THROMBOSIS OF THE Sinuses of the Dura Mater IN FATAL CASES OF DYSENTERY IN YOUNG CHILDREN. BY SAMUEL C. BUSEY, MJY, Professor of the Theory and Practice of Medicine, Medical Department of the University of Georgetown ; one of the Physicians to the Children’s Hospital, Washington, D. C, Reprinted from the American Journal of Obstetrics and Diseases of Women and Children, Vol. XIII., No. 1., January, 1880. NEW YORK: WILLIAM WOOD & CO., 27 GREAT JONES STREET. 1880. THROMBOSIS OF THE Sinuses of the Dura Mater IN FATAL CASES OF DYSENTERY IN YOUNG CHILDREN. tY , SAMUEL 0. BUSEY, M,D., Professor of the Theory and Practice of Medicine, Medical Department of the University of Georgetown ; one of the Physicians to the Children’s Hospital, Washington, D, C, Reprinted from the American Journal of Obstetrics and Diseases of Women and Children, Vol. XIII., No, L, January, 1880. NEW YORK: WILLIAM WOOD & CO., 37 GREAT JONES STREET. 1880. THROMBOSIS OF THE SINUSES OF THE DURA MATER IN FATAL CASES OF DYSENTERY IN YOUNG CHILDREN. BY SAMUEL C. BUSEY, M.D., Prof, of the Theory and Practice of Medicine, Medical Department, University of George- town ; one of the Physicians to the Children’s Hospital, Washington, D. C. It has been my misfortune to lose a number of cases of dysentery in young children; and, in every case, so far as I can recall the clinical histories, the fatal issue has taken place under precisely similar circumstances. In several cases during the acuteness of the attack, but more frequently after the characteristic symptoms had subsided and when convalescence seemed almost established, the child would be seized with convulsions, which, in occasional cases, recurred a second and a third time, and were followed by coma and death. In no instance has consciousness returned after the first convulsion. These observations have led me to suspect that in dysentery, as in fatal cases of exhaustive diarrhea in young children, the convulsions which so frequently precede death found their cause in thromboses1 of the sinuses of the dura mater, but in the absence of post-mortem examination, I could not verify it. The more commonly accepted opinion ascribes the final con- vulsions of exhaustive diarrheas to cerebral anemia, and it is undoubtedly true that both conditions not infrequently co-exist. Marshall Hall was the first to recognize and differentiate spurious hydrocephalus from other intercranial diseases with which it had been previously confounded; yet lie probably included in the clinical description of hydrocephaloid disease its congener, with which it is so closely allied in cause, symp- toms, course, and result. In fact, both are the proximate effects of exhaustion and wTaste, Hothnagel, Gerhardt, and others assert that thromboses of tbe cerebral sinuses occurring 1 Gerliardt found thrombi in the sinuses of the dura mater in seven autopsies of children who had died of profuse diarrhea, attended with cyanosis, coma, and convulsions. 4 Busey; Thrombosis of the Sinuses of the Dura Mater in young children, when the walls of the venous channels are free from disease, “originate in conditions of the nature of marasmus.” J. Lewis Smith, Steiner, and Yogel enumerate chronic gastro-intestinal diseases among the causes, and more recently Bouchut has definitely determined the fact that such formations may and frequently do occur in a variety of the chronic affections of young children, and occasionally at the termination of acute diseases. In such cases death is preceded by convulsions. I have also observed, in a limited number of fatal cases of protracted diarrhea in very young children, edema of the lower extremities; in two instances associated with discolora- tion of the integument of the feet and legs, supervening several days previous to death. Whilst I had learned to regard these phenomena as indications of a fatal issue, I had not until the recent researches of Bouchut recognized the formation of thrombi in the pelvic veins as the cause of the venous stasis and the serous transudation into the subcutaneous cellular tissue. Dysentery in young children is comparatively a rare form of intestinal disease in this locality, but three cases having been treated in the Children’s Hospital since its foundation in 1871, consequently opportunities to make post-mortem exam- inations are not often secured. But recently, and only in a single case, have 1 obtained permission to examine the brain of a child dead of this disease. This child was a patient in the Children’s Hospital, under the care of my colleague Dr. W. W. Johnston, who has permitted me to use the notes of the post-portem. From the date of admission I made daily inquiries concerning the course and progress of the case, and when informed by the house physician that the dysen- teric symptoms had all subsided, I replied that the child was very far from being out of danger; in fact, that the case had reached the stage when the danger of convulsions was imminent, and if such should occur, coma and death would follow. The next day he informed me that the patient had had three convulsions and was comatose. It died a few hours later. Post-mortem by Dr. A. C. Adams, twenty-four hours after death. Body emaciated, eyes sunken, abdominal walls retracted; rigidity slight. Brain: weight 2 lbs. 5J oz., anemic, effusion (estimated) into the arachnoid cavity 1 pint, slight in ventricles. Black clots in in Fatal Cases of Dysentery in Young Children. 5 all the sinuses, and a large white fibrinous thrombus at the junc- tion of the right lateral with the petrosal sinuses. Heart; effusion into pericardium; white fibrinous clots in supe- rior yena caya, extending into right auricle and firmly attached to base of tricuspid yalye. No blood in either ventricle; valves intact; weight ozs. Lungs: float in water; weight oz. ; left normal; right con- tained in middle lobe a cheesy mass as large as a hen’s egg; this lobe was firmly attached to the pleura. Lungs anemic; no tuber- cular deposits. A cheesy bronchial gland as large as a pigeon’s €SS- . . . Abdomen: abdominal walls thin, destitute of fat; omentum contained but little fat; mesenteric glands slightly enlarged and congested. Intestines contain small quantities of feces; nothing abnormal in the small, in the large intestines patches of inflam- mation were found all along the track from the cecum to the anus. Liver anemic, buff-colored. Gall-bladder distended. Large depots of pus at lower extremity of either kidney. Weight oz. The evidences of exhaustion, waste, and cachexia are obvi_ ous, and sufficient, perhaps, to account for the fatal result. But the inquiry cannot rest here, as the object is not so ranch to determine the cause of death as to ascertain the relation of thrombosis to the clinical phenomena; to study the means of prevention, and thereby avert the occurrence of a lesion which is incompatible with the long continuance of life. The intracranial effusion, fulness of the venous and anemia and lessened "weight of the brain-mass are the usual post-mortem conditions concurrent with thromboses of the sinuses, but are also found, especially, in fatal cases of spurious hydrocephalus, independent of the presence of thrombi. They are not necessarily the result either of partial or com- plete occlusion of the sinuses by thrombi, but may be and frequently are the morbid effe. ts of diseases characterized by great exhaustion, inspissation of the blood, and weak heart- action. Cases of such diseases as are complicated with intra- cranial effusion, shrinkage of brain-mass, and thickening of the blood are not necessarily fatal; they may be successfully met with timely and appropriate treatment. But those in which thrombosis may be either a superadded or a primary lesion, if not certainly fatal, acquire such gravity as to preclude any reasonable hope of recovery. The inquiries relate, then, espe- cially to the diagnosis and prophylaxis. 6 Busey: Thrombosis of the Sinuses oj the Dura Mater Intracranial lesions are among the most difficult of diagno- sis, and often the most cultivated and experienced diagnosti- cian will be baffled in his efforts to determine, in a given case, the anemic or hyperemic condition of the brain. But in such diseases as favor the development of spurious hydrocephalus or marantic thrombosis of the sinuses, the previous clinical history would establish the condition of cerebral anemia beyond a doubt. A long-continued exhaustive disease, characterized by ema- ciation, great prostration, a weakened heart, probably a sub- normal temperature, dilatation of the pupils, eyes sunken in their sockets, half-closed lids, in very young children a de- pressed fontanelle, followed by apathy, somnolence, coma, and death, together with the post mortem evidences of anemia and shrinkage of brain-mass; thickening and stasis of blood in the venous sinuses, and sub-arachnoid effusion would complete the clinical history and post-mortem appearances of a case of hy- drocephaloid disease. But even such an array of symptoms would not warrant an absolute diagnosis during life, to the exclusion of marantic thrombosis of the cerebral sinuses. If however, motor disturbances either of a paralytic or convul- sive character should be added, the presence of the latter com- pl.cation would be freed, in a measure, from ambiguity.1 It is nevertheless true that, occasionally, symptoms of brain-irri- tation co-exist with all the usual objective and subjective phe- nomena of marantic thrombosis, whilst the post-mortem discloses only-the conditions usually found in the hydrocepha- loid disease. The two affections so often co-exist, and both are so alike in their precursory symptomatology, that it is not possible always to make a positive diagnosis of either to the exclusion of the other. Nor is the differentiation a matter of undisputed practical utility, except so far as it enables the practitioner, in the case of marantic thrombosis, to express a hopeless, and in the case of hydrocephaloid disease a less hopeless prognosis. Marantic thrombosis may be the primary or a superadded lesion. That is, primary or secondary so far as regards the 1 In thirty-eight observations of final convulsions in cachectic children, Bouchut found thrombosis of the sinuses in thirty-five cases, and in three, overfilling with blood and encephalitis. in Fatal Cases of Dysentery in Young Children. 7 consecutive development of the intracranial lesions which are usually present in fatal cases of the hydrocephaloid diseases and of cerebral thrombosis. General anemia, waste, thicken- ing of the blood, a weakened heart, and brain-anemia and shrinkage, are the constant premonitory and causative condi- tions. Whether venous stasis from mechanical obstruction to the return current of the blood is ever a cause is a disputed question. Thrombosis may be single or multiple, and the obstructed channels may be partially or completely occluded. Stasis and clotting of blood in the sinuses, and effusion (when secondary to the formation of these tibrinous masses, as undoubtedly they are in a majority of cases of thrombosis), vary in extent according to the locality of the masses and consequent inter- ruption to the venous circulation. The amount of fluid in the cavity of the arachnoid (Nothnagel) and ventricles is not always increased. The cure of thrombosis of the sinuses of the dura mater is not probably within the resources of medical science. The few reported successful cases were most likely instances of mistaken diagnosis. It is only during the premonitory stage, when conditions which favor the development of thrombi are present, that treat- ment is of any use. In such cases the indications are expressed in exhaustion, weakened heart, and thickening of the blood. Stimulants, tonics, and diet are the resources at command. These must be employed promptly and vigorously. Unfortu- nately, it too often happens that the obstacles to nutrition are insurmountable, and treatment proves unavailing. With each recurring observation of final convulsions in dysentery, I have mentally reviewed and compared the man- agement of the case, hoping to discover the error which might be avoided in subsequent cases. Sometimes it has seemed that stimulants were too long delayed or inefficiently employed ; at others, that they were too lavishly used and too little atten- tion was given to the diet. In very young children, the pulse, condition of the anterior fontanelle, and symptoms of collapse, are safe guides in regard to the use of stimulants. After the closure of the fontanelle, the pulse and state of exhaustion constitute the only criteria by which the administration of 8 Busey; Thrombosis oj the Sinuses of the Dura Mater. stimulants can be regulated. I apprehend error more often consists in an inefficient rather than in the excessive adminis tration of stimulants. “It is better,” says Jacobi, “for chil- dren to take in the course of the day three or six ounces of brandy and ten or twelve grains of camphor . . . than it is for parents to bury them the next day.” Delay in commenc- ing their use is perhaps a more frequent mistake. Stimulants withheld until collapse threatens immediate death, accomplish,, as a rule, little more than the prolongation of life for a few hours. But, after all, nourishment constitutes the main reli- ance. Biood impoverishment progresses with extraordinary rapidity in dysentery. To counteract and stay the develop- ment of complications incompatible with life, believed to be the successive results of devastation of the blood, nutrition must be maintained during the acute stage of the disease, and not neglected or deferred until exhaustion is so far advanced and the blood has become so impoverished that digestion and assimilation are physiological impossibilities. The proper alimentation of sick children is one of the most complex problems of the present day. The routine dietary of the nursery and sick-chamber indiscriminately and uniformly supplied to every sick child and to every disease, without re- gard to the demands of the animal economy and to the dietary and digestive idiosyncrasies of the patient, is as reprehensible as routine medication without a knowledge of the nature and progressive stages of the morbid process. Death demonstrates failure, but recovery oftentimes falls far short of establishing the value of the treatment.