Megaesophagus is a frequently reported disorder in canines resulting in ineffective esophageal peristalsis, dilation, and regurgitation.1,2 The underlying causes of megaesophagus can be idiopathic, congenital, acquired, or secondary to a number of diseases, such as myasthenia gravis,3 hypothyroidism,4,5 or Addison disease.6 Complications such as esophagitis, weight loss, malnourishment, dehydration, and aspiration pneumonia are common, resulting in a guarded to poor prognosis in canines.2,7–9
Sildenafil has been investigated as a possible treatment in canines with megaesophagus.10,11 Sildenafil is a selective phosphodiesterase type 5 inhibitor that indirectly potentiates the action of endogenous nitric oxide by reducing cGMP degradation due to phosphodiesterase type 5.12 This results in smooth muscle relaxation as well as vasodilation.11,13 Notably, numerous studies11,13–17 have found that sildenafil can cause a significant reduction in muscle tone in the lower esophageal sphincter (LES). Decreased LES tone will reduce pressure inside the lumen of the esophagus, which could facilitate the movement of ingesta into the stomach.11 Sildenafil has been shown to be a promising treatment for canine congenital idiopathic megaesophagus, successfully reducing LES tone and resulting in both radiographic and clinical improvement in dogs.10,11
Megaesophagus is also a cause of morbidity and mortality in populations of phocids undergoing rehabilitation.18–21 However, information on treatment options for megaesophagus in phocids is limited.10–13 A retrospective review19 of records from 3 rehabilitation facilities reported a mortality rate of 92% for seals diagnosed with megaesophagus. Thus highlighting the need for developing treatment options to improve the prognosis and possible release of these animals.19
This study describes the treatment of 3 Pacific harbor seals (Phoca vitulina richardii) admitted to the Vancouver Aquarium Marine Mammal Rescue Society (VAMMR) between January 2021 and December 2023, diagnosed with megaesophagus, and treated with sildenafil. Clinical signs were closely monitored during and after 2 weeks of sildenafil administration, and radiographic changes were also evaluated after the treatment course. The goal of this case series was to explore a treatment option to improve rehabilitation outcomes in harbor seals diagnosed with megaesophagus.
Methods
Electronic medical records from harbor seals undergoing rehabilitation at VAMMR from January 2021 to December 2023 were reviewed. The inclusion criteria were harbor seals diagnosed with megaesophagus and treated with sildenafil during the study period. Diagnosis of megaesophagus was made based on clinical signs of regurgitation and/or hyporexia and radiographic findings of dilatation of the esophagus. Animals that did not have a confirmed case of megaesophagus on radiographs or were not treated with sildenafil were excluded. An IACUC approval was not obtained as this was a retrospective review of clinical cases. Extralabel drug use was performed in compliance with provisions of the Animal Medicinal Drug Use Clarification Act and 21 Code of Federal Regulations Part 530.
Rehabilitation process
All harbor seals undergoing rehabilitation at VAMMR received an admission physical examination, a CBC and serum biochemistry panel, as well as additional examinations and diagnostics (including radiographs and repeated bloodwork) if necessary. Body mass was measured at admission and twice weekly throughout the entirety of their rehabilitation. All seals’ ages were estimated based on pelage, dentition, umbilicus, and body mass as described previously.22–24 All seal pups admitted for rehabilitation were fed via gastric gavage a formula made from a combination of Zoologic milk matrix 30/52 (PetAg Inc) powder (1,000 g), water (2.5 L), Mazuri marine mammal supplement with vitamin C (6 g) (Mazuri Exotic Animal Nutrition), and herring/hake oil blend (800 mL) with volumes slowly increasing based on body mass. Once teeth were erupting and the animal was approximately 4 to 6 weeks of age, they were gradually weaned onto a diet of 100% herring until release. This is based on the timing of weaning in the wild, generally around 1 month of age.22,25
Diagnosis and treatment
Radiographs were obtained without sedation. Two view dorsal/ventral and lateral thoracic and abdominal views were obtained when possible, based on patient compliance but a minimum of dorsal/ventral thoracic and abdominal views were obtained in all 5 cases. After a diagnosis of megaesophagus was made, 3 animals were treated with sildenafil (25-mg tablets; Teva Pharmaceuticals) at a target dose of 1 mg/kg orally and placed in herring or fish formula delivered via gavage feeding twice a day for 14 days. This dose of sildenafil was chosen based on a previous study on canines.10
Release and follow-up
Radiographs were repeated within 2 weeks of discontinuing the medication and animals were monitored for a minimum of 1 month posttreatment. Before release, a physical examination was performed, and blood was drawn for CBC and serum biochemistry.
Results
From January 2021 to December 2023, 282 harbor seals were admitted to VAMMR. Of these, all records for juvenile animals that were diagnosed with megaesophagus based on radiographic findings (n = 5) were reviewed. Three of these 5 animals were treated with sildenafil (Table 1).
Sex, estimated age, clinical signs and time of onset, and outcome for harbor seals (Phoca vitulina richardii) in the study population.
| Case | Sex | Estimated age at admission (d) | Onset of clinical signs (d in rehabilitation) | Body mass at time of diagnosis (kg) | Clinical signs | Outcome |
|---|---|---|---|---|---|---|
| 1 | F | 7 | 24 | 13.4 | Regurgitation, diarrhea, bloating, and poor gain of body mass | Released |
| 2 | M | 10–14 | 12 | 10.5 | Regurgitation and bloating | Released |
| 3 | M | 10–14 | 55 | 13.5 | Bloating, poor gain of body mass, hyporexia, and diarrhea | Euthanasia |
| 4 | F | 5 | 12 | 11.75 | Lethargy and regurgitation | Euthanasia |
| 5 | F | 10 | 14 | 9.5 | Difficulty passing gavage tube, diarrhea, and regurgitation | Deceased |
F = Female. M = Male.
Case 1 was an approximately 7-day-old female harbor seal rescued due to maternal separation. On presentation, the animal was quiet and mildly dehydrated and had a body condition score of 2/9. There were no other significant findings on the initial physical examination. Admit CBC and serum biochemistry panel showed mild erythrocytosis (RBC, 5.8 X 1012/L; reference range, 3.6 to 5.4 X 1012/L), decreased BUN (7.2 mmol/L; reference range, 12.1 to 21.4 mmol/L), hypoproteinemia (49 g/L; reference range, 65 to 90 g/L), hypoglobulinemia (15 g/L; reference range, 27 to 64 g/L), increased GGT (29 IU/L; reference range, 8 to 23 IU/L), and hyperbilirubinemia (40.8 μmol/L; reference range, 3.4 to 13.7 μmol/L). This assessment was based on in-house reference ranges. One incident of regurgitation as well as diarrhea was noted starting on day 24 after admission at the end of her 5-day weaning process. Over the next month, the animal continued to have intermittent diarrhea and poor body mass gain and developed marked gastrointestinal gas resulting in positive buoyancy. Radiographs were performed revealing dilation of the esophagus throughout the thorax as well as severe gas distention of the stomach and small intestines (Figure 1). At this time, the patient was given sildenafil at 0.89 mg/kg, 12.5 mg by mouth twice daily for 14 days. The animal was also treated with simethicone at 1 mg/kg, 15.2 mg by mouth twice daily for 7 days due to gas accumulation throughout the gastrointestinal tract. Throughout the treatment period, clinical signs resolved and the animal began to gain body mass normally. The animal was monitored for 1 month after completion of treatment, and no clinical signs recurred. Recheck radiographs were performed just before release (1 month after completion of sildenafil treatment) showing resolution of esophageal dilation (Figure 2).
Radiographs from a harbor seal (Phoca vitulina; case 1) undergoing rehabilitation at the Vancouver Aquarium Marine Mammal Rescue Society at time of diagnosis with megaesophagus. Dorsoventral view (A) and right (R) lateral view (B) are shown.
Citation: American Journal of Veterinary Research 2025; 10.2460/ajvr.24.09.0281
Radiographs from a harbor seal (P vitulina; case 1) undergoing rehabilitation at the Vancouver Aquarium Marine Mammal Rescue Society at time of diagnosis with megaesophagus and 1 month after treatment with sildenafil at 1 mg/kg by mouth twice daily for 14 days. Dorsoventral view at diagnosis (A), dorsoventral view posttreatment (B), right lateral view at diagnosis (C), and right lateral view posttreatment (D) are shown.
Citation: American Journal of Veterinary Research 2025; 10.2460/ajvr.24.09.0281
Case 2 was admitted to the facility as an approximately 10- to 14-day-old male harbor seal, rescued due to maternal separation. On presentation, he was bright and moderately dehydrated, had a body condition score of 2/9, and had an approximately 2.5-cm-long laceration along the fourth digit of the right hind flipper with no associated swelling, erythema, or discharge. Initial CBC and serum biochemistry panel revealed hemoconcentration (RBC, 6.9 X 1012/L; reference range, 3.6 to 5.4 X 1012/L; and hematocrit, 0.65 L/L; reference range, 0.5 to 0.6 L/L), decreased BUN (10.3 mmol/L; reference range, 12.1 to 21.4 mmol/L), hypoproteinemia (51 g/L; reference range, 65 to 90 g/L), hypoglobulinemia (19 g/L; reference range, 27 to 64 g/L), increased ALP (277 IU/L; 52 to 224 IU/L), increased GGT (30 IU/L; reference range, 8 to 23 IU/L), and hyperbilirubinemia (14.2 μmol/L; reference range, 3.4 to 13.7 μmol/L). This assessment was based on in-house reference ranges. Regurgitation was noted starting on day 12 of rehabilitation. Initially, formula volume was broken into more frequent, smaller meals but regurgitation continued and bloating developed. Radiographs were taken 1 week later and revealed dilation of the esophagus throughout the thorax as well as gas distention of the stomach and small intestines (Figure 3). At this time, the patient was treated with sildenafil at 1.2 mg/kg, 12.5 mg by mouth twice daily for 14 days. The animal was also treated with simethicone at 1 mg/kg, 10.4 mg by mouth twice daily for 7 days due to gas accumulation throughout the gastrointestinal tract. This animal had not yet started the weaning process, but teeth had erupted so all gastric gavage was discontinued at the time of diagnosis and the animal was placed on an all-herring diet. Throughout the treatment period, clinical signs resolved and no further regurgitation was noted. Radiographs were taken at the end of the 14-day course of sildenafil and revealed marked improvement in esophageal dilation with only a small amount of gas visible in the esophagus. The animal was monitored for 3 months after completion of treatment. No clinical signs recurred, and he continued to gain body mass appropriately. Recheck radiographs were performed just before release, 3 months after completion of sildenafil treatment showing resolution of the dilation of the esophagus. This animal received a satellite-linked transmitter before release. The tag transmitted for 39 days during which time the animal was active and swam a daily average of 29.75 km/day as during that time. The animal was also photographed by a member of the public 30 days after his release and appeared to be in good body condition, active, and bright.
Radiographs from a harbor seal (P vitulina; case 2) undergoing rehabilitation at the Vancouver Aquarium Marine Mammal Rescue Society at the time of diagnosis with megaesophagus and after treatment with sildenafil at 1 mg/kg by mouth twice daily for 14 days. Dorsoventral view at diagnosis (A), dorsoventral view 1 day posttreatment (B), and dorsolateral view 3 months posttreatment (C) are shown.
Citation: American Journal of Veterinary Research 2025; 10.2460/ajvr.24.09.0281
Case 3 was admitted to another rescue facility as an approximately 14-day-old male harbor seal due to maternal separation and transferred for long-term rehabilitation to VAMMR 1 week later. At the time of initial rescue, the animal was quiet and moderately dehydrated and had a body condition score of 2.0/9. Once transferred to VAMMR, the animal was bright and well hydrated. The CBC and serum biochemistry panel on admission revealed a neutrophilic leukocytosis (WBC, 26.3 X 109/L; reference range, 6.9 to 12.3 X 109/L; and neutrophils, 21.0 X 109/L; reference range, 3.42 to 13.96 X 109/L) and increased GGT (38 IU/L; reference range, 8 to 23 IU/L). This assessment was based on in-house reference ranges. Clinical signs of hyporexia and abdominal distension were noted starting on day 55 of rehabilitation at the end of his 5-day weaning process. Regurgitation was first noted on day 60. This animal was treated with simethicone at 1 mg/kg, 14.8 mg by mouth twice daily for 7 days initially with no noted clinical improvement. Radiographs were taken 1 week after regurgitation was first seen and revealed dilation of the esophagus throughout the thorax as well as gas distention of the stomach and small intestines. At this time, the patient was treated with sildenafil at 0.93 mg/kg, 12.5 mg by mouth twice daily for 14 days. This animal was also treated with maropitant at 2 mg/kg, 30 mg by mouth for 4 days. Tube feedings were reinitiated 4 times per day due to the refusal of fish. Over the first 6 days of treatment, the animal became lethargic, started having diarrhea, and regurgitation and loss of body mass continued. At that time, euthanasia was elected. Euthanasia was performed with butorphanol at 0.25 mg/kg, 3.34 mg, IM, and midazolam at 0.2 mg/kg, 2.66 mg, IM, followed by pentobarbital sodium at 240 mg/mL, 2 mL/4.5 kg, 1,920 mg, IV. On postmortem examination, case 3 was found to have marked, segmental cylindrical dilation of the esophagus, scattered mucosal erosions, and occasional ulcerations. The small intestine was found to contain a small amount of fluid ingesta and gas, and the entire length of the descending colon was markedly dilated with gas and bright yellow mucoid feces. There was no evidence of aspiration. Histopathologic examination revealed moderate laminar, submucosal, subserosal, and perineuronal fibrosis multifocally throughout the esophagus (Supplementary Material S1).
Case 4 was an approximately 5-day-old female harbor seal rescued due to maternal separation. On presentation, the animal was quiet and mildly dehydrated and had a body condition score of 2/9. A corneal ulcer was observed in the left eye, but there were no other significant findings on initial physical examination. Admission CBC and serum biochemistry panel showed hemoconcentration (RBC, 6.6 X 1012/L; reference range, 3.6 to 5.4 X 1012/L; and hematocrit, 0.69 L/L; reference range, 0.5 to 0.6 L/L), a lymphocytic leukocytosis (WBC, 13.0 X 109/L; reference range, 6.9 to 12.3 X 109/L; and lymphocytes, 5.0 X 109/L; reference range, 0.7 to 3.57 X 109/L), decreased BUN (7.0 mmol/L; reference range, 12.1 to 21.4 mmol/L), hypoproteinemia (54 g/L; reference range, 65 to 90 g/L), hypoglobulinemia (19 g/L; reference range, 27 to 64 g/L), hyponatremia (143 mmol/L; reference range, 148 to 158 mmol/L), and increased GGT (37 IU/L; reference range, 8 to 23 IU/L). This assessment was based on in-house reference ranges. One incident of regurgitation as well as lethargy was noted starting on day 12 of rehabilitation, and the seal was treated with maropitant at 1 mg/kg, 11 mg, SC, once daily, and metoclopramide at 0.2 mg/kg, 2.2 mg, SC, twice daily, for 2 days during which regurgitation continued at 1 to 2 feeds per day and lethargy worsened. Three-view thorax and 2-view abdominal radiographs were performed revealing dilation of the esophagus. Due to dull mentation and overall decline in clinical status at the time of diagnosis, euthanasia was performed with butorphanol at 0.25 mg/kg, 2.9 mg, IV, and midazolam at 0.2 mg/kg, 2.35 mg, IV, followed by pentobarbital sodium at 240 mg/mL, 2 mL/4.5 kg, 1,200 mg, IV. Postmortem examination revealed aspiration and colitis but did not report megaesophagus.
Case 5 was an approximately 10-day-old female harbor seal rescued due to maternal separation. On presentation, the animal was quiet and moderately dehydrated and had a body condition score of 2/9. She had multiple small abrasions on her hind flippers on presentation, but there were no other significant findings on the initial physical examination. Admit CBC and serum biochemistry panel blood results showed erythrocytosis (RBC, 5.9 X 1012/L; reference range, 3.6 to 5.4 X 1012/L), decreased creatinine (16 μmol/L; reference range, 26.4 to 96.8 μmol/L), decreased BUN (2.8 mmol/L; reference range, 12.1 to 21.4 mmol/L), hypoproteinemia (49 g/L; reference range, 65 to 90 g/L), hypoglobulinemia (22 g/L; reference range, 27 to 64 g/L), increased ALP (306 IU/L; reference range, 52 to 224 IU/L), increased GGT (36 IU/L; reference range, 8 to 23 IU/L), and hyperbilirubinemia (20.0 μmol/L; reference range, 3.4 to 13.7 μmol/L). This assessment was based on in-house reference ranges. Difficulty passing the gavage tube and intermittent diarrhea were noted starting on day 14 of rehabilitation and regurgitation was noted on day 28. Regurgitation during and after gavage feeding occurred 1 to 2 times per day for the next 4 days along with diarrhea and the animal was treated with metronidazole at 10 mg/kg, 118 mg by mouth twice daily for 7 days, and maropitant at 1 mg/kg, 12 mg, SC, once daily for 4 days. Three view thoracic radiographs at this time revealed no major abnormalities. This animal had not yet started the weaning process, but teeth had erupted, so gastric gavage was discontinued and the animal was placed on an all-herring diet due to continued regurgitation and difficulty gavage feeding. Over the next 2 weeks, the seal continued to be difficult to feed, became progressively lethargic, and occasionally regurgitated after the fish meals. Two weeks after the initial imaging, radiographs were repeated revealing dilation of the esophagus throughout the thorax as well as mild gas distention of the small intestines. This patient was found deceased a few hours after radiographs were obtained before sildenafil treatment could be initiated. Postmortem examination revealed marked, diffuse cylindrical dilation of the esophagus with partially digested fish found within the lumen. The stomach was moderately distended with ingesta, and there was mucoid, firm dull brown, green feces found in the colon. Histologically, the esophagus was found to have myocellular degeneration, necrosis, and moderate esophagitis.
Discussion
In this study, 3 Pacific harbor seals diagnosed with megaesophagus based on clinical and radiographic findings were treated with sildenafil. This is the first study to describe the treatment of this disease in juvenile harbor seals. Previously, megaesophagus has been suspected to be a congenital disorder in harbor seals. However, the development of clinical signs only weeks after admission to the rescue facility as well as apparent resolution after short-term treatment raises questions about the underlying etiology. With congenital idiopathic megaesophagus, as in domestic canines, animals require lifelong management, which is not consistent with our findings. Cases 1 and 2 were monitored in the rehabilitation facility for 1 and 3 months, respectively, after discontinuing sildenafil and showed no return of clinical signs. Additionally, radiographs just before release showed full radiographic resolution of the previous esophageal dilation.
There was no indication of underlying systemic disease in any of these cases that could have resulted in a secondary megaesophagus. Noted bloodwork changes were consistent with hemoconcentration, poor nutritional status, and neonatal status. In 2 individuals, leukocytosis was also noted. All of these changes are common in seal pups rescued due to maternal separation. Based on this bloodwork, there was no indication of other underlying disease, but further diagnostics were not pursued to explore possible systemic pathologies such as hypothyroidism, hypoadrenocorticism, or myasthenia gravis, which are all known causes of secondary acquired megaesophagus in canines.11 Finally, no indication of other underlying pathologies, other than esophagitis (cases 3 and 5), was found on gross postmortem and histopathologic examination. The cause of megaesophagus in these cases could not be determined but was associated with mucosal ulceration and fibrosis of the esophagus.
Megaesophagus has been reported secondary to pharyngeal or esophageal trauma in ruminants caused by the use of balling guns, dose syringes, specula, rigid probe calf esophageal feeders, and stomach tubes.26 Additionally, megaesophagus secondary to nontraumatic esophagitis has been reported in both foals and cats and has been suspected in cattle.26–29 It is possible then that repeated passing of an orogastric tube could cause cumulative irritation and esophagitis in these seal pups, which could eventually lead to megaesophagus. In foals, esophagitis is usually secondary to reflux due to pyloric outflow obstruction,26 and in the reported feline case, it was suspected to be due to postoperation gastroesophageal reflux resulting in esophagitis and subsequent megaesophagus.27 This indicates that both acute trauma to the esophagus during gavage feeding and chronic repeated irritation and inflammation from passing an orogastric tube could be associated with the development of this pathology. To better understand the underlying etiology of these cases, more advanced diagnostics should be considered in future cases including endoscopy, contrast radiographs, and fluoroscopy to identify any mucosal lesions of the esophagus, anatomical abnormalities, esophageal motility disorders, or gastric changes that could be contributing to the development of megaesophagus.
There are some limitations to this study including a small sample size as well as possible effects of megaesophagus on oral absorption of drugs. It is possible that medications used remain in the esophagus due to the dilation present and do not effectively reach the stomach for systemic absorption. Future investigations into this treatment protocol should involve more animals from several different rehabilitation facilities. Additionally, a better understanding of the pharmacokinetics of sildenafil in this species would aid in the future use of this drug in harbor seals and other pinnipeds. Additionally, investigations of different formulations (tablet vs liquid) of sildenafil as well as delivery methods (in whole fish vs via gavage fed in formula) of the medication on effective oral delivery would help determine the best treatment method for future cases. Finally, a better understanding of the underlying etiology of megaesophagus in pinnipeds would help in determining which individuals may benefit from short-term treatment with sildenafil or other interventions.
Megaesophagus in seal pups undergoing rehabilitation has historically resulted in high mortality rates,19 emphasizing the need for continued investigation into possible treatment options. Based on the successful rehabilitation of some individuals with megaesophagus treated with sildenafil, this medication warrants further investigation. Although the underlying cause of megaesophagus in this species is still unknown, we hypothesize that repeated orogastric tube feeding could contribute to the development of this pathology in some cases of megaesophagus in harbor seal pups. Stomach tubes should be measured before each feeding to ensure the tube is placed appropriately into the stomach, not the esophagus, to avoid distention and trauma of the esophagus, and all staff should be thoroughly trained on proper tube placement. Further investigation into the underlying causes of megaesophagus in pinnipeds, and possible treatment options, could improve rehabilitation success rates.
Supplementary Materials
Supplementary materials are posted online at the journal website: avmajournals.avma.org.
Acknowledgments
The authors thank the veterinary technicians, staff, and volunteers at the Vancouver Aquarium Marine Mammal Rescue Society for their excellent care and assistance with these cases. Additionally, the authors thank Stephen Raverty, DVM, for all postmortem examinations and histopathology on these cases.
Disclosures
Dr. Wright is an Associate Editor for JAVMA and AJVR but was not involved in the editorial evaluation of or decision to accept this article for publication.
No AI-assisted technologies were used in the generation of this manuscript.
Funding
Funding was provided by Florida Fish and Wildlife Conservation Commission Marine Mammal Training Grant No. 20324.
ORCID
S. E. Wright https://orcid.org/0000-0002-0097-5575
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