The treatment of wound shock / (instructions produced by the Medical Research Council Committees on Traumatic Shock and on Blood Transfusion, in co-operation with the Army Medical Service).

Date:
1944
Catalogue details

Licence: Public Domain Mark

Credit: The treatment of wound shock / (instructions produced by the Medical Research Council Committees on Traumatic Shock and on Blood Transfusion, in co-operation with the Army Medical Service). Source: Wellcome Collection.

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    OTHER COMPLICATING FACTORS Fat embolism.—Blockage of pulmonary capillaries by fat globules from injuries of the long bones and limbs may contribute to the development of.a special form of circulatory collapse. Symptoms may develop after an interval of 6-72 hours from the time of injury. There may be cerebral symptoms, varying from irritability to coma, and petechiae in the skin, resulting from passage of fat globules through the lungs into the general circulation. Collapse from fat embolism does not respond to transfusion. The condition may be suspected if the cervical veins become engorged during transfusion. Toxic Gases. —Lung irritants, such as phosgene, cause delayed pulmonary oedema. In severe cases, the blood becomes concentrated and the patient passes into a state of circulatory collapse, with a rapid, feeble pulse and a clammy skin. The failure of the lungs to absorb oxygen makes this type of ‘shock ”’ particularly dangerous, but the cyanosis may be detectable only on the lips and the tips of the ears. The exposure of large areas of skin to vesicants, such as mustard gas or lewisite, may also cause haemoconcentration. This may be partly due to local fluid loss, but is mainly due to the effects of the poison after absorption into the general circulation. The effects of these substances are described in the Medtcal Manual of Chemical Warfare (H.M. Stationery Office, London, 1943). Severe carbon monoxide poisoning per se can produce a state of hypo- tension. The history of exposure to explosive or exhaust gases in a confined space—and the accompanying features, such as mental confusion, glycosuria, patchy pulmonary atelectasis—help in making the diagnosis. The cause of the low blood pressure is not completely understood. Infections.—Severe and overwhelming bacterial infections are well known to produce a fall in blood pressure. In abdominal wounds, peritonitis may be responsible. In muscle wounds, an infection may be established within a few hours, e.g. gas gangrene. Infection also complicates burns. Low blood pressure in such cases usually does not respond to transfusion, or the response is in- complete and transient. Anaesthesta.—Anaesthesia may add considerably to the complexities of the circulatory depression in the injured state. Patients who are “‘ shocked ’’, or who have just been resuscitated from ‘‘ shock’’, are peculiarly susceptible to the action of anaesthetic drugs, and relatively small amounts of any anaesthetic will provide adequate anaesthesia in such cases. The normal circulatory adjustments to change of posture are modified under general anaesthesia, and sudden alterations may lead to cerebral anaemia. Chloroform has a toxic action on the myocardium, especially in conditions of anoxia, and its use is likely to be followed by a high mortality in “shocked” patients. With increasing concentrations of ether, vaso-dilatation may become a factor leading to a further fall of blood pressure. If anoxia is allowed to accompany nitrous oxide anaesthesia, this will lead to further depression of the respiratory and vasomotor centres in the “ shocked.”’ patient. Respiratory depression, with consequent anoxia, may follow excess of pentothal sodium or hexobarbitone. As spinal and splanchnic anaesthesia lower blood pressure, they are contraindicated. Large-scale regional anaesthesia may cause vasodilatation of a whole limb, the possible effects of which should be borne in mind. Local anaesthesia is not known to have any deleterious effect in the ‘“ shocked” patient. (For further details regarding anaesthesia in “‘ shocked ”’ patients, see p. 16.) Dehydration.—After haemorrhage, extravascular fluid is drawn into the blood as a compensatory mechanism. Where, however, the subject is already dehydrated from any cause, this mechanism may be relatively ineffective, and the condition of the circulation may be made worse, e.g. by vomiting in abdominal injuries. ®
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