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Home , Resuscitation, Surgical shock

Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from

Postgrad. med. J. (September 1967) 43, 592-598.

Resuscitation- W. G. PROUT R. VAUGHAN JONES M.B., F.R.C.S. M.B., M.R.C.P., M.C.Path. Surgical Registrar, Consultant Pathologist, St Peter's , Chertsey, and St Thomas' Hospital, London North West Surrey Group Laboratory St Peter's Hospital, Chertsey

THIS short account will be confined to the dromes with no common single clinical manifesta- management of circulatory failure in the first few tion. hours after reception of the patient in a Casualty Bloch et al. (1966) define as a state of Department. Where shock is due to trauma the progressive circulatory failure in which the cardiac cause will usually be obvious, but many shocked output is insufficient to meet tissue requirements cases brought to Casualty Departments suffer for nutrition, oxygenation or waste disposal. This from other in which circulatory failure definition serves to emphasize the basic patho- may be complex in origin. For this reason we have logical feature, that of defective tissue . also discussed non-traumatic causes. For the different forms of shock, further terms have been introduced. Shires (1967) has suggested Traumatic shock subdivision into haematogenic, neurogenic, vaso-

It is generally agreed that reduction in the genic and cardiogenic forms, but these are termsby copyright. circulating is the main factor in the without therapeutic implication. McGowan & production of traumatic shock. When external or Walters (1966) point out that clinically two internal haemorrhage takes place, the fluid lost is, patterns of circulatory upset are most often seen of course, blood. When there is extensive burning -cold and warm hypotension, terms an increase in capillary permeability leads to a first suggested by Grant & Reeve (1951, p. 225). massive exudation of plasma-like fluid with reduc- tion in the plasma and extracellular fluid volumes. Cold hypotension Crushing may cause not only frank This refers to classical traumatic shock charac- haemorrhage but also the accumulation of a terized by low (systolic pressure plasma-like inflammatory exudate in the damaged less than 100 mmHg), high rate (greater than tissues with reduction in the plasma volume and 100/min) low pulse volume and usually cold pale http://pmj.bmj.com/ hence the blood volume. extremities. Central venous pressure (CVP) is low. Reduced and peripheral Electrolyte changes arteriolar constriction are associated with this type After trauma in the normal subject and of shock. reduced renal sodium output are the rule, whereas This condition may be the result of oligaemia, renal output is increased. Plasma acute myocardial failure, pulmonary , sodium levels are reduced but this does not infection especially that due to Gram-negative on September 30, 2021 by guest. Protected indicate sodium depletion and is not an indication organisms, or pancreatitis. for therapy with isotonic or hypertonic saline (Sevitt, 1966). Plasma potassium levels may rise, Warm hypotension sometimes rapidly if there has been considerable Here the blood pressure is low with high pulse damage to muscle. If oliguria persists hyper- rate and full pulse volume, while the extremities kalaemia may necessitate the administration of are commonly warm and dry. CVP is normal or a resins or some form of (Gallagher & little reduced. Polak, 1967). In this type of shock the cardiac output is probably undiminished but there is a decrease in Terminology arteriolar tone. Shock, a term hallowed by some 200 years Warm hypotension is found in response to usage, defies precise definition, for it represents infection, pancreatitis, following treatment of cold not a single syndrome but a collection of syn- hypotension, in response to drugs, e.g. anaesthetic Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from

Resuscitation-fluid replacement 593 agents and barbiturate or phenothiazine group (a) Intravenous infusion overdosage, and in alcoholism. In the last two In the severely injured patient, particularly if groups of patients circulatory reflexes are blocked old or suffering from concurrent , monitor- (Barraclough & Sharpey-Schafer, 1963) and shock ing of the central venous pressure is desirable and may develop when they are subjected to relatively an intravenous should be introduced so minor traumata. that its tip lies in a great . It must be emphasized that these two states are If oligaemia and venoconstriction make per- not clear-cut subdivisions, and intermediates may cutaneous cannulation difficult, time should not be found: indeed, the patient may pass from one be wasted on a prolonged search for a suitable to the other during the course of an illness. vein; instead a cut-down should be performed. A 12-in. catheter may be introduced via the Pathophysiology of shock antecubital vein into the axillary or subclavian The changes which occur in uncomplicated . If care is taken that the tip of the catheter oligaemic shock are well known. Reduction of does not impinge on the valve at the lower border circulating blood volume stimulates baroreceptors of the subscapularis, an accurate measurement of causing an increase in the rate and force of the the central venous pressure is obtained. cardiac beat, constriction of veins, venules and of the regional peripheral arteriolar beds, all the Note: If an Intracath (Bard-Davol) or Needle and result of adrenergic stimulation (Mollison, 1967, Cathether (Portex) is used at the elbow, care must be taken The that the needle cutting edge is guarded, and the elbow firmly p. 153). blood flow to the splanchnic area, splinted so that the catheter cannot be severed by play skin, muscle and kidneys is considerably reduced against the sharp end of the needle. and blood is diverted to the cerebral and coronary vessels (Freeman, 1963). Some authors (Borow et al., 1965) have In healthy young adults without cardio- suggested using the external jugular or cephalic pulmonary disease these changes occur after a loss veins, but there may be difficulty in negotiating the of about 30% of the blood volume (approximately valves which guard the terminations of those by copyright. 3 pints): as the blood loss approaches 50% the veins. compensatory vasoconstriction is no longer If none of these veins is suitable, percutaneous adequate and death is imminent if transfusion is cannulation of the femoral vein is performed: the withheld (Grant & Reeve, 1951, p. 205). needle is introduced just below the skin crease, 1 cm medial to the femoral . It is passed in a Irreversible shock backward and upward direction to enter the In recent years much experimental and clinical femoral vein where it is supported by the superior attention has been directed to this state. Many pubic ramus. Through it the catheter may be patients who would formerly have come within the this category are now effectively treated and the passed into inferior vena cava. A greater incidence of thrombo-embolic phenomena make http://pmj.bmj.com/ diagnosis of irreversible shock should only be this route less desirable (Wilson et al., 1962). made retrospectively when the patient dies of Long saphenous cut-down at the ankle is tech- shock. nically easy but makes CVP measurement impos- Nevertheless, the term is sometimes used loosely sible. to denote a state of persistent circulatory failure despite adequate blood volume replacement. Perhaps a better term is 'refractory shock' (Smith (b) Immediate investigations A specimen of blood for grouping and & Moore, 1962) from which the patient might match- on September 30, 2021 by guest. Protected recover or pass into true irreversible shock with ing should be despatched to the laboratory as soon ensuing death. as possible. This does not, however, take pre- The mechanisms involved in irreversible shock cedence over infusing the patient, should direct are beyond the scope of this article-an excellent venepuncture prove difficult. account is given by Bloch et al. (1966). Haemoglobin and haematocrit estimations are valuable as they provide a baseline for retrospec- Practical management of shock tive assessment even although they do not Shock from traumatic causes. In traumatic accurately reflect the blood loss until haemo- shock, oligaemia is the result of external or dilution has occurred over the first 48 hr. internal blood loss, or of plasma loss from Similarly, initial determination of the plasma damaged capillaries in the traumatized region. The electrolytes and blood urea may be useful, and a several facets of resuscitation of the shocked specimen of separated plasma, retained overnight patient are most conveniently considered in the refrigerator, may be analysed at a con- separately. venient time. Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from

594 W. G. Prout and R. Vaughan Jones (c) Fluids for infusion Abnormal has followed the use of large Whole blood. Where haemorrhage has occurred quantities of dextran (Hardisty & Ingram, 1965). blood is the correct replacement fluid, although There is evidence that the bleeding tendency is some other fluid may have to be given while it is most severe with fractions of large average mole- made ready. Unmatched blood should only be cular weight but no clear picture is available of the given in dire emergency and it clearly behoves'a quantity of dextran which can be tolerated with- new casualty officer to find out what arrangements out causing bleeding. Mollison (1967, p. 175) sug- exist in his hospital for the rapid matching of gests that in ordinary circumstances it is best to blood. limit to 1 litre the amount of dextran given but it When very large quantities of stored blood are is clear that in the treatment of this amount given rapidly, e.g. at the rate of 500 ml in 5 min, has often been exceeded without side effects. may occur. Administration of 10 ml Saline. Saline will frequently be the fluid of first of 10% calcium gluconate for each litre of blood choice in resuscitation, its administration allowing transfused has been recommended (Bull, 1963a). blood to be taken, before dextran is administered, For a discussion of this problem and methods of from veins which are no longer collapsed, or per- warming blood see Lancet (1966). mitting time for plasma to be dissolved or blood Plasma. In burns, plasma is perhaps the ideal to be matched. Saline is comparatively rapidly replacement fluid although some writers advocate removed from the circulation. dextran (Wilkinson, 1960). Small-pool plasma Mannitol. Acute renal failure is often encoun- carries a risk of hepatitis of less than 1% (Bull, 1963b), but supply is often a limiting factor in the tered following , e.g. 14% of use. American soldiers severely injured in the Korean Dextran. Several kinds of dextran solution are War developed this condition (Bourne & Cerny, available. Dextran Injection B.P. has an average 1964) emphasizing the importance of the kidney in molecular of and has shock.

weight (M.W.) 150,000 by copyright. recently been desig,nated Dextran 150. Blood Mannitol diuresis appears to protect the sludging and capillary blocking were observed in ischaemic kidney in the early phases of renal experimental animals given such dextran, and failure before demonstrable tubule cell damage significant histological damage, attributed to has occurred. Protection may be due to increased , was found especially in the liver and cardiac output (Camishion & Fishman, 1964), myocardium (Ricketts, 1966). increased renal blood flow (Teschan, Gagnon & Murphy, 1963; Bourne & Cerny, 1964) or irriga- Low-molecular weight dextrans (average 40,000) tion of pigment particles or casts from the tubules appear to have no sludging properties and are (Mueller, 1965). claimed to improve tissue perfusion when this is impaired (Lancet, 1964). They are much more Although a view to the contrary has been rapidly excreted in the urine so that plasma expressed (Saito et al., 1965), we feel that mannitol http://pmj.bmj.com/ volume expansion is relatively transient, compared should be given to all severely injured patients. with that achieved by other dextrans. Low mole- Twenty-five grams of mannitol (10% or 20% cular weight dextrans should not be given to solution) may be rapidly infused when urgent dehydrated patients because of the risk of pro- resuscitation has been completed. This dose should ducing oliguria (Eliasson, 1963). They may not be repeated unless a flow of urine of at least occasionally cause renal failure in patients who 100 ml/hr results, when, after 6 hr, a further dose

are not dehydrated (Morgan, Little & Evans, may be given. on September 30, 2021 by guest. Protected 1966). Their place in the treatment of shock is not Choice of fluid. Factors such as the haemo- yet clearly defined and the subject is reviewed by globin concentration and state of hydration of the Mollison (1967, p. 177). patient, which fluid has been lost and which are Dextran 110 (Ricketts, 1966) with an average available will dictate which fluids ought to be M.W. of 110,000 has few of the larger molecules administered. If dextran has been administered responsible for sludging but is well retained in the before a blood sample was taken for matching circulation. The Swedish and American dextrans tests, the laboratory should be warned as rouleaux of average M.W. 70,000 or 75,000 have a higher formation may be expected. urinary excretion rate and are retained in the cir- (d) Assessment of blood loss culation for shorter periods. As stated earlier, in a healthy young adult who We feel that Dextran 110 or dextrans of M.W. has been injured, and shows signs of oligaemic 70,000-75,000 are the products of choice for shock, the blood loss will be of the order of 3 resuscitation unless there are special rheological pints. For this reason, Jamieson & Kay (1966a) indications for low molecular weight dextran. suggest transfusing the patient till the systolic Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from

Resuscitation-fluid replacement 595 blood pressure reaches 100 mmHg and then trans- adequate blood flow and tissue perfusion are to be fusing a further 2 pints. attained, the blood volume must be sufficient for In limb injuries, the relation between the size of the capacity of the circulation, whilst the cardiac the wound and the blood volume led Grant & pump must be able to maintain its flow. Reeve (1951, p. 197) to suggest that an area of All three of these factors are mirrored in the damaged tissue less than the size of one hand central venous pressure, so that it is an index of represented a loss of less than 10% of the patient's the circulating blood volume relative to the com- blood volume; one to three hands, roughly bined capacities of the heart pump and the 20-40%; five hands, 50% approximately. Clarke vascular bed (Borow et al., 1965). & Fisher (1956), finding the volume of a clenched The normal range of CVP is from 6 to 17 cm hand to be about 500 ml, used this for estimating of water above the mid-point of the heart, which haematoma size. Thus, as a very rough guide, for is on a level with the mid-axillary line in the each 'hand' or 'fist' of wound or haematoma, a supine patient (Harkins, 1965). Whilst a single pint of blood will have been lost. Clearly, this measurement may be used as a therapeutic pointer method of estimating blood loss will not take (see Table 1), observation of the changes which account of haemorrhage into the chest, the pelvis occur in response to therapy provides the best or the retroperitoneal tissues. guide to fluid replacement. As up to 1-7 litres of blood may be lost in a closed fracture of femur (Clark, Topley & Flear, TABLE 1 1955) and as much as half the blood volume in Therapy according to CVP trunk fractures with visceral damage, the usual (after Borow et al., 1965) tendency is to under-transfuse these patients (Apley, 1963). The response to treatment is crucial CVP* Inference Therapy and will provide an index of its adequacy. Other methods of controlling fluid replacement 0-5 Hypovolaemia Active replacement are now available. of fluid by copyright. 6-12 Possible Trial administration Blood volume measurement hypovolaemia of fluid The relative complexity of these estimations, > 15 Heart failure Curtail fluid or over- administration and the time taken, have been reduced by com- transfusion danger of puterized semi-automatic machines measuring the pulmonary oedema dilution of 125I and 1311-labelled albumin. The expected blood volume can be calculated from the *Central venous pressure: cm of H20 above subject's height and weight (Nadler, Hidalgo & mid-thoracic point. Bloch, 1962) if the latter can be measured. This

method has been championed by Fine (Friedman, The actual measurement of CVP has been http://pmj.bmj.com/ Grable & Fine, 1966), but there appear to be greatly facilitated by the advent of the disposable major objections to control of infusion therapy venous manometer (Baxter, Capon-Heaton) by repeated blood volume measurements. (Hobbs, 1966). This is a double-ended transfusion Repeated venepuncture in the shocked patient, giving-set, one arm of which is attached vertically particularly if obese, may prove impossible. Fur- to the drip-stand and used as a saline manometer. thermore, it is now recognized that the capacity of An external measuring-gauge introduced earlier the circulation may increase following hypo- by McGowan & Walters (1963) now seems less tension, trauma, infection and administration of satisfactory, having the disadvantage that nursing on September 30, 2021 by guest. Protected drugs such as anaesthetic agents, alcohol, bar- staff are unable to use it as readily as the saline biturate or phenothiazine derivatives (MacLean, manometer. 1964; Barraclough & Sharpey-Schafer, 1963). The Measuring central venous pressure and arterial fact that blood volume is 'normal' does not pressure, transfusion and infusion is controlled indicate that it is necessarily adequate for the according to the therapeutic response: circulatory demands at that particular time (1) Rising systolic pressure: low or normal (McGowan & Walters, 1963). CVP. This occurs in the early treatment of shock For these reasons, the use of central venous due to oligaemia. The tendency to stop replace- pressure monitoring as a guide to fluid replace- ment prematurely must be avoided, remembering ment is to be recommended strongly. that normotension may be found with blood Central venous pressure (CVP) volume deficiencies of up to 30% (Grant & Reeve, MacLean et al. (1965) emphasize that shock is 1951, p. 198). Transfusion may, with advantage, a failure of blood flow, not blood pressure. If be continued until 2 pints in excess of that Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from

596 W. G. Prout and R. Vaughan Jones required to establish an arterial pressure of CVP. The management of these patients where 100 mmHg systolic have been given (Jamieson & the cause of shock is uncertain follows the same Kay, 1966), and so that the CVP rises to the general pattern, regardless of cause. normal range. Otherwise the patient remains liable If an infection cannot be excluded, after blood to return to the shocked state if further relatively culture large doses of antibacterial agents are small blood or plasma loss occurs. given. The choice will depend upon the organism (2) Persistent low systolic pressure: rapidly suspected, and its sensitivities if it is expected to rising CVP. If, after the administration of a small be a hospital strain. Usually two antibacterial volume (200-300 ml) of the appropriate intra- agents are given in combination. venous fluid, the arterial pressure remains low, Reduced tissue-perfusion leads to hypoxia and but the CVP starts to rise, the cause of the shock anaerobic metabolism, accumulation of lactate is not oligaemia. and pyruvate and a metabolic (Freeman, (3) Persistent low systolic pressure: slowly rising 1963). Correction of such an acidosis on the lines CVP. This is not seen in oligaemic shock, unless suggested by Astrup et al. (1960) is widely prac- delay in instituting treatment has caused it to tised (MacLean et al., 1965; Borow et al., 1965; become 'refractory' or 'irreversible' (see below). du Toit et al., 1966), although the view that clinical (4) Low systolic pressure: high CVP. This may acidosis impairs myocardial efficiency has been be found in cardiac disorders such as myocardial disputed (Shires, 1967). , and in cardiac It is clear that many patients with traumatic tamponade. shock who are adequately transfused do not Treatment is directed at the cause along stan- develop a metabolic acidosis and require no such dard medical or surgical lines. Treatment of correction. In refractory shock, however, the by intravenous infusion with acidosis should be corrected. peripheral vasodilators is under investigation, Plasma, blood, or other circulation expander is but its value is unproven (Brit. med. J., 1966). infused till the CVP approaches the upper limit of The treatment of categories (2) and (3) is dealt normal (unless there is a history of cardiac in-by copyright. with in the next section. sufficiency when a lower level is recommended). If warm hypotension persists, or if cold hypotension Shock from non-traumatic causes has become converted to warm hypotension Although the casualty officer is chiefly con- during this additional therapy, no further cerned with shock due to trauma, many cases of immediate action is taken. If cold hypotension shock due to other causes are dealt with initially persists, indicating poor peripheral tissue per- in Casualty Departments. A brief account of the fusion, certain other therapeutic agents may be management of fluid replacement in these patients used. is given.

, With the exception of those with severe uncon- (a) Phenoxybenzamine (dibenzyline) http://pmj.bmj.com/ trolled haemorrhage, most hypotensive surgical This is an a-adrenergic blocking agent. Block- patients will benefit from a period of rehydration ade of the a-receptors, which are chiefly concerned and electrolyte correction. If administration of an with vasoconstriction, results in decreased peri- anaesthetic is anticipated, it is particularly impor- pheral resistance with increased blood flow, tant that hypovolaemia should be corrected for the notably to the renal and splanchnic circulations overall effect of the anaesthetic is to enlarge the (Nickerson, 1966, p. 550). As well as increasing vascular space and diminish compensatory re- tissue perfusion, the cardiac load is considerably on September 30, 2021 by guest. Protected flexes (Wylie & Churchill-Davidson, 1966). Low decreased (Bloch et al., 1966). Also, movements serum potassium should be corrected if muscle of fluid from the pulmonary to the systemic cir- relaxants are to be used, although use of a non- culation and from the interstitial to vascular depolarizing muscle relaxant in hypokalaemia does compartments take place. not necessarily result in prolonged neuromuscular Nickerson (1966, p. 553) suggests that a dose of block (Evans & Gray, 1965). 1 mg/kg body weight is given intravenously in Early adequate fluid replacement, with appro- 500 ml of normal saline or 5 % dextrose over priate anti-bacterial therapy if there is an infective about 1 hr. By this time the effect is maximal and element in the cause of shock, will usually result in persists for up to 2 days. It affects only the a satisfactory peripheral circulation, with a state a-receptors and does not block the s-receptors. of normotension or warm hypotension. Once given it cannot be reversed. Delay in treatment may result in a response to The clinical use of this drug is described by as seen in groups (2) and (3) Lillehei et al. (1964) and Eckenhoff & Cooperman above; persistent low systolic pressure and rising (1965). Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from

Resuscitation-fluid replacement 597 (b) Hydrocortisone relatively larger head and smaller limbs. Intra- Hydrocortisone was initially used in shock as venous therapy should be instituted in children replacement therapy for supposed adrenal cortical with more than a 10% and in adults with a failure. This does not, in fact, occur, and the only 15% or larger burn (Bull, 1963a). Moyer (1966, place for doses of the order 100-200 mg is in the p. 353) points out that burns of less than 20% treatment of an Addisonian-type crisis. rarely produce shock, except in infants and very Lillehei et al. (1964) have used massive doses old people. (40-60 mg/kg body weight) which appears to Although the traditional view is that therapy exert an a-adrenergic blocking effect. should be directed towards restoring blood volume Smith & Moore (1962) report no beneficial effect (Mollison, 1967, pp. 169 et seq.), recently the im- from this drug in small doses, and Walters (1967, portance of extravascular sodium deficiency has personal communication) saw no beneficial effect been stressed, and Moyer (1966, p. 349) expresses in twelve of thirteen patients who were given the view that this is the major cause of burn massive doses after failing to respond to trans- shock, regarding oligaemia as a minor cause. A fusion. The conventional form of a-adrenergic series of cases with severe burns who made good blocker would seem a more hopeful prospect. recoveries when treated solely with large volumes of lactated Ringer's solution in spite of rising (c) Isoprenaline haematocrits, adds weight to the opinion. Other workers have used isoprenaline in the In this country at present, plasma, plasma sub- management of the hypotensive patient with raised stitute and normal saline form the sheet anchor of venous pressure (Maclean et al., 1966; Du Toit the early therapy of burns. Dextran would seem et al., 1966). an adequate substitute for plasma, though pro- A 83-adrenergic stimulator, this drug acts on the bably its use should be limited to 1 litre (see under heart and increases cardiac output by direct action infusion fluids). on rate and force of beat. Peripherally it causes The methods of deciding volume replacement arteriolar relaxation, chiefly in the muscle circula- have been reviewed by Bull (1963a). by copyright. tion, but also of the renal and splachnic beds to Evans et al. (1952) suggest that 1 ml of some degree. Improved tissue perfusion results. colloid/ % burn/kg of body weight should be One milligram of isoprenaline is diluted in given in the first 24 hr along with an equal volume 500 ml of saline or 5% dextrose and 50-100 ml of saline. Placing an upper limit of 50% on the infused every hour. The rate of infusion should burn to avoid the risk of pulmonary oedema, they not exceed that which raises the pulse rate above report good results in sixty-eight patients. 110/min, as higher rates may predispose to Such a formula provides only the roughest arrhythmias and decreased volume (Mac- guide. Further, although serial venous haemato- lean et al., 1965). crits, and urinary output may be measured, the http://pmj.bmj.com/ Note: It is of the utmost importance that if any of these variability of the individual response precludes three agents which expand the circulatory capacity is used, their use as the only criteria on which transfusion the patient must not be oligaemic before their administration. may be based. The adequacy of fluid replacement The reader is strongly recommended to consult the references should be assessed from the clinical condition of cited before using the drugs. the patient and the parameters described earlier Vasopressor agents such as , nor- under traumatic shock. adrenaline or metaraminol should not be used in Although in a full thickness burn of greater place of adequate blood volume replacement. than 15% appreciable destruction of red cells on September 30, 2021 by guest. Protected They have no part to play in the treatment of occurs, there seems to be little advantage in early oligaemic shock (Mollison, 1967, p. 153). replacement of this loss (Topley & Jackson, 1957) and transfusion of blood can wait until the Burns anaemia appears. The severely burned patient is usually treated in a specialist centre, and a brief account only of Summary the initial intravenous therapy is given. The resuscitation of patients with peripheral cir- The area of burning is estimated by Wallace's culatory failure using intravenous fluids has been 'rule of nine': The head plus the separate upper reviewed. limbs each account for 9% skin area, whilst the front of the trunk, back of the trunk and the Acknowledgment whole leg are each covered by about 18% of the We are grateful to Dr G. Walters who originally stimu- skin area (Wallace, 1951). A small child has a lated our interest in this subject. Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from

598 W. G. Prout and R. Vaughan Jones

References Lancet (1964) Dextrans for easing blood flow. Lancet, i, 28. Lancet (1966) Warm blood for massive transfusion. Lancet, APLEY, A.G. (1963) A System of Orthopaedics and Fractures, i, 1193. p. 283. Butterworths, London. LILLEHEI, R.C., LONGERBEAM, J.K., BLOCH, J.H. & MANAX, ASTRUP, P., JORGENSEN, K., SIGGAARD-ANDERSON, 0. & W.G. (1964) The nature of irreversible shock. Ann. Surg. ENGEL, K. (1960) The acid-base metabolism. Lancet, i, 160, 682. 1035. MACLEAN, L.D. (1964) Blood volume versus central venous BARRACLOUGH, M.A. & SHARPEY-SCHAFER, E.P. (1963) pressure in shock. Surg. Gynec. Obstet. 118, 594. Hypotension from absent circulatory reflexes. Lancet, i, 489. MACLEAN, L.D., DUFF, J.H., SCOTT, H.M. & PERETZ, D.I. BLOCH, J.H., DIETZMAN, R.H., PIERCE, C.H. & LILLEHEI, (1965) The treatment of shock in man based on haemody- R.C. (1966) Theories of the production of shock. Brit. J. namic diagnosis. Surg. Gynec. Obstet. 120, 1. Anaesth. 38, 234. McGOWAN, G.K. & WALTERX, G. 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