All of these symptoms may develop in twelve to twenty-four hours, or it may take several days. If there is no spontaneous disappearance of the threatening symptoms, or if operative interference is not resorted to, the symptoms of carbon dioxide poisoning conic on, and the stage of asphyxia is entered (von Rauchfuss).
The patient grows weaker and the activity of the accessory muscles of respiration lessens. The restlessness is followed by an ominous calm. The breathing becomes accelerated, more superficial and the dyspncua, seems to lessen, but the deathly pallor of the skin has a cyanotic tint. The features are drawn, the nose is pinched and prominent and the forehead is covered with a cold sweat. The extremities grow cool. The pulse may have the paradoxus type, it is rapid, thready and finally not countable. The patient falls into a dreamy doze from which he is roused time and again by the asphyxia, starting up with an expression of great anxiety. From time to time more severe attacks of dyspncea set in, without, however, causing a marked reaction. This condition persists or tracheal rattle comes on, and life ebbs away slowly after a more or less protract ed agonal period, with advancing paralysis of the centres of respira tion and circulation.
The course is not so severe in all cases. Some patients have only aphonia and mod erate dyspn ce a, but these may persist for weeks or exceptionally for months. Even the severe cases may re cover (a bout one sixth) from the stage of stenosis, by an in crease in the mucous secretion tending to dislodge the mem brane. Like the local symptoms, the symp toms of specific gene ral intoxication also show great variations. In the advanced stage of the disease it is difficult to sepa rate the action of the diphtheria-toxin from that of the carbon dioxide intoxication.
The successful outcome of operative interference depends first on how far the local process has advanced in the air-passages; and next, on the degree of general intoxication, especially on the extent to which the heart is capable of doing its work,—this influencing in no small degree the next important element, the disposition of the deeper air-passages to a primary diphtheritic infection or to a secondary infection with pneumobacteria (lleubner). If the bronchial tree is already involved at the time of operation, unless the fibrinous exudate becomes melted away by prompt administration of the antitoxin, the outlook for recov ery is very dark and the operation is not followed by improvement in oxygenation, the expectoration through the tracheal cannula is weak, respiration remains superficial and rapid, cyanosis and depression in crease and death follows in a few hours or days. If the process has been limited to the larynx and trachea, the symptoms of carbonic acid intox ication disappear after the operation and there remain only the effects of the toxin. The outcome is then practically dependent on the time of administration of the antitoxin.
Sometimes, in about half of the cases not treated with antitoxin, after the temporary success of the operation and even with a falling temperature, there comes a turn for the worse due to a descent of the fibrinous inflammation to the bronchial tree, involving in sonic cases the smallest bronchi. Its onset is marked by an elevation of temperature. Respiration becomes more superficial and accelerated, forty to eighty to the minute. Inspiratory recession is seen at times. The breath sounds over the lower lobes are weak or inaudible, over the upper lobes they are whistling, sibilant, coarse and accompanied by occasional riles. The further the process advances, the greater is the area of the lung shut off from respiration, increasing by so much the more the carbon dioxide poisoning to which the patient ordinarily succumbs in a day or two.
Far more frequently the fibrinous proceSs stops at the bifurcation of the trachea and the bronchial tree is subject only to catarrhal inflam matory processes, bronchitis, capillary bronchitis, lobular and pseudo lobar pneumonia. These are caused either by a diphtheritic infection, with the bacilli demonstrable in the affected parts, or by a secondary, non-specific infection with pneumobacteria or the pyogenic cocci. These latter infections are rendered possible through the resistance of the or ganism being lowered by the general weakness and the diphtheritic toxaemia, and are favored by the lessened expectoration with stasis of the mucus.
As in fibrinous bronchitis, these processes are accompanied by in creased fever which continues rather high and with only slight remissions throughout the duration of the illness. The breathing again becomes superficial and accelerated and, like the cough, is painful. Dyspncea and carbon dioxide poisoning are marked in the severe cases, like descending croup. Auscultation and percussion give no special signs. After a preliminary oedema of the lungs, death follows in collapse, or else there is a protracted course lasting long after the primary diphtheritic infection is overcome.
Sometimes serous or purulent pleurisy may arise to complicate the conditions. In other cases the diphtheritic infection produces a dark, hemorrhagic, infarct-like infiltration of the lung. In such cases there are found small, circumscribed areas of dulness over which bronchial breathing and scattered riles are heard. If the lung parenchyma becomes broken down, cavernous breathing and bubbling riles are heard, followed by septic fever. a putrid odor to the breath, and death. Another possible affection of the lung, which is also accompanied by very high fever and symptoms of widespread pulmonary involvement, is caused by the aspiration of foreign bodies such as particles of food. This is seen especially in operative cases and has as sequels abscess, gangrene or empyema.