III. The puerperal state has been considered by Behier, Dubreuilh, and others with some degree of reason as one closely resembling a condition of traumatism. In fact, the raw surface with widely-open uterine veins and sinuses which exists so soon as the placenta is fairly separated is analogous to that of a limb which has just been amputated. The differences which present themselves are those which arise from the special state of the patient herself. During gestation, and particularly toward its terminal period, the relative quantity of fibrin to the mass of the blood is greatly augmented. According to Andral and Gavarret, this excess of fibrin may become so great as to reach a third more than the normal quantity. After delivery of the foetus and placenta involution of the uterus begins. This process lasts several weeks, and during this period the blood is filled with effete material. Besides these favoring causes of thrombosis which are special to the puerperal state and mark its blood-dyscrasia, we have the fact of loss of blood, both during and after confinement, as an efficient and well-known cause of this accident. According to Leishman,35 who cites Merriam, this is doubtless the reason why after placenta prævia cases of phlegmasia alba dolens are so frequently observed. Not only does Richardson consider the loss of blood as predisposing toward pulmonary thrombosis, but also syncope or exhaustion in other depressed states of the system. In some such instances, however, we must not ignore possible disease of the myocardium or compression from an abscess of the broad ligament (Charcot and Ball). The coagula formed in the femoral or saphena veins may sometimes extend into the iliacs, venæ cavæ, and become a frequent source of pulmonary embolism. Owing to the rapid softening of clots formed in the uterine veins during septic endometritis, we have a special cause of pulmonary embolism accompanied by toxic phenomena (Virchow). Several of the operations necessary in certain complications of this condition, such as application of the forceps, detachment of the placenta, etc., have been followed by pulmonary embolism (Massari). It is not remarkable that with so many predisposing causes of thrombosis blood-clot should be of frequent formation in the puerperal state.
35 System of Obstetrics, p. 710.
Phlegmasia and pulmonary embolism have been well studied on account of their gravity; the other situations of fibrinous deposit are very imperfectly known. Playfair36 believes that clots may form in the right heart and pulmonary artery, just as they may be produced in other portions of the venous system and under the influence of the same causes. This conviction is opposed to that of Virchow and Bertin,37 who hold that an embolus must be the starting-point of a blood-clot, and that without its presence it cannot form. Virchow, indeed, considers stagnation of the blood as the most essential condition of the formation of a coagulum. It would seem, however, that the action of the heart is so feeble in certain debilitated persons, or in diseases in which there is strong tendency to adynamia, that this objection is at least partially met. Certainly, as Humphrey38 has shown, the pulmonary artery, owing to its numerous divisions and the prominent angles it offers, is favorable to coagulation by its anatomical formation. Moreover, if coagulation may form around an embolus, why cannot similar causes which bring this about also occasion a spontaneous deposit of fibrin? The greater number of cases of pulmonary embolism in the puerperal state occur in young women not many days after confinement (Hennig, Luzzato). Occasionally a case is seen as late as the fifth week. Cases also occur, though exceptionally, during pregnancy. Playfair39 has endeavored to show, partly by post-mortem appearances, partly by the date of the accidents, the distinctions to be drawn between pulmonary embolism and pulmonary thrombosis. After the nineteenth day from the date of delivery the accidents are usually due to embolism, before this date to thrombosis. This would appear to be rationally explained when we consider that the degenerative changes which alter the vascular clot sufficiently to permit its transport from the place of its formation to a distant organ take a certain time to become effected. The causes of the pulmonary thrombosis are those which produce coagulation elsewhere in the vascular circuit during the puerperal state. Pulmonary embolisms are more frequent with women than men on account of affections of the uterus and the puerperal condition (80 to 66, Luzzato). In children pulmonary embolisms generally come from clots first formed in some one of the peripheral veins (renal, umbilical, diploe, etc.). Autochthonous clots in the pulmonary artery may be due to direct pressure from enlarged ganglia of the neck. The great number of pulmonary embolisms form in the vessels of the lower extremities. Thus far, thrombi have not been shown in the larger lymphatic trunks of the body.
36 "The Puerperal State," being Part V. from a Treatise on Midwifery, p. 50, Philada., 1882.
37 Des Embolies.
38 On the Coagulation of the Blood in the Venous System during Life, quoted by Playfair.
39 Lancet, 1867.
SYMPTOMATOLOGY.—The symptoms thus far observed of pulmonary embolism are not usually very full or accurate. Many of the cases occur so suddenly and fill the beholders with such dismay that clinical observations are imperfect. Opposed to this statement we note the fact that what pertains to pathology and morbid anatomy of pulmonary embolism is particularly complete. Nevertheless, for the sake of clearness and in view of accidents really observed, we may divide the cases into—1st, sudden, fatal form; 2d, grave form; 3d, benign form.
1st. Sudden, Fatal Form.—In this category should be placed those instances in which the main trunk or both primary divisions of the pulmonary artery have become wholly obstructed in a sudden, almost instantaneous, manner. Immediately the patient is a prey to the most intense dyspnoea and anxiety; the chest-walls rise and fall in an exaggerated degree and with great rapidity; the heart-pulsations are tumultuous and irregular; there is intense pallor of the face; a groan or cry is heard; there is a vain and brief struggle for breath; and death may occur before aid can be offered, with symptoms resembling those of asphyxia. These rapidly fatal accidents are always deeply impressive, but never so appalling as when they take place in convalescence, when everything appears to be going on well, and there is no reason to apprehend such an occurrence had not numerous recorded facts affirmed their verity. Such cases have been observed40 particularly after fractures of the lower extremities and during recovery after confinement.41 The accidents are not always asphyxic in character, even though they be equally sudden and destructive. According to Trousseau,42 this is true where the embolus is arrested in the right ventricle and is of sufficient size to cause stoppage of cardiac contractions and an attack of fatal syncope. In instances which are not mortal in a few moments, and where the gasping and struggling for breath continue during half an hour, an hour, or more, the excessive pallor gives way to a deeply cyanosed tint of the face. When the face assumes a livid purple hue it has been considered as proof of a condition of spontaneous thrombosis rather than embolism.43
40 Azam, 1re Mémoire, Gaz. hébd. de Méd. et Chirurgie, 1864; Observ. II., reported by Levrat.