead to a water-retention to be recognized in an anasarca. I wish to distinguish clearly at this point the difference in finding an œdema in certain involved tissue structures in various parts of the body and arising through an inflammatory reaction due to the presence of peculiar focal irritation, as compared with the accumulation of fluid in many and irregular situations as it occurs through retention and faulty excretion by the kidneys. Various organs as we have found—as, for instance, the lung, heart and liver—showed a condition of œdema which was not to be reconciled with an inadequate circulation because of a cardiac or renal incompetency. These œdemas, which we will discuss later, are local and are the result of damaging influences inducted in and upon the tissues where they are found.
Muscle
In all of our cases we have been struck with the excellent physique of the individuals succumbing to this epidemic. All were youths in the best of health, of good muscular build and strong bony frame-work. Post-mortem rigidity set in fairly rapidly after death. Where this rigidity had “set” for six or more hours it required much force to change the position of the muscles. The voluntary muscles of the thorax and abdomen were always carefully observed, and in a number of instances the muscles of the thigh were also examined. It was not possible routinely to dissect the muscles of the extremities, so that we are unable to give an accurate account of the occurrence of degenerations in these structures. We have, however, observed the reactions taking place in the pectorals, psoas and muscles of the abdominal parietes. Changes were observed with greatest frequency in the recti of the abdomen. Degeneration occurred in these muscles in 14 instances, while the same tissues suffered rupture, in part or completely with hemorrhage, in six instances. It was not uncommon to find marked degeneration in the lower segment of the rectus muscle on one side, while degeneration and hemorrhage had occurred in its fellow on the opposite side. In four cases rupture of the entire belly of the muscle had taken place, so that a considerable space had occurred between the broken ends and a large clot of blood filled the intervening space. This degeneration, which was seen only in the voluntary muscles, was quite interesting and in its milder degrees was rather difficult to detect. All gradations of loss of muscle color were seen. In some instances the muscle simply seemed to have lost its meaty lustre, while again in the more severe instances the muscle color had changed from the bright red to an insipid yellow or clay color. The most marked degeneration occurred in the midportions, while the ends of the muscle masses at the points of attachment were less involved. Complete rupture of the rectus always occurred in the lowermost segment, a short distance above the insertion into the pubic bone. At times the distribution of the degeneration within the muscle was quite patchy, and irregular islands of yellow about 2 cm. in diameter were splashed through the muscle masses, which in themselves were paler than normal. Where the muscle degeneration was advanced the tissue was soft and at times even buttery. It resembled the character of the degeneration observed in typhoid fever, although I have no recollection amongst many enteric cases of having seen the degeneration of the muscle occur so acutely. Recklinghausen claimed that these hemorrhages were most unusual in influenza. This is contrary to our findings.
Degenerations of a similar kind as those of the abdominal recti were found in both pectorals. In the chest region, however, the degeneration was less frequent and less severe. We observed it only twice, and in neither instance had the degeneration led to a rupture and hemorrhage of the muscle bundles. Kuskow observed a single case of degeneration and hemorrhage of the pectoral muscles. In the psoas muscle we observed degeneration on two occasions, in one of which the lesion was associated with a partial separation of the muscle fibers and hemorrhages into its substance. In one case clinically, but not coming to autopsy, a lesion, which from its character we presume to have been a degeneration, occurred in the sterno-mastoid, being accompanied by hemorrhage and the development of a firm clot the size of a hazel nut. In the subsequent history of this case the lesion passed through an aseptic process of organization with contracture so that the patient has recently been developing a “wryneck.” Kohts in 1890 reported the finding of muscle degeneration and abscesses in the arm. The condition arose as a late complication of influenza.
From our experience at the autopsy table in observing the relative frequency with which muscle degeneration occurs in the severe cases of epidemic influenza, we feel convinced that numerous cases which recover pass undiagnosed of this condition. Furthermore we have evidence, as illustrated in a case observed by Dr. McMeans, wherein a lesion which occurred in the gluteal muscles was followed by a localizing infection at this site that these muscle degenerations and hemorrhages may have serious consequences. There are a number of instances in which post-influenzal complications of the nature of deep-seated abscesses of the extremities, thorax, and abdomen may have their explanation for the localization in a primary muscle damage accompanied by hemorrhage and followed by an infection of variable type. Cole also comments upon the development of abscess in the deep muscles where degeneration had taken place. In illustrating some of our findings to Dr. J. Anderson he immediately recognized such a condition in the pectoral muscles of a patient in which he was unable to arrive at a conclusion of the pathological events which had taken place. It is one of the noteworthy features in this disease that the voluntary muscles of certain regions are apt to suffer severe damage, while the heart and the various unstriped muscular tissues are little if at all affected by a similar process. It would be interesting to know whether the lack of response and the delayed functional recovery on the part of the muscles of the extremities in so many patients who have suffered influenza is the result of the damaging influence of a peculiar intoxication present in this disease. One of the features in influenza is the prostration of the patient, and with it there is definite muscular weakness. We have been prone to lay the responsibility of this state entirely at the door of the nervous tissues. Here, however, we are able to offer evidence that quite aside from the lesions arising in the nervous tissue, there is definite muscle damage which, as we shall again discuss when describing the microscopic features, incapacitates even to the point of complete destruction the muscle elements in various fields of the body. Before, however, being able to state that the muscular weakness of the extremities is the result of such damage by toxins it is necessary to obtain more definite information regarding the frequency with which these degenerations occur in the limbs. In our own material we are unable to discuss the matter with adequate figures. We are, however, impressed with the changes observed in the muscles which were available to us. Naturally, too, a certain number of muscle degenerations have escaped our detection because of our unfamiliarity with the mildest grades. In fact, we have already discovered in our microscopic studies that certain cases, which in the macroscopic had escaped us, showed well-marked lesions under the microscope.
TABLE IV
MUSCLE DEGENERATION
| Abdominal Recti | Pectoral | Psoas | |
|---|---|---|---|
| Toxic Degeneration | Hemorrhage Into Rectus | Toxic Degeneration | Toxic Degeneration |
| 745 on 10th day | 745 both on 10th day | 756 on 8th day | 756 on 8th day |
| 749 on 4th | 752 both on 13th | 770 on 11th | 792 on 6th |
| 752 on 13th | 756 both on 8th | ||
| 756 on 8th | 764 both on 9th | ||
| 757 on 6th | 765 both on 9th | ||
| 762 on 10th | 778 both on 23d | ||
| 763 on 11th | |||
| 764 on 9th | Rupture of | ||
| 765 on 9th | Rectus | ||
| 767 on 10th | |||
| 770 on 11th | 745 right on 10th day | ||
| 778 on 23d | 756 both on 8th day | ||
| 783 on 8th | 778 right on 23d day | ||
| 791 on 6th | |||
We have convinced ourselves that the marked hemorrhage taking place in the muscle tissue follows upon a primary degeneration of this tissue and its spontaneous rupture. The amount of hemorrhage is in proportion to the degeneration and fracture of the muscle elements. The hemorrhage does not precede the muscular change, nor does it have any antecedent relation to the actual tearing of the muscle fibers.
A much better appreciation of the muscle degeneration was obtained in the microscopic studies of these tissues. The various gradations of tissue change could be followed, which was not possible in the naked-eye examinations. Some points respecting this degeneration were quite noteworthy. Firstly, the process of degeneration in its early stages and advancing through the acute destructive periods was not accompanied by any inflammatory reaction. Evidence of inflammatory exudate was obtained only when the degeneration had proceeded to a degree permitting of rupture with hemorrhage, or in the late stages when the areas of marked muscle dissolution were undergoing repair. We have no evidence to indicate that bacteria were present during the beginning of the degenerative process. Bacteria could not be demonstrated in section. The appearance of the tissue suggested a purely toxic process which was selective in its action, picking out voluntary striped muscle tissue and attacking certain muscle groups in preference to others. It was also interesting to observe in the early stages of the degeneration that individual fibers lying amidst healthy and unchanged muscle elements would show degeneration in many of its stages. This appearance was often unique, particularly when in the early stages of the process the involved fiber would still retain its normal position and shape though markedly altered in its staining and chemical qualities.