- Email: [email protected]
Duodenal Stricture in a Foal
Vet Clin Equine 22 (2006) 37–42
Duodenal Stricture in a Foal Bonnie S. Barr, VMD Rood and Riddle Equine Hospital, 2150 Georgetown Road Lexington, KY 40580, USA
History A 3-month-old Thoroughbred filly was evaluated for colic, bruxism, ptyalism, hypersalivation, and depression. The filly had a history of hospitalization for enteritis. The initial visit to the hospital was 3 weeks earlier, and the clinical signs resolved with medical management, including fluids and muzzling. The most recent hospitalization was 5 days before this visit, and treatment was instituted as for the initial visit. The filly had been dewormed every 30 days and had not yet received her first set of vaccinations. Physical examination On physical examination the filly was quiet, grinding her teeth, and hypersalivating. Vital signs were as follows: temperature 38.3 C (101.4 F), pulse 52 beats/minute, and respiratory rate 36 breaths/minute. Auscultation of the heart and lungs did not detect any abnormalities. Borborygmi were quiet and decreased. There was minimal abdominal distension, and fecal consistency was soft. There was no evidence of lameness or joint effusion. Case assessment Causes for colic in a 3-month-old foal include enteritis, enterocolitis, colitis, gastric ulcers, intussusception, a strangulating lesion, or ruptured viscous. Bruxism usually indicates pain, most likely associated with the gastrointestinal tract. Ptyalism can occur with oral ulcers, oral foreign body, esophageal ulceration, slaframine toxicity, or gastric ulcers. Occasionally ptyalism is noted in the case of enteritis or enterocolitis. Oral examination did not identify any oral ulcers or foreign bodies, so these could be ruled out as a cause of the clinical signs noted in this foal. Additionally, slaframine toxicity is uncommon in young foals. To differentiate further E-mail address: [email protected] 0749-0739/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.cveq.2005.12.015 vetequine.theclinics.com
38
BARR
the cause of the colic, bruxism, and ptyalism in this foal, further diagnostics were necessary. Procedures Laboratory work included complete blood chemistry and a master panel. No significant abnormalities were noted on laboratory work. A nasogastric tube was passed, and 2 L of foul-smelling reflux was obtained. After gastric decompression the foal’s heart rate improved. Gastroscopy was performed with a 3-m endoscope, and severe gastric ulceration and distal (reflux) esophagitis with linear erosions were noted (Figs. 1, 2). A transabdominal ultrasound was performed with a 7.5-MHz transducer; there was no excessive peritoneal effusion, but there were several loops of mildly distended fluid-filled small intestine. After the results of the abdominal ultrasound were available, peritonitis and ruptured viscous were less likely. An abdominocentesis was not performed because there was not an excessive amount of peritoneal fluid, and the risk of inadvertent bowel wall perforation is higher in foals. Because of the concern of a potential gastric outflow obstruction, contrast gastrointestinal radiography was performed. Once the stomach was completely empty, barium (10 mL/kg) was administered through a nasogastric tube. Serial standing lateral radiographs of the abdomen were taken before administration of the barium, immediately after barium administration, and at 5, 10, 15, 20, 30, and 60 minutes after barium administration [1]. A normal foal should have evidence of barium in the duodenum by 5 to 10 minutes after barium administration. In this case the barium did not empty out of the stomach, even after 1 hour; therefore the diagnosis was delayed gastric emptying (Fig. 3). Differential diagnosis Delayed gastric emptying in a foal could result from a functional outflow disorder or a mechanical outflow disorder. A functional outflow disorder
Fig. 1. Severe, diffuse gastric ulceration.
DUODENAL STRICTURE IN A FOAL
39
Fig. 2. Distal (reflux) esophagitis. Note linear ulcerative lesions.
could result from inflammation, erosion, or ulceration causing impairment of gastric emptying by affecting the myoelectric activity of the gastrointestinal tract [2]. Diseases such as gastric/duodenal ulceration, anterior enteritis, peritonitis, endotoxemia, and enterocolitis could result in a functional outflow problem. On the other hand, disorders that result in a mechanical obstruction include pyloric/duodenal stricture, small intestinal volvulus, small intestinal intussusception, or large colon displacement [2]. A small intestinal volvulus and large colon displacement were ruled out because the foal’s pain level could be controlled with frequent gastric decompression; in this author’s experience, foals with a small intestinal volvulus or large colon displacement do not stay comfortable even with frequent gastric decompression. Enterocolitis could be ruled out because the foal had normal feces. The gastroscopy identified severe gastric ulceration and distal (reflux) esophagitis. In this author’s experience, the presence of distal esophagitis (along with
Fig. 3. Barium that has not emptied out of the stomach 60 minutes after administration.
40
BARR
the gastric ulcers) and the lack of emptying of barium from the stomach suggest inflammation or stricture of the pylorus or proximal duodenum. Often it is difficult to differentiate between inflammation without stricture and duodenal stricture. If the foal’s comfort level can be maintained with gastric decompression and other medical therapies, medical management is the initial treatment in the hope that there is no stricture.
Treatment Medical management included frequent decompression of the stomach, antiulcer medications, and intravenous fluids. Treatment with intravenous potassium penicillin (20,000–40,000 IU/kg every 6 hours) and gentamicin (6.6 mg/kg every 24 hours) was started. Because the foal initially was refluxing, intravenous antiulcer medication (ranitidine) was administered (Table 1). Often these foals have mild electrolyte abnormalities; thus balanced polyionic fluids with appropriate supplementation are administered. This author’s rule of thumb for fluid management is Fluid rate for 1 hour ¼ maintenance requirement ð2:24:4mL=kg=hourÞ þ fluid deficit ð% dehydratyion body weight in kg=24 hoursÞ þanticipated hourly losses ðcaused by refluxing or diarrheaÞ
A constant-rate infusion is best, but if it is not practical, fluids can be administered every 4 to 6 hours. Typically medical management is tried for 2 to 3 days. Signs of improvement include a decrease or resolution of gastric reflux, a decrease or resolution of bruxism and ptyalism, and the ability to nurse or eat without pain. If the ulceration has progressed to fibrosis, and medical management does not result in improvement, surgical intervention is needed [3,4]. After 3 days of medical management, this filly showed no signs of improvement. An exploratory celiotomy identified a duodenal stricture. A gastrojejunostomy was performed to bypass the duodenal stricture. Postoperative care typically includes allowing nothing by mouth for 2 days, appropriate fluid therapy, antimicrobials, antiulcer medication, and nutritional support if needed. The nutritional support can range from Table 1 Typical anti-ulcer medications for use in foals Drug
Dose
Route
Frequency
Sucralfate Cimetadine Cimetadine Ranitidine Ranitidine Omeprazole
10–20 mg/kg 10–20 mg/kg 6.6 mg/kg 5–10 mg/kg 0.8–2.2 mg/kg 4 mg/kg
po po iv po iv po
Q Q Q Q Q Q
6 hr 4 hr 4 hr 6–12 hr 6 hr 24 hr
DUODENAL STRICTURE IN A FOAL
41
intravenous dextrose (5% solution) as an additive to fluids to partial or total parenteral nutrition (TPN). The need for intravenous nutritional support is based on the debilitation or body condition of the foal. The author has had best success with a TPN formula of dextrose (10 g/kg/day), amino acids (2 g/ kg/day), and lipids (1 g/kg/day). The rate of administration varies according to the foal’s caloric needs, weight, and ability to tolerate the TPN. Usually the TPN is started at one fourth the foal’s caloric needs and then increased over a 12- to 24-hour period depending on the foal’s ability to tolerate the TPN, primarily the dextrose. The blood glucose level is initially monitored every 2 to 4 hours and then every 6 hours, depending on the patient. A dextrometer purchased from a human pharmacy is a cheap and accurate assessment of the blood glucose. Postoperatively, antiulcer medication should be switched to an oral medication (omeprazole or ranitidine) once the foal is no longer refluxing. Antimicrobial therapy should be continued for 7 days postoperatively. Foals that have undergone surgical correction have a fair longterm prognosis [5]. Immediate postoperative complications include ileus, colitis, incisional infection, or possible strangulation of the intestine. If surgery is not an option, medical management can be continued longer, and motility-enhancing drugs can be considered. In this situation one of the most commonly used prokinetic drugs used is bethanecol (Table 2). If the foal is to continue on medical therapy, intravenous nutrition such as 5% dextrose or TPN may be required. Response to continued medical treatment will be noted by the decrease/resolution of reflux, decrease/resolution of bruxism and ptyalism, and the foal’s ability to nurse without any signs of abdominal discomfort. In the author’s experience, medical management carries a poor prognosis unless the foal receives treatment early in the course of the disease, before stricture formation. Often, however, the problem is not diagnosed until the lesion is extensive. The exact cause of duodenal strictures is unknown. Probably the lesion begins as inflammation or ulceration of the proximal duodenum that progresses to fibrosis and stricture. Factors predisposing foals to gastroduodenal ulcers include use of nonsteroidal anti-inflammatory drugs, stress, or a disease process that results in an imbalance between the protective and aggressive factors of the gastric mucosa [6–8]. There have been a few reports of several foals on one farm being affected, leading to the belief that an Table 2 Common prokinetic agents for use in foals Drug
Dose
Route
Frequency
Bethanecol
0.02 mg/kg followed by 0.35 mg/kg 1.3 mg/kg followed by 0.05 mg/kg/min 0.1 mg/kg 0.5–2 mg/kg
sc po iv iv iv iv
Q 4–6 hr Q 8 hr Bolus in 1 L CRI Q 6 hr (in 1 L saline over 1 hr) Q 6 hr (in 1 L saline over 45 min)
Lidocaine 2% Metaclopramide Erythromycin
42
BARR
infectious agent may be involved, although one has not definitively been identified [3,4]. Because the exact cause of duodenal strictures is unknown, effective preventative measures can be hard to define. Minimal usage of nonsteroidal anti-inflammatory agents is recommended. If they are used, antiulcer medication can be administered at the same time. In addition, good management practices are avoiding overcrowding, reducing stress, and limiting exposure to possible infectious diseases [8]. A 12-month follow-up has shown this foal/yearling to be doing well. Overall the best treatment for a foal with delayed gastric emptying is surgical exploration. Unfortunately, the exact cause of this disease is unknown, but common clinical signs are bruxism, ptyalism, and colic
References [1] Campbell ML, Ackerman N, Peyton LC, et al. Radiographic gastrointestinal anatomy of the foal. Vet Radiol Ultrasound 1984;25(5):194–204. [2] Murray MJ. Stomach disease of the foal. In: Mair T, Divers T, Ducharme N, editors. Equine gastroenterology: gastrointestinal disease in the foal. London: W.B. Saunders; 2002. p. 469–76. [3] Campbell-Thompson ML, Brown MP, Slone DE, et al. Gastroenterostomy for treatment of gastroduodenal ulcer disease in 14 foals. J Am Vet Med Assoc 1985;188(8):840–4. [4] Orsini JA, Donawick WJ. Surgical treatment of gastroduodenal obstructions in foals. Vet Surg 1986;15(2):205–13. [5] Zedler ST, Embertson RM. Surgical resolution of gastric outflow obstruction in the horse. In: Programs and abstracts of the 8th International Equine Colic Research Symposium. 2005. [6] Borrow HA. Duodenal perforations and gastric ulcers in foals. Vet Rec 1993;(March):297–9. [7] Murray MJ. Gastroduodenal ulceration in foals: a tutorial article. Equine Vet Educ 1999; 11(4):199–207. [8] Barr BS. Gastric ulcer prophylaxis in the critically ill equine neonate. In: Wilkins PA, Palmer JE, editors. Recent advances in equine neonatal care. International Veterinary Information Service; 2001.
Duodenal Stricture in a Foal Bonnie S. Barr, VMD Rood and Riddle Equine Hospital, 2150 Georgetown Road Lexington, KY 40580, USA
History A 3-month-old Thoroughbred filly was evaluated for colic, bruxism, ptyalism, hypersalivation, and depression. The filly had a history of hospitalization for enteritis. The initial visit to the hospital was 3 weeks earlier, and the clinical signs resolved with medical management, including fluids and muzzling. The most recent hospitalization was 5 days before this visit, and treatment was instituted as for the initial visit. The filly had been dewormed every 30 days and had not yet received her first set of vaccinations. Physical examination On physical examination the filly was quiet, grinding her teeth, and hypersalivating. Vital signs were as follows: temperature 38.3 C (101.4 F), pulse 52 beats/minute, and respiratory rate 36 breaths/minute. Auscultation of the heart and lungs did not detect any abnormalities. Borborygmi were quiet and decreased. There was minimal abdominal distension, and fecal consistency was soft. There was no evidence of lameness or joint effusion. Case assessment Causes for colic in a 3-month-old foal include enteritis, enterocolitis, colitis, gastric ulcers, intussusception, a strangulating lesion, or ruptured viscous. Bruxism usually indicates pain, most likely associated with the gastrointestinal tract. Ptyalism can occur with oral ulcers, oral foreign body, esophageal ulceration, slaframine toxicity, or gastric ulcers. Occasionally ptyalism is noted in the case of enteritis or enterocolitis. Oral examination did not identify any oral ulcers or foreign bodies, so these could be ruled out as a cause of the clinical signs noted in this foal. Additionally, slaframine toxicity is uncommon in young foals. To differentiate further E-mail address: [email protected] 0749-0739/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.cveq.2005.12.015 vetequine.theclinics.com
38
BARR
the cause of the colic, bruxism, and ptyalism in this foal, further diagnostics were necessary. Procedures Laboratory work included complete blood chemistry and a master panel. No significant abnormalities were noted on laboratory work. A nasogastric tube was passed, and 2 L of foul-smelling reflux was obtained. After gastric decompression the foal’s heart rate improved. Gastroscopy was performed with a 3-m endoscope, and severe gastric ulceration and distal (reflux) esophagitis with linear erosions were noted (Figs. 1, 2). A transabdominal ultrasound was performed with a 7.5-MHz transducer; there was no excessive peritoneal effusion, but there were several loops of mildly distended fluid-filled small intestine. After the results of the abdominal ultrasound were available, peritonitis and ruptured viscous were less likely. An abdominocentesis was not performed because there was not an excessive amount of peritoneal fluid, and the risk of inadvertent bowel wall perforation is higher in foals. Because of the concern of a potential gastric outflow obstruction, contrast gastrointestinal radiography was performed. Once the stomach was completely empty, barium (10 mL/kg) was administered through a nasogastric tube. Serial standing lateral radiographs of the abdomen were taken before administration of the barium, immediately after barium administration, and at 5, 10, 15, 20, 30, and 60 minutes after barium administration [1]. A normal foal should have evidence of barium in the duodenum by 5 to 10 minutes after barium administration. In this case the barium did not empty out of the stomach, even after 1 hour; therefore the diagnosis was delayed gastric emptying (Fig. 3). Differential diagnosis Delayed gastric emptying in a foal could result from a functional outflow disorder or a mechanical outflow disorder. A functional outflow disorder
Fig. 1. Severe, diffuse gastric ulceration.
DUODENAL STRICTURE IN A FOAL
39
Fig. 2. Distal (reflux) esophagitis. Note linear ulcerative lesions.
could result from inflammation, erosion, or ulceration causing impairment of gastric emptying by affecting the myoelectric activity of the gastrointestinal tract [2]. Diseases such as gastric/duodenal ulceration, anterior enteritis, peritonitis, endotoxemia, and enterocolitis could result in a functional outflow problem. On the other hand, disorders that result in a mechanical obstruction include pyloric/duodenal stricture, small intestinal volvulus, small intestinal intussusception, or large colon displacement [2]. A small intestinal volvulus and large colon displacement were ruled out because the foal’s pain level could be controlled with frequent gastric decompression; in this author’s experience, foals with a small intestinal volvulus or large colon displacement do not stay comfortable even with frequent gastric decompression. Enterocolitis could be ruled out because the foal had normal feces. The gastroscopy identified severe gastric ulceration and distal (reflux) esophagitis. In this author’s experience, the presence of distal esophagitis (along with
Fig. 3. Barium that has not emptied out of the stomach 60 minutes after administration.
40
BARR
the gastric ulcers) and the lack of emptying of barium from the stomach suggest inflammation or stricture of the pylorus or proximal duodenum. Often it is difficult to differentiate between inflammation without stricture and duodenal stricture. If the foal’s comfort level can be maintained with gastric decompression and other medical therapies, medical management is the initial treatment in the hope that there is no stricture.
Treatment Medical management included frequent decompression of the stomach, antiulcer medications, and intravenous fluids. Treatment with intravenous potassium penicillin (20,000–40,000 IU/kg every 6 hours) and gentamicin (6.6 mg/kg every 24 hours) was started. Because the foal initially was refluxing, intravenous antiulcer medication (ranitidine) was administered (Table 1). Often these foals have mild electrolyte abnormalities; thus balanced polyionic fluids with appropriate supplementation are administered. This author’s rule of thumb for fluid management is Fluid rate for 1 hour ¼ maintenance requirement ð2:24:4mL=kg=hourÞ þ fluid deficit ð% dehydratyion body weight in kg=24 hoursÞ þanticipated hourly losses ðcaused by refluxing or diarrheaÞ
A constant-rate infusion is best, but if it is not practical, fluids can be administered every 4 to 6 hours. Typically medical management is tried for 2 to 3 days. Signs of improvement include a decrease or resolution of gastric reflux, a decrease or resolution of bruxism and ptyalism, and the ability to nurse or eat without pain. If the ulceration has progressed to fibrosis, and medical management does not result in improvement, surgical intervention is needed [3,4]. After 3 days of medical management, this filly showed no signs of improvement. An exploratory celiotomy identified a duodenal stricture. A gastrojejunostomy was performed to bypass the duodenal stricture. Postoperative care typically includes allowing nothing by mouth for 2 days, appropriate fluid therapy, antimicrobials, antiulcer medication, and nutritional support if needed. The nutritional support can range from Table 1 Typical anti-ulcer medications for use in foals Drug
Dose
Route
Frequency
Sucralfate Cimetadine Cimetadine Ranitidine Ranitidine Omeprazole
10–20 mg/kg 10–20 mg/kg 6.6 mg/kg 5–10 mg/kg 0.8–2.2 mg/kg 4 mg/kg
po po iv po iv po
Q Q Q Q Q Q
6 hr 4 hr 4 hr 6–12 hr 6 hr 24 hr
DUODENAL STRICTURE IN A FOAL
41
intravenous dextrose (5% solution) as an additive to fluids to partial or total parenteral nutrition (TPN). The need for intravenous nutritional support is based on the debilitation or body condition of the foal. The author has had best success with a TPN formula of dextrose (10 g/kg/day), amino acids (2 g/ kg/day), and lipids (1 g/kg/day). The rate of administration varies according to the foal’s caloric needs, weight, and ability to tolerate the TPN. Usually the TPN is started at one fourth the foal’s caloric needs and then increased over a 12- to 24-hour period depending on the foal’s ability to tolerate the TPN, primarily the dextrose. The blood glucose level is initially monitored every 2 to 4 hours and then every 6 hours, depending on the patient. A dextrometer purchased from a human pharmacy is a cheap and accurate assessment of the blood glucose. Postoperatively, antiulcer medication should be switched to an oral medication (omeprazole or ranitidine) once the foal is no longer refluxing. Antimicrobial therapy should be continued for 7 days postoperatively. Foals that have undergone surgical correction have a fair longterm prognosis [5]. Immediate postoperative complications include ileus, colitis, incisional infection, or possible strangulation of the intestine. If surgery is not an option, medical management can be continued longer, and motility-enhancing drugs can be considered. In this situation one of the most commonly used prokinetic drugs used is bethanecol (Table 2). If the foal is to continue on medical therapy, intravenous nutrition such as 5% dextrose or TPN may be required. Response to continued medical treatment will be noted by the decrease/resolution of reflux, decrease/resolution of bruxism and ptyalism, and the foal’s ability to nurse without any signs of abdominal discomfort. In the author’s experience, medical management carries a poor prognosis unless the foal receives treatment early in the course of the disease, before stricture formation. Often, however, the problem is not diagnosed until the lesion is extensive. The exact cause of duodenal strictures is unknown. Probably the lesion begins as inflammation or ulceration of the proximal duodenum that progresses to fibrosis and stricture. Factors predisposing foals to gastroduodenal ulcers include use of nonsteroidal anti-inflammatory drugs, stress, or a disease process that results in an imbalance between the protective and aggressive factors of the gastric mucosa [6–8]. There have been a few reports of several foals on one farm being affected, leading to the belief that an Table 2 Common prokinetic agents for use in foals Drug
Dose
Route
Frequency
Bethanecol
0.02 mg/kg followed by 0.35 mg/kg 1.3 mg/kg followed by 0.05 mg/kg/min 0.1 mg/kg 0.5–2 mg/kg
sc po iv iv iv iv
Q 4–6 hr Q 8 hr Bolus in 1 L CRI Q 6 hr (in 1 L saline over 1 hr) Q 6 hr (in 1 L saline over 45 min)
Lidocaine 2% Metaclopramide Erythromycin
42
BARR
infectious agent may be involved, although one has not definitively been identified [3,4]. Because the exact cause of duodenal strictures is unknown, effective preventative measures can be hard to define. Minimal usage of nonsteroidal anti-inflammatory agents is recommended. If they are used, antiulcer medication can be administered at the same time. In addition, good management practices are avoiding overcrowding, reducing stress, and limiting exposure to possible infectious diseases [8]. A 12-month follow-up has shown this foal/yearling to be doing well. Overall the best treatment for a foal with delayed gastric emptying is surgical exploration. Unfortunately, the exact cause of this disease is unknown, but common clinical signs are bruxism, ptyalism, and colic
References [1] Campbell ML, Ackerman N, Peyton LC, et al. Radiographic gastrointestinal anatomy of the foal. Vet Radiol Ultrasound 1984;25(5):194–204. [2] Murray MJ. Stomach disease of the foal. In: Mair T, Divers T, Ducharme N, editors. Equine gastroenterology: gastrointestinal disease in the foal. London: W.B. Saunders; 2002. p. 469–76. [3] Campbell-Thompson ML, Brown MP, Slone DE, et al. Gastroenterostomy for treatment of gastroduodenal ulcer disease in 14 foals. J Am Vet Med Assoc 1985;188(8):840–4. [4] Orsini JA, Donawick WJ. Surgical treatment of gastroduodenal obstructions in foals. Vet Surg 1986;15(2):205–13. [5] Zedler ST, Embertson RM. Surgical resolution of gastric outflow obstruction in the horse. In: Programs and abstracts of the 8th International Equine Colic Research Symposium. 2005. [6] Borrow HA. Duodenal perforations and gastric ulcers in foals. Vet Rec 1993;(March):297–9. [7] Murray MJ. Gastroduodenal ulceration in foals: a tutorial article. Equine Vet Educ 1999; 11(4):199–207. [8] Barr BS. Gastric ulcer prophylaxis in the critically ill equine neonate. In: Wilkins PA, Palmer JE, editors. Recent advances in equine neonatal care. International Veterinary Information Service; 2001.