CIRCULATORY COLLAPSE AND WOUND SHOCK*

By J. McMICHAEL, M.D., F.R.C.P.Ed. Reader in Medicine, University of London

The problem of death from grievous bodily injury without damage to vital organs cannot be better introduced than by quoting Crile's classical description of such a case. " the The patient was young and strong ; every organ of body was sound : he had lost but little blood, although both legs had been crushed by a locomotive. As I watched him slowly sink into death, the mental and physical prostration, the cold sweating skin, the fading pulse fixed the picture in my ? mind. Autopsy revealed no lesion in any vital organ. . ? As I watched the pulse fading so inevitably, I thought that death was due to want of circulation. . . In civil life this tragic picture is seldom seen, but war has once again made shock a major problem of practical medicine. The clinical picture of pallor, rapid thready pulse of loW pressure, and the subnormal temperature is similar to that in severe haemorrhage, and the pioneer work of N. M. Keith in the last war established that the basic fault was similar in haemorrhage and traumatic shock. Both are the result of a depletion of the volume of the circulating blood. Basic physiological knowledge enables us to piece together a reasonably complete picture of the sequence of events in the circulation once the blood volume is reduced. Appreciation of these now commonplace facts saved many lives towards the end of the last war, and with the beginning of this war we have been much better prepared to face the problem of shock- The knowledge culled by the efforts of the Shock Committee of the last war was at our disposal. Transfusion was obviously to be the basis of all treatment, and the Blood Transfusion of Depots set up throughout the country have been a bulwark of great strength in combating the tragic circulatory sequels grave injury. * Honyman Gillespie Lecture delivered in the Royal Infirmary) Edinburgh, 28th November 194?- I

Circulatory Collapse and Wound Shock In spite of these measures, however, mortality from shock stlH remains high. In spite of surgical skill and assiduous attention to transfusion, our efforts may frequently be made in Vain. Blood transfusion saves many patients, but seems to fail ln others. Three principal questions are therefore raised. V1) Are our transfusions adequate ? (2) Are they given too a e ^ (3) Are there other, as yet unknown or inadequately appreciated, factors at work which are not met by the standard methods of treatment ? The challenge to medical science is ?rave and urgent.

The Physiological Mechanisms of Shock Disproportion between the Content and Capacity of the Vascular System (Reduction of Blood Volume or increased capacity of the smaller blood vessels)

! Diminished Pressure in Great Veins near the Heart

Decreased DiastolicI Filling of Heart I Decreased Cardiac Output {Starling''s Law) I Fall in Blood Pressure Decreased Pressure in Carotid Sinus

J I " " Acceleration.1 of Pulse Compensatory Sympathetic Vaso- constriction and Visceral Pallor) i (Skin stimulation) i Sweating (Sympathetic Owing to the somewhat unexpected course of this war, vv studies could be made in cases of shock during the first * ^e^r- During that time we made basic studies mainly on types of circulatory collapse, usually from haemorrhage. ^nerecent air-raids, however, have broadened our clinical and a description of three types of case will serve 0 ^xperience,^lustrate the major problems. Thereafter I shall discuss

The team on Shock at Hammersmith Hospital includes ^ working E. p. Sharpey-Schafer, Dr E. G. L. Bywaters, Mr D. K. Hill and D. a service of Beall ; Dr J. Clegg and Professor J. H. Dible maintain ??d and recalcified serum saline for transfusion. To these colleagues I e used for this y express my indebtedness for much of the material lecture. N-s- IV., XLVIII. NO. 3 161 M L J. McMichael of experimental observations and venture on an integration the knowledge gained.

i. Shock due to Loss of Plasma Constituents

Case i. A male, aged 16, was buried under a collapsed house for eight hours before admission, the left thigh being" pinned down by a heavy load of masonry. The clinical course is illustrated in the adjoining chart (Fig. i).

" " Fig. X.?Shock due to Plasma Fluid Loss.

On admission the- systolic pressure was 140 mm. .Hg- Superficial abrasions were present on the left thigh, but apart from some limitation of movement, apparently due to pain, there was no evidence of any injury other than crushing of the soft tissues. He fainted on getting out of bed a few hours later, but no observation of blood pressure was made. Nine hours after admission he collapsed, the blood pressure falling to 40 mm- Hg. The haemoglobin had risen to 140 per cent., and the 162 Circulatory Collapse and Wound Shock

P'asma proteins were also concentrated to 9-1 per cent. The superficial abrasions had become whealed, and it was obvious at the thigh was more swollen. It was therefore assumed at the capillaries of the injured area had become permeable protein, and that an albuminous fluid was leaking from the o?u. This idea was observations W supported by subsequent lch showed that the oedema fluid in the thigh contained 9 per cent, of protein, while the albumin/globulin ratio of e plasma was altered in favour of globulin. An infusion of serum-citrate reduced the haemoglobin to *4 per cent, with restoration of the blood pressure. Subse- quently the course seemed satisfactory for about a day, but Welling of the thigh increased and the haemoglobin again to 135 per cent, with a fall in blood pressure to ^oncentratedrnm. Hg ; serum infusion again restored the circulation 0 a more normal state. Throughout the second day the left foot had been giving ause for anxiety, as it had become increasingly cold and the j^salis pedis pulse had become feeble. By the third day the an^eS *nc*P*ent gangrene were present. It was thought that th had resulted from pressure of the oedema fluid in the thigh an operation was undertaken to relieve this. Incisions were |||ade into the oedematous thigh which seemed partially effective Sieving the circulation in the limb, as a feeble pulse became Perceptible in the posterior tibial artery. the second also other had made th -^Ur*n? day symptoms h^11" aPPearance- The patient began to vomit and the . ?men was so tense as to rouse the of an internal " suspicion with peritonism." The urine output was scanty. ls ^JUry. clinical picture became dominant the third and u by day, sPite of all the measures which had been tried, circulatory apse occurred, temporarily alleviated by oxygen through ?L.B. mask, leading to death. So far as the picture of shock is concerned, this case .,Ustrates clearly that the loss of fluid from the plasma into e . Jnjured area may be the main factor. A biopsy of the lnJUred muscle at the operation showed patchy necrosis of the Muscle with a polymorph reaction. This aseptic inflammatory reaction may also have contributed to the picture in allowing some pooling of blood in the injured muscle. The immediate CraPeutic response to serum replacement, however, indicates at " plasma loss was the principal factor. 163

^ ? J. McMichael

2. Shock due to Haemorrhage CASE 2 (Fig. 2).?Male, aged 32. Admitted soon after injury with a compound fracture of right ankle, swelling of the left thigh with punctured wound, and punctured wound of the arm. External haemorrhage was negligible- His condition on admission was quite good, blood pressure being 110, pulse 100, and Hb 86 per cent. He was treated by warmth, morphia, and raising the foot of the bed, but after about one hour the blood pressure fell to 70, the

Fig. 2.?Shock due to Hemorrhage.

Hb remaining much the same. Owing to the arm wound, the blood pressure could not be followed all the time, but by palpation there was clearly a rise of blood pressure after a litre of serum. The level of the Hb after serum suggested that haemorrhage had probably occurred; and so it proved, incision into the thigh revealed a large quantity of blood in the thigh and buttock. The further haemodilution gives some idea of the extent of the original haemorrhage. This case illustrates that haemorrhage into the injured area may be the main primary factor. After haemorrhage, plasma 164 Circulatory Collapse and Wound Shock Volume is made up by withdrawal of tissue fluids. We all know after severe gastro-intestinal haemorrhage in man, blood i?n to the extent of 15 or 20 per cent, (haemoglobin falling m 100 . to 80 per cent.) takes place quickly, but thereafter ls a slow process, a day or two before the ^ long, taking n^oglobin reaches a level (e.g. of 50 per cent.) which gives us \ny indication of the initial volume of blood lost. In traumatic an k?Ur or two after the injury, haemoglobin levels of 8o? Per cent. or so are with the idea , therefore quite compatible simple haemorrhage into or from the injured area may be the primary cause. 3* Shock due to Haemorrhage combined with Plasma Loss Case 3 (Fig. 3).?A woman aged 56 was admitted following Severe crushing injuries involving a compound fracture of the

Fig. 3.?Shock due to Plasma Loss plus Haemorrhage. eft leg-. Blood pressure was 70/50, and the haemoglobin 100 per cent. 1600 c.c. of serum were given, and the blood Pressure rose to 140/90, with a fall of Hb to 72 Per cent- An h?ur and a half later the Hb had risen to 90 per cent. aSain, which meant that the serum given had been almost c?mpletely lost from the circulation. After further transfusion patient was operated on. It was found that the skin of the had been torn from the underlying fascia and a large pool N-S. IV., XLVIII. NO. 3 165 M 2 J. McMichael of blood had formed, containing several pints. In spite of further post-operative transfusion this patient died. That the two factors of haemorrhage and plasma loss may be mixed is thus indicated by Case 3. Plasma transfused may be rapidly lost as indicated by the failure to maintain blood dilution and circulatory improvement. This evidence of abnormal capillary permeability was combined with the operative demonstration of blood loss in a colossal haematoma- Quantitative Studies in Shock Leaving aside for the moment the biochemical observations in shock, let us turn to some quantitative observations on the circulation.

SYSTOLIC BLOOD PRESSURE. Fig. 4.? Relation between Blood Pressure and Lowered Blood Volume.

Keith's estimations of blood volume were made with a dye ?vital red?the size of the molecular aggregates of which were considered to be such that they would remain in the circulation. This method is of great value in normal subjects, but in cases of shock, in which we have just shown that the capillaries are often unduly permeable to large protein molecules, it seems possible that his measurements were fallacious. It was therefore necessary to review the relationship between blood volume and the degree of circulatory collapse. A neW and ingenious spectrophotometric carbon monoxide method was developed in our laboratory by Mr D. K. Hill. This was applied to a number of patients with circulatory collapse resulting from haemorrhage. A further development of Hill s 166 Circulatory Collapse and Wound Shock Work involved the use of a transfusion of concentrated " corpuscles the dye." This is probably the most ideal method of crmining- blood volume, as it enables estimations to be ^ade with a material which does not leave the circulation r?ugh permeable capillaries, and which is at the same time nehcial to the patient. Using these methods (Fig. 4) we Und that the reduction in effective circulating blood volume may be extreme?down to 30-40 per cent, of the normal in with a blood pressure of 60 mm. Hg. In such cases ?^Seseith usually found the blood volume to be 60 per cent, of SO readings appear to us to have been too high. en the blood pressure is down to mm. the blood 0 90 Hg, ume has usually been reduced to about 3 litres from the n?rmal value of 5 litres.

TABLE I Effect of Blood Loss on Cardiac Output in Man

Normal at = Rest Recumbent 4 litres/mins.

A.V.Oo B.P. Pulse. Hb. Cardiac diff. Output.

acute gastro-intestinal 110/60 96 45 48 5-00 litres 2 p "^ding over a week ecent haematemesis 81 120/65 94 94 2-96 ? 3 Recent severe haematemesis 90/70 120 84 I5S

Cardiac output standardised to 02 consumption rate of 240 c.c./minute.

We have already mentioned that the cardiac output is lowered by the reduction in venous and venous return ^hich filling results from depression of the circulating blood volume. ?^?easurements made in cases of indicate that at a blood haemorrhage pressure of 90 mm. Hg the cardiac output may be less than half the normal. If this is associated, as it often is, low ^ith haemoglobin values, the of oxygen to the tissues supply may be in severe jeopardy. Owing to the sluggish c*rculation the haemoglobin in the circulating blood returns the lungs practically fully reduced. If these preliminary figures are substantiated, severe oxygen lack ts bound to occut when the blood pressure below 90 mm. in sh?ck. falls Hg secondary The classical observations of Cohnheim and, latei, of andis, have shown that severe and prolonged oxygen depriva- tion leads to abnormally great capillary permeability. J. McMichael

A synthesis of our data so far may now be attempted. " " 1. Trauma leads to blood loss and plasma transudation in the injured area. 2. As a result of the lowering of plasma and blood volume, a severe depression of cardiac output occurs resulting in oxygen deprivation. 3. Oxygen deprivation leads to a further increase in capillary permeability. This makes treatment difficult, as plasma is not retained. In favourable cases, however, the deleterious effect on capillary permeability is reversed if a good state of the circulation can be maintained. Early treatment and assiduous and continuous attention are necessary in the management of shock to secure this end. If the serum trans- fused is not retained, as will be shown by rising haemoglobin and falling blood pressure figures, further transfusion must be given. The Pulse Rate in Shock

I have purposely evaded any reference to pulse rate up to this point. We all know the value of a rising pulse rate as

5

LU 3

60 80 100 120 140 160 PULSE RATE Fig. 5.?Relation between Pulse Rate and Blood Volume. indicating deterioration in cases of circulatory collapse, and in a general way this also holds in shock. A rising pulse rate corresponds to the fall in blood pressure and blood volume. The adjoining diagram (Fig. 5), however, indicates that racing pulse rates are seldom encountered even in severe shock. Pulses of 100-120 are common, but more rapid pulses are rare. 168 Circulatory Collapse and Wound Shock Slow pulses, however, are encountered and these do not exclude shock. Furthermore, the pulse may not fall much with the restoration of blood pressure in treatment. It often continues to be rapid for a day or two after the blood pressure has been restored to a satisfactory level.

Biochemical Changes in Shock An increased permeability of capillaries may be indicated a by rise in plasma proteins and a leakage of albumin from the blood. This has already been noted. Rising blood urea is common to a number of conditions of cardiovascular collapse, haematemesis, diabetic coma and the Crises of Addison's disease. High values are also encountered ln shock, but not so high as those in haematemesis. Scudder and his co-workers in New York have recently stressed the importance of rising serum potassium and falling s?dium and chloride. A survey of his work indicates that these changes only appear after the blood pressure has been at a low level for a long time. In many instances they are ante- mortem changes. The distribution of inorganic ions is normally s?dium and chloride extracellularly, and potassium and phos- phate intracellularly. As death approaches, it would appear that this important differential cell-membrane permeability is l?st, with resulting rise in serum potassium and fall in sodium. Suprarenal cortical hormone and sodium chloride injections have been recommended for the treatment of this change, but So far without much success. The essence of our therapeutics should be to prevent these changes occurring by the early treatment of shock.

" Toxaemia "

Case 4.?A man aged 30 sustained severe crushing iftjuries to both legs and the left arm. The haemoglobin rose to 160 per cent, and the oedema was widespread. After a course of four days similar to that in Case 1, terminal collapse occurred without further haemoconcentration. Vomiting was a pro- nc>unced feature in the last three days of life, and the patient developed a curious mental state in which drowsy disorientation alternated with periods of mental clarity in which the patient was acutely aware of the gravity of his illness. The urinary output became scanty, and the blood urea steadily rose towards 345 169 J. McMichael per cent., while the plasma chloride fell from 600 to 461 nig- per cent. Serum potassium was high from an early stage. The course of this illness was similar to that seen in some " cases of severe burns. The toxaemic" phase of burns, described by Professor Wilson, has been closely paralleled in our cases of traumatic oedema which follows prolonged crushing- Wilson has suggested that the transuded fluid may develop lethal properties. Our experience suggests that these bio- chemical changes result from profound renal insufficiency which is in some way dependent on the restoration of circulation through dead muscle tissue.

Nervous Factors in Shock Primary shock occurs immediately after an injury, and seems to resemble a very prolonged faint. The pulse is sloiv,

FEAR OR OTHER EMOTION.

ALTERATION OF THRESHOLD OF SENSITIVITY SO THAT V. M.C. BECOMES SENSITIVE EVEN TO NORMAL PRESSURE.

PRESSURE INCREASE IN \< CAROTID SINUS.

CARDIAC SLOWING Fig. 6.?The Mechanism of the Vaso-vagal Syndrome.

and the systolic pressure is low. This stage usually recovers with rest alone ; it is not necessarily associated with severe injury or even with any injury. The vaso-vagal mechanism described by Lewis is probably responsible (Fig. 6). It is 170

A Circulatory Collapse and Wound Shock

lrnP?rtant in that it is frequently observed among air-raid casualties, and it should be differentiated from severe secondary shock. It is possible, however, that it may persist until Sec?ndary shock develops and confuse the picture. The evidence that nervous impulses from the injured area ring about a reflex fall in blood pressure has not found much experimental support. The clinical application of this hypo- . sis, which should be local or regional anaesthesia of the area, has not met with any degree of success as treatment jnjured?r shock, although it may conceivably be the anaesthetic of choice in limb injury. Diagnosis The diagnosis of shock is best made by blood pressure and Pulse records, and by observations of the clinical state of the Patient. Of these, blood pressure records are all-important, as e pulse may be misleading and the clinical state may be simu- a ed by other conditions. The most important of these are :?

1 * Primary shock : this tends to spontaneous recovery. 2- Acute CO-poisoning. Patients may be admitted un- conscious from badly ventilated shelters when gas-mains have een ruptured or glowing coals used in an attempt at e heating. patients are a collapsed and cold, with low blood pressure, ut there no is sign of external injury. The history is important ln diagnosis. 3- Blast contusion of the lungs may produce an alarming PJcture of blood-stained froth at the mouth, but the blood Pressure is not lowered unless other injuries are present to cause shock. Therapeutic Considerations Shocked patients should be treated in a special resuscitation ^ard. General measures such as relief of pain, arrest of ^morrhage, warmth, raising the foot of the bed, and the administration of fluid are well known. I only wish to emphasise s?rne special points. l- Early and adequate transfusion is the sheet-anchor of treatment. In the accompanying table (p. 172) I have given s?me sample data. Blood, plasma or serum should be given until the blood pressure is normal, and if the blood pressure falls a?am further transfusions must be given. Modern observations ?n blood volume in shock indicate the gross inadequacy of quantities like one pint of blood. These patients may be nearly 171 J. McMichael

completely exsanguinated, and yet if blood is given adequately and promptly recovery can take place.

TABLE II Relation between Blood Loss, Volume Transfused and Degree of Recovery

Estimated Volume Transfused Percentage Result- Case Blood Loss. (Serum-Citrate or Replace- B.P. Rise. Final Litres. Citrated Blood). ment.

, 2*7 Death 4*? (slowly) 67 Imperceptible- n? I 3-o i-6 53 60-^140 Improvement maintained 2-6 66 6o->io6 Slow recovery- i-7 t0 Pulse 140-160 2 days f?r 3 3'7 2-2 60 6o->io8 Pulse 140 days. Recovery 1-4 I'l 79 40-^130 Immediate improvement (?) 2-2 3-5 100 (?) 6o->iiS Recovery (bleeding)

2. Oxygen may be raised to a concentration of 90 per cent, a in the lung alveoli by the use of a B.L.B. mask. This may be useful adjuvant in shock. It should certainly be used in any periods of delay, for example before transfusion is started. 3. Severe crushing injuries constitute a special problem- The danger to the limb circulation, and the risk of toxaemia make it important to limit transudation as much as possible. Crushed limbs should be bandaged and elevated to achieve this end. Once the toxaemic picture has developed as manifested by vomiting, diminished urinary output, rising blood urea and blood potassium, the therapeutic problem is very great. Even amputation of the damaged limb may fail to save life. Decap- sulation of the kidneys has not yet been tried. It may be that we shall have to find some biochemical index of the severity ' " of the damage to muscle, and resort to early prophylactic amputation. the Finally, we must remember that traumatic cases fall to surgeon for local treatment. The continued effort now being and made by surgeons and physicians, aided by^ biochemists physiologists, seems to be recreating a unity of purpose in the whole range of medical science. Let us look on this collabora- tion as a great gain for the present and a great hope for fuller development of the healing art in a not too distant future. 172 1