Shock

SHOCK A STUDY OF THE PARTIAL

AVAILABLE L. M. hYERS, BERKELEY,

MODERN

LITERATURE

OF SHOCK

M.D.

CALIFORNIA

0

Definitions of Shock. Webster’ defines shock by the use of words such as “collapse” and “concussion.” Roget2 at greater length uses “attack, paroxysm, seizure, apoplexy, paralysis; thrill, excitement, agitation; concussion, crash, cohision, impact; bIow, ordeal.” We at once sense in a reconsideration of these terms that the word shock has come in the field of medicine to have special signihcance, one not conveyed usually by such terms as “ coIlapse ” or “concussion.” It has, in other words, become a technical term and has acquired somewhat exact limits to its meaning. Dorland3 describes shock as a

NE is tempted when undertaking a review of the literature of shock to enter his subject rather lightly and with at least as much assurance as he thinks he feels when called to meet its emergency in the surgery. However confident one feels in the early phases of the perusal, it is not long before a slow sense of consternation enters as one is deluged with conflicting theories, and data which refuse to integrate. In reading the numerous articles one finds that there is no satisfactory account of shock, and he is led to believe that it is stilI a chaotic held where individuals, committees and commissions wander, while in the hospitals the emergency of shock is met daily in hard practice, now and then successfully. When sufficient time has elapsed, one realizes that a few well supported principles have appeared gradually, which seem well worth our search. No attempt has been made to make a complete survey of the literature; we have confined ourselves to a review embracing the literature available through a fairly comprehensive list of libraries. We have rareIy expressed our own opinions, either those which might be derived from experimentaI work or those acquired through clinical experience. Both principles and emphasis have been left largely to the actual content of the literature as it exists. On the completion of this fairIy Iong review specific acknowledgment is made each Iibrary mentioned at the end of the paper other than the author’s own. This particmar acknowledgment is extended aIso to each author quoted and each pubIisher mentioned in the reference Iist. AcknowIedgment is aIso due my secretary, Myra Keplinger, A.B., for her assiduous heIp in abstracting and coIIating the materiaIs with which we have dealt.

sudden vital depression, due to an injury or emotion which makes an untoward impression upon the nervous system. Shock may be slight and transient, or profound and even fatal. In severe shock the prostration may amount to immobility or syncope; but in other cases the patient is restIess and excited. Recovery from shock is folIowed by more or less quickening of the puIse and respiration and abnormaIIy high temperature. Schorcher4

defines shock as

a cIinica1 state resulting from a sudden trauma of the nervous eIements inffuencing the centra1 nervous system by way of the refIex arc. It is accompanied by a rise in the bIood pressure foIIowed later by a fall. CoIIapse, on the other hand, while cIinicaIIy simiIar to shock, differs from it causaIIy in that it is the result of a chemical action. It is caused by the absorption of toxic substances and their effect primarily in the circuIatory system. It is sIower in deveIopment and is characterized by a primary faI1 in the bIood pressure. Rutherford5 speaks interference with the mechanism of life-an

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of shock as “an most fundamental interference with

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the mechanism for the transformation energy.” Bickham6 defines shock as

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a reflex depression on the vita1 functions due to bodiIy injury, traumatic or operative, due to proIonged operation, or error of anesthetization, due to psychic inff uence, especially strong mentaI emotions of a distressing nature, or due to any other cause resuhing in the exhaustion of inhibition of the vasomotor mechanism. According of traumatic

to Wright’ shock,

in his discussion

“Shock” is a condition in which the sensory and motor parts of the reflex arc are paraIyzed to a greater or Iess degree, together with a profound disturbance of the circuIation, subnormal temperature, and usuahy frequent shaIIow beathing; it may be seen typicaIIy foIIowing severe injuries. According

to Sherrington,s

The whoIe of that depression or suppression of nervous functions which ensues forthwith upon a mechanical injury of some part of the nervous system and is of temporary nature may be convenientIy included as “shock.” GoItz considered it entirely a coIIection of inhibition phenomena. In a dissertation on operative shock Rehn,g Professor of Surgery at the University of Freiburg, Germany, says, AI1 of these considerations have served to contribute to the conception of shock the idea of a sudden occurrence precipitated in one way or another by some factor acting from without and foIIowed by severe circuIatory manifestations of a periphera1 and centra1 nature together with disturbances of other vegetative centers.

Definition of Shock Quoted from Early Literature. In Mann’slO consideration of “The Peripheral Origin of Surgical Shock,” he includes a brief historica review of the subject, quotingearlydefinitionsof “shock” by various authors. An example follows: “Travers (‘An Inquiry Concerning Irritation,’ London, 1826) states that ‘shock is a species of functional concussion by which the influence of the brain over the organ of circulation is deranged or suspended. ’”

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Analogy between the Chemical Pathology of Cholera and Shock. With reference to the history of the subject of shock, Atchley and Loebl’ say “In 1831 Dr. W. B. O’Shaughnessy of Newcastle-upon-Tyne wrote a brief letter to the London MedicaI Gazette which embodied the results of several years of what he termed his ‘experimental inquiries’ into the cholera.” These authors have taken time to trace the deveIopment of the chemica1 pathoIogy of choIera because it presents probabIy the earIiest instance in which there was an understanding recognition of the physioIogic processes invoIved in the deveIopment of this common compIication of many disease conditions, viz., dehydration, saIt depIetion, and shock. . . . ChronoIogicaIIy, the next correct appraisal of the fundamenta1 probIem may be found in the Guy’s HospitaI reports of 1874. Dr. C. Hilton Fagge described, therein, “A Case of Diabetic Coma, treated with partia1 success by the injection of a saline soIution into the bIood.” The most impressive feature of this pioneer experiment in therapy was the rationaIe which he offered. . . What suggested to my mind the advisabiIity of injecting a saIine soIution into the bIood in this case was the idea that coma was due to the drain of water from the system, caused by the diabetes. I suppose that the hypothesis upon which I acted was essentiaIIy simiIar to that which formed the basis of the Iike treatment in the coIIapse of choIera.

Characteristics of tbe Shock Syndrome as Recognized in Modern Surgical Practice. Orr12 states that “James Latta, in I 795, is said to have been the first to use the term ‘shock’ to describe this condition,” referring to a syndrome occurring in surgical practice. Today in the syndrome of surgical or traumatic shock, according to Cannon13 the foIlowing characteristics are recognized, a singIe case illustrating several or all of them: Iow venous pressure; low or falling arterial pressure; rapid, thready pulse; diminished blood volume; normal or increased peripheral red cell count and blood hemoglobin; leucocytosis; increased blood nitrogen; reduced blood alkali ;

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lowered metaboIism; subnormal temperature; coId skin, moist with sweat; paIIid, grayish or cyanotic appearance; thirst; shaIIow, rapid respirations; vomiting; restIessness; and anxiety progressing to mentaI duIIness. Symptoms and Signs Characterizing Shock Continued. According to Wright,7 Breathing is characterized by Iong deep sighing respirations aIternating with very superficia1 ones. The patient reacts very slightly and only to very painfuI stimuh. The Iimbs are toneIess. Spontaneous movements are not made, but in response to urgent orders very brief Iimited movements may be executed. Complaint may be made of cold, faintness and deadness of a11 parts of the body. Marsha11 and Piney14 in&de in their enumeration of symptoms characterizing shock, “profound ff accidity of the muscuIar system.” Bickham6 says, The puIse increases in rate, whiIe decreasing in tension and volume-respiration increases in rapidity and shaIIowness-temperature is lowered, the pupiIs dilate . . . and in advanced shock nausea, hiccoughing, and vomiting may occur-incontinence of feces and retention of urine may be present-reflexes are lost-response to stimuIation Iessens-and coma and death supervene. Crile’”

says,

. . . whatever the cause of exhaustion (shock) certain basic phenomena are the same. . . , diminished reserve aIkaIinity, and in acute phases, increased H-ion concentration of the blood; intraceIIuIar changes in the brain, the liver, and the adrenaIs; decreased eIectric conduction of the brain and increased eIectric conductance of the liver. _Moon’6 points out that “shock occurs not only foIIowing extensive surgery or trauma. It is seen in a wide variety of clinicaI conditions incIuding extensive burns, poisoning with various substances, metaboIic intoxications, abdomina1 emergencies, and severe acute infections.” Consideration of the “ Constitutional Condition and Shock.” The origina subject

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for this paper was “The Constitutiona Condition and Shock,” which suggests primariIy, consideration of the predisposing causes in the physica constitution which mihtate for or against the state caIIed shock. Are some body types more susceptibIe to shock than others? It seems a fertile subject for investigation but very IittIe reference to it is made in the Iiterature dealing with shock. CriIe17 says in his Iecture dehvered before the Harvey Society in January, 1908, “It is axiomatic to state that the better the physica condition the Iess the shock.” Factors Predisposing to Shock. Rutherford,” discussing the significance and management of shock, Iists the fohowing predisposing causes of shock: I. Age: The aged do not endure shock weI1. The risk is determined, not by the age of the patient but by the age of his circuIatory apparatus. When aged patients are subjected to injury, the immediate circulation and other changes may be sIight; but, under these conditions, the power of compensation or rebound is IikeIy to be equaIIy sIight.

Mortimer’* reIationship

says with regard of age to shock:

to

the

Shock is more IikcIy to occur in infants and young chiIdren than in aduIts, for the whole nervous system is more responsive to impressions, and diffusion of these readiIy occurs, as is found in the Iiability of infants to genera1 convuIsions from causes which do not have the same effects Iater in Iife . . . Rutherford

continues

as foIIows :

II. Sex: Before puberty there is IittIe or no difference in the susceptibiIity of the sexes. After puberty, especiaIIy after the menstrual period (begins), the femaIe becomes Iess stabIe. The maIe grows more hardy. During the chiIdbearing period the femaIe deveIops an increased capacity for shock. During the menopause the femaIe again becomes more susceptible to shock. After the period of deveIoping menopause the femaIe has entered upon an unbroken period of quietness and her resistance is increased. At the corresponding age, the maIe is carrying the greatest burden of his career,

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subject exhibiting the phenomena. One has consequently : I. Physic&I shock; 2. ChemicaI shock; 3. Electric shock; 4. MentaI or psychic shock; She11 shock; :: Litigation “shock.” Wound shock, surgiI. Physical Shock. cal shock, and traumatic shock are examples of physica shock. PIeuraI shock, discussed, for exampIe, by HamiIton and Rothstein and also by Cocke23 is to be mentioned as a subheading under trauWakeIey and Buxtonlg mention race in matic shock. HamiIton and Rothstein addition to age, sex, and time of day: define pIeura1 shock thus: “ PIeuraI shock “Race is of some importance; the coIored (pIeural reff ex, pIeura1 eclampsia, pIeural races are not so easiIy shocked as the white epiIepsy) is a syndrome caused by irritaraces.” These authors say aIso, “Nervous tion or puncture of the pIeura and is characpatients are notoriousIy bad subjects for terized by the appearance of a group operation. So-caIIed ‘psychic shock’ may of symptoms not unIike those of air supervene in a patient anxious about an emboIism.” operation. This shock may even come on Obstetric shock, aIso, is a form of during the operation while the patient is traumatic shock under the genera1 heading stiI1 unconscious, and it certainIy tends to of physica shock. TayIor,24 discussing this be a rea1 danger afterwards.” form of shock, says “It is my growing Among additional factors predisposing beIief that separation of the pIacenta, in to shock Robertson20 mentions the fact that whoIe or in part, is rapidIy foIlowed by the “Injury to the Iiver by chIoroform or formation of histamine or aIIied substances phosphorus greatIy reduces the power of an . . . then a major fail of bIood pressure anima1 to withstand depletion of its pIasma takes pIace. This faI1 has Nature’s desired proteins.” effect of stopping further hemorrhage on a CriIe15 says, large scaIe. . . . ” Shock due to freezing is a form of physiWe have found that exhaustion may be ca1 shock, although the resuIts of severe produced by an excess of, no Iess than by the freezing which contribute to the shock want of thyroid or adrena or brain activity. state have been shown by Harkins to be We have found that Ioss of Iiver function, similar to those foIIowing severe burns want of oxygen, want of cardiac power, want of norma vasomotor action, of themseIves, which wiI1 be mentioned under chemical individuaIIy or in any combination, may pre- shock. “ Speed ” shock is another variety of dispose to or cause exhaustion (shock). physica shock. It is the syndrome which Wangensteenzl incIudes “ anemia, infechas been described as resuIting from rapid intravenous injections. Milbert,26 quoting tion, maIignancy, inanition, fever, obesity,” Hyman et al., says that these workers “are as some of the conditions that predispose toward shock. of the belief that a rapid injection of any Varieties of Shock. There are severa moIecuIe into the vein may result in widevarieties of shock, depending upon the spread systemic disturbances . . . ” MiIagents giving rise to the syndrome, and bert’s own conclusions, however, are “That also upon the sequence of events in the the roie of veIocity does not pIay a cIinicaIly and from this period on to the end he is not so good a surgica1 risk as is a woman. III. Time of Day: There is a marked daily variation in the process of metaboIism of the body, beginning in the morning and ending in the evening. The vita1 processes are more active, reserved forces are at a maximum, the psychic factor at a minimum on rising in the morning. The most unfavorabIe time is from one to two o’cIock in the morning. Night accidents are IikeIy to be more grave than equaIIy severe ones occurring during the day. In lingering iIInesses, more deaths occur after midnight than during the day.

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perceptibIe part in administering Auids intravenously.” 2. Chemical shock in&ides anaphyIactic shock, insulin shock, coIIoid shock, etc.; but aIso, no doubt, is reIated in many of its ramifications to physica shock. Shock folIowing severe burns may aIso be cIassified as chemica1 shock. Harkins, considering experimental burns, writes in summary: Iocal accumuIation of Auid in cases of bGs . . . begins at the time of the burn and continues in the form of a decelerating curve unti1 death. Accompanying the coIIection of fIuid is a simultaneous increase in the concentration of bIood as shown by an increase in the percentage of hemogIobin and in the hematocrit readings. After most of the Auid has accumulated, the faI1 in bIood pressure sets in and continues rapidIy unti1 death occurs in a state of secondary shock. ChemicaI shock is aIso probabIy reIated in many of its ramifications to the third division, i.e., 3. Electric Shock. This variety of shock may easiIy be reIated immediateIy or remoteiy to both physical shock and chemica1 shock. According to PaIfrey,2s “The effect of eIectric shock is predominantIy a paralysis of respiration.” Among PearI’s2g concIusions we find the folIowing: (3) It is probable that death from eIectricity in higher animals is due, in a majority of cases, to primary fibriIIation of the ventricIes. In man this condition is hopeIess unIess prompt and heroic treatment is instituted. (4) Postmortem findings fai1 to expIain the cause of electric death. Changes in the waIIs of the vesseIs are noteworthy. Heat rather than eIectroIysis is probabIy responsibIe for most pathoIogic changes . . . (IO) The sequeIae of electric shock are many and varied. The most important ones affect the skeIeta1 and nervous systems.

4. Mental or Psychic Shock. “Psychic shock,” says Mortimer,ls “has been defined as the effect on the meduIlary centres of impuIses from the centres of consciousness (pain, fear, and other emotions).” This type of shock obviousIy is or may be present in some degree in physical, chemi-

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ca1, and eIectrica1 shock, and may derive some of its reinforcements from any combination of them. It may, on the other hand occur spontaneousiy from pureIy psychic causes and then run off into phenomena identifiable as having physica1, chemical, and eIectrica1 shock characteristics. 5. Shell Shock. This term, says Wigin the Iiterature for gers, 3o “is reserved more distinctly nervous disturbances which more or Iess permanentIy disquaIify the patient but do not lead to circuIatory faiIure and death.” 6. Litigation “shock” is a condition, says Fraser31 (quoting McKendrick) which is incapabIe of medica definition or of proof or disproof. True shock is the resuIt of excessive pain, of severe bodiIy damage or due to some very terrifying experience. Litigation or “nervous shock” as it is often termed, on the other hand is a condition that is not suddenIy produced but has a gradua1 onset. Somewhat obscureIy, in a statement having possibly more IegaI than medical value, we read that SpiIsbury32 regards “‘shock’ . . . as one of the most overworked terms in the medico-Iegal vocabuIary, as many deaths said to be due to shock shouId reaIIy be ascribed to such conditions as Ioss of bIood, exhaustion, injury to a vita1 organ or concussion of the brain, etc.” According to its behavior in the anima1 organism, surgica1 shock is divided into two stages : Primary shock is very frequentIy seen in those cases in which injury has been so severe that death is inevitabIe, or may quickly supervene, unIess proper treatment is instituted at once. The symptoms of primary shock deveIop as soon as ,the wound is received, with the onset of paIIor, profuse perspiration, chiIIy sensations and sometimes Ioss of consciousness. The puIse rate is increased, but the bIood pressure reading may earIy be somewhat increased or normaI.12 CannonI observes that may be seen . . . either

“Primary shock in the mortahy

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wounded, or after extensive hemorrhage, or in the reIativeIy rare instances in which nervous eIements seem to pIay an important roIe.” According to Mann and Essex,33 There seems to be compIete agreement that the primary feature, whether the shock is immediate or deIayed, is Iow arteria1 blood pressure. In either type of shock, if a Iow bIood pressure persists. for an hour or more, the secondary condition appears and is attended by the phenomena associated with oxygen Iack, such as decreased metaboIic rate, and decreased aIkaIine reserve. Speaking of primary shock, FriedIander34 remarks that “it is aItogether probabIe that as a consequence of wounding, there is a reflex reIaxation of bIood vesseIs simiIar to that which occurs in fainting.” Wright7 states that, “ EarIy or primary shock, which sets in immediateIy foIlowing an injury . . . is probabIy due to afferent impulses causing reffex vasodiIation and a profound faI1 of blood pressure.” Primary and Secondary Shock. “ Recovery from primary shock may be quite prompt or it may deveIop into the secondary type.“12 Wright7 says secondary shock is “due chieffy to a capiIIary poison, probabIy histamine or some substance with a simiIar action which is Iiberated from the injured tissues.” Cannon13 in this regard says: “The theory of a secondary shock which has the strongest support . . . is that of a toxic factor operating to cause an increased permeabiIity of the capiIIary waIIs and a consequent reduction of bIood voIume by escape of pIasma into the tissues.” In quoting Quenu, “who has also coIIected and summarized the studies of other French surgeons made during the war,” FriedIander34 says, “Secondary shock does not appear immediateIy after the reception of wounds. So that it is not of the nature of a nervous effect. The state is commonIy we11 estabIished before infection, and therefore is not of bacteria1 origin.”

Cannon13

says further:

Exposure to coId, Iack of water, rough carriage and absence of spIinting of broken bone have been recognized as circumstances favorabIe to the onset of the symptoms. A stiI1 Iater aspect of secondary shock is that which is attended by infection, especiaIIy with gas baciIIi. Or+? says, “Secondary wound shock is the type usuaIIy encountered in the severely wounded. It is also the type frequentIy seen folIowing serious or proIGnged surgica1 operations.” Primary and Secondary Forms of Sboci Distinguished. HoIt, opening a discussion on traumatic shock at a recent meeting of the Section of Surgery of the RoyaI Society of Medicine, compared circuIatory changes in neurogenic (primary) shock and traumatic (secondary) shock thus: Secondary Shock (Hematogenic) Blood pressure maintained. Rise in puIse rate. Vasoconstriction. Diminution in bIood voIume. 02 consumption diminished. FaII in bIood pressure serious.

Primary Shock (Neurogenic) FaII of arteria1 pressure. No rise in puIse rate. VasodiIation. not Blood voIume diminished. No change in 02 consumption. FaII in bIood pressure not serious so Iong as respiratory center maintained.

New Descriptive Terms Suggested to Re“Primary ” and “ Secondary ” as place He thought Applied to Shock. . . . that some other cIassification than the division of shock into primary and secondary was necessary. American writers had suggested the foIIowing .cIassification: bematogenic, resuiting from Ioss of circuIating bIood voIume (muscIe trauma); neurogenic, resuIting from Ioss of centra1 vascuIar tone (trivia1 injury, emotional distress) ; vasogenic, resulting from Ioss of periphera1 vascuIar tone (histamine and other drug reactions). The adoption of some such cIass&cation would do much to remove the present confusion in which the pathoIogy of this subject had been pIaced.35

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Is There Such a Condition as “Secondary ” Shock? At the same meeting at which these recommendations were made, it is noted that O’Shaughnessy declared “he had never seen a case of secondary shock nor read a satisfactory acccmnt of such a case, nor seen it experimentally According to his experience, produced.” “ following trauma the syndrome progressed either to recovery or to a fatal end. There was never an initial recovery followed by a later onset of shock.” OPINIONS

REGARDING

CAUSATION

OF

SHOCK I. Accumulation of Blood in the Capillaries. Crile15 uses the term “shock” to denote a state of exhaustion which has been developed rapidly by psychic, traumatic, toxic or thermal stimuli. HewIett,36 in resume, says

The marked hypotension of surgical and traumatic shock is not due in the main to a Ioss of arteria1 tone or to a faiIure on the part of the heart. It is due to a lessened flow of blood to the right auricIe, caused mainIy by an accumuIation of blood in the smaIIer venuIes and capiIIaries. This accumuIation may be due to a direct injury of the part or it may be caused by vascuIar poisons absorbed from the damaged tissues. There is no good evidence that nerve Iesions pIay a dominant role in the pathogenesis of the more serious forms of surgical or traumatic shock. 2. Loss of CO2 from the Blood. In discussing the causation of shock, McDowal137 says,

Of specia1 importance in reIation to central failure as a cause of surgical shock is undoubtedIy sensory stimuIation. . . . The rea1 expIanation has . . . been shown by YandeII Henderson to be due to the washingout of carbon dioxide brought about by the hyperpnoea occasioned by the sensory stimulation. The acapnia or Ioss of carbon dioxide . . . brings about a reduction in the tone of the vaso-motor centre . . . In such anesthesia (light ether), as pointed out by Henderson, it is important to remember that apart from the faI1 in bIood pressure, there may be brought about death from failure of respiration as a

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resuIt of the washing-out of the normal stimulus-carbon dioxide. The amount of this gas in the bIood becomes insuffrcient to stimuIate the partIy anesthetized centre and respiration becomes inadequate to suppIy the oxygen requirement of the body, especiaIIy of the heart and the meduIIa. 3. Role of Anesthesia as a Causative Factor in Shock. Statements by Knoefe138 with reference to the role of anesthesia as a cause of shock may be quoted here. He says in part: . . . the secondary or delayed shock that may be produced by prolonged anesthesia with ether or chloroform is due to a corcentration and reduction in voIume of the circuIating blood resulting from genera1 stimulation of the sympathetic nervous system incIuding the outpouring of adrenin . . . Banerji and Reid have just shown that in the hypergIycemia caused by ether and chloroform, the adrenaIs are importantIy concerned, and have again demonstrated that such production of hyperglycemia is inhibited by amyta1. Does amytal, with reIated substances prevent the general hyperactivity of the sympathetic nervous system that ether and chloroform produce? If they do, and there is some evidence for such a concIusion, then their use as basa1 narcotics receives important support in that the tendency of such voIatiIe anesthetics to produce shock may be markedly counteracted. Local Nerve Block in Shock Prophylaxis. The utility of local nerve block in prophyIaxis of shock is mentioned by certain workers. Jones3g decIares that “Local nerve bIock with a cocaine derivative (nupercain) lessens damage to the centraI nervous system, allows relaxation with a minima1 anesthesia, and prolonged freedom from pain in the postoperative period.” 4. Precipitation ofParticles in Capillaries, Lymphatics, etc. McDonagh40 makes the foIlowing assertion : Shock is due to the precipitation of the protein particIes of the pIasma in the perivascular lymphatics, capiIIaries, and occasionaIIy the arterioIes of an important viscus. The particIes are precipitated because they have become too Iarge or too aggIutinated to

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circuIate, therefore any agent that can cause these two physica changes to occur in excess may produce shock. The chemico-physical changes the protein particles in the plasma undergo to cause disease, are the same whether they be caused by a parasitic or a chemical invasion . . . When protein particles are dispersed the particIes become smaher, more numerous, their Brownian movements increase, and their negative eIectric charge becomes more pronounced. Excessive dispersion resuIts in intra-vascular clotting and causes one of the forms of shock. ExperimentalIy, this form of shock is occasioned best by an overdose of para-thyroid extract.40 THEORIES

OF SHOCK

The fohowing theories of shock are those having support of the majority of investigators deahng with the subject: I. “Acapnia” (Henderson).41 The fundamenta1 condition (in the deveIopment of shock) is a disturbance of the respiratory metabolism of the tissues which leads, through processes which are stiI1 obscure, to the acapniaI state. That this state may properIy be defined as acapnia is proved by the fact that, given an adequate oxygen supply and a restoration of the hemoglobin to transport it, no other known procedure brings al1 the functions of the body back to their norma state so effectiveIy and so rapidIy as does inhalation of carbon dioxide. 2. “Acidosis,” or hydrogen-ion increase in the blood. Cannon13 says of the “acidotic ” process : “ Non-respirable acid, such as Iactic acid, develops in the tissues because of oxygen-want and, uniting with the Naz of Na2C03, drives off CO, which is breathed out.” 3. “AdrenaI.” Theories on the basis of an “adrenal” factor are apparently poorly supported. “Neither the suggestion of overactivity nor the suggestion of underactivity of the adrenals has sufficient evidence in its favor to warrant attributing shock to the adrena gIands,” according to Cannon. l3 Wiggers30 more recently has expressed a like opinion. Conclusions of other investigators who have experimented with animals

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with and without adrenal gIands in a shocked state are quoted below.86-88~etc~ 4. “CapiIIary

congestion.”

BIaIock42

says of this theory: “StarIing . . . thought the lost blood (in shock) was mainIy in the capiIIaries of skeIeta1 muscIes . . . “ Erlanger and his associates . . . noted (in experimenta shock) that the capiIIaries and venuIes of the intestina1 villi were distended with soIid masses of red corpuscles.” “ Fat emboIism.” Quoting MoynihanT;a The presence of fat emboli in the Iungs and other viscera of patients dying with a11 the symptoms of acute surgical shock has been reported by Bissell (1917), who aIso remarked upon the large amount of fat in the venous blood of such patients, as we11as in the blood of patients with broken bones. The frequency of shock in the wounded among patients with broken bones, or with muItipIe wounds of the soft parts, was also pointed out by Porter (1916) (and aIso by Porter4 in 1920) as evidence of the part pIayed by fat emboIism in the production of shock.

6. “Inhibition.” theory :

BIaIock42 says of this

It was developed by Meltzer before the reduction of the blood volume in shock was recognized. He noted that dissection of the skin of the abdomen caused an inhibition of peristalsis. . . . However, as Cannon has emphasized, the cessation of intestina1 movements is not due to the inhibition of activity in the centrai nervous system, but rather to activity there. 7. “LocaI

vessel injury

of fluid.” This theory BIaIock,42 who says,

with Iocal Ioss by

is mentioned

Many different types of experiments have been performed and the results indicate that the Ioss of bIood at the site of injury and not the absorption of toxins is responsible for the diminution in the blood volume and the decline in bIood pressure folIowing trauma to an extremity. 8. “Traumatic

toxemia.”

The present outIook, Cannon13 says, seems to be that not onIy the shock foIIowing burns,

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but also the shock consequent on severe trauma, is properly in the same category with other forms of genera1 depression of bodily functions and defective circuIation due to the setting free of toxic materiaI in the body, and that the nervous factors, which for so Iong a time have been regarded as of primary importance, shouId be reIegated in most cases to a secondary position. g. “Vasoconstriction.” Cannon’s13criticism of this theory is as foIIows: “The chief defect in the argument (in favor of vasoconstriction as a cause of shock) Iies in a faiIure to account for a primary vasoconstriction capabIe of inducing the effects which MaIcoIm62 describes . ” IO. “Vasomotor exhaustion.” CriIe15 says, We have found that excessive emotion, loss of sIeep, exertion, injury, infection, hemorrhage, or the injection of acids, aIike may cause exhaustion; and that, whatever the cause of exhaustion certain basic phenomena are the same-muscuIar and menta1 weakness; diminished adaptive metabolism; increased respiration; increased puIse rate; sweating; diminished reserve aIkaIinity and in acute phases, increased H-ion concentration of the bIood; intra-ceIIuIar changes in the brain, the liver, and the adrenaIs; decreased eIectric conductance of the brain and increased eIectric conductance of the liver.

Medical

Shock.

AtchIey45

emphasizes

the importance of shock as a fairIy frequent and very vita1 complication of certain medical conditions. It can be seen that the internist may find two types of shock. There is anhydremic shock, dependent on simpIe Ioss of blood voIume, an exampIe of which is diabetic coma; and there is toxemic shock, dependent on possible capiIIary paraIysis from some bacteria1 or protein substance, an exampIe of which is vasomotor coIIapse in pneumonia. This author45 reports the case of an intravenous rattIesnake bite with subsequent shock and eventua1 recovery. Moon and Crawford4’j report the case of a man exhibiting the shock syndrome in mercuric chIoride poisoning.

American Journal of Surgery

63’

MuIIer, Myers, et aI. describe shock symptoms which occasionaIIy foIIow “the intravenous injection of arsphenamine and other drugs or serums.”

Fatal Shock Following Intracutaneous in Test with Horse Serum. Freedman,48 reporting a fata case of acute anaphyIactic shock foIIowing intracutaneous test for sensitivity to horse serum, reviews the Iiterature of related fatalities. In his opinion “ FataI reactions foIIowing the subcutaneous, intramuscuIar or intravenous injection of horse serum comprise the largest group of such anaphyIactic deaths. Fatal reactions foIIowing the intracutaneous injection of a protein, however, are extremeIy rare.” Gus Bacillus and Shock. Buerger4g points out a practica1 point in that, “The earIy local signs of gas baciIIus infection when deep seated may be mistaken for IocaI shock, a11 the more so since the Iimbs, aIready in the condition of IocaI shock, were found especiaIIy prone to this type of bacteria1 invader.”

Further Observations Regarding Traumatic Toxemia. Number 8 of the theories of shock causation, i.e., that of “Traumatic may be elaborated somewhat. Toxemia,” It is significant that surgeons who served on the battIe front during the Great War observed that some toxic agent very definiteIy pIayed a part in so-caIIed “shock” cases. Thus in the specia1 report of the MedicaI Research Committee, DaIe, Laidlaw, and Richards50 make the foIIowing statements : Shock, as produced by histamine, seemed to . . . to be a condition in which the circuKion failed, and the arteria1 pressure feI1 to a Iow IeveI, in spite of arteria1 constriction, because the bIood drained away into the capiIIary network and tended to stagnate there, instead of returning to the heart through the veins. And in seeking for an explanation of this condition it seemed to us that, while Ioss of pIasma and consequent thickening of the bIood, when they occurred, would accentuate the tendency of the bIood thus to accumulate at the periphery, the essentia1 cause must be a genera1 loss of the norma tone of the

632

American

Journal

Boyers-Shock

of Surgery

capiIIary wails. AI1 observations on the Iiving circuIation supports the idea that onIy a small part of the capiIIary network is at any one moment functioning as a channe1 for the bIood. ’ ‘fiistamine Shock. . . . An investigation carried out by two of UP (DaIe and Richards, 1918) . . . furnished us with positive evidence in favor of the view that histamine, and by impIication the group of substances having the same type of action, owe their effect on the circuIation, whether the evanescent depressor effect of small doses or the shock-Iike effect of Iarge doses, to their power of obIiterating the normaI tone of the capiIIaries. Over against this factuaI data we read reports exemplified by the foIIowing excerpts : MiIIer,51 of Los AngeIes, observes that “the cIassicaIIy accepted theory that the production of histamin in the tissues by trauma increases capiIIary permeabiIity, permitting the escape of ffuid from the vascuIar bed is now being questioned.” He quotes resuIts obtained by FreedS1’” who “has shown that rats which are very resistant to histamin, are not shocked by extensive trauma unIess they have been previousIy adrenaIectomized.” ” Vicious Circle” of Causal Events in Production of Shock. MiIIerS1 considers the causa1 sequences of events in shock to be as foIIows : Dehydration produces increased viscosity of the bIood which in turn produces anoxemia, aIready shown to give sympathetic stimuIation. Sympathetic stimuIation resuIts in increased secretion of epinephrin, which increases the rate of the denervated heart; thus demonstrating that dehydration produces sympathetic stimuIation. (Note former quotation concerning sympathetic stimuIation by ether and chIoroform-KnoefeI.38) In shock the vicious circIe is compIeted by the observation that proIonged sympathetic hyperactivity producing vasoconstriction reduces bIood ffow in Iarge areas of the body, resuIting in anoxemia and increased permeabiIity of the smaIIer bIood vesseIs with the Ioss of proteins and fIuid. We find Wright’ observing:

quoting

Cannon,

and

JUNE, 1937

(i) Histamine is present in a11 tissues and is readiIy Iiberated as a resuIt of even trivia1 injuries. (ii) Many of the features of surgica1 shock are identica1 with those of histamine . . polsonmg, e.g., the low venous return, the diminished cardiac output, the Iow bIood pressure, the rapid puIse, the diminished bIood the increased viscosity of the voIume, bIood and the rise in the haemogIobin percentage, visibIe distension of the minute vesseIs in the bowe1 and the increase in the weight of intestina1 Ioops. Injuries which Iiberate quite smaI1 quantities of this capiIIary poison may induce shock in the presence of (a) an anesthetic which sensitizes the bIood vesseIs to the action of histamine, (b) other compIicating factors which of themseIves tend to lower the bIood pressure, e.g. (i) exposure to cold; (ii) Iack of food and water . . . ; (iii) considerabIe sweating which for some unknown reason often accompanies severe injuries, causes further Ioss of fluid, and aIso tends to lower the body temperature; (iv) hemorrhage by itseIf, even if twenty-five per cent of the bIood voIume is Iost, does not give rise to a permanent faI1 of bIood pressure, but hemorrhage combined with injury produces shock.

Histamine-like Various Names.

Tissue Extract Culled by

For many years numerous investigators beIieved that histamine or a histamine-Iike substance reIeased in the bIood stream has been an accompaniment of, and a causative factor in the production of (secondary) shock. We find in the Iiterature different terms referring to this toxic tissue product. In the accounts of his researches TurckK2 has given the name “ cytost ” to the tissue extract derived from injured tissues. De Nito,53 discussing bIood pressure reducing hormones and protein shock, designates “IymphogangIin” which is beheved by him to be formed in the most important Iymph nodes as the “hormone” of this kind.

In Defense of the Role of Histamin Substance in Shock Production. CIark54 says in his concIuding surgica1 shock,

paragraph

of an articIe

on

AIthough it wouId now appear as a resuIt of recent work that Ioss of Auid from and into the

NEW

SERIES VOL. XXXVI,

Boyers-Shock

No. -,

injured area and not histamine is the cause of shock, it would be as we11 to remember, as Dale (1933) puts it, that “we should be unwise on the ground of negative results of experiments on the crushing of the histamine-poor voIuntary muscIes to discount aItogether the possibiIity that irritative handIing and exposure of abdomina viscera, for exampIe, which are reIativeIy rich in it, might Iiberate histamine into the circuIation in shock-producing amounts.”

Traumatic

vs. Histamin

Shock.

HoIt3j

beIieves No observer has satisfactoriIy demonstrated the presence of any depressor substance in the venous bIood from a traumatized area; . . . The circulatory changes of traumatic shock differ considerabIy from those produced by the injection of histamine or other depressor substances obtained from tissue extracts. Marked differences were found in the changes which followed traumatic and histamine shock respectively. The changes indicated . . . are best set out in the foIIowing tabuIar form: Traumatic Shock Diminished circuIating blood voIume. Diminished output of heart before arteria1 bIood pressure faIIs.

Removal of quantity of causes death.

smaI1 bIood

Marked paIIor of viscera. Lungs paIe and heart containing very IittIe blood. Very IittIe bIood when soIid viscera sectioned.

Histamine Shock No marked change in bIood volume. in arteria1 Decline blood pressure before any diminution in cardiac output. Much larger quantity of blood must be removed to cause death. appearCongested ante of viscera. Lungs congested and heart we11 fiIIed with bIood. Solid organs bIeeding freeIy on section.

Experimental Surgery on Animals Tells Less than the Whole Truth When Applied to Human Beings. O’Shaughnessy and SIome,“5 discussing etioIogy of shock on the basis of experimenta work, decIare that “our first conctusion is that a toxemia due to the elaboration of histamine, or any other depressor substance manufactured in the traumatized area, plays no part in the

American Journal of Surgery

633

syndrome of traumatic shock.” Speaking of the variance of resuIts of the experimenta work of these investigators and that of Cannon, MiIIerS6 says, “As is so often the case, experimenta surgery on animaIs teIIs Iess than the whoIe truth when applied to human beings, for in this instance it can take no account of that most important human factor, the psychoIogica1 attitude of the patient.” Roome and WiIsonS7 aIso record results of experimenta work which Iead to the concIusion that “The findings do not support the ‘toxic theory’ of the etioIogy of traumatic shock.” Injury of Certain Parts of the Body Causes Shock M’ore Readily than Injury of Other Parts. With regard to traumatic shock, asserts that shock foIlows Wangensteen2i injury of certain parts of the body more readiIy than others : Fractures of the lower extremities, especially if accompanied by considerabIe bruising of the muscIes, are very IikeIy to be accompanied by of the Iower extremity shock. . . . Fractures are more frequentIy foIIowed by shock than simiIar injuries in the upper, accounted for IargeIy by the presence of Iarger muscIes in the Iower extremity giving rise to more bIeeding when injured. Fractures of the femur and peIvis are frequentIy attended by shock. Head injuries, unIess accompanied by a good dear of external hemorrhage, rareIy give rise to shock. Fractures of the skuI1, unIess associated with intraventricuIar hemorrhage or injury of the meduIIary centers, rareIy give rise to depression of bIood pressure or shock. fractures of the spine rareIy . . . IsoIated produce shock. And in a patient with a fracture

of the spinal column presenting shock, concommitant injuries elsewhere such as intraperitoneal damage or a broken femur, should be looked for. (ItaIics ours.) Wounds of the thorax in which muItipIe fractures of ribs occur may give rise to shock, owing to the formation of numerous hematomas. Severe shock may aIso foIIow the fracture of a singIe rib, in which the lung is punctured with the accumuIation of bIood in the pIeura1 cavity. . . . Zntraperitoneal Injury and Shock.21 Intra-

peritonea1 injury, unless accompanied by severe

634

American

Journal

of Surgery

Boyers-Shock

hemorrhage, does not give rise to significant depression of blood pressure. Contrary to genera1 beIief, the perforation of a hoIIow intraperitonea1 viscus is not foIIowed by shock with immediate reduction of arteria1 pressure. CoIIapse and disability, however, are the rule, owing to the pain produced by irritation of the parieta1 peritoneum.

Condition

of Blood

Vessels in Shock.

With regard to the state of bIood vesseIs in shock there is difference of opinion as to whether the vesseIs are diIated or constricted. FriedIander3* decIares that “the faI1 in blood pressure is due to diIatation

(and congestion) of the Iarge venous trunks of the splanchnic area with coincident meduIIary anemia.” On the other hand Or+ says that “ WalIace, Fraser, and Drummond, after operating upon many hundreds of patients with abdomina1 injuries in a11 degrees of traumatic shock, have not found any splanchnic congestion to exist.” Parsons and Phemister,68 discussing experimental results, say, “We necropsied dogs which died as a result of traumatism of the extremities and found no diIatation or engorgement of the blood vessels of the intestines and other abdomina1 viscera. On the contrary the intestines were paIe.” HewIett’s36 concIusions regarding the mechanica factors which Iead to the Iow arteria1 pressure of shock are that “aIthough some reduction in arteria1 resistance and in cardiac efEciency may be present, the chief cause of the hypotension is withdrawa of bIood from the circuIation partIy through the passage of pIasma into the tissues but mainIy through stasis of blood in capiIIaries and smaI1 veins.” Buerger4g quotes Dale, Cannon, and Hooker, who account for faI1 of bIood pressure in shock as “due to the fact that capiIIaries become paraIyzed and dilated with stagnation within them, thus rendering the arteriole contractions ineffective.” BIaIock6g says, The initia1 changes in bIood pressure (in shock) are to be considered as secondary to (I) compensatory vasoconstriction, and (2) dimin-

JUNE, r937

ished output per beat. The minute output is usuaIIy diminished, but in those experiments in which tachycardia deveIops earIy the minute output may remain norma whiIe the initial changes in blood pressure occur. CutIer diIatation

and Scott,6o without reference to or contraction of vesseIs, say,

It now seems cIear that shock is but a symptom compIex resuIting from a rapid diminution in the circuIating bIood voIume beIow the point of circuIatory efficiency. When a certain point (the critica IeveI) is reached, the Iow blood pressure and insuffIcient suppIy of blood acts in a vicious circIe as an added injury to the capiIIary bed. RostG1 remarks

that

investigations of Mauthner and Pick have shown (that) there is a constriction of the blood vesseIs both of the Iiver and the intestines. During the contraction of the Iiver capillaries, the venous bIood in the intestina1 vessels is choked back. A constriction also occurs in the capiIIaries of the Iungs. The bIood pressure faIIs because the heart receives nothing to pump. . . . According to the opinion of CriIe and Mummery the bIood pressure sinks because of paraIysis of the vasomotor center. But numerous investigations of other writers, such as Malcolm, Seelig and Lyon, Mann, have shown that the blood vesseIs in shock are not diIated but constricted. MaIcoIm,62 in setting forth his views as opposed to those of CriIe in the matter of the condition of bIood vesseIs during shock, decIares : CriIe’s concIusion requires further proof . . . because the assertion . . . that a Iowering of bIood pressure in the carotids must depend on a reIaxation of some part of the vascuIar system is open to question. It is, in my opinion, an altogether untenabIe proposition. It appears to be founded on the idea that a contraction of the arteries causes a rise of blood pressure and a reIaxation causes a faI1. But this is a very incompIete and inexact statement of the we11 recognized law that the smaII arteries exercise a reguIating or stopcock action on the flow of bIood to the tissues. When fuIIy set forth an essentia1 part of the

NEW SERIES VOL. XXXVI.

No. j

Boyers-Shock

stopcock mechanism is that a contraction raises the pressure in the Iarge vesseIs, but at the same time Iowers the pressure in the smaIIer ones, in those beyond the point where the stopcock is supposed to act. Hence, if any vessel has its Iumen suffIcientIy contracted, the bIood pressure in it wiI1 be Iowered. I beIieve that in this fact we have the true expIanation of the faII of blood pressure in shock. McDowaI13’ says, When the shock is due to capiIIary diIation as a resuIt of toxins, the arteries are undoubtedIy constricted, as has been emphasized by MaIcoIm. This has indeed been shown experimentaIIy by the writer and may be taken as evidence of an attempt at compensation, such as we know occurs in hemorrhage. According

to Parsons

and Phemister,58

Handy and Phemister found that re-injection or circuIation by means of a vivi-perfusion apparatus of severa cubic centimeters of sIightIy traumatized or sIightIy haemoIyzed bIood in the femora1 artery caused vasodilation in the Iimb of a dog, but that these same amounts of severely traumatized or compIeteIy haemoIyzed bIood caused vasoconstriction when circulated in the Iimb. We have tested this further by the injection of compIeteIy haemoIyzed or severeIy traumatized bIood in smaI1 quantities (1-50 c.c.) into the Ieft heart or first portion of the aorta, so that it reaches the genera1 capiIIary bed in high diIution. It produces a sharp declhe in blood pressure which with 25-50 C.C. may be as much as 70 mm. of mercury. But the recovery was always very prompt (one-haIf to two minutes) and when it was injected more graduaIIy the bIood pressure would return to the previous IeveI before the injection was compIeted . . . It seems that passage of the damaged bIood through the Iung capiIIaries robs it very IargeIy of its vasodiIator property, and passage through the capiIIaries of a limb compIeteIy destroys it. The cause of the vasodiIation is unknown. It was thought that it might be due to a histamine-like substance Iiberated from the broken down ceIIs, but this is not so, since, when the amount of histamine injected into an anima1 is increased, the faI1 in blood pressure becomes more marked and proIonged,

American

Journal of Surgery

635

whereas very Iarge amounts of extensiveIy haemoIyzed or severely traumatized bIood (200-400 c.c.) circuIated through a periphera1 artery do not Iower genera1 bIood pressure at a11 and when circulated through a vein produce only an initia1 faI1 for one to two minutes. This parodoxica1 behavior when varying concentrations and amounts of damaged bIoods are injected may be due in part or whoIe to physica chemical changes, not to a toxin acting on the ceIIs. The Cause of Experimental Vasodilation Is Unknown. According to WakeIey and Buxton, lg In shock the Iips are pale, and the skin is cold, a state of affairs not at a11 suggestive of diIatation of the surface capillaries. The splanchnic area is quite Iarge enough to accommodate a great deal of bIood. Experimenta1 production of spIanchnic diIatation resuIts in a faI1 of bIood pressure. In shock, however, the practica1 observations of the surgeon show that no such diIatation occurs. Tbe Blood Vessels in tbe Intestinal Tract in Shock. The intestines are paIe in shock, and not red and engorged as wouId be the case with spIanchnic dilatation. The capiIIaries of the muscIes are under different conditions from the capiIIaries of the viscera and skin. Their activity is dependent on the state of the muscIe, and it is possible that the loss of tone in the muscles in shock aIIows of passive diIatation of a Iarge mass of capiIIaries.lg Petroff, Filatov, et aI. conducted experiments with voIume determinations of

kidneys,

spleen, hind Iegs, and brain which

indicate

that

the introduction

of hemoIyzed

or foreign bIood causes a marked narrowing in the Iumen of the renaI and spIenic bIood vesseIs. The circuIation in the brain and in the hind legs was affected onIy slightly. . . . These experiments demonstrated that the main alterations in the circuIatory system in hemolytic shock proceed from the aIterations in the waIIs of the arteries and the veins. “have been abIe to Wesselkin et aI. substantiate the basic experiments of Hesse and FiIatov as to the spasm of the renal arteries constituting a characteristic symptom of the acute stage of shock.”

636

Boyers-Shock

American Journal of Surgery

Deoxygenation of Body Tissues in Shock. MacFee and BaIdridge65 say, the essentia1 fact of shock is deoxygenation

of body tissues, occurring from impairment of circuIation . . . (which) results from diminution of bIood voIume in circulation. This Ioss is due to stagnation of bIood in the capiIIary areas and to escape of pIasma from capiIIary channeIs. Hemorrhage and dehydration are frequent factors.

Blood Cell Counts in Shock. Cannon13 and his co-workers at Bethune made bIood counts in a series of 27 cases of severe traumatic shock. “AI1 but eIeven had a capiIIary count which amounted to 6,000,ooo red corpuscIes or higher, and in eight corcases it was more than 7,000,000 puscIes.” Venous counts the same time, and

were aIso made at

from these considerations it seems evident that the difference between capiIIary and venous red counts varies roughIy with the degree of shock, and, since the venous count is approximately at the norma IeveI or beIow it, the difference is due to concentration of the bIood or stagnation of corpuscIes in the capiIIaries. Wright? says, “The pIasma bicarbonate content is Iowered in shock; this has been which causes attributed to anoxemia, incompIete combustion of carbohydrates and possibIy of fats in the tissues with the formation of acid products which pass into the bIood.” Reduction of Alkali Reserve in Shock. BayIiss states that “a part of the norma bicarbonate content becomes neutraIized by combination with some fixed acid (Iactic, etc.) produced in the tissues on account of the defective oxygen suppIy.” Henderson and Haggard attribute this to over-ventiIation of the Iungs by rapid breathing. Cannon states that “the reduction of the aIkaIi reserve is an indication of a fundamenta1 diffIcuIty occurring in the body, nameIy, an insuffrcient oxygen suppIy.“‘2 Continuing 0Iogy :

in

Cannon’s13

own

phrase-

JUNE, 1937

The faiIure of deIivery of sufficient oxygen to the brain is IikeIy to affect profoundIy the norma metaboIism of nerve ceIIs in particuIar, and to Iead to a disturbance of their functions. It becomes a matter of importance, therefore, to know at what point in an impaired circulation the oxygen deIivery to organs becomes inadequate. and VaIte . . . RosP says, “Cobbett of the blood as see an increased viscosity the cause of shock. . . . Short couId not demonstrate this condition.” In a discussion of fat embolism in surgical shock, Moynihan43 says, “That the presence of fat in the bIood stream in shock greatIy increased its viscosity was demonstrated bsGauss.”

Viscosity of the Blood in Shock. CannonI says the increase in the number of corpuscIes per C.C. increases the viscosity of blood in shock. He says aIso that “another way in which the viscosity factor might become prominent is through concentration of the corpuscIes due to sIowness of the bIood Aow itself.” (Work of Cohnstein and Zuntz and by Ma11 and Welch cited.) H-ion Concentration of the Blood in Shock. According to KiIduffe,66 “When the bIood pressure is Iowered by shock, there is a faI1 of pH, and the same is true of hemorrhage.” BIaIock42 disagrees : The faII in bIood pressure precedes a significant increase in the hydrogen-ion concentration of the blood. It is onIy in the terminal stages of shock that the aIkaIi reserve is markedIy reduced. CriIe,15 aIso, says that H-ion concentration of blood is increased “in every type of intense overwheIming activation-by intense exertion, by intense emotion, by intense trauma; it was increased aIso by inhaIation anesthesia, by hemorrhage . . . (etc.). Aub and Cunningham67

conclude

that

I. There is a markedIy diminished oxygen content of the venous bIood in experimental traumatic shock. This change occurs before the blood pressure faIIs to a shock level and

NEW

SERIES VOL. XXXVI,

is &II shock.

present

after

No.

Boyers-Shock

3

apparent

recovery

from

. . .

Are the Blood and Lymph in Shock Toxic? EIman and CoIe68 carried out anima1 experiments to discover if possibIe whether or not blood and lymph in shock describing in detai1 are toxic. “Without these experiments it was apparent that none of the injected material proved toxic; and, when it was, there was no essentia1 difference over the controIs.” Earlier investigators and advocates of the “traumatic toxemia” theory of shock wouId disagree with the foregoing statement on the basis of experimenta work as we11 as cIinica1 observation. findings which “preOrrl* summarizes sent rather strong evidence that following trauma there is an absorption of toxic protein materia1 from the damaged tissues which is a factor in the production of the shock state.” The Factor of Toxins in the Production of Shock. In their “Note on MuscIe Injury in ReIation to Shock,” BayIiss6g and Cannon say in part: “And, just as in the animal experiments recorded above, the injured muscIe wouId produce metabolites, which, on being absorbed into the bIood stream, would indicate their presence by a decrease in the blood pressure, with other signs of shock.” Robertson” notes that ” IncoaguIabiIity of the blood is one of the symptoms of profound anaphylactic shock. . . . ” Leucocytes in Shock. Other statements with regard to bIood characteristics in shock foIlow: 0rr12 says, Following severe trauma a leucocytosis as high as 20,000, or even higher, may deveIop within one or two hours. This Ieucocytosis rapidIy diminishes and usuaIIy disappears within forty-eight hours. The reason for this rapid rise in the white cel1 count is certainIy not infection. It is apparently due to the absorption of traumatic products. These clinica observations do not correspond to the observations of CriIe and Mann, who found a decrease in Ieucocytes in experimental shock.

American

Journ al of Surgery

637

Sugar Content of the Blood in Shock. With regard to the sugar content of the bIood in shock, Cannon13 says, . . . there is no Iack of sugar in the bIood; indeed, is actuaIIy above the . . . the amount norma (0.1 per cent). Furthermore, there appears to be no reIation between the variations of the carbon dioxid capacity of the bIood and the percentages of sugar.” Aub and Wu,‘O studying experimenta traumatic shock, con&de: ” I. AnimaIs with marked muscIe trauma but without true shock showed onIy sIight changes in total non-protein nitrogen, urea, creatin and sugar in the blood. These constituents, especiaIIy the creatin and the sugar, rose markedIy as shock deveIoped. In contro1 animaIs the determined constituents showed no appreciable change. . . . ” induce him to ScarpeIIo’s71 researches concIude that . . . in traumatic shock the increase in the blood sugar is due chiefly to an aIteration of the gIucoreguIatory functioning of the hepatic ceIIs. It is not easy to give an expIanation of this phenomenon. It is probabIe that various factors act on the Iiver and increase the gIycogenie functioning. By way of a simple hypothesis, it might be assumed that the traumatic shock causes disturbances in the fieId of the sympathetic nervous system which in turn act on the hepatic ceIIs and increase the gIycogenoIytic functioning. On the other hand, it is not impossible that the disturbing movements of the intestine cause an absorption by the porta system of toxic substances, which, as has been shown for various toxins (Delbet, Marmier), may stimuIate the hepatic ceIIs to an increased gIycogenoIysis.

Nitrogen Content of the Blood in Shock. CannonI says, “By a chemical analysis of the bIood of wounded men, DuvaI and Grigaut determined that, paraIIe1 with a diminution of the non-protein nitrogen of traumatized tissues, there was an increase of non-protein nitrogen and of residual nitrogen (i.e. total non-protein nitrogen minus urea nitrogen) in the bIood.” In his study of “Certain Aspects of the Metabolic Response to Injury,” Cuthbertson72 con-

638

Boyers-Shock

American Journal of Surgery

cIudes: “ (7) Th e curves of urinary excretion of nitrogen and the basa1 consumption of oxygen are generahy paraIIe1.”

The Basal

Metabolic

Rate

in Shock.

With regard to the basa1 metaboIic shock, Aub73 says in concIusion,

rate in

. . . (2) Experimenta traumatic shock causes a marked faII in the rate of basal metaboIism to 70 per cent of the original IeveI. The degree of faI1 is dependent upon the severity of the shock produced. . . . (4) The effect of hemorrhage is not constant. It may temporariIy lower, or have no immediate effect on the metabolic rate. (3) Recovery from shock after bIood transfusion is usuaIIy associated with a prompt return of the metabolic rate to a norma level.

Systemic Efects the systemic Loeb” say,

effects

of Shock. of shock,

Regarding AtchIey and

The most significant effect is the interference with tissue function which results from circuIatory stasis and diminished bIood suppIy. No organ shows this disturbance more strikingIy than does the kidney. Rena1 function is compromised and anuria frequentIy resuIts. This, in turn, definiteIy upsets the acid base equiIibrium of the body and in the case of diabetic shock prevents the excretion of ketone bodies, thus adding to the seriousness of the disease state. The tissues of the centra1 nervous system are aIso incIuded in the genera1 damage and the resuIting pathology doubtIess pIays a large part in the termina1 stages.

Shock and Hemorrhage. Reference may be made briefly to the distinction between shock and hemorrhage. CriIe” writes as foIlows : “In the absence of a history of either trauma or bIeeding, without evidence of free ffuid in cavities, and without a bIood examination, . . . we beheve it (differentiation between shock and hemorrhage) cannot with certainty be done.” 0rr,12 discussing changes in the blood picture in shock, quoting from CriIe’s work, states that there is either a sIight or no faI1 or a rise in hemogIobin, and in hemorrhage there is at first IittIe or no faI1, but after the Ioss of a fourth, a sixth, or a tenth of the fata amount

JUNE, 1937

of bIood the hemogIobin begins steadiIy to faI1. The red ceI1 count foIIows rather closeIy the curve of the hemoglobin in both hemorrhage and shock. CriIe found reIativeIy sIight change, sometimes a fall in the Ieucocytes in shock, and in hemorrhage in every instance a rising Ieucocyte count. He then concIudes that repeated and accurate observations upon the blood picture may differentiate between hemorrhage and shock. BIaIock74 quotes from JournaI of the American tion’ll which summarizes and Kennedy:

an editoria1 in the Medical Associawork by Moon

In shock the bIood becomes more concentrated, as shown by specific gravity, hemogIobin, and erythrocyte count; foIIowing hemorrhage, diIution of bIood occurs. In shock there is widespread capiIIary diIatation of the congestion accompanied by edema viscera, and petechia1 hemorrhages; foIIowing hemorrhage the tissues are anemic. The differentiation of hemorrhage and shock is of more than academic importance. It is we11 known that recovery foIIows the introduction of physioIogic soIution of sodium chloride into the circuIation of patients suffering from the simpIe Ioss of bIood. The futiIity of this procedure in shock has been proved beyond question. The increased permeabiIity of the capiIIaries, which is a characteristic feature of shock, aIIows saIine soIution to escape rapidly into the tissues. SoIutions containing acacia or dextrose have been found more effective than saline soIutions but not so effective as transfusion of blood. Even the Iatter is ineffective in profound shock.14

Is Diferentiation between Shock and Hemorrhage Possible? ArchibaId and McLean, quoted by Orr, l2 aIso observed “that in hemorrhage intravenous saIine soIution was heIpfu1, but useIess in severe shock.” diagnosis (i.e. beMacIeod76 says, “The tween surgica1 shock and hemorrhage) is cIinched by the effect of, transfusion; the hemorrhage case quickIy recovers whereas that in shock onIy sIowIy, if at alI.” According to Bickham,‘j “marked hemorrhage resuIts in coIlapse, rather than in shockahhough differentiation of the phenomena is not easiIy made.” Cannon13 is even less

NEW SERIES VOL. XXXVI,

Boyers-Shock

No. 3

discriminatory: “Shock is hemorrhage hemorrhage is shock.” Mann and Essex33 point out that

and

shock and hemorrhage are identica1 in one respect, namely, that there is a decrease in the amount of circulating blood in both conditions. Thus there is a simiIarity in the physioIogic aspects of the two conditions, although the pathoIogic fmdings may be quite different. This conception of the reIationship between shock and hemorrhage explains the fact, which has been demonstrated so frequently both cIinicaIIy and experimentally, that a hemorrhage which wouId be insignificant in the norma state wiI1 aggravate or prove fatal in the condition of shock. CutIer

and ScottGo say:

The immediate effects of severe hemorrhage and shock produce the same syndrome by the same mechanism, viz., a diminution in the circulating bIood voIume. There is the difference that in shock uncomplicated by hemorrhage the blood is concentrated without loss from the body of the erythrocytes which to a Iarge extent remain in the capiIIary bed, whereas in case of active hemorrhage the red ceIIs and their contained hemogIobin are Iost to the body. This fact is demonstrated by a study of the difference in the recovery of the two types. Thus, after making up the bIood volume Iost by a Iarge hemorrhage the hemoglobin figure is much Iower than after a corresponding degree of shock not caused chiefly by hemorrhage for in the Iatter instance viabIe ceIIs are brought back into the circuIation.

Rhodes and McKenney76 lowing distinctions :

make

the fol-

If hemorrhage is the major factor, the cIinica1 picture is aItered in that: (I) The apathy is repIaced by anxious alarm. (2) Instead of the passive immobility of shock there is restIessness and often a marked degree of muscuIar activity. (3) The shaIIow rapid respiration is replaced by deeper and more Iabored breathing, which is terminaIIy aptIy described as typica air hunger. (4) The examination of the peripheral bIood shows a diminution in red blood ceIIs and hemogIobin as in secondary anemia, thus differing markedly from the findings in shock. There is aIso a Ieukocytosis with a reIativeIy high percentage of poIymorphonucIear ele-

American

Journal

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639

ments, and when the hemorrhage is internal there is a rapid and very marked increase in white bIood ceIIs. PaIfrey28 beIieves

that

the constitutiona effects of hemorrhage have one important difference in their course from those of shock. . . . In shock, the symptoms and the faI1 in the bIood-pressure readings occur progressively. In gradual hemorrhage, on the contrary, aIthough the pulse rises progressiveIy, the symptoms tend for a time to be in abeyance, and the blood-pressure tends to maintain itself until at Iast, quite suddenly, there is a great faI1 in blood-pressure with serious symptoms of coIIapse.

Recent Work on Surgical Shock. Concerning recent work on surgical shock, there is in a late issue of the JournaI of the American MedicaI Association113 the folIowing announcement: Dr. John Beattie, conservator of the museum of the RoyaI CoIIege of Surgeons, (London), described recent work at the coIIege Iaboratories on surgical shock. Experimental animals showed three stages. The first faI1 in bIood pressure after trauma was due to Ioss of fluid. The period of recovery might Iast thirty minutes and then a gradua1 faI1, terminating in death, took place. The work done in the Iaboratories pointed to the concIusion that the Ioss of fluid during the first phase was not the cause of death, which was due to something happening in the second stage, probabIy associated with impuIses passing aIong the sympathetic nerve. Perhaps these impulses brought about some change in the central nervous system that was irreversible, and in consequence the bIood pressure kept on faIIing unti1 it became so Iow that death was inevitable. An anima1 shocked by trauma of the hind Iimb might die in two and one-haIf hours. But if the spina cord was bIocked by procaine hydrochIoride the bIood pressure was maintained and the anima1 was prevented from passing into a condition of shock. Cross circuIation experiments confirmed the concIusion that the Iethal factor in shock was abnorma1 nerve impulses.

Introduction to Consideration of Treatment of Shock. As an introduction to a discussion statement

of the treatment of shock, a by McDowaIP’ is a propos: “I

640

American

Journal

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propose to . . . emphasize that shock is not a singIe entity, but may be produced experimentally and cIinicalIy from a variety of causes, and that any singIe remedy used without understanding of the case in hand is bound to give most contrary resuIts.”

Measures Directed toward Prevention of Shock. Or+ says, In the civi1 practice of surgery, serious consideration shouId be given to the prevention of surgica1 shock. Much can be done to avoid this compIication by properIy studying and preparing the patient for operation. It appears obvious that a patient with dxiseased kidneys, impaired function of the Iiver, faiIing circuIatory system, cachexia, anemia, toxemia or other conditions which Iower the genera1 bodiIy resistance, might more quickIy deveIop shock than the patient whose vita1 functions are practicaIIy normal. In addition to the carefu1 study of the patient’s physica condition, care shouId be taken not to Iower his resistance by iII-advised preoperative surgica1 preparation. Depleting purges, starvation, dehydration and excessive anxiety shopId be avoided as much as possible. In many cases, transfusion, hypodermocIysis of physioIogic sodium chIoride or infusion of gIucose soIution before or during an operation wiI1 prevent shock. The proper seIection of an anesthetic is of utmost importance. Every surgeon shouId have a good working knowIedge of the various types of anesthesia and shouId make this choice to suit the patient. . . Carefu1 protection of the patient from coId before, during and after operation is essential. Trauma shouId be minimized aIways. The judicious use of sedatives to reIieve pain and restIessness is not onIy fair to the patient, but may Iessen the shock of anesthesia and operation.

Spinal Anesthesia Advocated in Shock. O’Shaughnessy and SIome55 advocate anesthesia for shock sufferers. They

spina say in

part, The one’ therapeutic measure which (we have found) succeeded in raising and maintaining the bIood pressure of a traumatized cat whose pressure had sunk to 20 mm. of mercury was the induction of spina anesthesia. In some cases this measure has been combined with injection of saIine into the peritoneum,

JUNE,I937

with apparentIy beneficial results. It is of course possibIe that some better method of controIIing nociceptive impuIses may be devised -the injection of a IocaI anesthetic into the traumatized area suggests itself as one possibiIity-but we are convinced that contro1 in some form is essentia1 to the successfu1 treatment of the syndrome. Even if we are wrong in the emphasis we lay upon the discharge of nociceptive impuIses, the beneficia1 effect of spina anesthesia remains a fact which seems worthy of note and further investigation.

Anesthesia and Shock Prevention. Another note regarding anesthesia in shock previousIy quoted from an articIe by Jones3g is repeated here: “ IocaI nerve bIock with a cocaine derivative (nupercain) Iessens damage to the centra1 nervous system, aIIows reIaxation with minimal anesthesia, and prolonged freedom from pain in the postoperative period.” CriIe’+ testimony is that “We have founb, that the acute exhaustion (shock) of gurgica1 operations may be minimized or prevented by bIocking the fieId of operation with IocaI anesthetics, or by preventing the response of the brain-ceIIs to the stimuIus of traumatic impuIses by nitrous oxide anesthesia.” CutIer and ScottGo decIare that If the bIood voIume can be maintained in the earIy stages before the capiIIary permeabiIity has been irreparabIy depressed, the serious phases of shock and hemorrhage never appear and the circulatory efficiency is kept above the critical Ievel. This makes it cIear how important it is to be able to estimate the avaiIabIe voIume of circulating bIood. These authors say aIso concerning vention of shock:

pre-

Postoperative hemorrhage and shock are prevented (I) by operating upon patients onIy when they are in a condition at least as regards their circuIatory mechanism, which we designate as “good risk,” i.e. their heart action, their vasomotor tone and their bIood voIume are as near norma as possibIe; and (2) by utiIizing careful surgical technique. This means perfect hemostasis during the operation, care-

Now SEHIES

VOL.

XXXVI.

No.

ful tying of ligatures, tissues, and asepsis.

3

gentIeness

Boyers in handIing

Low Blood The Dangers of Persisting Pressure. Under caption of “ PrincipIes underIying proper treatment,” Rhodes and McKenney76 say, . . . If the low blood pressure with its reduced voIume ffow is suffIcientIy persistent, permanent ceIIuIar changes are brought about in the higher nerve centers, and these uItimateIy resuIt in paralysis of the vasomotor center. Herein lies the great need for early treatment in shock for once the vasomotor center has become permanentIy damaged by the anoxemia, vascular tone is lost. When this Ioss of vascular tone exists, our efforts to combat shock, particuIarIy those endeavoring to restore fIuids, wiI1 be fruitless. The probIem accordingly resoIves itseIf into an attempt to interrupt the chain of events which Ieads to these typica vicious circIe reactions. WaIIace,78 who had an extensive experience with shocked patients at the battle front, states that “a11 the estabIished methods of treatment were used, but warmth combined with rest greatIy outstripped a11 others in favour.” Treatment of Shock More or Less IndeAtchIey45 says, pendent of the Cause. The treatment of shock is more or Iess independent of its cause. Whether it is due to trauma, toxemia, hemorrhage or anhydremia, the physiologic probIem is the same; namely, a disproportion between the bIood voIume and vascuIar bed. On one hand there is primarily decreased bIood voIume from hemorrhage or fluid loss; on the other increased vascuIar bed from capiIIary diIatation. The need for immediate measures to increase bIood voIume is common to a11 types. A point of view opposite from that quoted is found in an articIe by Andrews.7g He says, “The treatment for the various sorts (of surgica1 shock) is quite specific and if appIied to the wrong kind, may be definiteIy detrimenta1.” Shock a Safety Reaction of Nature. In considering the treatment of burns CIark and Cmickshankso make an interesting observation : “Shock in itseIf may be

Shock

American

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641

Nature’s effort to deaden pain and tide the patient over the initia1 phase of his injury, and its treatment shouId be conservative. Loss of fluid shouId be prevented as far as possibIe and repIaced by the most suitabIe methods.” Principles Underlying Selection of Proper Says JohnDrugs for Treatment of Shock. son,81 of Chicago, The method of treatment of acute surgica1 shock or of shock due to hemorrhage when the predominating symptoms are low bIood pressure, weak and thready puIse, and depression of the centra1 nervous system has always been unsatisfactory as far as the use of drugs is concerned. As a ruIe, in this type of shock a vicious circle is estabIished in which depression of the bIood pressure causes further depression of the centra1 nervous system and vice versa. In some instances it appears as if the centra1 nervous system depression is the predominant factor which Ieads to Ioss of vasomotor tone with a Iowering of bIood pressure. In other cases the Iow bIood pressure seems to be the essentia1 factor with consequent central nervous system depression. In the choice of a drug designed to overcome this vicious circIe, severa factors ought to be considered, the most important of which are as foIIows: I. The drug shouId be non-toxic with a high margin of safety; i.e., a drug that wiI1 not cause a toxic reaction in aIready depressed circulaIatory and nervous systems. 2. It shouId have a pronounced hemodynamic action as we11as a marked stimuIant action on the centra1 nervous system. 3. These actions of the drug shouId be of a Iasting character in order that the various body systems may regain the physiologic state Iost by the previous inadequate circuIation of bIood through them. If the drug has a Iasting action, time wiI1 be avaiIabIe for the institution of other supportive measures. This author*’ states that “ephedrine seems to exhibit these characteristics.” Wood,“2 reUse of Coramine in Shock. porting on the efficacy of coramine, says, I. Coramine is a definite stimulant to respiration and circuIation depressed by avertin, novo1, or in surgica1 shock.

642

American Journal of Surgery

Boyers-Shock

2. The toxicity of coramine is Iow; so that Iarge and repeated doses may be empIoyed if the necessity exists. This is we11 iIIustrated in one of our cases, where 28 C.C. were given in a period of sixteen hours with apparently excelIent results. Further, that in this series there was no evidence of depression after the immediate stimuIation . . .

Use of Morphine in Treatment of Shock. Orr12 says, “UndoubtedIy morphine shouId be given in many cases of shock. . . . CriIe and Lower have recommended giving morphine unti1 the respiration is reduced to I 2 per minute.” According to SoIis-Cohen,83 “In conditions of surgica1 shock, morphine is sometimes the best agent that can be employed. In other cases, strychnine or epinephrine may be preferabIe.” In Marshali’s opinion, “the severeIy wounded do not make good recover& from operation if deepIy morphinized.“12 Orr12 quotes Cannon’s report of experimenta1 observations made by CatteII at Dijon upon the relationship between the use of morphine and the change in aIkaIi reserve. The resuIts show that morphine prevents the faI1 in aIkaIi of the blood and that, in cases of low blood pressure with an aIready Iow carbon dioxide combining power, there is a rise in aIkaIi approaching normal. The expIanation for this effect of morphine is not cIear, but it is probabIy due to a reduction of bodiIy activity, with a resuIting decrease in tissue demand for oxygen. Hendersons4 points out aIso that “one of the principa1 effects of morphine is to decrease and in suf%cientIy Iarge dosage, finaIIy aImost to abolish the sensitivity of the neurorespiratory system to its normal stimuIus, carbon dioxide.” Regarding the use of adrenaIin in shock, MacFee and BaIdridge66 say, AdrenaIin to raise bIood pressure is to be condemned. Acting as it does upon the arterioIes, its effect is to raise the bIood pressure in the arteria1 tree. But, as pointed out by Cannon, this does not improve the voIume ffow in the capiIIaries. “ . . . MereIy a higher arteria1 pressure is not the desideratum in the treatment of shock, but a higher pressure

JUNE, 1937

which provides an increased nutritive flow through the capiIIaries a11 over the body.” These authorss5 decIare that “cardiac stimuIants, in the absence of organic cardiac disease, are generaIIy uncaIIed for.”

Adrenalin

Insuficiency

(?)

in Shock.

SwingIe, Pfiffner, et aI. express the suggestion that “the signs and symptoms of adrenaIin insuffIciency, and of traumatic or secondary shock are possibIy due to one and the same thing, i.e. failure of the blood volume and bIood-diIuting reguIator mechanism, the adrena cortex.”

Tbe Relationship of Adrenal Cortex Hormone to Shock. There has been considerabIe criticism and discussion of SwingIe’s work and pubIications. Freemans believes The investigators (under discussion) have cIearIy demonstrated that the cortico-adrenal hormone is a specific therapeutic agent for the shock which is associated with absence of the adrenaIs, but they have not reported experiments in which the effect of cortin has been assayed in traumatic shock. . . . AIthough the anaIogy between deficiency of corticoadrena hormone and traumatic shock is a cIose one, no convincing evidence has been presented that the two conditions have a common etioIogy or that the cortica1 hormone is of benefit in the treatment of shock. Britton

and SiIvettes7

say,

Our own observations Iead us to conclude that changes in bIood pressure and in the amount of circuIating blood are indirect and illustrative onIy of the genera1 effects of adrenaIectomy throughout the body. . . . Our data compe1 adherence to our first proposed theory of the adrena cortex-that of the regulation, in cooperation with other tissues or secretions, of carbohydrate metaboIism in the organism. .

Functioning of Adrenal Cortex as Related to Shock. Parkins and his co-workers have done considerabIe experimenta work on the subject of resuIts of adrenaIectomy in relation to the shocked state of animaIs. Their experimentation Ieads SwingIe and Parkinss8 to report in part that “The data

NEW

SERIES VOL. XXXVI,

No.

3

Boyers-Shock

indicate that the unoperated dog has sufficient reserve hormone in his intact functioning adrenai cortica1 tissue to prevent shock foIIowing hemorrhage and . . . The adrenaIectomized anitrauma. mal enjoying good heaIth but lacking such reserve hormone, succumbs to shock as a result of trivial injury.” Shock Causes Marked Reduction in Functional Eficiency of Adrenal Cortex. Experimenta1 data is presented by Donahue and Parkinssg indicating that foIIowing trauma and the onset of secondary shock the adrena cortex is subjected to severe functiona strains Ieading to a marked depletion of Iipoid, gross hemorrhages into the gIand and vacuoIization of ceIIs. These changes are indicative of marked reduction in the functiona efficiency of the cortex in this syndrome (i.e. shock).

eviParkins et aI.g0 have aIso reported dence that “The adrenaIectomized dog aIthough in equaIIy good physioIogica1 condition is far more susceptible to the decrease in serum sodium and chloride and associated disturbance in ff uid baIance foIIowing intraperitoneal injections of isotonic glucose than is the anima1 with intact adrenaIs.” Use of Stimulant Drugs in Shock during the Great War. Cannon13 says with regard to the use of drugs in treatment of shock: “In British and American services the use of stimuIant drugs, such as strychnin, and aIso vasoconstrictor drugs, such as pituitrin and adrenaIin, practicaIIy disappeared during the course of the recent War.” The resuIts of such experience as that on which Cannon bases his statements must aIways take precedence over concIusions such as those expressed by Harrower,g1 e.g., who says : “For years it has been known that adrenaIin offers a Iife-saving service in shock and heart faiIure. The best method of administering adrenaIin in cases of ordinary shock is by intravenous infusion of high diIutions in saIine soIution.” Epinepbrine and Pituitary Solutions in Treatment of Shock. Summarizing their recent experimental work with pituitary

American

.lournal

and with epinephrin et aI.g2 say:

643

of Surgery

soIutions,

BIaIock

Experiments were performed in which a decline in blood pressure was produced by the introduction of histamine, of unpurified acacia and of incompatible blood, and saIt solution was injected continuousIy intravenousIy. The introduction of soIution of pituitary or of epinephrine in the amounts used in these experiments did not prevent the Ioss of protein from the circuIation. FriedIander,34

aIso,

concIudes

that

Epinephrin and pituitary extract are of no vaIue in the treatment of secondary shock. . . . And Cannon adds that the desideratum in shock is a higher pressure which provides an increased nutritive ffow through the capiIIaries a11 over the body. This cannot be brought about by any medication, but onIy by such measures as wiI1 definitely increase the bIood voIume and thus heIp the voIume Aow through the capillaries. AtchIey

and Loebl’ beIieve

that

The use of vasoconstrictors, such as epinephrine, is not heIpfu1 and may, indeed, be dangerous. From a physioIogica1 standpoint they are contraindicated because the bIood vesseIs which they affect are aIready constricted to the disadvantage of the capiIIary circuIation, as has been shown by studies of both the skin and viscera1 arterioIes.

Parathormone in Treatment of Shock. McDonagh40 proposes that parathormone be used, decIaring that “ Parathormone is a conductor, it causes dispersion of hydrated particIes, and is of equal vaIue in preventing histamine from producing shock, insulin from producing convuIsions as it is in preventing guanidine, etc., from producing tetany.” says that of the stimuIant PaIfrey28 sodio-benzoate, grs. 2-3, drugs, “caffein given intravenously, is the one most generally beIieved in.” He thinks “epinephrin (I : I oo), minims xv, added to norma saIt soIution and given intravenously is of vaIue.” Cagein and Digitalis in Treatment of Shock. Rhodes and McKenney76 decIare

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American Journal of Surgery

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that “Caffein in Iarge doses is used aImost routineIy as the proper stimuIant for the patient in the shock state. Certain observers recommend aIso various cardiac stimuIants of the digitalis group for these patients. The value of both caffein and digitaIis is probabIy over-estimated, as apparentIy there is no intrinsic myocardia1 fauIt demonstrabIe.” Wangensteenzl says “ BIaIock found that digitaIis in shock Iowered the minute cardiac output, and he concIuded that its use in shock is actuaIIy harmfu1. It is to be remembered that the contractiIe power of the heart is norma in shock and that it is not in need of stimuIation.” The Use of Drugs in Treatment of Surgical Shock. Wangensteen says eIsewhere,g3 with regard to use of drugs in treatment of surgica1 shock, In the faI1 of bIood pressure accompanying spinal anesthesia and that occurring after sudden remova of Iarge quantities of fluid from the body cavities, the administration of vasospastic agents is urgentIy indicated, for in these conditions there is an actual Iowering of the tone of the vessels. In these conditions too, the TrendeIenburg posture has its greatest value. Later in this same articIe the author says, “ Even though patients in shock suffer more from depIetion of bIood voIume than from want of oxygen carriers, the most effectual means of restoring a diminished bIood voIume ,is transfusion of bIood.” The concIusions of Cutler and ScottGo regarding treatment of shock may represent the genera1 consensus of opinion: “Other than transfusion and the administration of fluid, heat and morphia wiI1 do more to restore vasomotor tone than a11 the other procedures advocated.” “Of a11 methods of intravenous treatment in shock,” says 0rr,12 “bIood transfusion most nearIy approaches the ideaI. It wiI1 raise the bIood pressure, increase the bIood voIume and, in addition, suppIy oxygen-carrying corpuscIes.” FIuids shouId be introduced into the body by whatever means is best suited to

the particuIar many4 say,

case.

Brandson

and

HiIIs-

The use of fluids is invariabIy directed towards maintaining the acid-base baIance, electronic concentration and blood voIume. . . . To resist the various disturbances to which the organism is constantIy subjected these processes have formed a defensive alliance. A disturbance in any one is resisted as far as possibIe by the specific process invoIved. When this process is unabIe to further cope with the situation the other two are caIIed upon for aid, unti1 by mutua1 assistance the biochemica1 baIance is again estabIished. Saline Solution in Treatment These authorsg4 say further:

of Shock.

In saIine we have a soIution that wiII restore very promptIy in a11 surgica1 conditions the acid-base baIance, electronic concentration and the bIood volume. The chief base of the bIood is sodium; the chief acid is chlorine; the great buIk of the bIood voIume is water; and the eIectronic concentration is chiefly maintained by retention, excretion and diffusion of sodium, chlorine, and water. Give to the organism a sufficient quantity of isotonic saIine soIution and it wiI1 by seIective action retain sodium and discard ‘chIorine in the presence of an acidosis, retain chIorine and discard sodium in the presence of an aIkaIosis, and utiIize the sodium, chIorine and water to distribute between bIood stream, tissue space and body cel1, to estabIish eIectronic baIance and restore bIood volume. In order to correct a11 three processes simuItaneousIy the saline must be isotonic, as saIine in any other concentration wiI1 affect the eIectronic concentration and force readjustment of the other two processes. Hypertonic Solutions. Padgett and Orrg5 say that “hypertonic solution of crystaIIoids have not been used with compIete success in the past in the treatment of we11 deveIoped shock. RecentIy, evidence is accumulating that intravenous therapy with hypertonic soIutions of crystaIIoids, unIess introduced with the greatest care, may be actuaIIy harmfu1.” CutIer and ScottGo state that It has been shown that the administration of Iarge amounts of fluids (by rectum, by

NEW SERIES VOL. XXXVI,

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645

mouth, and subcutaneousIy or intravenousIy) washes out into the genera1 circuIation ceIIs which presumabIy are stored against such an emergency. . . . The spIeen may .be such a reservoir. The investigations of Robertson and Bock seem to indicate that even immature forms of red ceIIs, possibIy from the bonemarrow, are freed into the circuIation folIowing the administration of Iarge amounts of fluid. Such ceIIs, of course, have a greater permanency of value than transfused ceIIs, and in a11 such cases a high fIuid intake is essential.

gives resuIts which, in this series, seems more satisfactory than those obtained in cases treated by saline or gIucose alone. (3) Cases of traumatic shock respond most readiIy to this treatment. (4) Cases of postoperative shock treated in this manner show marked improvement. (5) The optiona dosage is 1000 C.C. of a 5 per cent or 10 per cent soIution of gIucose with one unit (~20) of insuIin to three grams of glucose. BeneficiaI results are usuaIIy apparent after 800 C.C. of fluid have been injected.

Temporary E$ect of NaCl or Ringer’s Solution. “ Bayliss (Intravenous Injection in Wound Shock, London, I 9 I 8) has proved quite conclusiveIy,” says 0rr,12

The conclusion in regard to the gIucoseinsuIin treatment reached by Padgett and Orr,g6 however, is that “from the experimental standpoint the glucose-insuIin treatment of shock recentIy advocated by Fisher seems to be no more beneficia1 then treatment with a hypertonic soIution of glucose or sodium chIoride.” More recent is the opinion expressed in an editorial notell pubIished by the JournaI of the American MedicaI Association in response to a query submitted by a Kentucky physician with regard to the use of dextrose intravenously in the treatment of shock:

that the injection of physioIogic sodium chloride or Ringer’s soIution has onIy a temporary effect in the treatment of severe shock. A rise in the bIood pressure foIIows the injection, but within an hour it usuaIIy returns to its previous IeveI. The solution IiteraIly Ieaks out of the bIood stream into the tissues. Hypertonic sodium chloride soIution raises the blood pressure, but its effect is usuaIIy transitory. The high osmotic pressure of the hypertonic soIution probabIy draws additiona fluid into the bIood stream, but this again passes out through the capillaries as soon as diIution takes pIace. 0rr12 quotes Cannon, Fraser, and Cowell as recommending use of 4 per cent sodium bicarbonate solution in treatment of shock, stating that “before or during operation it raises the bIood pressure during the critica period. This soIution aIso increases the aIkaIi reserve.” SheItons6 recommends the use of “a pure 5 per cent dextrose solution in Ringer’s solution (which) may be given intravenousIy continuousIy for days . . . UsuaIIy an intravenous cannuIa is empIoyed, but for a period of a few hours the intravenous hypodermic needIe is often satisfactory. In cases of shock this method is of great vaIue.” Glucose-insulin Treatment in Shock. Wade,s7 in 1929, wrote in summary, . . . (2) GIucose intravenousIy with insuIin subcutaneously in the treatment of shock

. Aside from suppIying water and sodium ;hIoride-the latter is important and shouId be provided in the solution-during a state when there is a drain on the system without chance for repIenishment through the ordinary channels, the dextrose may antagonize starvation acidosis, and that is a11 the good dextrosesaIine soIution can do in shock. As this is therefore mereIy a matter of replacement of nutritiona essentials, it has no pIace in the earIy treatment of shock. . . . When bIood has been Iost, it may be of detriment rather than of advantage, as it is IikeIy to Iower stiI1 further the percentage of corpuscIes in the circuIating bIood. . . . When there has been a great Ioss of saIt from the system, as by excessive emesis, hypertonic (IO per cent) sodium chIoride soIution may be the most important emergency remedy. Hypertonic dextrose soIution should be avoided, as it causes crenation and possibIe destruction of bIood corpuscles when none can be spared; and it wiII stiI1 further increase the existing state of hypohydration of the tissues. . . . One shouId therefore empIoy drip phIebocIysis,

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using equa1 parts of 5 per cent dextrose and 0.9 per cent sodium chloride solution, as the first offering of diet to a patient who is emerging from shock and who is presumabIy or actually in such a condition that he is not IikeIy to benefit from the ingestion of fluid by mouth. Excepting in a case of diabetes meIIitus, insulin shouId be empIoyed onIy when sugar appears in the urine of a patient who is given dextrose phIebocIysis and then onIy in guarded dosage to make hypogIycemia impossibIe. As has been noted in the foregoing, Cannon13 found that the blood sugar in shock is above normal, and that it is not related to the decreased alkali reserve. Acetone bodies were absent from the urine . . . “ It seems probable that the beneficial effects of glucose are due largely to the water introduced with it.” This statement is made by MacFee and Baldridge. Glucose and Histamine Shock. Mention should be made of an abstract of an article by Djuricicss on the subject of “glucose and histamine shock” which says, “Contrary to in anaphylactic shock, what happens glucose exerts no protective action in histamine shock. This is another fact which is not in accord with the view that the two forms of shock have the same mechanism.”

Gum Solution in the Treatment of Shock. “ In 1919” says Friedlander, ErIanger and Gasser* pubIished the resuIts of their experimental studies of shock treated with hypertonic gum soIutions. They used soIutions containing 25 per cent of gum acacia and 18 per cent of gIucose. They found that such a soIution acts beneficiaIIy in the treatment of shock, (a) by drawing fluid from the tissues to the bIood stream, thus aiding in restoring bIood voIume, (b) by maintaining this increased voIume through some property of the acacia, (c) by diIating arterioIes through some specific action of the hypertonic crystalIoid, (d) by increasing the energy of the heartbeat in the same way, aIso through the direct action of gIucose on the heart muscle, (e) by augmenting metaboIism through increase in the suppIy of gIucose to the organism. *Ann.

Surg., f$: 389,

1919.

??

JUNE,1937

Randall,gg reporting on the use of intravenous solution of acacia in the Mayo CIinic in the treatment of shock, makes the foIlowing statements : The tota number of patients in a11 services at Mayo CIinic who received intravenous injections of soIution of acacia in 1928 was fuIfiIs a11 the II8 . . . Acacia apparentIy requirements for intravenous treatment of shock except furnishing erythrocytes. It has been proved to be innocuous in severa series of cases. It increases the voIume of pIasma and blood and keeps it increased unti1 the normal IIuid-regulating mechanism of the body is restored. As preventive of shock I fee1 that it is often we11 to give an injection of soIution of acacia in cases in which the patient is fatigued or debiIitated and in which obstetric operations are to be performed. HuffmanloG summarizes his findings with acacia and sodium chloride solution as follows : Gross evidence of toxicity was not seen foIIowing the intravenous injection of soIution of acacia and sodium chIoride in shock. The bIood pressure increased, the puIse rate decreased, the respiration deepened and the genera1 condition of the patient improved. The need for transfusion was often obviated. In some cases, increased output of urine was noted. Injurious effects on the kidneys were not seen. ChemicaI changes in the bIood of a harmfu1 nature were not apparent. Physicochemica1 changes in the bIood did not Iead to harmfu1 aIterations in physioIogic processes. Six days is usuaIIy required to rid the bIood of acacia. PathoIogic change resuIting from the acacia was not demonstrated at necropsy. The therapeutic usefulness of soIution of acacia and sodium chIoride is confirmed. Macleod75 notes “two precautions necessary to success in using the gum solution, first they must be properly prepared, and second they must not be injected so rapidly that their high viscidity would slow the circulation and so embarrass the heart’s action.” Erlanger, Gasser, et al.101~102early presented several articIes reporting favorable experimenta results with gum acacia in treatment of shock. Good and Boyerio3

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are among more recent advocates of the use of this solution. Unfavorable Comment Regarding Intravenous Use of Acacia. Lund, of Boston, in discussing an article by Frazierlo says, I think . . . that the acacia problem is not finished. Acacia stays in the bIood a Iong time. It has been recovered six months or longer after introduction. It is a gummy soIution and, according to a pharmacologist, tends to coat and cIog the capiIIaries in the liver. In reasonabIe amounts, I am sure that it can do nothing but good, but I think that repetitions of doses of acacia, say, 500 C.C. three or four times in twenty-four hours, and three or four times more in the next twenty-four hours, might be bad, and I would Iike to see anima1 work done to find what the upper limit of tolerance of acacia in the way of dosage is.

In the consideration of ways and means of administering fluids by the intravenous routes, Wengerlo5 says, I have found it d&uIt to give large quantities of fluid intravenously with the usual gravity method. Among other objections, this gravity method is too slow. Because of these inconveniences, the ScannelI apparatus for transfusion was used. However, it is cumbersome and somewhat compIicated. The apparatus described below is an outgrowth of these diffrcuIties. Apparatus for Intravenous Treatment of A glass T-tube is inserted between the Shock.

gravity tube and the needIe, which needle should preferably be of the type with a shieId to rest on the patient’s arm. To the perpendicuIar of the T-tube, by means of rubber tubing, a 50 C.C. Luer syringe is attached. The other equipment required is the ordinary infusion bottIe for transfusion and an artery clamp. The artery cIamp is pIaced on the tubing just above the T-tube. When the cIamp is removed the fluid Aows into the vein and into the syringe displacing the pIunger. When the syringe is fuI1, the cIamp is reapplied; gentIe pressure is exerted on the syringe, thus forcing the fluid into the vein. The clamp is removed and the procedure repeated unti1 sufficient fluid has been given. In my cases 500 C.C. are given in a period of from thirty to forty

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minutes. In no case has there been any iI effect from giving the fluid at this rate.

Wenger lo5 decIares

that

of the apparatus Iie in its simplicity; in the fact that the treatment can be given at the bedside; that the patient is but sIightIy disturbed; that a Iarge voIume of fluid may be given in a minimum of time; and that the flow into the vein is continuous. Thus there is no clotting in the needle. the advantages

Four Dangers Associated with Administration of Solutions Intravenously. In his discussion of an articIe deaIing with the roIe of intravenous drip in therapy by Hyman and Touroff,’ Orr points out four major dangers attendant on administering solutions intravenoudy : (I) the immediate reaction; (2) the possibiIity of overloading the circuIatory tree; (3) the production of edema; (4) the embolism.

production

of puImonary

Treatment of Electrical Shock. Brief notice may appropriateIy be made of the treatment of eIectrica1 shock. PearI’szg summary and concIusions on this subject incIude the foIIowing : . . . (6) The treatment of eIectricaIIy induced ventricuIar fibriIIation is prompt cardiac massage, preceded if possibIe by the intraventricuIar injection of potassium saIts folIowed by caIcium salts. The carotid route for administration of these salts may prove sufficient without the use of cardiac massage. If avaiIabIe an appropriate current may be passed through the heart, foIIowed by cardiac massage.

Electrosurgery Technique. It is interesting to note that Schorcher4 found that “trauma of an eIectrosurgica1 procedure produced Iess shock than that produced by ordinary mechanica means . . . EIectrocoaguIation destroys the toxicity of the rapidIy working toxins because it generates a temperature of 60 to 80 degrees, whereas their activity is inhibited at 59 degrees of heat.” The author “believes that he demonstrated in experiments that eIectrosurgica1 trauma produces IittIe reaction on the part of the nervous and circuIatory systems.” Artificial Respiration in Electrical Shock. “Jaffe . . . joins with other recent stu-

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says an editoria1 in the Current dents,” Comment sectionlo of the JournaI of the American MedicaI Association under date “in stressing the imporof June 16, 1928, tance of vigorous attempts at artificia1 respiration. This may effect resuscitation of a paraIyzed respiratory center. The passive movements of the chest should be started as soon as possibIe and continued for a sufficient time, even for hours.” In discussing appIication of heat as an important procedure in the therapy of surgica1 and traumatic shock, it may not be amiss to caI1 attention to the use of diathermy for this purpose. The first paragraph of a paper read at the sixth annual meeting of the American CoIIege of Physica1 Therapy by Portmann,lo8 of the CIeveland CIinic follows :

Diatbermy in Treatment of Shock. The use of diathermia in the treatment and prevention of surgica1 shock is based upon certain experiments which were made a number of years ago. Dr. CriIe found that coohng of the Iiver is one of the most important factors in the production of shock in abdomina1 operations. In a series of anima1 experiments NageIschmidt found that the ampIitude and voIume of respiration and the heart beat are increased when diathermia is appIied through the mediastinum. Description of a Device for Application of Heat in Treatment of Shock. Hitchcock an apparatus and ReynoIds log describe originaIIy fashioned to expedite cast drying where more or Iess extensive body casts are required, and Iater utiIized to prevent and to treat cases of shock. The apparatus consists, essentiaIIy, of a cabinet with electrica coiIs for heating, together with a blower which deIivers this warmed air into fIexibIe tubes. These tubes fit, by means of simple coupIing devices, into a coiIed spring mat which can be Iaid on a bed or folded around a patient, as any ordinary bIanket or mat wouId be. The coiIed springs are covered by fabric, which makes the whole unit into a fIexibIe chamber or a flexible hoIIow wrapping, through which the heated air circulates, to Ieave by a vent at its dista1 end. The principa1 mat, which enveIopes the body and

legs, is augmented by an auxiIiary mat, which can be fitted over an arm to which a separate pipe can deIiver heated air. The amount of heat deIivered is subject to simpIe reguIation by means of switches, so that a greater or lesser degree of heat can be obtained, depending on the needs. . . . This apparatus provides “quick, generabzed heat” which “is an important factor in recovery from shock.”

Carbon Dioxide and Oxygen in Treatment of Shock. Hendersona has pointed out recently that “hemorrhage produces its iI effects IargeIy through asphyxia. This is tacitIy recognized by surgeons in their preference for transfusion of bIood over any mere infusion of a saline or gum solution. The victim of acute exsanguination exhibits air hunger.” He recommends treatment with resuscitation methods-the administration of carbon dioxide and oxygen. He says in part: In shock without hemorrhage there is, however, no loss of red corpuscIes from the body, and the blood aIkaIi is mereIy dispIaced. Both corpuscIes and aIkaIi may be recaIIed into use. To effect such recaI1, both the asphyxia and the acarbia may be combated with inhaIation of carbon dioxide and oxygen. One of the oIdest and aIso the Iatest of many conceptions of the underIying cause of the depression of the circulation in shock and in iIIness is that the tonus of a11 the muscIes of the body, both skeIeta1 and visceraI, is depressed, and that the bIood stagnates in the atonic tissues. Stimulation of respiration with carbon dioxide increases the effective differences of pressure between the tissues of the body and the thorax and thus promotes the venous return to the heart.84

Support for the Theory of the Value oj Carbon Dioxide in Treatment of Shock. Support for Henderson’s cIaims are found in reports of work by other investigators. McDowaI13’ says, The tone of the bIood-vesseIs is kept up by the vasomotor center, the activity of which Dale and Evans have shown to be dependent on the carbon-dioxide content of the blood. It wiI1 be cIear, then, that any condition which separates the centre from the vessels or which causes the carbon dioxide to he reduced must

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resuIt in a fall in blood pressure from not only an increased capacity of the circuIation but aIso a Ioss of the periphera1 resistance of the arteries. War Experience with Carbon Dioxide in Treatment of Shock. War experience, aIs0, serves to estabIish vaIidity for Henderson’s theory of treatment for shock. Porter44 says in the summary of his Iectures on shock: “#13. Increased action of the thoracic pump, brought about by the inhaIation of carbon dioxide IiberaIIy mixed with pure air, wiI1 raise the bIood pressure from 15-20 miIIimetres in norma and wounded men. When the bIood pressure is near the critica IeveI this procedure is of advantage.” PreviousIy this author44 had made a point of the fact that “A few mms. above the critica IeveI, recovery wiI1 usuaIIy occur spontaneousIy; a few mms. beIow, death wiI1 foIIow unless skiIIed aid be at hand.” Keen, l lo quoting Porter IaigeIy, says : A11 physioIogists know that the pumping action of the diaphragm is an important aid in the movement of bIood from the abdomen into the chest. At the height of a strong inspiration the venous pressure in the chest may be more than 40 mms. Iower than the venous pressure in the abdomen. I produced strong respiratory movements of the diaphragm by aIIowing the anima1 to breathe an atmosphere rich in carbon dioxide. The diastolic arteria1 pressure (which shouId always be the guide; the systoIic pressure shouId not be used as the standard) was thereby increased rg and even 30 mms. In June, IgI 7, I successfuIIy applied this new method to the treatment of wounded soIdiers. In cases aImost pulseless, cases in which a11 other means of raising the bIood pressure had failed, the carbon dioxide respiration strengthened the puIse and raised the diastoIic bIood pressure IO mms. This rise is of great vaIue when the pressure is at the critica IeveI. Postmortem Findings in Shock. Moon and Crawford46 give the foIIowing postmortem changes as characteristic of shock: “widespread diIatation of capiIIaries and venuIes, with edema and capiIIary hemor-

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rhages. These were most marked organs of respiration.” WakeIey and Buxtonls say that

in the

Postmortem, very Iittle of importance is found in shock, the only reIiabIe findings being in the centra1 nervous system, where . . . ChromatoIysis occurs, commencing on the afferent side, and extending to the important vita1 nuclei. This is regarded as due to the nociceptive stimuli received wearing out the afferent nucIei first, extension being a secondary matter. ChromatoIysis in the cerebeIIum has been shown to be very constant. Hence we see how profound is the benefit of sleep. Moon16 says that “Shock produces characteristic changes demonstrabIe by postmortem examination. These consist of marked capiIIary and venous congestion of the viscera, edema of Iungs and mucosae, petechial hemorrhages in serous and mucous surfaces, and effusion of fluid into serous cavities.” SUMMARY

A very IittIe reflection on the part of the reader wiI1 Iead to the reaIization that, Iong as this review is, it represents in its present extent a virtua1 summarization of the avaiIabIe Iiterature of the subject. It is probabIy not possibIe to condense further, i.e., to summarize, and at the same time to keep the review representative of the actual Iiterature. REFERENCES

The reading materia1 reviewed in this articIe has been drawn from the (I) Library of the American MedicaI Association, Chicago; (2) American CoIIege of Surgeons Library, Chicago; (3) Library of the University of CaIifornia, Berkeley, CaIif.; (4) University of California MedicaI SchooI Library, San Francisco; (5) Lane MedicaI Library, Stanford University MedicaI SchooI, San Francisco; (6) Library of the AIameda County MedicaI Association, AIameda County HospitaI, OakIand, CaIif. ; and (7) Private Iibrary of the author, BerkeIey, CaIif. I. Webster’s abridged)

New International 1929.

Dictionary

(Un-

650 2.

3.

4.

5.

6. 7. 8.

g. IO.

I I.

12.

13. 14.

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MAWSON, X. 0. S. The Roget Dictionary of Synonyms and Antonyms. N. Y., G. P. Putnam’s Sons, 193 I. DORLAND, W. A. N. The American IIIustrated Medical Dictionary. PhiIa., W. B. Saunders, 1927. SCHORCHER,F. Shock, coIIapse and eIectrosurgery. Deutscbe Zeitscb. f. Cbir., 243: 225 (May 14) 1934. Reviewed by the J. A. M. A., 103: 146 (JuIY 14) 1934. RUTHERFORD,A. G. The significance and management of shock. West Virginia Med. Jour.. 26: 26-28 (Jan.) 1930. BICKHAM, W. S. Operative Surgery. Phila., W. B. Saunders, 1924, I: 143 and 306-309. WRIGHT, S. AppIied PhysioIogy. London, Oxford Medical PubIications, 1928, pp. 290-300. SHERRINGTON, C. S. The-Integ~a& Action of the Nervous Svstem. New Haven. Yale Univ. hZSS, 191 I, pp. 240-247. REHN, E. Operative Shock. Internat. Clin., 2: 57-65 (June) cmMANN, FRANK C. The peripheral origin of surgical shock. Bull. Jobns Hopkins Hosp., 25: 205-212 (JuIY) 1914. ATCHLEY, D. W. and LOEB, R. F. Dehydration and medica shock. Med. Clin. N. Amer., 17: 117o1391 (Mar.) 1934. ORR, T. G. Hemorrhage and Traumatic Shock. Dean Lewis’ Practice of Surgerv. Hanerstown. Md., W. F. Prior Co,, I: 1-35 khap. gj 1928. CANNON, W. B. Traumatic Shock, N. Y., D. AppIeton Co., 1923, pp. I-192. MARSHALL, C. J. and PINEY, A. Textbook of SurgicaI Pathology. N. Y., D. Appleton, 1925.

PP. 5-9. 15. CRILE, G. W. A Physical Interpretation of Shock. London, Oxford Press, 1921, pp. 1-208. 16. MOON, V. H. The shock syndrome in medicine and surgery. Ann. Znt. Med., 8: 1633-1648

(June) m5.

17. CRILE, G. W. Surgical Shock, Harvey Lectures for Igo7-1908, 3: 132-154. PhiIa., Lippincott co., 1909. 18. MORTIMER, J. D. Shock, anesthesia, analgesia. Med. Press and Circular, I 28: 5 15-5 I 7 (Dec. 25) ‘929. 19. WAKELEY, C. P. G. and BUXTON, ST. J. D. SurgicaI PathoIogy. N. Y., Wm. Wood, 1929, pp. 859-862. 20. ROBERTSON, T. B. Principles of Biochemistry. Phila., Lea & Febiger, 1924, pp. 202, 207-208, 380-381. 21. WANGENSTEEN, 0. H. Present concept of traumatic shock and its treatment.. Lancet, 51: 711-718 (Dec.) 1931. Abstr. Sect., Znternat. Surg. Digest, 13: 121-126 (Feb.) 1932. 22. HAMILTON, C. E. and ROTHSTEIN, E. Air embolism. J. A. M. A., 104: 2226-2230 (June 22) 1935. 23. COCKE, C. H. Pleura1 shock. Am. Rev. Tuberc., 3 I : 404-412 (Apr.) 1935. 24. TAYLOR, W. Postpartum hemorrhage and obstetric shock. Cl&. Jour., 64: 203-205 (May) 1935. 25. HARKINS, H. N. Shock due to freezing: I. shift of body Auids and associated bIood concentra-

Shock

26.

27.

28.

29. 30. 31. 32. 33.

34. 35.

Jo%

I937

tion changes. Proc. Sot. Exper. Biol. and Med., 32: 432-434 (De.) 1934. MILBERT, A. H. Infusion reactions with special reference to “speed shock.” Am. Jour. Surg., 26: 479-485 (Dec.) 1934. HARKINS, H. N. Experimenta burns: I. The rate of Auid shift and its reIation to the onset of shock in severe burns. Arch. Surg., 31; 71-85 (JuIy) 1935. PALFREY, F. W. The SpeciaIties in Genera1 Practice. Phila., W. B. Saunders, 1927, pp. 641-642. 654-655. PEARL, F. L. Electric shock. Arch. Surg., 27: 227-249 (Aug.) 1933. WIGGERS, C. J. Physiology in HeaIth and Disease. PhiIa., Lea & Febiger, 1934, pp. 699-706. FRASER, A. J. Trauma, Disease, Compensation. Phila., F. A. Davis, 1630, p. 93. SPILSBURY. SIR B. Some MedicoIeeaI asoects of shock. iancet, 2: 1038-1040 (No;. 4) I’g33. MANN, F. C. and Essur, H. E. The present status of the probIem of traumatic shock. Am. Jour. Surg., 28: 160-165 (Apr.) 1935. FRIEDLANDER, A. Hypotension. Baltimore, WiIIiams & Wilkins, 1927, pp. 22-42. HOLT, R. L., et a1. A discussion on traumatic shock. Brit. Med. Jour., I: 792-793, (Apr. 13)

1935. PhysioIogy of In36. HEWLETT, A. W. Pathologica ternal Diseases. N. Y., D. Appleton, 1923, pp. I 18-122. 37. MCDOWALL, R. J. S. CIinicaI Physiology. N. Y., D. Appleton, 1927, pp. 123-130. 38. KNOEFEL. P. K. The nature of anesthetic shock and the vaIue of premeditation. California and West, Med., 39: ;44 (Nov.) 1933; Banergi, H. and Reid. C. lauoted bv KnoefeI1. Jour. Pbysiol., 7jl: 370, ‘1\33. LI 39. JONES, W. C. Prophylaxis of shock. Soutbern Med. Jour., 28: 166-168 (Feb.) 1935. 40. MCDONAGH, J. E. R. Shock. Med. Press and Circular, 124: 27 (JuIy 13) 1927; 47 (JuIy 20) 1927; 70 (JuIy 27) 1927; 8g (Aug. 3) 1927; IIO (Aug. IO) 1927. 41. HENDERSON, Y. Acapnia as a factor in postoperative shock, ateIectasis and pneumonia. j. A. M. A., 95: 572-575 (Aug. 23) 1930. 42. BLALOCK, A. A consideration of the causes and treatment of shock associated with inury to tissues. Internal. Clin., I: 144-161 (Mar.) 1933. of operations 43. MOYNIHAN, SIR B. Complications upon the stomach &d intestine&shock. Oxford Surg., 2: 643-648 (Pt. 2) 1928. Shock, The Harvey 44. PORTER, W. T. Traumatic Lectures, 13-14: 21-43, PhiIa., LippinCOtt CO., 1920. 45. ATCHLEY. D. W. Medical shock. J. A. M. A., 9s: (Aug. 9) 1930. 46. MOON, V. H. and CRAWFORD, B. L. Shock syndrome in mercuric chIoride poisoning. Arch. Patbol., 15: 509-515 (Apr.) 1933. 47. MULLER. E. F.. MYERS. C. N. and PETERSEN, W. F. The nature of shock symptoms occasionaIIy foIIowing drugs or vaccines. J. A. M. A., 88: I 128-1132 (Apr. g) 1927. 48. FREEDMAN, H. J. Acute anaphylactic shock following intracutaneous test for sensitivity to horse

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serum; report of a fatal case. New England Jour. Med., 212: IO (Jan. 3) 1935. 49. BUERGER, L. CircuIatory Disturbances of the Extremities. Phila., W. B. Saunders, 1924, pp. 62 and 526-527. 50. DALE, H. H., LAIDLAW, P. P. and RICHARDS,A. N. The action of histamine-its bearing on traumatic toxemia as a factor in shock. ~Med. Res. Corn., Special Rep. #26, London, rgrg, pp. 8-15. 5 I. MILLER, H. The mechanism of traumatic shock. Caltfornia and West. Med., 39: 344-345 (Nov.) 1933.

51~. FREED, S. C. Quoted by MiIIer. Proc. Sot. &per. Biol. and Med., 30: 677 (Feb.) 1933. 52. TURCK. F. B. Shock and fatigue with acute and chronic (cytost-anti-cytost) reaction. Med. Rec., IOO: 705 (Oct. 22) 1921. 53. DE NITO, G. BIood pressure reducing hormones as cause of protein shock. Deutsch. med. Wcbnscbr., 61: 339 (Mar. I) 1935. Abstr. J. A. M. A., 104: 1865 (May 18) 1935. 54. CLARK, ALFRED. Surgical shock. Glasgow Med. Jour., 5: 1-6 (Jan.) 1935. 55. ~‘SHAUGHNESSY, L. and SLOME, D. EtioIogy of traumatic shock. Brit. Jour. Surg., 22: 589-618

(Jan.) 1935.

$6. MILLER, I. D. SurgicaI shock Med. Jour. Australia, I: 522-523 (Apr. 27) 1935. 57. ROOME. N. W. and WILSON. H. ExnerimentaI shock-the effects of extracts from traumatized limbs on the bIood pressure. Arch. Surg., 31: 361-370 (Sept.) 1935: ~8. PARSONS. W. and PHEMISTER, D. B. Hemorrhage in traumatized Iimbs. Surg., and “shock” Gynec. and Oh., 51: 196-207 (Aug.) 1930. 59. BLALOCK, A. Mechanism and treatment of experimenta1 shock. Arch. Surg., 15: 762-798 (Nov.) 1927. 60. CUTLER, E. C. and SCOTT, J. M. Postoperative CompIications, Graham’s SurgicaI Diagnosis. PhiIa., W. B. Saunders, I: 136-145, 1930. 61. ROST, F. PathoIogicaI PhysioIogy of SurgicaI Diseases (S. P. Riemann transIation). PhiIa., BIakiston’s, 1923, pp, 229230. 62. MALCOLM, J. D. On the condition of bIood vessels during shock. Lancet. I : 497-499 (Feb. 23) 1907. 63. PETROFF, J. and FILATOV, A. et a1. Experimentat studies of hemoIytic shock in blood transfusion. Arch. j. klin. Cbir., 181: 2og (Nov. 12) 1934; J. A. M. A., 104: 430 (Feb. 2) 1935. 64. WESSELKIN, P., LINDENBAUM, J., et a1. Role of the central nervous system in pathogenesis of vascuIar disturbances in hemolytic shock. Arch. j. klin. Cbir., 181: 227 (Nov. 12) 1934; J. A. M. A., 104: 430 (Feb. 2) 1935. 65. MACFEE, W. F. and BALDRIDGE, R. R. Postoperative shock and shock-Iike conditions. Ann. Surg., 91: 329-341, 1930. Reviewed in Internat. Surg. Digest, g: 316-320 (May) 1930. 66. KILDUFFE, R. A. CIinicaI Interpretation of BIood Examinations. Phila., Lea & Febiger, 1931, P. 587. 67. AUB, J. C. and CUNNINGHAM, T. D. Studies in experimenta traumatic shock-II. The oxygen content of the bIood. Am. Jour. Pbysiol., 54: 408-415 (Dec.) 1920.

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68. ELMAN, T. and COLE, W. H. Hemorrhage and shock as causes of death foIIowing acute portal obstruction. Arch. Surg., 28: I 166-1175 (June) 1934. 69. BAYLISS, W. M. and CANNON, W. B. Note on muscle injury in reIation to shock, special report. Ser. #26, Med. Res. Corn., London, IgIg, PP. 19-23. 70. AUB, J. C. and Wu, H. Studies in experimental traumatic shock--rrr. Chemical changes in the blood. Am. Jour. Pbysiol., 54: 416424 (Dec.) 1920. 71. SCARPELLO, A. Experimenta researches on glycogenic functioning of the liver in traumatic shock. Rij. Med. Naples, 46: I 198 (JuIy 28) 1930. Abstr. J. A. M. A., 95: 1460 (Nov. 8) 1930. 72. CUTHBERTSON,D. P. Certain aspects of the metabolic response to injury. Glasgow Med. Jour., 3: 41-56 (Feb.) 1934. 73. AUB, J. C. Studies in experimental traumatic shock-r. The basal metabolism. Am. Jour. Pbysiol., 54: 388-407 (Dec.) 1920. 74. BLALOCK, A. Further studies with particuIar reference to the effects of hemorrhage. Arch. Surg., 29: 837-857 (Nov.) 1934. 75. MACLEOD, J. J. R. PhysioIogy and Biochemistry in Modern Medicine. St. Louis, C. V. Mosby CO., 1926, pp. 514-525. 76. RHODES. G. K. and MCKENNEY. C. Traumatic shock-its newer aspects and treatment. Calijornia and West. Med., 33: 665-670 (Sept.) ‘930. 77. MCDOWALL, R. J. S. Experimental shock, with specia1 reference to anesthesia. Brit. Med. Jour., I: 6go (Apr. 22) 1933. 78. WALLACE. C. S. Traumatic toxemia as a factor in shock. Med. Res. Corn., London, IgIg, Special Rep. Ser. f26, pp. 3-8. 79. ANDREWS, EDMUND. Surgical shock. Northwest Med., 34: 122-126 (Apr.) 1935. 80. CLARK, A. M. and CRUICKSHANK,R. Observations on the treatment of burns. Lancet, I: 201-204 (Jan. 26) 1935. 81. JOHNSON, C. A. Ephedrin suIphate in treatment of acute shock from trauma or hemorrhage. J. A. M. A., 94: 1388%1390 (May 3) 1930. 82. WOOD. P. M. Coramine in denarcotization and resuscitation. Am. Jour. Surg., 22: 8691 (Oct.) 1933. 83. SOLIS-COHEN, S. and GITHENS, T. S. Pharmacotherapeutics. N. Y., D. AppIeton, 1928, p. 1695 and index re: shock. 84. HENDERSON, Y. Resuscitation. J. A. M. A., 103: 834-837 (Sept. 15) 1934. 85. SWINGLE, W. W., PFIFFNER, J. J., et a1. The function of the adrena cortical hormone and the cause of death from adrena insuffrciency. Science, 77: 58-64 (Jan. 13) 1933. 86. FREEMAN, N. E. Cortin and traumatic shock. Science, 77: 211-212 (Feb. 24) 1933. 87. BRITTON, S. W. and SILVETTE, H. Theories of cortico adrena function. Science, 77: 366-368 (Apr. 14) 1933. 88. SWINGLE, W. W. and PARKINS, W. M. A comparative study of the effect of trauma on healthy, vigorous dogs with and without adrena gIands.

American

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Journal of Surgery

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1935. 89. DONAHUE, J. K. and PARKINS, W. M. Lipoid and hemorrhagic changes in adrena cortex foIlowing traumatic shock, Proc. Sot. Exper. Biol. and Med., 32: 12491253 (May) 1935. go. PARKINS, W. M., TAYLOR, A. R. and SWINGLE, W. W. A comparative study of sodium chloride, and bIood pressure changes induced by adrena insufficiency, etc. Am. Jour. Pbysiol., I 12: 581590 (Aug. I) 1935. gr. HARROWER, H. Practical EndocrinoIogy. GIendaIe, CaIif., 1932, pp. 334 & 341-342. 92. BLALOCK, A., WILSON, H., et a1. Loss of protein from the blood stream. Effects of the injection of soIution of pituitary and of epinephrine. Arch. Surg., 26: 330-334 (Feb.) 1933. 93. WANGENSTEEN, 0. H. The recognition and treatment of surgical shock. Surg., Gynec., and Obst., 54: 970-71 (June) 1932. 94. BRANDSON, B. J. and HILLSMAN, J. A. FIuids in surgery. Canad. Med. Assn. Jour., 26: 689-698 (June) 1932. 95. PADGETT, E. C. and ORR, T. G. The insuIinglucose treatment of traumatic shock. Surg., Gynec., and Obst., 46: 783-788 (June) 1928. 96. SHELTON, H. J. The influence of physioIogic research on modern surgery. Virginia Med. Montbly, 55: 790-796 (Feb.) 1929. Abstr. Sect. Znternat. Surg. Digest, 7: 242-247 (Apr.) 1929. 97. WADE, P. A. The present status of glucose-insulin in the treatment of shock. Anestb. and Analg., 1929. 8: 298-301 (Sept.-Ott.) 98. DJURICIC. GIucose et choc histaminique. Compte.rend. Sot. de biol., I 13: 432, 1933. Physiologic Abstr., lg: 74 (Apr.) 1934. gg. RANDALL, L. M. Shock in obstetrics. J. A. M. A., 93: 845-847 (Sept. 14) ‘929. IOO. HUFFMAN, L. D. Solution of acacia and NaCI in hemorrhage and shock. J. A. M. A., 93: 16g81702 (Nov. 30) 1929. IOI. GASSER, H. S. and ERLANGER, J. Studies insecondary traumatic shock: v. Restoration of the pIasma vohrme and of the alkali reserve. Am.

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Jour. Pbysiol., 50: 104-118; VI. Statistical study of the treatment of measured trauma with solutions of gum acacia and crystaIIoids. Ibid., I 19-148; VII. Note on the action of hypertonic gum acacia and ghrcose after hemorrhage. Ibid., 149-156 (Oct.) rgrg. 102. WHITE, H. L. and ERLANGER, J. The effect on the composition of the bIood of maintaining an increased bIood voIume by the intravenous injection of a hypertonic sohrtion of gum acacia and glucose in normal asphyxiated and shocked dogs. Am. Jour. Pbysiol., 54: I-29 (Nov. I) 1920.

103. GOOD, R. W. and BOYER, B. E. Intravenous use of acacia solution in shock. Jour. Med.. 12: 630-636 (Feb.) 1932. 104. FRAZIER, C. H. The modern treatment of surgical shock. J. A. M. A., 105: 1731-1734 (Nov. 30) . 1935. 105. WENGER, H. L. Present conception and treatment of shock. Am. Jour. Surg., 13: 307-310 (Aug.) 1931. I 06. HYMAN, H. T. and TOUROFF, A. S. W. Therapeutics of the intravenous drip. J. A. M. A., 104: 446451 (Feb. 9) 1935. 107. The dangers from eIectrica1 shock. J. A. M. A., Current Comment, go: rg4g (June 16) 1928. I 08. PORTMANN, U. V. Observations on the use of diathermia for the prevention and treatment of surgica1 shock. Arch. Pbys. Tber., X-ray, Radium, g: 385-388 (Sept.) rgz8. 109. HITCHCOCK, H. H. and REYNOLDS, T. E. Shock treated by warmed ‘air. California and West. Med., 44: 98-99 (Feb.) 1936. I IO. KEEN, W. W. The Treatment of War Wounds. PhiIa., W. B. Saunders, rgr8, pp. 22-36. III. Editorial. Shock, J. A. M. A., IOO: 46 (Jan. 7) 1933. 112. Queries and Minor Notes: Use of dextrose intravenously in shock. J. A. M. A., 107: 300-301 (July 25) 1936. I 13. Am. Med. Assn. London Correspondent: Recent Work on Surgical Shock. J. A. M. A., 107: 725 (Aug. 29) 1936.