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Acute Blood Loss Therapeutics in Practice Acute Blood Loss Column Editor K. Gary Magdesian, DVM, DACVIM, DACVECC, DACVCP University of California, Davis Debra Deem Morris, DVM, MS, DACVIM Acute hemorrhage, a form of hypovolemic shock, can result from external or internal 190 State Route 10 blood loss. Distinguishing between these two types of hemorrhage is important to ren - dering proper therapy because cases of controllable hemorrhage must be treated differ - East Hanover, NJ 07936 ently than cases of uncontrollable hemorrhage. • phone 973-599-1191 • fax 973-599-1193 PATHOPHYSIOLOGY OF HEMORRHAGIC SHOCK • email stretchdee m@ yahoo.com Acute hemorrhage results in hypovolemia and a reduction in oxygen-carrying capac - ity (hemoglobin). A blood volume loss of 15% to 20% is clinically detectable, while life-threatening circulatory failure occurs with a blood volume loss of 30% to 40%. 1 Compensatory physiologic mechanisms include vasoconstriction, increased cardiac contractility, and tachycardia (activation of the sympathetic nervous system). In addi - tion, the drop in hydrostatic pressure due to hypovolemia causes filtration fraction to diminish and lymphatic flow to increase as a result of sympathetic activation and a reduction in central venous pressure (CVP). These changes result in a net movement of interstitial fluid into the vascular space. Simultaneously, the renin–angiotensin– aldosterone system is activated, resulting in a decreased glomerular filtration rate, decreased urine production and enhanced renal sodium resorption, increased thirst, and vasoconstriction. Vasopressin contributes to vasoconstriction and thirst. These compensatory mechanisms can maintain circulation in cases of mild blood loss (up to a volume loss of 15%). Losses exceeding this amount require volume replacement and are beyond physiologic compensation. If the patient’s condition is left unchecked, shock results from persistent hypoperfusion, leading to cell dysfunction and, ulti - mately, apoptosis and necrosis. CLINICAL SIGNS OF HEMORRHAGIC SHOCK Vital signs can be misleading as to the degree of hemorrhage, particularly in young and healthy animals; therefore, monitoring tools are critical in evaluating the bleeding patient. Because of compensatory vasoconstriction and contractility, the heart rate may Therapeutics in Practice not reflect the severity of blood loss. features current medical In general, the signs of blood loss reflect hypovolemia, including pale mucous mem - branes, prolonged capillary refill time, progressive deterioration of mental status, protocols used to treat a tachypnea, hypothermia, poor pulse quality (narrow pulse pressure), and cool extremi - variety of conditions ties. Tachycardia often does not develop until severe loss has occurred. Colic, sweating, in horses. and ileus may also occur in horses with significant blood loss. Send comments/questions via email MONITORING TOOLS [email protected] Because a physical examination can underestimate the quantity of blood lost, moni - or fax 800-556-3288 . toring tools should be used to enhance the sensitivity of detecting clinically significant Visit CompendiumEquine.com for hemorrhage. The hematocrit and total protein concentration are poorly correlated with full-text articles, CE testing, and CE blood volume deficits in acute hemorrhage because it takes several hours (>8 to 12) for test answers. fluid redistribution to occur and for the renin–angiotensin–aldosterone system to affect COMPENDIUM EQUINE 80 March 2008 Acute Blood Loss 81 the hematocrit. Decreased systolic blood pressure (<100 Measuring Indirect Blood Pressure mm Hg in adult horses) and fluid responsiveness are Indirect blood pressure is measured using an occlusion consistent with hypovolemia due to blood loss. Labora - cuff over an artery. Possible sites of cuff placement include tory data can be particularly useful as well. Markers of the coccygeal, dorsal metatarsal, median, and palmar significant blood loss include decreased blood pH, digital arteries. The tail is the most convenient and increased base deficit, increased lactate, and decreased reliable. Oscillometric monitors (Dinamap Veterinary mixed venous (or estimated by central venous) oxygen Blood Pressure Monitor [Critikon, Tampa, FL]) monitor tension. Coagulopathies with increased prothrombin systolic, diastolic, and mean blood pressures as well as time and partial thromboplastin time can develop. In pulse. This is significant because mean blood pressure is humans, the combination of progressive metabolic aci - the most important of the three in determining end-organ dosis, coagulopathy, and hypothermia are considered perfusion. The appropriate-size cuff (provided by the “the lethal triad,” which precedes circulatory failure in company) should be firmly placed around the tail or patients with blood loss. 2 With currently available diag - appendage. Once the cuff is in place, readings can be nostic tests, most of this monitoring can be performed measured. If the pulse rate displayed is not consistent with stall-side. Indirect blood pressure and portable blood gas the actual pulse rate, the blood pressure readings should analyzers (e.g., i-STAT handheld clinical analyzer not be trusted. Another means of double checking the accuracy of indirect blood pressure measurements is to [Heska, Loveland, CO]) are practical means of obtain - repeat them three times and evaluate the consistency ing these data (see the box on this page). among the different readings. In an experimental model of modest blood loss in horses, CVP decreased and blood lactate concentration increased significantly before the heart rate changed. 3 Normal CVP in adult horses is 5 to 15 cm H 2O, and the goal in treating controlled hemorrhage, hypoten - after 16 ml/kg of blood loss, CVP values decreased to –4 sive resuscitation is the approach used when managing to 5 cm H 2O. Lactate increased from 0.7 ± 0.2 mmol/L uncontrolled hemorrhage. With hypotensive resuscita - (range: 0.4 to 1.1) to 2.2 ± 1 mmol/L (0.5 to 6.7). 3 tion, the goal is to maintain a minimal mean arterial blood pressure to ensure end-organ perfusion without TREATMENT potentiating blood loss. Normalization of blood pres - Therapy for hemorrhage consists of the following: sure should be avoided to prevent worsening of hem - orrhage. The optimal blood pressure target for this Providing hemostasis when possible • type of resuscitation is unknown in horses; however, a • Increasing cardiac output with fluid resuscitation mean blood pressure of 60 mm Hg is a reasonable • Increasing oxygen-carrying capacity by providing goal. On the other hand, controlled (ligated or hemoglobin in the form of blood products stopped) hemorrhage is treated more aggressively with fluids, with the goal of normalizing perfusion (see the Hemostasis box on page 82). Controllable hemorrhage can be stopped by ligation Several types of resuscitation fluid used to treat acute of vessels, cautery, pressure bandages, manual pressure, hemorrhagic shock, including isotonic crystalloids, syn - the application of topical procoagulants (“fibrin thetic and natural colloids, and blood products, are dis - sealants” [e.g., thrombin, fibrin]), or a combination of cussed in the following sections. these therapies. After cessation of bleeding, fluid resus - citation is the primary aim in treating affected horses. Fluid Management of Controlled Hemorrhage Acute blood loss results in loss of cardiac output and Fluid Resuscitation Strategy hemoglobin—two components in the oxygen uptake Therapy of acute blood loss depends on the form of and delivery equations (see the box on page 84). Each hemorrhage. The treatment goals for uncontrolled of these is corrected using distinct strategies. 1 The con - hemorrhage (e.g., intraabdominal, uterine arterial, or sequences of a low cardiac output are more life-threat - pulmonary hemorrhage) are very different than those ening than those of anemia; therefore, the primary for controllable hemorrhage. Whereas normalizing initial aim in treating controlled hemorrhage is rapid blood pressure (through increasing cardiac output) is restoration of cardiac output through increasing preload March 2008 COMPENDIUM EQUINE 82 Therapeutics in Practice Fluid Choices Available for Controlled restoration of microcirculation as indicated by normal - Versus Uncontrolled Hemorrhage ization of blood pH (7.4), lactate (<2 mmol/L), mixed (or estimated from central) venous oxygen tension Goal in treating controlled hemorrhage (normal partial pressure of central venous oxygen Rapid normalization of blood pressure and cardiac output [PcvO 2] in horses is 32.3 ± 1.2 mm Hg [range: 27.4 to 36.2]), and urine output. Urine output can be measured Fluid choices through the use of indwelling urinary catheters. Mares • Early in the course of hemorrhage (during are easily instrumented with a 24- to 28-Fr Foley hypovolemic shock) for rapid administration of catheter, while males can either be catheterized with a fluids stallion urinary catheter or have a collection harness — Isotonic crystalloids — Hypertonic saline placed (with the collection bucket near the sheath). — Colloids Alternatively, urine output can be estimated through • Later in the course of hemorrhage (after volume urination frequency and spot checks of urine volume has been replaced) with intermittent collection of urine into a bucket. Car - — Isotonic crystalloids diac output can also be measured directly in horses in — Plasma for correction of hypoproteinemia or advanced monitoring settings through the use
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