Indirect measurement of blood pressure as a guide to the efficacy of fluid therapy in equine shock: A case report

Indirect measurement of blood pressure as a guide to the efficacy of fluid therapy in equine shock: A case report

INDIRECT M E A S U R E M E N T OF BLOOD P R E S S U R E AS A GUIDE TO THE EFFICACY OF FLUID THERAPY IN EQUINE SHOCK: A CASE REPORT B.W. Parry, BVSc, P...

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INDIRECT M E A S U R E M E N T OF BLOOD P R E S S U R E AS A GUIDE TO THE EFFICACY OF FLUID THERAPY IN EQUINE SHOCK: A CASE REPORT B.W. Parry, BVSc, PhD; B.A. Christie, BVSc, MACVSc; C.C. Gay, DVM, MVSc, FACVSc; and R.N. Haywood, BVSc

CASE SUMMARY A case of acute circulatory failure in a horse is described. The response to intravenous fluid therapy was monitored by measurement of heart and respiratory rates, and arterial and central venous pressures. Heart rate was an unreliable guide to improved circulatory status. Central venous pressure and indirect arterial blood pressure were valuable guides to the efficacy of fluid therapy.

INTRODUCTION Easy and accurate indirect measurement of blood pressure in the horse is a comparatively recent innovation, s 6 79 The present case report documents the clinical usefulness of indirectly measured blood pressure when monitoring equine colic cases post-operatively. MATERIALS AND METHODS Blood pressure was measured indirectly at the middle coccygeal artery, using an ultrasonic blood flow detector a technique s and a bladder width to tail girth ratio of about 0.5.16 The horse was gently restrained in a normal, relaxed standing position ~4 for all readings. All values were q u o t e d as coccygeal uncorrected values (CUCV), 4 that is they were not corrected to heart level or adjusted for the bladder width to tail girth ratio used. Central venous pressure was measured by an intravenous cather b system, zeroed to shoulder level. 8 Heart rate (H R) was determined by cardiac auscultation and respiratory rate (RR) by observation o f thoracic excursions.

Authors' address: Department of Veterinary Clinical Medicine and Surgery Washington State University Pullman, WA 99164-6610 From the Department of Veterinary Clinical Sciences University of Melbourne, Werribee, Victoria, 3030, Australia Acknowledgement: The assistance of K. Carey, M. Gebert and P. Waldo are gratefully acknowledged.

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REPORT

History A 12-year-old Palomino mare (weighing 405 kg) was referred to the University of Melbourne Veterinary Clinical Centre for treatment of an acute abdomen. One month previously, an exploratory laparotomy had been performed to relieve a small intestinal strangulation caused by a fibrous band thought to be either an ovarian adhesion or a pedunculated lipoma. At the same time, the terminal 2.5 m of the ileum was resected and an end-to-side ileocecal anastomosis performed. The second bout of colic also required exploratory surgery. This revealed an obstruction of the terminal ileum caused by a constrictive band of omentum which ran to an adhesion between a loop of small intestine and the cecum. (The adhesion did not compromise the gut.) The omental band was transected and a small section of cecum, together with about 30 cm of small intestine, were resected to remove the adhesion. The horse made an uneventful anesthetic recovery.

Clinical Findings and Treatment The morning after surgery the horse was mildly depressed with H R t05 beats/minute, R R 28 breaths/minute, blood pressure 89/64 mm Hg C UCV and rectal temperature 37.9 °. Gut sounds were markedly decreased over most areas of the abdomen. The oral mucosae, facial arterial pulse and jugular filling rate were all normal and there was no skin tenting. The hematocrit was 43% with a refractometric protein of 6.2 g/dl. The leukogram revealed a total count of 7,500/ul with a normal neutrophil count and a left-shift with a marked toxic change. A peritoneal fluid sample contained 102,600 nucleated cells/ul, 95% of which were

a Ultrasonic blood flow detector BF4A, Medasonics Inc., Mountain View, CA. bTuta Laboratories (Australia) Pty Ltd, St Kilda, Victoria, Australia. EQUINE VETERINARY SCIENCE

cloudy and blood-tinged fluid, which had an erythrocyte count of 1,200,000/ul and a leucocyte count of 53,400/ul (98% of which were neutrophils). The following peritoneal fluid concentrations were noted: refractometric protein 4.6 g/dl, biuret protein 4.2 g/dl, glucose 64.7 mg/dl and lactate 46.8 mg/dl. A diagnosis of persisting peritonitis with acute circulatory failure was made and fluid therapy commenced. A total of 22 liters of Hartmann's solution and 200 mg of dexamethasone were administered intravenously, as shown in Figure I. Three grams of ampicillin was given intravenously at the beginning of fluid therapy. The response to treatment is shown in Figure I. On the following day, rectal temperature was 37.5°C, HR 48 beats/minute, RR 6 breaths/minute and blood pressure 139/106 m m H g CUCV. Treatment with butazolidine was discontinued after 2 days. After 3 days the antibiotic was changed to procaine penicillin (10,000 I U/kg SID) and dihydrosktreptomycin (10 mg/kg BID) for 2 days, then trimethoprim (3 mg/kg) and sulphadiazine (l 5 mg/kg BID) for 14 days. Peritonitis continued as a clinical problem for about a week. A few skin sutures broke down about l ! days after surgery. Throughout this period blood pressure, RR and rectal temperature remained within normal limits, but the horse had bouts of tachycardia. There

( p r e d o m i n a n t l y i n t a c t ) n e u t r o p h i l s a n d 5% were mononuclear-type cells, with refractometric protein of 4.5 g/dl. P o s t - o p e r a t i v e peritonitis was d i a g n o s e d and antibiotic treatment with ampicillin (initial dose 4 g, then 3 g, intravenously TID). The mare was also favoring her left hind leg and was treated with b u t a z o l i d i n e (I g intravenously SID). Throughout the day blood pressure was observed to vary between 89/61 and 116/86 m m H g CUCV, H R between 80 and 104 beats/minute, RR between 16 and 32 breaths/minute and rectal temperature between 37.8 and 39.0°C. On the following day the horse was mildly depressed, but showed no overt signs of pain. Rectal temperature was 39.5°C, H R 94 beats/minute and RR 36 breaths/minute. The facial arterial pulse was weak and the distal limbs were palpably cold, however, jugular filling rate was good, the oral mucosa was pink, moist and had a capillary refill rate of 1 second, and there was no skin tenting. Blood pressure was 48/20 m m H g CUCV. The hematocrit was 39% and the total leucocyte count was 10,000/ul, with a normal neutrophil count and marked toxic change. The following blood concentrations were noted: refractometric protein 6.8 g/dl, biuret protein 7.1 g/dl, glucose 90.8 mg/dl, urea nitrogen 20.2 m g / d l and lactate 15.8 m g / d l . Abdominocentesis produced a plentiful flow of moderately

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Figure I. Response to intravenous fluid therapy. Cumulative totals of Hartmann's solution (Fluids) and corticosteroids (CCS) are indicated.

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were no clinical signs of a b d o m i n a l pain. The mare was discharged 3 weeks after admission.

Clinical Findings and Treatment The morning after surgery the horse was mildly depressed with H R 105 beats/minute, R R 28 breaths/minute, blood pressure 89/64 m m H g C U C V and rectal temperature 37.9°C. Gut sounds were markedly decreased over most areas of the a b d o m e n . The oral mucosae, facial arterial pulse and j u g u l a r filling rate were all n o r m a l and there was no skin tenting

DISCUSSION Normal equine blood pressure ranges f r o m 80/49 to 144/105 m m H g CUCV.~5 After the administration of a b o u t 4 liters of fluids to the present case, b l o o d pressure was within low n o r m a l limits, however, central venous pressure was still below the normal of 5 to 15 cm water. 3 Thus, although systemic perfusion, as reflected by coecygeal blood pressure, had improved, blood volume, as reflected by central venous pressure, was still inadequate. Continued fluid administration sustained blood pressure in the m a r g i n a l l y h y p o t e n s i v e range a n d f u r t h e r i m p r o v e d circulatory status, as indicated by normalization of central venous pressure and R R by 1 hour. On completion of fluid therapy, blood pressure, R R and central venous pressure were all normal, however, tachycardia persisted. The reason for the s u s t a i n e d t a c h y c a r d i a in spite o f i m p r o v e d cardiovascular function was unclear; pain was not a clinical problem. The decreased R R was presumably due to correction of metabolic acidosis, however, blood gas and acid/base measurements were not made. Reliance on a decreasing H R to indicate improved circular status would have been misleading in this case. Measurement of arterial and central venous pressures permitted quantification of circulatory improvement. These measurements compliment each other. Central venous pressure gives a measure of cardiac venous return. Theoretically, high central venous pressure m a y result from cardiac failure or over-hydration. However, over-hydration is considered an i m p r o b a b l e sequela to fluid therapy in the horse.3 ,7 Thus, while increasing central venous pressure may indicate efficacious fluid therapy, it could also indicate impending cardiac failure. A high central venous pressure may be presumed to be due to cardiac failure. Arterial blood pressure measurement provides a means of differentiating between these two causes o f increasing central venous pressure. When the rate of intravenous infusion is sufficient to restore circulating blood volume, arterial hypotension will be corrected, concomittant with increased central venous pressure. However, with cardiac failure in the face of fluid therapy, central venous pressure may increase, but arterial hypotension persists. In the present case, acute circulatory failure was diagnosed during a routine post-operative examination. Successful treatment involved early and intensive therapy. The degree of arterial hypotension reflected the magnitude of the problem, however, the hemotocrit and total protein

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values apparently belied the severity of the situation. Slightly elevated blood urea nitrogen and blood lactate values suggested the condition was probably of short duration. J2 ~3 In the normal horse, peritoneal fluid lactate concentration is less than that in blood (which is normally below 14 mg/dl), l° while mean peritoneal fluid glucose concentration is slightly greater than corresponding blood levels.2 ii In cases with peritonitis, peritoneal fluid glucose v a l u e s d e c l i n e , p r e s u m a b l y d u e to m e t a b o l i s m b y inflammatory cells a n d / o r bacteria, l ]2 Anerobic glycolysis by inflammatory cells a n d / o r bacteria would decrease the peritoneal fluid glucose level and increase the peritoneal fluid lactate concentration as was observed in the present case. Inverted b l o o d / p e r i t o n e a l fluid lactate and glucose ratios, with a b n o r m a l peritoneal fluid concentrations, have been c o m m o n l y found in cases of peritonitis, severe intestinal infarction and visceral ruptureJ 2 Peritoneal fluid glucose concentrations were almost undetectable in some cases, resulting in very high b l o o d / p e r i t o n e a l fluid glucose ratios. Such horses may have a p o o r prognosis.13 A l t h o u g h peritoneal fluid glucose concentration was less that the corresponding blood value, in the present case it was not m a r k e d l y decreased as would p r o b a b l y be the situation in a severe (septic) peritonitis.

REFERENCES 1. Brownlow, M.A.:Abdominal paracentesis in the horse--a clinical M.V.Sc. Thesis, University of Sydney, N.S.W., Australia, 1979. 2. Brownlow, M.A., Hutchins, D.R., and Johnston, K.G.: Reference values for equine peritoneal fluid.Eq Vet J 13:127-130, 1981. 3. Donawick, W.J., and Alexander J.T.: Laboratoo, and clinical

evaluation.

determinations in the management o f the horse with intestinal obstruction.

Proc 16th Ann Conf Am Assoc Eq Prac, pp. 343-353, 1970. 4. Gay, C.C., McCarthy, M., and Carter, J.:Indirect measurement of arterial blood pressure in horses. Proc Ann Conf Aust Vet Assoc 54:107108, 1977. 5. Gay, C.C., McCarthy, M., Reynolds, W.T., and Carter, J.: A method for indirect measurement of arterial blood pressure in the horse.Aust Vet J 53:163-166, 1977. 6. Geddes, LA. Chaffee, V., Whistler, S.J., Bourland, E.E., and Tacker, W.A.: Indirect mean blood pressure in the anesthetized pony. A m J Vet Res 38:2055-2057, 1977. 7. Hahn, A.W., Garner, H.E., Coffman, J.R., and Sanders, C.W.: [ndirect measurement of arterial blood pressure in the laboratory pony.Lab Anita Sci 23:889-893, 1973. 8. Klein, L, and Sherman, J.: Effects of preanesthetic medication, anesthesia and position of recumbency on central venous pressure in horses. J A m Vet Med Assoc 170:216-219, 1977. 9. Latshaw, H., Fessler, J.F., Whistler, SJ., and Geddes, L.A.: Indirect measurement of mean blood pressure in the normotensiveand hypotensive horse.Eq Vet J 11:191-194, 1979. 10. Moore, J.N., Traver, D.S., Turner, M.F., White, F.J., Huesgen,J.G. and Butera, T.S.: Lacticacid concentration in peritoneal fluid of normal and diseased horses.Res Vet Sci 23:117-118, 1977. 11. Nelson, A.W.: Analysis of equine peritoneal fluid. Vet Clin N Am: Lge Anita Prac 1:267-274, 1979. 12. Parry, B.W.:Studies on the clinical usefulness o f indirectly measure blood pressure in the horse, with special reference to prognosis in cases o f equine colic. Ph.D. Thesis, Melbourne University, Victoria, Australia,

1982. 13. Parry, B.W., Anderson, G.A., and Gay, C.C. :Prognosis in equine colic: a study of individual variables used in casse assessment.Eq Vet J submitted, 1982. EQUINE VETERINARY SCIENCE

14. Parry, B.W., Gay, C.C., and McCarthy, M.A.: Influence of head height on arterial blood pressure in standing horses.Am J Vet Res 41:16261631, 1980. 15. Parry, B.W., McCarthy, M.A., and Anderson, G.A.: Resting blood pressure values of clinically normal horses. Eq Vet J, submitted, 1982. 16. Parry, B.W., McCarthy, M.A., Anderson, G.A. and Gay, C.C.: Correct occlusive bladder width for indirect blood pressure measurement in horses. A m J Vet Res 43:46-50, 1982. 17. Rose, R.J.: A physiological approach to fluid and electrolyte therapy in the horse.Eq Vet J 13:7-14, 1981.

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