SHOCK and COLLAPSE. A severe injury which is not sufficient to kill may yet so derange the mechanism of the body that even a casual observer can correctly judge how little extra hurt would be necessary to cause death. In lesser degrees of in jury a trained observer is able to detect derangements which must be regarded as early stages of the more serious conditions which compel observation. The name given to this depressed condition of the body is "shock" and when consequent on injury it is known as traumatic shock.
Shock has been studied chiefly in connection with injury and many would limit use of the term to the results of trauma. It is undeniable however that conditions of the body very similar to those produced by severe external injury may follow various accidents of disease, e.g., perforation of a gastric ulcer or stran gulation of a coil of intestine—so that it is wise to take a broader view of the subject. This is the more necessary since Dale has shown that injection into the body of minute doses of histamine— a protein decomposition product—will produce an almost exact simulation of shock. Similar symptoms may also be produced by the entry into the circulation of poisons formed in obstructed small intestines, or of products of muscle-disintegration after injury, or of bacterial products in peritonitis. It is convenient therefore to apply the term shock to the common state and to designate the particular type by a qualifying adjective, e.g., traumatic, toxic, protein or haemorrhagic shock. The word col lapse is rather loosely used to indicate the same condition as shock. Various contradictory and unsatisfactory efforts have been made to distinguish between shock and collapse. There is no doubt that collapse suggests something rapid and a close approximation to the common significance of the term would be "the rapid onset or aggravation of the symptoms of shock." The symptoms of severe shock are very characteristic and con sist chiefly of a failure of the peripheral circulation with ac companying (and partly consequent) diminution of all the meta bolic processes of the body. There is in addition some increased activity of the sympathetic system as shown by the sweating and dilated pupils. The affected person is usually pale or livid, the extremities and nose cold, the pulse small and weak, and fre quently more rapid than normal. The blood-pressure is as a rule
lowered and tends to diminish as the condition progresses. The mental processes are commonly sluggish and the muscles relaxed. The secretions are diminished with the exception of sweat which may be poured out in great quantities. Though pain itself may produce shock yet in severe cases of shock, pain is usually not a complaint. The temperature is usually subnormal, registering 95° or 96° F. The clinical measure of the degree of shock is usually made by an estimation of the blood-pressure. In severe shock the systolic blood-pressure usually goes below ioomm. of mercury and sometimes drops to 8o or even 6omm. Recovery rarely takes place if a lower register than somm. is reached. Sometimes the systolic pressure does not fall so low but the pulse-pressure (difference between systolic and diastolic pressures) drops from the normal 5o down to as little as 2omm. These measurements afford a ready proof of circulatory failure.
Though in well-defined shock all the indications are present there are many occasions when one or more of the classical symp toms are wanting. Occasionally a slow pulse may accompany even severe shock whilst very obvious appearance of shock (sub normal temperature, sweating, pallor) may exist with only a slight or even no fall in blood pressure. Mental dullness is another rather variable factor for in many cases of toxaemic shock the mind may be very alert.
The pathology of shock has been the subject of much research and difference of opinion. Most of the experimental work has been concerned with traumatic shock and has been performed on animals. Clinical work has been concerned chiefly with shock following operation—a particular type of traumatic shock. It is agreed that prolonged over-stimulation of penpheral nerves will cause shock in proportion to the intensity of the stimulus and the number of nerve endings involved. Crile showed that if the nerve was anaesthetized so that the nerve impulse could not pass, then shock was diminished. He thought that shock resulted from exhaustion or inhibition of the vasomotor centre in the medulla whereby blood stagnated in some of the smaller paralysed and dilated arterioles, and the circulation in the vital centres be came insufficient. It has since been shown that the vasomotor centre is not paralysed in shock.