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resuscitation in small animals - Maravet

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36 Shock<br />

Often the <strong>in</strong>fusion of a synthetic colloid <strong>in</strong> the fluid therapy program allows a reduction <strong>in</strong> the<br />

crystalloid fluid requirement by 40-60%.<br />

43. What is oxyglob<strong>in</strong>? When is it used <strong>in</strong> a shock patient?<br />

Oxyglob<strong>in</strong> is a member of a group of compounds know as hemoglob<strong>in</strong>-based oxygen carriers<br />

(HBOC). The molecule is polymer of bov<strong>in</strong>e hemoglob<strong>in</strong> that recently was approved for use<br />

<strong>in</strong> dogs <strong>in</strong> the United States. The HBOCs have evolved from more than 50 years of research <strong>in</strong>to<br />

acelluar blood replacement solutions. The oxygen-carry<strong>in</strong>g characteristics of this product are<br />

similar to those of blood with several important differences. Oxyglob<strong>in</strong> b<strong>in</strong>ds and releases<br />

oxygen more readily than whole blood, requires no typ<strong>in</strong>g or cross-match<strong>in</strong>g, requires no special<br />

adm<strong>in</strong>istration set or filter, does not depend on levels of 2,3-diphosphoglycerate to regulate its<br />

oxygen-b<strong>in</strong>d<strong>in</strong>g site, and is shelf-stable for more than I year at room temperature. Oxyglob<strong>in</strong> has<br />

demonstrated its effectiveness <strong>in</strong> restor<strong>in</strong>g oxygen delivery <strong>in</strong> anemic dogs or dogs <strong>in</strong> hemorrhagic<br />

shock. Recent research has demonstrated that Oxyglob<strong>in</strong> adm<strong>in</strong>istered at low doses improves<br />

oxygen delivery to tissues by <strong>in</strong>creas<strong>in</strong>g the transfer of oxygen across the <strong>in</strong>terstitial fluid<br />

barrier and by reach<strong>in</strong>g tissues that red blood cells cannot. Label directions must be followed<br />

closely. Oxyglob<strong>in</strong> has significant colloidal osmotic properties and can <strong>in</strong>duce circulatory overload<br />

if adm<strong>in</strong>istered too rapidly or <strong>in</strong> excess of recommended dosages.<br />

44. What is the rationale beh<strong>in</strong>d low-volume <strong>resuscitation</strong> <strong>in</strong> hemorrhagic shock?<br />

The rationale is simple: adm<strong>in</strong>istration of <strong>small</strong> volumes of fluids dur<strong>in</strong>g traumatic or hemorrhagic<br />

shock reduces the risk of disrupt<strong>in</strong>g clotted vasculature and exacerbat<strong>in</strong>g hemorrhage<br />

until def<strong>in</strong>itive care is available. Although this concept recently has been popularized based on<br />

one paper, no currently available data determ<strong>in</strong>e how low or for how long a patient can be ma<strong>in</strong>ta<strong>in</strong>ed<br />

before irreversible shock will result. The efficacy and safety of this theory are unproved <strong>in</strong><br />

the cl<strong>in</strong>ical sett<strong>in</strong>g and warrant further study.<br />

BIBLIOGRAPHY<br />

I. Aldrich J: Shock. In K<strong>in</strong>g L, Hammond R (eds): Manual of Can<strong>in</strong>e and Fel<strong>in</strong>e Emergency and Critical<br />

Care. Cheltenham, UK, BSAVA, 1999, pp 23-36.<br />

2. Astiz ME, Rackow EC, Weil MH: Pathophysiology and treatment of circulatory shock. Crit Care Cl<strong>in</strong><br />

9: 183-203, 1993.<br />

3. Crystal MA, Cotter SM: Acute hemorrhage: A hematologic emergency <strong>in</strong> dogs. Compend Cont Educ<br />

Pract Vet 14:60-68, 1992.<br />

4. Ford SL, Schaer M: Shock syndrome <strong>in</strong> cats. Compend Cont Educ Pract Vet 15: 120-125, 1993.<br />

5. Hansen B: Fluid therapy <strong>in</strong> the shock patient. Proceed<strong>in</strong>gs IVECCS VI, San Antonio, TX, 1998, pp<br />

216-221<br />

6. Hask<strong>in</strong>s SC: Therapy for shock. In Bonagura JD (ed): Current Veter<strong>in</strong>ary Therapy, vol. XIII.<br />

Philadelphia, wn. Saunders, 2000, pp 140-146.<br />

7. Hughes D: Lactate measurement: Diagnostic, therapeutic, and prognostic implications. In Bonagura JD<br />

(ed): Current Veter<strong>in</strong>ary Therapy, vol. XIII. Philadelphia, WB. Saunders, 2000, pp 140-146.<br />

8. Kirby R: Septic shock. In Bonagura JD (ed): Current Veter<strong>in</strong>ary Therapy, vol XII. Philadelphia, WB.<br />

Saunders, 1995, pp 139-146.<br />

9. Kl<strong>in</strong>e lA. Shock. In Rosen D (ed): Emergency Medic<strong>in</strong>e: Concepts and Cl<strong>in</strong>ical Practice, vol I. SI. Louis,<br />

Mosby, 1998 pp 86-106.<br />

10. Rackow Ee. Astiz ME: Mechanisms and management of septic shock. Crit Care Cl<strong>in</strong> 9:219-237, 1993.<br />

I I. Schertel ER, Muir WW: Shock: Pathophysiology, monitor<strong>in</strong>g, and therapy. In Kirk RW (ed): Current<br />

Veter<strong>in</strong>ary Therapy, vol X. Philadelphia, wn. Saunders, 1989, pp 316-330.<br />

12. Walley KR, Wood LD: Shock. In Hall JB (ed): Pr<strong>in</strong>ciples of Critical Care. New York, McGraw-Hill,<br />

1998, pp 277-301.<br />

13. Ware WA: Shock. In Murtaugh RJ, Kaplan PM (eds): Veter<strong>in</strong>ary Emergency and Critical Care Medic<strong>in</strong>e.<br />

Chicago, Mosby-Year Book, 1992, pp 163-175.<br />

14. W<strong>in</strong>gfield WE. How much fluid should you adm<strong>in</strong>ister? Proceed<strong>in</strong>gs VECCS, 1997, pp 17-19.

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