Hemorrhagic shock

HEMORRHAGIC CHARLES M.

SHOCK

SWINDLER,

M.D.

New York, New York

T

HE purpose of this paper is to describe in some detaiI the probIems of hemorrhagic shock as seen in the European Theater together with their method of handhng and the Iessons Iearned. The detaiIs outIined herein are a summation of the experience of the various surgeons and shock officers of an AuxiIiary SurgicaI Group. The materia1 has been cuIIed from the persona1 fries of the surgeons, ofIicia1 reports of the surgica1 team heads and from a monograph on acute traumatic surgery by the consuItant surgeon for the Mediterranian-ItaIian Theater. Experiences are drawn from TacticaI Operations of the Fifth and Seventh Armies. They commence with the beachhead operation of North Africa and end with the drive for centra1 Germany. These experiences have for their background : (I ) the airborne operation in the Low Countries, (2) Tunisian desert campaign, (3) various ItaIian river crossings and (4) battIes associated with the BuIge and the Seigfried Line. The shock ofhcer is primarily concerned with the probIems of shock and his duties are the supervision and treatment of a11 shock which occurs in battIe casuaIties. This offrcer works in the most forward FieId HospitaIs where the patients treated are so criticaIIy wounded that they cannot be transported to the rear. Treatment of acute bIood Ioss in these patients is the first responsibihty of the shock officer. It is his duty to see that suitabIe bIood repIacement is carried out by bIood transfusions and bIood pIasma. The amount and type of bIood used or the use of bIood derivatives are decisions which the shock off’cer has to make and are predicated on the cIinica1 condition of the patient when he arrives in the shock tent. ChurchiII states : “ Restoration of bIood

voIume and the reIief of hypo-tension and anoxia must be done without Ioss of time. RepIacement therapy forms the basis of resuscitation. WhoIe bIood in Iarge amounts is mandatory. One can speed resuscitation by simuItaneous infusion of bIood into one vein and pIasma into another vein or into the sterna1 meduhary cavity.“l The important thing to remember, however, is that whoIe bIood must be rapidIy infused into the circuIatory system even under pressure if the periphera1 vasomotor coIIapse is so profound as to prevent the norma operation of the cIassica1 Baxter sets which we empIoyed routineIy. (By rapidIy we mean 500 to 1,500 cc. in twenty minutes). UnfortunateIy, the idea has deveIoped that the treatment of shock rests upon the restoration of bIood voIume. This is faIse reasoning. “The dominant factor in shock is the Ioss of blood into the wounded tissues, into body cavities, and to the surface. The successfu1 treatment of shock, therefore, not onIy rests upon the restoration of bIood voIume, but aIso upon the restoration of hemogIobin as weI1. Infusions of pIasma aIone wiI1 not suffice. Beyond a certain point, pIasma may do harm by diIuting the remaining red bIood ceIIs at a time that the rising bIood pressure increases hemorrhage. A faIse sense of security may be created by the eIevation of the systoIic bIood pressure under these circumstances. A bIood pressure brought to norma or nearIy norma IeveIs by pIasma aIone, may fai1 precipitousIy with the induction of anesthesia, operative manipuIation, or mereIy moving the patient.“‘v2 The preparation of the criticahy injured battIe casuaIty for surgery requires the utmost in keen surgica1 judgment and astute surgica1 diagnosis. AppraisaI of the patient’s condition demands the sum tota of the surgeon’s cIinica1 knowIedge. So, too,

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the shock ofhcer must be ever aIert and mentaIIy active for it is he who wiI1 care for the patient during the surgeon’s absence or until such time as the surgeon can render his opinion. Reactivation of hemorrhage may occur as the circuIation improves. If continuing hemorrhage is suspected, the surgeon must proceed with the indicated operation whiIe bIood is being transfused into one or more veins. If the state of shock does not improve and/or respond rapidIy to infusion of bIood and pIasma, it is a fair assumption that there is continuing hemorrhage, estabIished infection or that the continuing shock is associated with other injuries, for exampIe, intracrania1 damage, transection of the spina cord or open wounds of the thoracic cavity with the resuItant disturbance of the cardiorespiratory physioIogy. One of our probIems of shock is: When is a patient ready for surgery? There is no specific answer. Each case is a probIem in itseIf, but the shock officer must hoId the key to the situation. His duty is to save Iife; it is aIso his duty to restore a patient to a state of equiIibrium which wiI1 permit the necessary surgica1 procedures. The shock officer outIines and carries out an individuaIized pIan of shock therapy for each criticaIIy injured battIe casuaIity admitted to his tent. Of a11 the drugs and procedures deveIoped for the treatment of hemorrhagic shock, none has stood up under the critica test of forward surgery with the exception of repIacement therapy. ExternaI appIication of heat and the use of morphine are two time-honored measures in the treatment of shock which, if used injudiciousIy, couId cIoud the picture considerabIy. “The externa1 apphcation of heat can be dangerous if overdone.“2 FIuid Ioss in the desert campaign and the drive for Rome was great even in the norma man. What wouId it be Iike in a man with dysfunction of the vasomotor system due to shock? Morphine is advisabIe onIy in moderate amounts and its use is Iimited to the excited patient. “Morphine is not indicated for the

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treatment of restIessness of hemorrhage, which is IargeIy due to anoxia.“2 The prescription for mor“q.s. ad Iibitum” phine can Iead onIy to dire end resuIts in two types of patients: (I) the patient with acute hemorrhagic shock and (2) the patient with an invasive anaerobic ceIIuIitis infection. The patient with acute hemorrhagic shock has no functioning periphera1 vascuIar system an8consequentIy no functioning route of assimiIation. Morphine given to this type of patient by the usua1 route of administration does nothing more than pile up in the tissues adjacent to the site of injection. This produces a pernicious situation because there is deIayed absorption of the drug. When the periphera1 circuIation is improved by resuscitation therapy, a manifoId absorption of the piIed up morphine ensues with resuItant acute morphine poisoning. A patient with acute invasive anaerobic ceIIuIitis wiI1 have his diagnostic findings masked if injudicious morphine medication is given- him. “The diagnosis of cIostridia1 myositis in a fieId hospita1 is entireIy cIinica1 and is based in great part on minute aIterations of the patient’s psychic pattern.“3 CIostridium Welchii infections make for the apprehensive, hyperexcitabIe, occasionaIIy maniaca type of personaIity change, whereas infections caused by CI. perfringens and oedematiens project the menta1 pattern into the comatose category. In a case of cIostridia1 myositis the menta1 base Iine must be estabIished. Morphine medication miIitates against such a procedure and makes the diagnostic estimateamost diffIcuIt. We know that morphine is a good drug but it is aIso a two-edged sword. In the types of patients which we have described, morphine is indicated for definite and unequivoca1 pain only, and the route of administration shouId be intravenous to avoid additive effect. Use the drug to the Iimit but use it wiseIy and judiciousIy. The differentia1 diagnosis between acute fuIminating cIostridia1 oedematiens infec-

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tion and morphinism is not easy; the treatment of acute hemorrhagic shock comphcated by morphine poisoning is not a simpIe task. TYPICAL

CASES

OF SHOCK

Head and Face Injuries. The average head injury, if the patient Iives for six hours, usuaIIy does not present much of a probIem. In most cases the injury is such that the patient decompresses himseIf. The probIem with head injuries is not as a ruIe too diffIcuIt to soIve because the shock is not primariIy due to acute bIood Ioss unIess there is an associated transection of one of the major vascuIar bundIes. From the point of view of the shock officer straight forward head injuries are best managed by estabIishing an adequate airand supplying hypertonic fI uids. way “Twice concentrated plasma” and serum aIbumin are the usuaI agents avaiIabIe in front Iine hospitals for this form of therapy. The estabhshment of an airway, especiaIIy in patients with associated facia1 injuries, resoIves itseIf into performing a tracheotomy. If there is any doubt as to the embarrassment of the airway in a faciaI injury, it shouId manditoriaIIy point to a tracheotomy. We aIways beIieved that adequate oxygenation was a very important phase of shock therapy and faiIure to maintain adequate oxygenation was to sign and sea1 the death warrant of the patient invoIved. Chest Injuries. In chest wounds the important probIem is the restoration of the normaI physioIogy of the cardiorespiratory system. Shock treatment in this type of injury is based upon the aIIeviation of the asphyxia, controI of the puImonary edema and the negation of tension pneumothorax. ActuaIIy, surgery in chest wounds is a secondary consideration. The primary consideration is shock due to aItered respiratory function. The treatment of this specia1 form of shock is immediate and rapid aspiration of the pneumothorax, cIosure of the perforation if there be one, contro1 of pain by intercostal bIock, drying out of the tracheobronchia1 tree by cathet-

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erization and nasa1 oxygen medication and the prompt reIease of tension pneumothorax through a water seal. FinalIy, the crux of shock therapy in chest injuries is adequate stabilization. The knowing when to operate on a chest injury is just as important as knowing how. One must answer these questions: Is that portion of the functioning Iung fieId dry? Has the

hemogIobin been restored to patient’s reasonabIy norma IeveIs? Can the patient withstand additiona asphyxia in the form of anesthesia? Abdominal Injuries. Penetrating wounds of the abdomen wiI1 test the shock ofl?cer’s diagnostic acumen to the nth degree. Patients with traumatic, intra-abdominaI wounds have a most unstabIe vasomotor system. WhiIe their shock may we11 be ascribed to hemorrhage, one must keep in mind that irritative peritonea1 contamination in the form of feces, biIe, bIood and urine aIone cause profound shock and death. This untoward reaction is most often seen after injuries to right colon, iIeum, and cecum whose contents are notabIy irritative. The heat and fIuid Ioss of intestina1 eviscerations and the acute pain of stomach avuIsions are also major contributory factors in the cause of shock in abdomina1 injuries. The treatment of these patients is perforce bIood. How much bIood one wilI give is predicated upon severa factors : (I ) rise in bIood pressure, (2) stabiIity of blood pressure, (3) hematocrit and pIasma protein readings as determined by the Evans copper suIfate method, (4) clinica appearance of the patient and (5) the tactica situation with its associated operating Ioad. In addition to bIood there are other therapeutic agents which are essentia1 in the treatment of shock in abdomina1 injuries. The stomach should be decompressed as soon as the patient arrives in the shock tent. The reasons for the use of a gastric suction tube in gut injuries are obvious. The empIoyment of the gastric suction tube in other conditions is aIso of vaIue. In pregnancy the processes of

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gastric motiIity cease with the onset of Iabor. So, too, when a man is criticaIIy injured, his gastric functions temporarily cease. Immediately acute gastric diIatation sets in. This causes pain but it aI.so raises the diaphragm on the Ieft side and thereby reduces puImonary ventilation. The reduction of avaiIabIe aeration space in the Iung is the one thing one does not want in shock; certainly it is an undesirabIe factor in thoracic, abdomina1 and thoraco-abdominaI wounds. Another factor which wiII reduce vita1 capacity is the voIuntary spIinting of the abdomina1 muscuIature and its concomitant decrease of the Costa1 excursion. Penetrating wounds of the upper abdomen notoriousIy deveIop wet Iung and it is our opinion that part of this may be attributed to this abdomina1 spIinting. The we11 trained shock officer wiI1 be thinking about muscuIar spIinting at a11 times. Sensation of the abdominal waII arises from the ninth thoracic through to the tweIfth. Treatment of upper abdomina1 wounds, in part, shouId be directed toward bIocking the previousIy mentioned innervation. It is in this fashion onIy that the patient can be prevented from reducing his vita1 capacity by muscuIar spIinting of the abdomina1 waI1. A shock officer has onIy to treat the pulmonary edema which arises from poor ventiIation once; he wiI1 ever after keep this important matter in mind. Extremity Injuries. The cause of shock in straight forward fracture cases seen in civiIian Iife has never been too we11 accepted by aI1. Various theories have been advanced, a11 of which are basicaIIy sound. But the cause of shock in extremity wounds due to she11 fire and mines is obvious. These patients manifest such pathoIogic conditions as fracture of the Iong bones with and without extensive comminution and/or soft tissue Ioss, major vascular injuries complicated by hemorrhage, traumatic amputations both partia1 and compIete, penetrating wounds of the joints, transections of the major nerves and penetrating wounds of the thighs with asso-

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ciated perforations of the bIadder, rectum and peritonea1 cavity. A compIication not infrequentIy seen in extremity wounds is anaerobic ceIIuIitis both invasive and noninvasive. Any one or a combination of these factors wiII produce shock of a profound degree. The probIem for the shock 0ffIcer in evaIuating a given case is to determine what factor or factors are producing the shock. The Ioss of bIood from a Iacerated artery is apparent, but the Ioss of bIood from venous back pressure due to an improperIy appIied tourniquet is often without reckoning. FrequentIypatients have been exsanguinated because of a tourniquet suff?ientIy tight to occIude the venous return but not the arteria1 suppIy. This is not the fauIt of the tourniquet but rather the method by which it was appIied. The shock oficer must be ever watchfu1 of this procedure because it does happen more often than one reaIizes and it can be not a IittIe embarrassing. The use of tourniquets in any case is very Iimited. The good shock officer can contro1 a11 hemorrhage in extremity wounds either by direct pressure over the wound or by Iigature of the offending vesse1. If a tourniquet must be appIied, it shouId be appIied as Iow as possibIe. There are good reasons for this remark. In the first pIace, why compromise the vitaIity of the entire Ieg by pIacing a tourniquet over the femora1 trigon when the patient has a traumatic amputation through the ankIe. To compromise the vitaIity of an extremity in this fashion not onIy reduces the prospects of getting a good operative resuIt but it aIso invites the development of anaerobic ceIIuIitis in tissue which would otherwise be heaIthy had its bIood suppIy not been impaired. Another reason for pIacing the tourniquet so Iow is that we wish to prevent the dissemination of myogIobin and exotoxins of cIostridia from the IocaI site of trauma. Extremity wounds present another situation which at times can be most confusing. This is infection with anaerobic organisms. Anaerobic infections are important to the

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shock officer because they are so often the etioIogic basis for the patient’s shock. Patients with extremity wounds can and do go into shock three hours after wounding and a frequent cause is acute invasive anaerobic ceIIuIitis. UnfortunateIy, the diagnosis of such conditions is entireIy cIinica1. Were we to see infections due primariIy to CIostridium WeIchii and CIostridium perfrigens, the matter wouId be reIativeIy simpIe. The crux of the argument is that infection caused by these organisms is not aIways the common finding. “Intensive studies carried out in SiciIy, ItaIy, and France disclosed that CL Bi-fermentens, Oedematiens, and SordeIIi infections were aIso frequent offenders.“3 It was the toxemia eIaborated by these organisms which threw the patient into decisive, profound and rapidIy fata shock. The existence of these organisms with their fuIminating type of infection shouId be borne in mind at a11 times because their diagnosis a11 too often hangs by the fine thread of an unstabIe bIood pressure, a rapid puIse, minute changes in the genera1 condition with aIterations in.the psychic pattern and menta1 behavior. UNFAVORABLE

RESULTS

The shock ofFicer wiII have many disappointments no matter how astute he might be or how hard he works. He wiI1 have many mistakes written to his credit; his work by definition wiI1 make for a high mortaIity rate. The author in an attempt to Iearn wherein he had faiIed spent severa months in the PathoIogy Department of a medica Iaboratory studying the postmortem findings of his errors. When the protocoIs of the various cases were studied, and this incIudes many of those patients who were operated upon by surgica1 teams of the auxiIiary surgica1 group but who never fuIIy recovered from shock, two contributory causes of death were noted: (I) fat embolism and (2) hemogIobinuric nephropathy. “There were two significant points noted in cases of fat emboIism: (I) It was seen

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in cases who had severe fractures and/or traumatic amputations and (2) it was rareIy diagnosed cIinicaIIy.“4 In the medica Iaboratory fiIes there were records of approximateIy 200 patients who died from wounds in which major fractures were a predominating compIication. AnaIysis of the tissue sIides of these cases showed thirty of them to have fat emboIi and this condition was apparentIy not recognized cIinicaIIy. The author is not without guilt in this matter. He had two patients who died presumabIy of cIostridia1 myositis. Microscopic examination of the tissues taken from these two reveaIed the diagnosis to be in reaIity fat emboIism. As further study of the autopsy protocoIs was carried out, it appeared that fat emboIism had its origin in four types of amputations, conditions: (I) t raumatic (2) fractures, (3) extensive tissue injuries to buttocks and (4) burns. The clinica picture of fat emboIism is CharacteristicaIIy, the highIy imitative. condition seemed to manifest itseIf fortyeight hours after operation or major manipuIative procedure. But we often saw patients with severe cornminuted fractures of the forearm who wouId arrive in the shock tent four hours after injury and then promptIy die for no apparent cause. The mode of demise in these cases was “wet Iung”; the cause of the wet Iung-puImonary fat emboIism. In those patients who manifested their symptoms fortyeight hours after operation one saw initiaIIy respiratory embarrassment usuaIIy dyspnea, cyanosis and uItimateIy frank puImonary edema. Further findings were those of a cerebra1 nature such as menta1 confusion, hyperexcitabiIity, amnesia, aphasic phenomena and sometimes convuIsions and coma. Various cIinicaIIy unexpIained IocaIizing signs presented themseIves. The cIinician’s diagnostic acumen was severeiy tested when such conditions as retina1 hemorrhage or edema, motor paraIysis and disturbance of the vegetative centers in the form of hyperthermia became apparent. Manifestations of this sort can be confused

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with possibIe head injury and indeed they often were. One patient was diagnosed as a Waterhouse-Friedrichson’s syndrome and another case was written up as “Typhus fever, acute severe.” According to the histories both of these patients manifested mentaI confusion, hyperthermia, shock, petechia1 hemorrhages in the skin and meningismus. Th ese were IogicaI conclusions. PathoIogicaIIy, the story was a different matter. The sIides showed fat emboIi in the brain, kidney, Iungs and connective tissue. Another contributory cause of death in severa of these cases studied was hemogIobinuric nephropathy. HemogIobinuric nephropathy is the sword of DamocIes in those patients receiving massive transfusions (3,000 to 6,000 cc.). HemogIobinuric nephropathy (shock kidney-transfusion kidney-kidney of crush syndrome) is and proIiferative type a degenerative of Iesion. The first thing seen in the microscopic section of the kidney are ,the pigmented casts Iocated in the tubuIes. With formation of this cast an obstruction and a concomitant $Iatation of the proxima1 nephrons deveIop. Edema of the interstitia1 tissue ensues and one sees connective tissue stroma i&Itration with histiocytes, Iymphocytes and eosinophiles. The tubuIar epitheIium, as a compensatory measure for the bIocking, proIiferates occasionaIIy to the extent of granuIoma formation. The casts are derived from one of two substances: (I) hemogIobin and (2) myogIobin. On the microscopic sIide both of these substances have the same chemica1 characteristics. To differentiate them one has to resort to spectroscopic procedures. From the surgica1 point of view, hemo-

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gIobin, as seen in hemogIobinuric nephropathy, can be derived from three sources: (I) Transfusion of bIood which is frankIy incompatibIe, which may be due to mismatching or to the Rh factors which manifest themseIves Iate (one to two months) and after many transfusions; (2) transfusion of hemoIyzed bIood, which has been stored bIood past its expiration date or has been poorIy prepared and/or cared for in the bIood bank. (3) transfusions of large amounts of type “0” bIood in a short time. The factor here is that with rapid transfusions hemoIysis of the recipient’s red bIood ceIIs takes pIace by A and B aggIutinins contained even in Iow titer “0” bIood. In other words, the protective factor of diIution, neutraIization and excretion are negated. SUMMARY

The dominant factor in shock is a Ioss of bIood. The successfu1 treatment of shock is predicated upon the rapid restoration of the norma hemogIobin content. To have a thoroughIy dry, patent, tracheobronchia1 tree with fuIIy aerated, freeIy expansiIe, Iung tissue is axiomatic. Tracheotomy, bronchia catherterization, intercosta1 bIocks and oxygen medication are adjuvant procedures to which you must resort if you wiI1 treat shock successfuIIy. REFERENCES I. CHURCHILL, EDWARD D. Penetrating abdominal wounds. Mediterranean Tbeater Circular Letter, January, 1944. 2. CHURCHILL, EDWARD D. Abdominal war wounds. Persona1 communication. 3. JERGESEN, FLOYD H. Anaerobic infections. Personal communication. 4. ROTHENBERG, JOSEPH. Fat embolism. Personal communication.