Symposium on Shock
Clinical Evaluation and Management of Shock in the Equine Patient D. M. Meagher, D.V.M., M.S., Ph.D.*
Shock has been described as peripheral circulatory collapse leading to tissue hypoxia and cell death. Although this may be a broad statement, it describes the basic disease process of all types of shock. There are numerous conditions which can result in shock, but the final result is failure of tissue perfusion and loss of energy production. Aside from the clinical signs related to the primary disease, the signs seen in a horse in shock follow the same pattern. They are signs of a failing circulatory system. The heart rate is elevated, peripheral pulse is reduced, and the capillary refill time is prolonged. The mucous membranes will be congested to cyanotic. The body temperature will be dropping, and the extremities will feel cold. The patient will be depressed and will exhibit an anxious expression. The respiratory rate will be elevated, and the respirations will be shallow and labored. Cardiogenic shock is not a problem in the horse. Therefore, failure of the cardiovascular system is a result of loss of volume through loss of whole blood, loss of the fluid component of blood, or pooling from loss of integrity of the system.
CLINICAL EVALUATION A careful clinical evaluation of the horse in shock cannot be overemphasized. The state of the disease will change constantly with the body responses and treatment. Consequently, it is important that clinical observations be made and laboratory tests be performed at regu*Associate Professor of Surgery and Chief of Equine Surgery, Veterinary Medical Teaching Hospital, University of California, Davis Veterinary Clinics of North America- Vol. 6, No. 2, May 1976
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Jar intervals throughout the course of the disease. The following clinical evaluations should be made, and the results recorded: 1. Temperature. 2. Pulse rate and character. 3. Respiratory rate and character. 4. Presence of peripheral pulse and temperature of extremities. 5. Capillary refill time. 6. Color and appearance of oral and ocular mucous membranes. 7. Careful auscultation of the thorax and abdomen. 8. The frequency of urination and volume of urine production. 9. Type and frequency of defecation. Ideally, the following parameters would be measured along with the clinical observations: 1. Packed cell volume. 2. Plasma proteins. 3. Blood urea nitrogen. 4. Central venous pressure. 5. Complete blood count. 6. Serum electrolytes: sodium, chloride, and potassium. 7. Blood pH, pC02 , HC03 , and a calculation made of the base excess or base deficit. 8. Screening urinalysis, including pH. Although it would be ideal to have these tests readily available and to repeat them as often as necessary, at present, most shock patients are treated on the basis of considerably less laboratory data. The hematocrit, plasma proteins, and central venous pressure, if measured at regular intervals, will provide a good indication of response to therapy. These parameters should be measured at 30-minute intervals during early therapy, and later at one- or two-hour intervals. The results of these tests, combined with clinical observations, will allow the clinician to make a fairly sound judgment of the patient's response and of the need for further treatment. Many equine clinicians do not have laboratory facilities or equipment readily available. Careful observations of the clinical signs will often determine if fluid therapy is needed. By following the clinical signs and recording them, it is possible to restore circulating blood volume without overhydrating the patient. Once there is evidence of clinical response, the intravenous fluids should be administered slowly. As the circulating blood volume increases, arterial pressure and urine pJ:oduction will increase. As the volume of urine increases and the urine becomes more dilute, the rate of administration of fluids can be further reduced. As shock develops, acidosis will also develop. The pH of the horse's urine will decrease. It would be ideal to measure blood gases and calculate the amount of buffer (e.g., sodium bicarbonate) needed,
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based on the calculations of base deficit. However, if the necessary laboratory support is not available, pH paper may be used to follow the changes in urine pH, and a slow drip of a solution containing sodium bicarbonate may be administered until the pH of the urine has returned to normal.
SEPTIC SHOCK Septic or toxic shock occurs frequently in the horse and may be caused by acute bacterial infection, endotoxemia produced by enteric organisms, or acute obstructive colic. Severe enteritis resulting from salmonellosis or colitis X can rapidly lead to shock. Large volumes of body fluids are lost through . profuse diarrhea. The result is severe hemoconcentration. Initially, the horse may show signs of mild discomfort accompanied by a moderate rise in pulse and respiratory rate. The mucous membranes will be slightly congested, and capillary refill time will be slightly increased. The temperature will be slightly elevated, and the horse may be somewhat depressed. The plasma protein and total white cell count will be elevated. In the early stages of these diseases, ileus rather than hypermotility may occur. Rectal palpation will frequently reveal fluid-distended loops of intestines. These horses are frequently thought to have some type of obstructive colic, although the clinical signs may not support that diagnosis. In attempting to differentiate severe obstructive colic from acute enteritis, it is important to auscultate the abdomen very carefully on both sides for evidence of fluid sounds. Within a few hours after the initial signs, intestinal hypermotility and severe diarrhea will often occur. A mature horse may lose 50 to 100 liters of fluid in a 24-hour period from the profuse diarrhea associated with these diseases. As fluid accumulates in the intestinal lumen, the horse may show signs of abdominal pain. Marked congestion and cyanosis of the oral mucous membranes will develop rapidly. The heart rate will be elevated, usually over 100 beats per minute, with a weak peripheral pulse. The horse will be uncomfortable but, usually, not extremely violent. There will be fluid sounds in the abdominal cavity which will increase to hypermotility as the disease progresses. Large volumes of fluid may be drained from the stomach via a stomach tube. The horse may sweat profusely and usually has a very anxious expression. There is an increase in the amount of peritoneal fluid, and the fluid will contain increased neutrophils and plasma protein. The diseases are often associated with some form of stress, such as prolonged transportation or major surgery. It has been demonstrated that there are clinically normal horses that are Salmonella carriers.
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Hemoconcentration occurs rapidly in these diseases. Within a few hours from the onset of clinical signs, the horse can be in severe shock as a result of loss of body fluid into the intestinal tract. The hematocrit will increase to levels of 50 to 70 per cent, and the plasma proteins may increase to 7.5 to 9 gm per cent. There will be peripheral venous congestion, and the peripheral pulse may not be palpable. The body temperature at this stage will usually be below normal, and the extremities will be cold and clammy to the touch. The urine will be concentrated with a decrease in pH, and there may be an elevation in the blood urea nitrogen. The respiratory rate will be increased and, frequently, will be shallow and labored. Large amounts of sodium, potassium, and bicarbonate will be lost with the fluid feces. As severe hemoconcentration occurs, the horse will develop metabolic acidosis as a result of severely impaired peripheral circulation. Large volumes of intravenous balanced electrolyte solutions are indicated, along with a buffering agent (e.g., sodium bicarbonate) to overcome the acidosis. It is very important that these acute enteritis cases be differentiated from severe obstructive colic. The signs of severe shock, combined with abdominal pain and palpable distended loops of intestine, can be mistaken for severe obstructive colic. Endotoxic shock, caused by the release of endotoxins from rapidly multiplying gram-negative organisms in the intestinal tract, occurs in the horse. This may be the result of a severe obstructive colic, such as torsion, or may occur independently. The onset of endotoxic shock in the horse is sudden and acute. There is rapid hemoconcentration, marked increase in pulse and respiratory rates, peripheral venous congestion, and prolonged capillary refill time. The horse may break out in a profuse sweat. The peripheral pulse will be absent or difficult to palpate. The arterial and central venous pressures will decrease rapidly. Large amounts of the circulating blood volume are lost as a result of peripheral vasodilatation and loss of capillary wall integrity. Metabolic acidosis and marked leukopenia will develop rapidly. The horse will have a very anxious expression and may show some signs of moderate discomfort. Pulmonary congestion and edema may develop early in the disease. The onset of endotoxic shock is rapid. Within a few hours, the horse will be in severe shock. Massive intravenous fluid therapy is indicated. A balanced electrolyte solution, combined with sodium bicarbonate to control the acidosis, is necessary. In the horse, this type of shock appears clinically to respond to corticosteroid therapy in combination with the fluid therapy. Shock is often a complicating factor in acute obstructive colic in the horse. This is particularly true when malpositioning of some organ or part of an organ has occurred and the circulation has been compromised or completely occluded. Although there is no doubt that endo-
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toxins play a role in this type of shock, several other factors are involved. Dehydration results from the profuse sweating, from pain, and from violent behavior. The compromised section of intestinal tract loses fluid and protein into its own lumen, as well as into the abdominal cavity. As the disease progresses, avascular necrosis occurs, and the toxic materials from cell breakdown are released into the body. Finally, when the lesion is corrected or straightened out, toxic material will enter the general circulation if the venous return and the lumen of the affected part have not been clamped or ligated. A severe strangulation or large volvulus is difficult to reduce surgically in the horse. It is often not possible to ligate or clamp the affected portion before the malpositioning is reduced. Therefore, after the lesion has been reduced, shock in the horse may become more severe. Horses that are showing sigris of colic or abdominal pain should be examined for signs of hemoconcentration or dehydration. The pliability of the skin, the rate and character of the pulse, the color of the mucous membranes, and the capillary refill time will give an indication of the degree of hemoconcentration. If there is any evidence that colic is caused by anything other than a simple impaction, indigestion, or spasmodic colic, the state of hydration should be evaluated. The hematocrit and plasma protein levels, although not reliable as abso'lute values, give an indication of hemoconcentration. If these tests are done at regular intervals during the course of the disease, they will provide a measure of the relative hemoconcentration and the effectiveness of the fluid therapy. Horses with severe colic frequently show signs of marked hemoconcentration and shock. The pulse rate may be 100 to 150, the capillary refill time may be increased to 3 or 4 seconds, and the mucous membranes may be severely congested and cyanotic. Usually, it is not possible to make an immediate definitive diagnosis. However, if the horse can be reasonably restrained, shock therapy should be started. Large intravenous volumes of balanced electrolyte fluids with an additional intravenous drip of sodium bicarbonate solution are used. Analgesics or sedatives may be required io control pain and allow for the intravenous therapy. Hypotenisve drugs, such as phenothiazine derivative tranquilizers, should be avoided initially. There is danger of further decreasing peripheral circulation by lowering the blood pressure before adequate fluid volume has been administered. While the intravenous fluid ther~py is being administered, a more thorough clinical examination and appropriate diagnostic tests can be carried out in an attempt to determine the cause of the acute abdominal disease. If the disease is such that a laparotomy is needed, fluid therapy prior to surgery will make the horse a better surgical risk. Fluid therapy is continued during and after surgery. Some types of acute abdominal disease in the horse may be so
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severe, and the horse may be in such pain, that it is not possible to sedate or restrain the horse sufficiently to administer a significant volume of intravenous fluids. If exploratory surgery is to be done, it may be necessary to induce general anesthesia and proceed with rapid fluid therapy as the horse is being prepared for surgery. Massive volvulus of the small intestine, complete torsion of the large colon, and strangulated inguinal hernia in the stallion are examples of such severe abdominal diseases in the horse. Many horses that are in shock or in impending shock will be extremely anxious and restless without the presence of painful lesions. These horses will paw, lie down and get up repeatedly, wander about aimlessly, or continuously throw their heads. As fluid therapy is administered and the horse becomes hydrated, these signs will frequently disappear. Colic can often be managed medically. Adequate fluid therapy is an important component of the treatment. As hemoconcentration occurs, shunting of blood and reduction in flow to peripheral tissues occur. The gastrointestinal tract may have impaired function as a result of inadequate circulation. Adequate hydration will play an important role in returning intestinal function to normal. Paralytic ileus may follow severe colic or may occur as a complication following abdominal surgery in the horse. Large amounts of body fluid will be lost into the gastrointestinal tract. Since the horse cannot regurgitate, frequent drainage of the stomach via a stomach tube will be necessary. Large volumes of intravenous electrolyte solutions are then needed to maintain hydration. Adequate potassium must be provided to prevent ileus as a result of potassium depletion. Oral electrolyte solutions or water, administerea by stomach tube or given free choice, are ineffective and, in fact, are contraindicated in the horse with paralytic ileus. Ileus is often refractory to smooth muscle stimulants. Horses with impaction colic of several days' duration and horses that have been deprived of water during prolonged strenuous exercise or transportation may become severely dehydrated. Dehydration also occurs in horses that have been severely ill, simply as a result of lack of water. Usually, the dehydration is recognized before it has progressed to the point of shock. However, if the condition persists, shock from severe hemoconcentration can occur. These animals simply need to be rehydrated. This can be done with oral fluids or a combination of oral and intravenous balanced electrolyte solutions.
ANAPHYLACTIC SHOCK Horses develop anaphylactic-like reactions to some drugs and biologicals. The reaction can occur a few minutes to a half-hour after ad-
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ministration of the agent, depending on the drug and the route of administration. Horses have shown acute reactions to penicillin, iron preparations, and tranquilizers. The respiratory rate 'will increase rapidly, and the horse usually breaks out in a profuse sweat. The heart rate increases, the pulse becomes weaker, and sounds of fluid accumulation in the thorax or pulmonary edema can be auscultated. The horse will show signs of weakness and may tremble. Intestinal hypermotility may develop, and soft feces may be passed frequently. The extremities will become cold, and the mucous membranes will become injected to cyanotic. The capillary refill time will be prolonged. Epinephrine and antihistamines may be effective in controlling the condition in its early stages. If response is not rapid, corticosteroids and intravenous electrolyte therapy should be given. On .some occasions, the reaction is so rapid and so severe that there is little time for therapy to be effective. In fact, the horse may die before treatment can be instituted.
SURGICAL SHOCK During general anesthesia and surgery, hemoconcentration occurs in the horse as a result of exposure and dehydration of tissues and water loss from breathing dry gas mixtures. Blood volume will be reduced as a result of hemorrhage during surgery. If the procedure is long and involves a large amount of tissue exposure, as in a laparotomy, shock may develop as a result of hemoconcentration. If excessive blood is lost during the procedure, hypovolemic shock may occur. Horses that are ill, debilitated, or anemic may develop shock following a very short procedure under a light plane of anesthesia. The use of intravenous balanced electrolyte solutions during all major surgical procedures is very important in the prevention of intraoperative shock. This precaution should be taken even during elective procedures in normal horses. By expanding the blood volume, it is possible to greatly improve tissue perfusion during anesthesia. Both peripheral arterial pressure and circulating volume will be increased or maintained within normal limits. Adequate arterial pressure and peripheral tissue perfusion play an important role in the prevention of postoperative myositis. This complication has been common following p;rolonged procedures, particularly since the widespread use of inhalation anesthetics in the horse. Hypovolemic or hemorrhagic shock occurs in the horse as a result of traumatic accidents, as a complication to surgery, and following spontaneous rupture of large vessels. The internal carotid artery may be eroded by chronic guttural pouch infection. The uterine artery may rupture at the time of parturition. Strongylus larvae induce aneurysms of the anterior mesenteric artery which may rupture spontaneously or
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following the administration of a hypertensive agent. Many of these animals die before treatment can be given, since the ruptured vessel is large and blood loss is massive. At present, no satisfactory surgical techniques are available for the repair of these vessels. When the site of hemorrhage is accessible, ligation or packing combined with fluid therapy may prevent the development of shock. Tranquilizers that are hypotensive should be avoided in horses that have known large blood losses. If the hematocrit remains above 20 per cent, the use of large volumes of balanced electrolyte solutions is preferable to blood transfusion. Many incompatibilities exist in horse blood. Before blood transfusion, major and minor cross-matches should be done. Several possible donors should be sampled in order to find a suitable one. The use of plasma or plasma expanders may be helpful in the horse with early hypovolemic shock. These are of particular benefit when the plasma protein has decreased below 4.5 gm per cent and additional fluid therapy might lead to pulmonary edema. The collection and storage of horse plasma is time consuming, expensive and is not a common practice at this time. Low molecular weight dextrans are useful as plasma expanders in the horse. However, they are expensive in the volumes required. If facilities for cross-matching are not available and the situation is critical, a horse of the same breed should be selected as a donor, and the blood administered as soon as possible after collection. Whole blood should be given only until red blood cell and plasma protein levels are adequate. The circulating volume should be maintained with balanced electrolyte solutions. Horses suffering from severe myositis, or so-called "tying up syndrome," may not be in shock, but do have some degree of hemoconcentration, severe pain, and localized metabolic acidosis. The excess lactic acid produces necrosis of muscle fibers, and myoglobin is released and excreted through the kidneys. If excess myoglobin is released, or if dehydration reduces kidney circulation, the rate of excretion of myoglobin may be slowed, and kidney tubular blockage may occur. Maintenance of an alkaline urine will prevent the precipitation of myoglobin within the renal tubules. Balanced electrolyte fluid therapy combined with the administration of sodium bicarbonate will help prevent kidney damage. With an adequate circulating blood volume, tissue perfusion is improved in the affected muscle tissue and kidney function is maintained.
TREATMENT OF SHOCK IN HORSES GENERAL PRINCIPLES OF TREATMENT OF EQUINE SHOCK
l. Ensure adequate ventilation. This may require a tracheostomy and a supplemental supply of oxygen that can be administered by flowing oxygen through a small tube directly into the trachea.
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2. Expansion of the circulating blood volume by the rapid intravenous infusion of balanced electrolyte solutions. 3. Replacement of lost body fluid. 4. Replacement of specific lost electrolyte ions. 5. Control of acidosis. 6. Antibacterial therapy. 7. Control of immunological disease (e.g., anaphylactic shock). 8. Support of the cardiovascular system by drugs which act directly on this system. 9. Support of the cardiovascular system and control of the effects of toxin in endotoxic shock. 10. The use of whole blood, plasma, or plasma expanders in hemorrhagic shock. This may be necessary if there has been excessive loss of red cells or plasma protein. The use of large intravenous volumes of balanced electrolyte solutions is essential in all types of shock. Sodium bicarbonate, to control and help prevent acidosis, should also be a portion of the treatment. A large-diameter, indwelling intravenous catheter should be used to facilitate fluid therapy. In the severely shocked horse, intravenous therapy should be started at the rate of 1 ml per kg per minute. After 15 to 30 minutes, the rate is reduced to 0.5 to 0.25 .ml per kg minute. In severe cases, it may be necessary to administer at least 50 ml per kg during the initial two or three hours. If suitable laboratory facilities are available, the amount of sodium bicarbonate needed is calculated and given by slow intravenous drip. A rule of thumb, when blood gas measurements are not available: Dissolve 0.25 gm per kg of sodium bicarbonate in 3 liters of 5 per cent dextrose and administer as a slow intravenous drip over a two- to three-hour period. This may be repeated as needed. The urine pH, measured at regular intervals with pH paper, will give a rough estimation of the response to bicarbonate therapy. Horses suffering from shock and dehydration may receive part of their fluid therapy orally if they do not have paralytic ileus or intestinal obstruction. Ringer's solution and lactated Ringer's solution are relatively low in potassium. Since total body potassium is reduced in shock, additional potassium at the rate of 10 mEq per liter, should be added after the first 30 ml per kg of fluid therapy has been administered. After initial therapy, the volume of fluid required and the rate of administration will be determined by the condition and the response. Some horses with severe abdominal crises or severe septic shock may require 150 ml per kg or more of electrolyte solution during a 24-hour period. Thirty to 100 liters of intravenous fluid are often needed to treat a single horse in shock. The clinician needs to find an economical means of obtaining large containers of electrolyte solutions. Large doses of antibiotics are indicated in shock. Initially, potas-
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sium penicillin (40,000 units per kg) should be given. Depending on the cause, further antibiotic therapy is changed as needed. In endotoxic and anaphylactic shock in the horse, corticosteroids should be given (0.5 to 1 mg per kg). Although the question of the value of large doses of corticosteroids in shock has not been resolved, it seems clear that they do have a beneficial effect in endotoxic and anaphylactic shock. They may be useful in other forms of shock, also. Initially, a rapid-acting corticosteroid, such as prednisolone sodium succinate*, is given as an intravenous bolus at the rate of 1 mg per kg. The balance may be in the form of dexamethasonet and mixed with the intravenous fluids. During surgical procedures, unless hemoconcentration has already occurred, 10 ml per kg per hr of intravenous fluids, plus an amount equal to the estimated volume of blood lost, is usually adequate to prevent shock. If the horse is seriously ill and hemoconcentration is already present, larger amounts of fluid will be needed. It is important to recognize the amount of fluid needed to maintain the circulating blood volume and to continue the administration of fluids based on individual response. Careful monitoring should be continued until the horse is capable of maintaining its own hydration. Vasoactive drugs, including corticosteroids, should be administered only after or in conjunction with adequate fluid therapy. Vasoconstrictive drugs, such as epinephrine or norepinephrine, should not be used unless there is danger of cardiac arrest. Hypotensive drugs, such as phenothiazine derivative tranquilizers, should be avoided or withheld until the blood volume has been expanded with large amount of intravenous fluids. During the last 15 years, equine practitioners have become aware of the large volumes of fluids that are needed to treat shock in the horse. Although the management and monitoring of the shock patient IS time consuming and expensive, the results can be very gratifying. *Solu-Delta-Cortef- Upjohn Co., Kalamazoo, Michigan. tAzium-Schering Corp., Kenilworth, New Jersey.
REFERENCES 1. Brasmer, T. H.: Shock- basic pathophysiology and treatment. VET. CLIN. NoRTH AM., 2:219, 1972. 2. Burrows, G. E., and Cannon, J.: Endotoxemia induced by rapid intravenous injection of Escherichia coli in anesthetized ponies. Am . .J. Vet. Res., 31:1967, 1970. 3. Burrows, G. E.: Hemodynamic alterations in the anesthetized pony produced by slow intravenous administration of Escherichia coli endotoxin. Am. J. Vet. Res., 31:1975, 1970. 4. Carrol, E. J., Schalm, 0. W., and Wheat, J. D.: Endotoxemia in a horse. J Am. Vet. Med. Assoc., 146:1300, 1965.
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5. Nelson, N. A., and Meagher, D. M.: Septic shock in the horse. Proceed. Eighteenth Ann. Conv. A.A.E.P., 1972, p. 531. 6. Tasker, J. B.: Electrolyte therapy in gastrointestinal disease. Vet. Med. S.A.C., 61:765, 1966. 7. Tasker, J. B.: Fluids, electrolytes and acid base balance. In Kaneko J. J., and Cornelius, C. E. (eds.): Biochemistry of Domestic Animals. New York, Academic Press, 1971. 8. Tasker, J. B.: Fluid therapy in the severely dehydrated horse. Proc. Am. Assoc. Equine Pract., 1964, p. 63. 9. Vaughan, J. T.: The acute colitis syndrome-colitis X. VET. CLIN. NoRTH AM., 3:301, 1973. Department of Surgery College of Veterinary Medicine University of California at Davis Davis, California
Clinical Evaluation and Management of Shock in the Equine Patient D. M. Meagher, D.V.M., M.S., Ph.D.*
Shock has been described as peripheral circulatory collapse leading to tissue hypoxia and cell death. Although this may be a broad statement, it describes the basic disease process of all types of shock. There are numerous conditions which can result in shock, but the final result is failure of tissue perfusion and loss of energy production. Aside from the clinical signs related to the primary disease, the signs seen in a horse in shock follow the same pattern. They are signs of a failing circulatory system. The heart rate is elevated, peripheral pulse is reduced, and the capillary refill time is prolonged. The mucous membranes will be congested to cyanotic. The body temperature will be dropping, and the extremities will feel cold. The patient will be depressed and will exhibit an anxious expression. The respiratory rate will be elevated, and the respirations will be shallow and labored. Cardiogenic shock is not a problem in the horse. Therefore, failure of the cardiovascular system is a result of loss of volume through loss of whole blood, loss of the fluid component of blood, or pooling from loss of integrity of the system.
CLINICAL EVALUATION A careful clinical evaluation of the horse in shock cannot be overemphasized. The state of the disease will change constantly with the body responses and treatment. Consequently, it is important that clinical observations be made and laboratory tests be performed at regu*Associate Professor of Surgery and Chief of Equine Surgery, Veterinary Medical Teaching Hospital, University of California, Davis Veterinary Clinics of North America- Vol. 6, No. 2, May 1976
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Jar intervals throughout the course of the disease. The following clinical evaluations should be made, and the results recorded: 1. Temperature. 2. Pulse rate and character. 3. Respiratory rate and character. 4. Presence of peripheral pulse and temperature of extremities. 5. Capillary refill time. 6. Color and appearance of oral and ocular mucous membranes. 7. Careful auscultation of the thorax and abdomen. 8. The frequency of urination and volume of urine production. 9. Type and frequency of defecation. Ideally, the following parameters would be measured along with the clinical observations: 1. Packed cell volume. 2. Plasma proteins. 3. Blood urea nitrogen. 4. Central venous pressure. 5. Complete blood count. 6. Serum electrolytes: sodium, chloride, and potassium. 7. Blood pH, pC02 , HC03 , and a calculation made of the base excess or base deficit. 8. Screening urinalysis, including pH. Although it would be ideal to have these tests readily available and to repeat them as often as necessary, at present, most shock patients are treated on the basis of considerably less laboratory data. The hematocrit, plasma proteins, and central venous pressure, if measured at regular intervals, will provide a good indication of response to therapy. These parameters should be measured at 30-minute intervals during early therapy, and later at one- or two-hour intervals. The results of these tests, combined with clinical observations, will allow the clinician to make a fairly sound judgment of the patient's response and of the need for further treatment. Many equine clinicians do not have laboratory facilities or equipment readily available. Careful observations of the clinical signs will often determine if fluid therapy is needed. By following the clinical signs and recording them, it is possible to restore circulating blood volume without overhydrating the patient. Once there is evidence of clinical response, the intravenous fluids should be administered slowly. As the circulating blood volume increases, arterial pressure and urine pJ:oduction will increase. As the volume of urine increases and the urine becomes more dilute, the rate of administration of fluids can be further reduced. As shock develops, acidosis will also develop. The pH of the horse's urine will decrease. It would be ideal to measure blood gases and calculate the amount of buffer (e.g., sodium bicarbonate) needed,
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based on the calculations of base deficit. However, if the necessary laboratory support is not available, pH paper may be used to follow the changes in urine pH, and a slow drip of a solution containing sodium bicarbonate may be administered until the pH of the urine has returned to normal.
SEPTIC SHOCK Septic or toxic shock occurs frequently in the horse and may be caused by acute bacterial infection, endotoxemia produced by enteric organisms, or acute obstructive colic. Severe enteritis resulting from salmonellosis or colitis X can rapidly lead to shock. Large volumes of body fluids are lost through . profuse diarrhea. The result is severe hemoconcentration. Initially, the horse may show signs of mild discomfort accompanied by a moderate rise in pulse and respiratory rate. The mucous membranes will be slightly congested, and capillary refill time will be slightly increased. The temperature will be slightly elevated, and the horse may be somewhat depressed. The plasma protein and total white cell count will be elevated. In the early stages of these diseases, ileus rather than hypermotility may occur. Rectal palpation will frequently reveal fluid-distended loops of intestines. These horses are frequently thought to have some type of obstructive colic, although the clinical signs may not support that diagnosis. In attempting to differentiate severe obstructive colic from acute enteritis, it is important to auscultate the abdomen very carefully on both sides for evidence of fluid sounds. Within a few hours after the initial signs, intestinal hypermotility and severe diarrhea will often occur. A mature horse may lose 50 to 100 liters of fluid in a 24-hour period from the profuse diarrhea associated with these diseases. As fluid accumulates in the intestinal lumen, the horse may show signs of abdominal pain. Marked congestion and cyanosis of the oral mucous membranes will develop rapidly. The heart rate will be elevated, usually over 100 beats per minute, with a weak peripheral pulse. The horse will be uncomfortable but, usually, not extremely violent. There will be fluid sounds in the abdominal cavity which will increase to hypermotility as the disease progresses. Large volumes of fluid may be drained from the stomach via a stomach tube. The horse may sweat profusely and usually has a very anxious expression. There is an increase in the amount of peritoneal fluid, and the fluid will contain increased neutrophils and plasma protein. The diseases are often associated with some form of stress, such as prolonged transportation or major surgery. It has been demonstrated that there are clinically normal horses that are Salmonella carriers.
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Hemoconcentration occurs rapidly in these diseases. Within a few hours from the onset of clinical signs, the horse can be in severe shock as a result of loss of body fluid into the intestinal tract. The hematocrit will increase to levels of 50 to 70 per cent, and the plasma proteins may increase to 7.5 to 9 gm per cent. There will be peripheral venous congestion, and the peripheral pulse may not be palpable. The body temperature at this stage will usually be below normal, and the extremities will be cold and clammy to the touch. The urine will be concentrated with a decrease in pH, and there may be an elevation in the blood urea nitrogen. The respiratory rate will be increased and, frequently, will be shallow and labored. Large amounts of sodium, potassium, and bicarbonate will be lost with the fluid feces. As severe hemoconcentration occurs, the horse will develop metabolic acidosis as a result of severely impaired peripheral circulation. Large volumes of intravenous balanced electrolyte solutions are indicated, along with a buffering agent (e.g., sodium bicarbonate) to overcome the acidosis. It is very important that these acute enteritis cases be differentiated from severe obstructive colic. The signs of severe shock, combined with abdominal pain and palpable distended loops of intestine, can be mistaken for severe obstructive colic. Endotoxic shock, caused by the release of endotoxins from rapidly multiplying gram-negative organisms in the intestinal tract, occurs in the horse. This may be the result of a severe obstructive colic, such as torsion, or may occur independently. The onset of endotoxic shock in the horse is sudden and acute. There is rapid hemoconcentration, marked increase in pulse and respiratory rates, peripheral venous congestion, and prolonged capillary refill time. The horse may break out in a profuse sweat. The peripheral pulse will be absent or difficult to palpate. The arterial and central venous pressures will decrease rapidly. Large amounts of the circulating blood volume are lost as a result of peripheral vasodilatation and loss of capillary wall integrity. Metabolic acidosis and marked leukopenia will develop rapidly. The horse will have a very anxious expression and may show some signs of moderate discomfort. Pulmonary congestion and edema may develop early in the disease. The onset of endotoxic shock is rapid. Within a few hours, the horse will be in severe shock. Massive intravenous fluid therapy is indicated. A balanced electrolyte solution, combined with sodium bicarbonate to control the acidosis, is necessary. In the horse, this type of shock appears clinically to respond to corticosteroid therapy in combination with the fluid therapy. Shock is often a complicating factor in acute obstructive colic in the horse. This is particularly true when malpositioning of some organ or part of an organ has occurred and the circulation has been compromised or completely occluded. Although there is no doubt that endo-
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toxins play a role in this type of shock, several other factors are involved. Dehydration results from the profuse sweating, from pain, and from violent behavior. The compromised section of intestinal tract loses fluid and protein into its own lumen, as well as into the abdominal cavity. As the disease progresses, avascular necrosis occurs, and the toxic materials from cell breakdown are released into the body. Finally, when the lesion is corrected or straightened out, toxic material will enter the general circulation if the venous return and the lumen of the affected part have not been clamped or ligated. A severe strangulation or large volvulus is difficult to reduce surgically in the horse. It is often not possible to ligate or clamp the affected portion before the malpositioning is reduced. Therefore, after the lesion has been reduced, shock in the horse may become more severe. Horses that are showing sigris of colic or abdominal pain should be examined for signs of hemoconcentration or dehydration. The pliability of the skin, the rate and character of the pulse, the color of the mucous membranes, and the capillary refill time will give an indication of the degree of hemoconcentration. If there is any evidence that colic is caused by anything other than a simple impaction, indigestion, or spasmodic colic, the state of hydration should be evaluated. The hematocrit and plasma protein levels, although not reliable as abso'lute values, give an indication of hemoconcentration. If these tests are done at regular intervals during the course of the disease, they will provide a measure of the relative hemoconcentration and the effectiveness of the fluid therapy. Horses with severe colic frequently show signs of marked hemoconcentration and shock. The pulse rate may be 100 to 150, the capillary refill time may be increased to 3 or 4 seconds, and the mucous membranes may be severely congested and cyanotic. Usually, it is not possible to make an immediate definitive diagnosis. However, if the horse can be reasonably restrained, shock therapy should be started. Large intravenous volumes of balanced electrolyte fluids with an additional intravenous drip of sodium bicarbonate solution are used. Analgesics or sedatives may be required io control pain and allow for the intravenous therapy. Hypotenisve drugs, such as phenothiazine derivative tranquilizers, should be avoided initially. There is danger of further decreasing peripheral circulation by lowering the blood pressure before adequate fluid volume has been administered. While the intravenous fluid ther~py is being administered, a more thorough clinical examination and appropriate diagnostic tests can be carried out in an attempt to determine the cause of the acute abdominal disease. If the disease is such that a laparotomy is needed, fluid therapy prior to surgery will make the horse a better surgical risk. Fluid therapy is continued during and after surgery. Some types of acute abdominal disease in the horse may be so
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severe, and the horse may be in such pain, that it is not possible to sedate or restrain the horse sufficiently to administer a significant volume of intravenous fluids. If exploratory surgery is to be done, it may be necessary to induce general anesthesia and proceed with rapid fluid therapy as the horse is being prepared for surgery. Massive volvulus of the small intestine, complete torsion of the large colon, and strangulated inguinal hernia in the stallion are examples of such severe abdominal diseases in the horse. Many horses that are in shock or in impending shock will be extremely anxious and restless without the presence of painful lesions. These horses will paw, lie down and get up repeatedly, wander about aimlessly, or continuously throw their heads. As fluid therapy is administered and the horse becomes hydrated, these signs will frequently disappear. Colic can often be managed medically. Adequate fluid therapy is an important component of the treatment. As hemoconcentration occurs, shunting of blood and reduction in flow to peripheral tissues occur. The gastrointestinal tract may have impaired function as a result of inadequate circulation. Adequate hydration will play an important role in returning intestinal function to normal. Paralytic ileus may follow severe colic or may occur as a complication following abdominal surgery in the horse. Large amounts of body fluid will be lost into the gastrointestinal tract. Since the horse cannot regurgitate, frequent drainage of the stomach via a stomach tube will be necessary. Large volumes of intravenous electrolyte solutions are then needed to maintain hydration. Adequate potassium must be provided to prevent ileus as a result of potassium depletion. Oral electrolyte solutions or water, administerea by stomach tube or given free choice, are ineffective and, in fact, are contraindicated in the horse with paralytic ileus. Ileus is often refractory to smooth muscle stimulants. Horses with impaction colic of several days' duration and horses that have been deprived of water during prolonged strenuous exercise or transportation may become severely dehydrated. Dehydration also occurs in horses that have been severely ill, simply as a result of lack of water. Usually, the dehydration is recognized before it has progressed to the point of shock. However, if the condition persists, shock from severe hemoconcentration can occur. These animals simply need to be rehydrated. This can be done with oral fluids or a combination of oral and intravenous balanced electrolyte solutions.
ANAPHYLACTIC SHOCK Horses develop anaphylactic-like reactions to some drugs and biologicals. The reaction can occur a few minutes to a half-hour after ad-
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ministration of the agent, depending on the drug and the route of administration. Horses have shown acute reactions to penicillin, iron preparations, and tranquilizers. The respiratory rate 'will increase rapidly, and the horse usually breaks out in a profuse sweat. The heart rate increases, the pulse becomes weaker, and sounds of fluid accumulation in the thorax or pulmonary edema can be auscultated. The horse will show signs of weakness and may tremble. Intestinal hypermotility may develop, and soft feces may be passed frequently. The extremities will become cold, and the mucous membranes will become injected to cyanotic. The capillary refill time will be prolonged. Epinephrine and antihistamines may be effective in controlling the condition in its early stages. If response is not rapid, corticosteroids and intravenous electrolyte therapy should be given. On .some occasions, the reaction is so rapid and so severe that there is little time for therapy to be effective. In fact, the horse may die before treatment can be instituted.
SURGICAL SHOCK During general anesthesia and surgery, hemoconcentration occurs in the horse as a result of exposure and dehydration of tissues and water loss from breathing dry gas mixtures. Blood volume will be reduced as a result of hemorrhage during surgery. If the procedure is long and involves a large amount of tissue exposure, as in a laparotomy, shock may develop as a result of hemoconcentration. If excessive blood is lost during the procedure, hypovolemic shock may occur. Horses that are ill, debilitated, or anemic may develop shock following a very short procedure under a light plane of anesthesia. The use of intravenous balanced electrolyte solutions during all major surgical procedures is very important in the prevention of intraoperative shock. This precaution should be taken even during elective procedures in normal horses. By expanding the blood volume, it is possible to greatly improve tissue perfusion during anesthesia. Both peripheral arterial pressure and circulating volume will be increased or maintained within normal limits. Adequate arterial pressure and peripheral tissue perfusion play an important role in the prevention of postoperative myositis. This complication has been common following p;rolonged procedures, particularly since the widespread use of inhalation anesthetics in the horse. Hypovolemic or hemorrhagic shock occurs in the horse as a result of traumatic accidents, as a complication to surgery, and following spontaneous rupture of large vessels. The internal carotid artery may be eroded by chronic guttural pouch infection. The uterine artery may rupture at the time of parturition. Strongylus larvae induce aneurysms of the anterior mesenteric artery which may rupture spontaneously or
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following the administration of a hypertensive agent. Many of these animals die before treatment can be given, since the ruptured vessel is large and blood loss is massive. At present, no satisfactory surgical techniques are available for the repair of these vessels. When the site of hemorrhage is accessible, ligation or packing combined with fluid therapy may prevent the development of shock. Tranquilizers that are hypotensive should be avoided in horses that have known large blood losses. If the hematocrit remains above 20 per cent, the use of large volumes of balanced electrolyte solutions is preferable to blood transfusion. Many incompatibilities exist in horse blood. Before blood transfusion, major and minor cross-matches should be done. Several possible donors should be sampled in order to find a suitable one. The use of plasma or plasma expanders may be helpful in the horse with early hypovolemic shock. These are of particular benefit when the plasma protein has decreased below 4.5 gm per cent and additional fluid therapy might lead to pulmonary edema. The collection and storage of horse plasma is time consuming, expensive and is not a common practice at this time. Low molecular weight dextrans are useful as plasma expanders in the horse. However, they are expensive in the volumes required. If facilities for cross-matching are not available and the situation is critical, a horse of the same breed should be selected as a donor, and the blood administered as soon as possible after collection. Whole blood should be given only until red blood cell and plasma protein levels are adequate. The circulating volume should be maintained with balanced electrolyte solutions. Horses suffering from severe myositis, or so-called "tying up syndrome," may not be in shock, but do have some degree of hemoconcentration, severe pain, and localized metabolic acidosis. The excess lactic acid produces necrosis of muscle fibers, and myoglobin is released and excreted through the kidneys. If excess myoglobin is released, or if dehydration reduces kidney circulation, the rate of excretion of myoglobin may be slowed, and kidney tubular blockage may occur. Maintenance of an alkaline urine will prevent the precipitation of myoglobin within the renal tubules. Balanced electrolyte fluid therapy combined with the administration of sodium bicarbonate will help prevent kidney damage. With an adequate circulating blood volume, tissue perfusion is improved in the affected muscle tissue and kidney function is maintained.
TREATMENT OF SHOCK IN HORSES GENERAL PRINCIPLES OF TREATMENT OF EQUINE SHOCK
l. Ensure adequate ventilation. This may require a tracheostomy and a supplemental supply of oxygen that can be administered by flowing oxygen through a small tube directly into the trachea.
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2. Expansion of the circulating blood volume by the rapid intravenous infusion of balanced electrolyte solutions. 3. Replacement of lost body fluid. 4. Replacement of specific lost electrolyte ions. 5. Control of acidosis. 6. Antibacterial therapy. 7. Control of immunological disease (e.g., anaphylactic shock). 8. Support of the cardiovascular system by drugs which act directly on this system. 9. Support of the cardiovascular system and control of the effects of toxin in endotoxic shock. 10. The use of whole blood, plasma, or plasma expanders in hemorrhagic shock. This may be necessary if there has been excessive loss of red cells or plasma protein. The use of large intravenous volumes of balanced electrolyte solutions is essential in all types of shock. Sodium bicarbonate, to control and help prevent acidosis, should also be a portion of the treatment. A large-diameter, indwelling intravenous catheter should be used to facilitate fluid therapy. In the severely shocked horse, intravenous therapy should be started at the rate of 1 ml per kg per minute. After 15 to 30 minutes, the rate is reduced to 0.5 to 0.25 .ml per kg minute. In severe cases, it may be necessary to administer at least 50 ml per kg during the initial two or three hours. If suitable laboratory facilities are available, the amount of sodium bicarbonate needed is calculated and given by slow intravenous drip. A rule of thumb, when blood gas measurements are not available: Dissolve 0.25 gm per kg of sodium bicarbonate in 3 liters of 5 per cent dextrose and administer as a slow intravenous drip over a two- to three-hour period. This may be repeated as needed. The urine pH, measured at regular intervals with pH paper, will give a rough estimation of the response to bicarbonate therapy. Horses suffering from shock and dehydration may receive part of their fluid therapy orally if they do not have paralytic ileus or intestinal obstruction. Ringer's solution and lactated Ringer's solution are relatively low in potassium. Since total body potassium is reduced in shock, additional potassium at the rate of 10 mEq per liter, should be added after the first 30 ml per kg of fluid therapy has been administered. After initial therapy, the volume of fluid required and the rate of administration will be determined by the condition and the response. Some horses with severe abdominal crises or severe septic shock may require 150 ml per kg or more of electrolyte solution during a 24-hour period. Thirty to 100 liters of intravenous fluid are often needed to treat a single horse in shock. The clinician needs to find an economical means of obtaining large containers of electrolyte solutions. Large doses of antibiotics are indicated in shock. Initially, potas-
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sium penicillin (40,000 units per kg) should be given. Depending on the cause, further antibiotic therapy is changed as needed. In endotoxic and anaphylactic shock in the horse, corticosteroids should be given (0.5 to 1 mg per kg). Although the question of the value of large doses of corticosteroids in shock has not been resolved, it seems clear that they do have a beneficial effect in endotoxic and anaphylactic shock. They may be useful in other forms of shock, also. Initially, a rapid-acting corticosteroid, such as prednisolone sodium succinate*, is given as an intravenous bolus at the rate of 1 mg per kg. The balance may be in the form of dexamethasonet and mixed with the intravenous fluids. During surgical procedures, unless hemoconcentration has already occurred, 10 ml per kg per hr of intravenous fluids, plus an amount equal to the estimated volume of blood lost, is usually adequate to prevent shock. If the horse is seriously ill and hemoconcentration is already present, larger amounts of fluid will be needed. It is important to recognize the amount of fluid needed to maintain the circulating blood volume and to continue the administration of fluids based on individual response. Careful monitoring should be continued until the horse is capable of maintaining its own hydration. Vasoactive drugs, including corticosteroids, should be administered only after or in conjunction with adequate fluid therapy. Vasoconstrictive drugs, such as epinephrine or norepinephrine, should not be used unless there is danger of cardiac arrest. Hypotensive drugs, such as phenothiazine derivative tranquilizers, should be avoided or withheld until the blood volume has been expanded with large amount of intravenous fluids. During the last 15 years, equine practitioners have become aware of the large volumes of fluids that are needed to treat shock in the horse. Although the management and monitoring of the shock patient IS time consuming and expensive, the results can be very gratifying. *Solu-Delta-Cortef- Upjohn Co., Kalamazoo, Michigan. tAzium-Schering Corp., Kenilworth, New Jersey.
REFERENCES 1. Brasmer, T. H.: Shock- basic pathophysiology and treatment. VET. CLIN. NoRTH AM., 2:219, 1972. 2. Burrows, G. E., and Cannon, J.: Endotoxemia induced by rapid intravenous injection of Escherichia coli in anesthetized ponies. Am . .J. Vet. Res., 31:1967, 1970. 3. Burrows, G. E.: Hemodynamic alterations in the anesthetized pony produced by slow intravenous administration of Escherichia coli endotoxin. Am. J. Vet. Res., 31:1975, 1970. 4. Carrol, E. J., Schalm, 0. W., and Wheat, J. D.: Endotoxemia in a horse. J Am. Vet. Med. Assoc., 146:1300, 1965.
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5. Nelson, N. A., and Meagher, D. M.: Septic shock in the horse. Proceed. Eighteenth Ann. Conv. A.A.E.P., 1972, p. 531. 6. Tasker, J. B.: Electrolyte therapy in gastrointestinal disease. Vet. Med. S.A.C., 61:765, 1966. 7. Tasker, J. B.: Fluids, electrolytes and acid base balance. In Kaneko J. J., and Cornelius, C. E. (eds.): Biochemistry of Domestic Animals. New York, Academic Press, 1971. 8. Tasker, J. B.: Fluid therapy in the severely dehydrated horse. Proc. Am. Assoc. Equine Pract., 1964, p. 63. 9. Vaughan, J. T.: The acute colitis syndrome-colitis X. VET. CLIN. NoRTH AM., 3:301, 1973. Department of Surgery College of Veterinary Medicine University of California at Davis Davis, California
