VETERINARY ANESTHESIA

Veterinary Surgery 24:69-72. 1995

Postoperative Myositis in a Neonatal Foal: A Case Report

MELANIE MANNING, DVM, RICHARD DUBIELZIG, DVM, DipACVP, and SHEILA MCGUIRK, DVM, DipACVIM

A foal with azotemia, acidemia, and electrolyte abnormalities was diagnosed with uropentoneum. The foal was anesthetized with isoflurane, and throughout the 4 hours of anesthesia and abdominal surgery, its mean arterial pressure ranged between 45 and 65 mm Hg. The foal developed a myopathy postoperatively and died 24 hours after surgery. OCopyright I995 by The American College of Veterinary Surgeons

N 18-DAY-OLD 95-kg Thoroughbred colt was A admitted to the Veterinary Medical Teaching Hospital with a history of abdominal distention and depression. Twelve days previously, the foal had been discharged from the Veterinary Medical Teaching Hospital after recovery from surgical re- section of a patent urachus. Five days after being discharged, the owner noticed that the foal was hav- ing difficulty defecating and he administered both mineral oil and psyllium orally. Five days later, the owner noticed that the foal was markedly depressed, had abdominal distention, and was no longer nursing the mare. The following day, the foal was taken to the referring veterinarian for evaluation. After ab- dominocentesis, a large volume of clear yellow fluid was collected, and it was consistent with urine. An abdominal drain was placed, and the foal was given oral electrolytes and an intramuscular injection of penicillin and streptomycin. The foal was referred to the Veterinary Medical Teaching Hospital the next day.

On clinical examination, the foal was depressed and had abdominal distention. Its heart rate was 1 10 beats/minute, and the respiratory rate was 120 breaths/minute. The rectal temperature was 102.6"F. Mucous membranes were pale, and capillary refill

time was within normal limits. Within 15 minutes of arrival, the foal collapsed. At this time, the primary diagnosis was ruptured bladder, An intravenous cath- eter was placed in the jugular vein, and 0.9% NaCl was administered at a rate of 950 mL/hr. A complete blood count (CBC) was not abnormal, and serum bio- chemical analysis indicated hyponatremia ( 106 mmol/ L), hypochloremia (70 mmol/L), hyperkalemia (6.7 mmol/L), and a high serum creatinine (10.7 mmol/ L). Blood glucose was 220 g/dL. Arterial blood gas analysis showed primary metabolic acidosis (pH, 7.293; HC03, 13.4 mEq/L; base excess (BE), -10.9; arterial oxygen pressure [Pa02], 76 mm Hg) with par- tial respiratory compensation (arterial carbon dioxide pressure [PaCOJ, 27.5 mm Hg). The strong ion dif- ference was normal (42.7), and the anion gap was el- evated (29.3). Analysis of the peritoneal fluid showed a high concentration of creatinine ( 15.2 mmol/L) and potassium (7.7 mmol/L). Protein and leukocyte con- tent of the abdominal fluid were low (<2.5 g/L and 8,700 cells/pL, respectively). Based on these findings, the history, and clinical examination, a diagnosis of uroperitoneum was confirmed, and the foal was taken to surgery for an exploratory laparotomy.

The foal was nasotracheally intubated and in- duced with 5% isoflurane in oxygen. An arterial

From the Department of Surgical Sciences, Department of Pathobiological Sciences, and the Department of Medical Sciences,

Address reprint requests to Melanie Manning. DVM, WL Gore and Associates. 4100 West Kiltie Ln, Flagstaff, AZ 86001. OCopyright 1995 by The American College of Veterinary Surgeons 0 I6 1-34991951240 1-00 I2$3.00/0

School of Veterinary Medicine, University of Wisconsin-Madison. Madison, WI.

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70 POSTOPERATIVE MYOSITIS IN FOAL

blood sample showed that the foal was hypercapnic (PaCO,, 58 mm Hg), which was treated with con- trolled ventilation. After surgical preparation, the foal was placed on a pad that contains beadlike ma- terial. When the air is evacuated from the pad, it conforms to the patient and helps hold the patient in position (VacPac, Olympic Medical, Seattle, Washington). In this case, the pad was used to hold the foal in dorsal recumbency. During surgery, the foal was maintained on isoflurane (0.5% to 1.5%) in oxygen. The oxygen flow rate was set at 2 L/min. A maintenance dose (950 mL/hr) of intravenous 5% dextrose in 0.9% NaCl was administered over the course of the surgery, which lasted 3.5 hours. A 20- gauge catheter was placed in the facial artery and connected to a pressure transducer. Blood pressure was monitored continuously throughout the pro- cedure, and arterial blood samples were submitted for analysis of pH, PaOz, and PaCOz. Mean arterial blood pressure ranged between 45 and 65 mm Hg throughout the entire procedure. The initial analysis of arterial blood indicated a metabolic acidosis (pH, 7.22; HC03, 17.2; BE, -9.5; PaCO,, 41.6; Pa02, 283), which was consistent with the preoperative evaluation. The foal's rectal temperature was mon- itored continuously and ranged from 98.7"F to 98.3"F. A pulse oximeter probe was placed on the foal's tongue, and oxygen saturation ranged from 97% to 99%.

Surgical findings were extensive and included an impaction of the small colon, a ruptured bladder, and adhesions of the ileum to the apex of the bladder. An enterotomy was performed, and several firm psyllium "plugs" were removed. Adhesions to the bladder were reduced manually. Forty percent of the apex of the bladder was resected, and samples were submitted for histopathologic examination, fungal culture, and aerobic bacterial culture,

The foal was given ampicillin, flunixin meglu- mine, and fluids postoperatively. On recovery from anesthesia, the foal remained sternal and did not attempt to stand. When the foal was assisted, the forelimbs could bear weight but there was knuckling of the fetlock and general weakness in the hindlimbs. Pain perception and reflexes remained in both hind- limbs. Over the next few hours, the foal began strug- gling to rise once or twice a minute. Serum electro- lytes, blood urea nitrogen (BUN), creatinine, creatinine phosphokinase (CPK), and arterial blood were submitted for analysis. The serum CPK was

greater than 45,000 IU/L. Primary metabolic aci- dosis (pH, 7.31; PCO,, 17.0 mm Hg; HC03, 8.7 mEq/L; BE, - 14.1 ; PaOz, 7 1.5), hyponatremia ( 1 17 mmol/L), hyperkalemia (6.3 mmol/L), hypochlo- remia (83 mmol/L), and azotemia (BUN, 101 mg/ dL; serum creatinine, 9.5 mmol/L) were present. The strong ion difference was normal (40.2), and the an- ion gap was elevated (3 1.6). Three hours postoper- atively, a diagnosis of postoperative myositis was made. The dose of flunixin meglumine was increased from 0.25 mg/kg three times a day to 0.5 mg/kg three times a day, and 0.5 g sucralfate was given orally. Twenty-five grams dimethyl sulfoxide (DMSO) was administered intravenously as a 10% solution of DMSO in 5% dextrose over a period of 4 hours. The foal developed pitting edema of the gluteal muscles, neutropenia, leukopenia, and ab- dominal distention. The hindlimbs began to feel cool. Reflexes in the hindlimbs were absent, but deep pain could be elicited. The foal spiked a fever ( 104.O"F) 24 hours postoperatively. An abdomi- nocentesis was performed. The foal went into cardiac arrest and died soon thereafter.

Preserved serum was retrospectively tested for creatinine phosphokinase. The CPK values before and during surgery were 2,267 IU/L and 1,448 IU/ L, respectively. A fresh postmortem examination was performed. On gross evaluation, the foal's body was that of a well-muscled dehydrated animal. The ab- dominal cavity contained 500 mL brown fluid. Throughout the abdominal cavity, there were nu- merous fibrinous exudates on the serosal surfaces, and some of these contained entrapped ingesta. The esophageal portion of the gastric mucosa had broad coalescing erosions. There were deep ulcerative le- sions in the glandular gastric mucosa, one of which perforated through the serosal surface. The entero- tomy site and urinary bladder were intact. The pro- visional diagnosis was perforating gastric ulcer with acute fibrinous peritonitis. Tissues were also sub- mitted for histopathology. Muscle samples taken from the sublumbar spine, thigh, and intercostal muscle showed individual granular basophilic myo- fibrosis indicative of necrosis and mineralization (Fig 1). The kidneys were normal.

The cause of postoperative myositis is multifac- torial. I The clinical course of postoperative myopa- thy (POM) has been replicated using prolonged re- cumbency, hypotension, hard surfaces, and poor positioning.'-3 Although controversy surrounds the

MANNING, DUBIELZIG, AND MCGUIRK 71

Fig 1. Photomicrograph of skeletal muscle from the internal intercostal muscle. Several individual myofibers show granular degeneration with an early macrophage infiltration. Hematoxylin- eosin (HE); original magnification X300.

clinical course of POM, muscle damage occurs be- cause of a direct decrease in muscle p e r f u ~ i o n . ~ . ~ , ~ Decreased perfusion results in tissue hypoxia and subsequent metabolic disturbances. Mean arterial blood pressures less than 65 mm Hg during anes- thesia predispose adult horses to POM.',2,6 This foal was maintained in a light plane of surgical anesthesia characterized by intermittent nystagmus, a palpebral reflex, and skeletal muscle tone. Despite the light plane of anesthesia, the foal's arterial blood pressure remained below 65 mm Hg throughout the surgery. A combination of decreased mean arterial pressure and prolonged surgical time have been shown to be significant factors in the development of POM in adult horses.' Many ill foals with low mean arterial pressures are anesthetized each year. It is unclear if the anesthesia contributed to this foal's myopathy. The foal in this report was not given any drugs to support cardiovascular function. Positive inotropic drugs provide a pharmacologic means to increase the arterial blood pressure without compromising tissue perfusion. Drugs such as dobutamine have a direct effect on betal receptors in the myocardium. Neonates have an underdeveloped sympathetic ner- vous system and are unable to increase cardiac out- put through c~n t rac t i l i t y .~~~ Neonates can, however, increase cardiac output to a small extent by increas- ing heart rate.' At higher doses, dobutamine affects beta2 receptors, thereby increasing heart rate and to- tal peripheral resistance. Although this may increase mean arterial blood pressure, it does not increase tissue perfusion.

Administering large volumes of intravenous fluids is another means of maintaining blood pressure for short periods. However, neonates cannot tolerate fluid overload because of cardiac and renal imma- turity. Glomerular and renal tubular balance of so- dium and water is poorly maintained in neonates."

Hypertonic saline has also been used to treat hy- potension. Because this foal was both hyponatremic and hypochloremic, hypertonic saline could have been administered. It is unlikely that hypertonic sa- line would have maintained this foal's blood pressure for the entire procedure because its effects are tran- sient. Hypertonic saline is believed to produce its effects through transient shifting of fluid to the in- travascular space from the interstitial and intracel- lular spaces as well as having a direct positive ino- tropic effect on the heart. This foal's extravascular space already was dehydrated, and hypertonic saline may have worsened its condition. Furthermore, the use of hypertonic saline in this case might have raised the serum sodium concentration too quickly and caused deleterious effects. Hypertonic saline contains 75 mg sodium per liter. Although the serum sodium concentration of this foal was low, the sodium con- centration in the interstitial spaces and intracellular fluid may have been normal given that the strong ion difference was normal (42.7). The foal was not showing neurologic signs that are typically associated with hyponatremia. Volume expansion was indi- cated in this foal. The strong ion difference was nor- mal (42.7), and anion gap was high (29.3). This sug- gests that therapy to correct the acid-base status should include fluid replacement with balanced electrolyte solutions rather than sodium bicarbonate administration. Because neonates do not tolerate rapid volume expansion, the foal was placed on a maintenance dose of fluids during anesthesia (10 mL/kg/hr). The strong ion difference was still normal (40.2) 4 hours postoperatively, and the anion gap remained elevated (3 I A). The lack of improvement in acid-base status might be explained by high con- centration of lactic acid caused by myositis. The slight increase in the anion gap may be insignificant and may simply correlate with a slight increase in serum protein values.

Proper positioning and adequate padding of ani- mals during anesthesia is i r n p ~ r t a n t . ~ ~ ~ ~ ' I VacPacs conform to the body and allow proper positioning and heat retention. They provide structural support, but they do not protect or pad muscles and nerves.

72 POSTOPERATIVE MYOSITIS IN FOAL

Lack of adequate cushioning may have contributed to this foal's postoperative condition.

The foal's preexisting metabolic derangements also may have contributed to POM. However, at- tempts to cause POM secondary to acid-base ab- normalities in properly padded adult horses under- going surgery have been unsuccessful.'~3 In addition, many horses undergoing surgery develop increased aspartate aminotransferase, creatine kinase, and lac- tic acid without developing clinical signs of myositis. Very little has been reported about the incidence and cause of POM in neonatal foals. Most of the literature pertains to postoperative myositis in adult horses and the potential for compression of their large muscle masses, which causes reduced tissue perfusion. Because this case of POM occurred in a 95-kg foal, it may be that more cases of myositis have gone undiagnosed or underdiagnosed in sick foals after anesthesia and surgery. Furthermore, this case reinforces the evidence that POM is a result of tissue hypoperfusion in animals of any size.

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