A certain amount of capillary haemorrhage generally accompanies all larger bleedings. The explanation of this seems to be that the pressure of blood produces such obstruction of the vessels around, that frequent leakage occurs from the capillaries. In thrombosis of the sinuses and veins there is also capillary haemorrhage (see above). Again, embolism may cause capillary haemorrhage, and, as we have seen, the blood is often mixed with the softened brain tissue. Septic embolism, as in ulcerative endocarditis and pyaemia, leads to capillary haemorrhage. Lastly/we may have leakage from the capillaries in scurvy, purpura, leukaemia, and other morbid states of the blood.

In capillary haemorrhages the collections of blood are generally small in size, forming a congeries of red puncta. But if very frequent and closely set they may run together and form a considerable effusion.

Appearances Of The Brain In Haemorrhage

The appearances presented when a person dies soon after the occurrence of haemorrhage are sufficiently characteristic. The effused blood increases the contents of the skull, and in order to its accommodation there must be some displacement and crushing of the brain substance. If the haemorrhage be at all extensive we find on opening the skull that the corresponding hemisphere is bulged outwards and perhaps projects beyond the middle line. The convolutions are more or less flattened, and there is a certain dryness and glazing of the surface which indicate that all available fluid has been absorbed to make room for the addition made to the contents of the skull. These are all indications of increased pressure within the skull, and during life this increase of pressure causes symptoms referable to the brain as a whole or to parts removed from the seat of haemorrhage. It sometimes happens that the appearance of blood in the membranes suggests the existence of haemorrhage before the brain is laid open, and this will be especially the case when rupture of an aneurysm of a larger artery or thrombosis in the sinuses has been the cause. On cutting into the brain substance the appearances will vary to some extent according to the cause and extent of the haemorrhage. If there are numerous small haemorrhages closely set there will be much softening of the brain, and the brain substance will be mixed with blood. If the haemorrhage be large the blood will be more pure. In any case the blood produces softening in the parts around, which may be stained with the blood colouring-matter. As already mentioned, there are usually red spots from capillary haemorrhage around the clot. The clot itself is mixed with the debris of brain substance, and the internal wall of the cavity in which it lies has an irregular character.

If the patient die almost immediately, the. clot is exactly like an ordinary gelatinous post-mortem coagulum. But if he survive a day or two, the clot has already drawn together somewhat and become firmer and has more of a brown colour. This is sometimes peculiarly manifest at the peripheral parts, so that a kind of capsule may be formed of condensed fibrine.

In washing away the clot from a cavity made by a haemorrhage one often isolates many small arteries with round knobs at their extremities. These are arteries which have been torn across by the accumulating blood. The torn arteries have withdrawn within their sheaths, and these latter have become distended with little plugs of blood which have, in the manner already described, contributed to the stilling of the haemorrhage. These little swellings may be readily mistaken for miliary aneurysms.

The obsei-vations of Durck are interesting in regard to the changes which occur in the blood-corpuscles and their pigment after haemorrhages in the brain. These changes, which have been already referred to, consist mainly in swelling up of the red corpuscles, discharge of their pigment, and the conversion of the latter first into hasmosiderin, and then into haematoidin. The presence of hemosiderin is detected (either in the fresh state or in sections made after hardening in Miiller's fluid or alcohol) by the use of dilute solutions of ferrocyanide of potassium and hydrochloric acid, in which sections may lie for several hours. From his experiments in the lower animals, a kind of timetable has been constructed by Durck, which may approximately be applied to human pathology. From the second day after a cerebral haemorrhage the corpuscles begin to swell and give up their pigment. On the third day amoeboid cells containing red corpuscles are first seen. These red corpuscles undergo shrinking from the fifth day. On the sixth day there is the first appearance of haemosiderin, which is diffused in the tissues. On the tenth day the haamosiderin is collected into the contractile cells, but still in solution. On the twelfth it begins to become granular inside the cells. By the eighteenth the granular pigment begins to get free by disintegration of the cells. About the twenty-fifth day there begins a finely granular precipitation of the pigment and loss of its iron, which by the thirty-fifth day has made essential progress. From this time the hsematoidiri increases, and by the sixtieth day it is the only form of pigment present, and it is entirely extra-cellular. By this time crystals, which are identical with those of bilirubin, may be present.

Disposal Of The Clot. The Apoplectic Cicatrix And Cyst

The pigment of the coagulum is disposed of in the manner indicated above. It first stains the surrounding brain tissue, in which we often find a rosy or rusty colour. It finally assumes the form of haematoidin, crystals of which are frequently met with in connection with old haemorrhages, even years after their occurrence.

The further disposal of the blood-clot is effected by a process analogous to the organization of a thrombus in a vein or artery. The process is one of chronic inflammation with the result that a vascular tissue is produced, which, forming around the clot, takes part in its absorption by penetrating its substance, while also forming a capsule and fencing it off from the surrounding tissue.

Through time the contents are absorbed and there may result, as in the case of softening of the brain, a Cicatrix. In many cases, however, the absorbed matter is replaced by clear fluid and a kind of cyst is the result, the so-called Apoplectic cyst. The cyst is not merely a sac containing fluid, but it is generally intersected by connective-tissue trabecular in the form of a network. It is indeed more an cedematous cicatrix than a cyst. It has already been noticed that similar cysts and cicatrices occur as a result of softening of the brain. These latter, however, do not commonly show blood crystals in their walls, whereas the true apoplectic cyst may present them even at a late date.

The apoplectic cyst may be compared in its origin with a cicatrix; it arises by the formation of connective tissue and fills the place of tissue lost, and it is only because, being situated in the midst of the brain substance, it does not readily contract that we have a cyst rather than a cicatrix. In this respect it may be compared with the organized thrombus as shown in Figs. 29 and 30, in which the shrinking of the new-formed connective tissue produces dilated blood-vessels, whilst here it is merely spaces which are produced. If the haemorrhage has been near the surface of a ventricle or of the brain itself we may have a cicatrix; or a cyst, by thickening of the trabecular and gradual drawing together of the parts, may be converted into a cicatrix. In the case of cicatrices occurring thus on the surface of the brain the soft membranes are depressed and puckered and firmly adherent to them. The cicatrices, like the cysts, often present some remains of blood-colouring matter.

Literature

Durand-Fardel, Arch, gen., 1844, and Traite des maladies des vieillards, 1854; Burrows, Disorders of cerebral circulation, 1846; Copeland, Nature and treatment of apoplexy, 1850; Nothnagel in Ziemssen's Encyclop. Aneurysm of larger arteries - Smith, Dublin Quart., iv., 1847; Ogle, Med. times and gaz., 1866, i.; Church, St. Barth. Hosp. Rep., vi., 1871; Tufnell, Dubl. Quart., xv., 1853; Holmes' Syst. of surg., Art. "Aneurism"; Ponfick, Virch. Arch., lviii., 1873; Coats, Glasg. Med. Jour., v., 1873 (with list of 87 cases and tabulation of results) and Trans, of Internat. Med. Congress, 1881, i., 415. Aneurysm of nutrient arteries - Charcot et Bouchard, Arch, de physiol., 1868, i., and Charcot, On senile dis., Syd. Soc. transl., 1881; Turner, Path trans., xxiii., 1882; Eichler, D. Arch. f. klin. Med., xxii. Blood-pigment in cerebral ha-morrhage - Durck (with references), Virch. Arch., vol. cxxx., p. 29, 1892.