Chronic Splenic Torsion in Two Dogs
A 5 yr old spayed female poodle (case 1) was presented with a 4 mo history of lethargy, inappetence, and nonregenerative anemia. A 5 yr old castrated male French bulldog (case 2) was presented with a 2 wk history of mild abdominal pain, dyschezia, and intermittent anorexia. Both dogs were diagnosed with chronic splenic torsion based on changes in splenic position, echogenicity, and/or echotexture identified on B-mode abdominal ultrasonography, as well as either decreased or absent splenic blood flow on color-flow Doppler ultrasonography. Both dogs underwent splenectomy and had full resolution of clinical signs. Presentation of chronic splenic torsion is variable, and clinical signs can be nonspecific. Abdominal ultrasound with Doppler evaluation is an important diagnostic step that can lead to appropriate surgical intervention and good long-term prognosis.
Introduction
In the emergent setting, acute splenic torsion is an important differential diagnosis for hemoabdomen as well as acute onset abdominal pain. Predisposed breeds include the Great Dane and German shepherd dog; however, any breed can be affected.1–3 Dogs with splenic torsion can also present with more chronic, nonspecific clinical signs. Those signs can include, but are not limited to, lethargy, anorexia, vomiting, and abdominal discomfort.4 Chronic splenic torsion presents a diagnostic challenge in that clinical signs may not permit organ localization and can mimic those of a variety of other conditions. Abdominal ultrasonography with color-flow Doppler, is a valuable tool in the diagnosis of splenic torsion and identifies the need for prompt surgical intervention.2
In this report, two cases of chronic splenic torsion are described. These cases highlight the variable presentation of chronic splenic torsion and the importance of diagnostic imaging in the diagnosis of this disease.
Case Report
Case 1
A 5 yr old spayed female poodle was presented to the internal medicine service at the Kansas State University Veterinary Health Center (KSU-VHC) with a 4 mo history of progressive lethargy and inappetence. The dog was initially presented to the primary care veterinarian 4 days after onset of clinical signs. A regenerative anemia (the hematocrit was 23.9%; reference range, 37–55% and reticulocyte count was 115.6 × 109 cells/L) and normal bilirubin (3.42 μmol/L; reference range, 0–15.4 SI units) were identified on blood work, and splenomegaly was identified on abdominal radiography and ultrasonography. The dog was presumptively diagnosed with immune-mediated hemolytic anemia (IMHA) and immunosuppressive therapy with prednisone [1 mg/kg per os (PO) q 12 hr] was initiated. After 5 days of prednisone therapy, a Coombs' test was performed that was negative. Serial complete blood counts revealed initial improvement followed by progression to a nonregenerative anemia with the hematocrit ranging from 15 to 35.1% and reticulocyte counts ranging from 29.8 to 205.9 × 109 cells/L. Adjunctive therapy with azothiaprine (1 mg/kg PO q 24 hr) was instituted 2.5 mo after initial presentation to the primary care veterinarian. Due to lack of response to therapy, the dog was referred to the KSU-VHC 4 mo after initial presentation to the primary care veterinarian. Prior to that illness, the dog had no major health concerns, was up to date on vaccinations, and received monthly heartworm prophylaxis. The dog was fed a commercially available canine maintenance diet and was the only dog in the household.
On presentation to the KSU-VHC internal medicine service, the dog was bright, alert, and responsive with vital parameters were within normal limits. Physical exam findings included generalized muscle wasting (particularly along the epaxial muscles), a thin coat, a pendulous abdomen, and an ulcerated skin lesion at the caudal aspect of the left elbow. Those findings were attributed to chronic steroid administration. Significant laboratory findings included leukocytosis (33.4 × 109 cells/L; reference range, 6–17 SI units), neutrophilia (30.0 × 109 cells/L; reference range, 3–11.5 SI units) with the presence of bands (0.7 × 109 cells/L; reference range, 0–0.3 SI units), lymphopenia (0.3 × 109 cells/L; reference range, 1.5–5 SI units), and monocytosis (2.3 × 109 cells/L; reference range, 0.1–0.8 SI units). A nonregenerative anemia [the hematocrit was 27% (reference range, 37–55%), the reticulocyte count was 59.5 × 109 cells/L, and the % reticulocyte was 1.7%] was present. Marked codocytes and occasional polychromatophils, schistocytes, and keratocytes were observed on a blood film. Significant serum biochemical abnormalities included hypoproteinemia (51 g/L; reference range, 54–76 SI units), hypoalbuminemia (33 g/L; reference range, 34–42 SI units), and elevated liver enzyme activities [alanine aminotransferase (ALT) was 17.07 μkat/L; reference range, 0.47–2.86 SI units and alkaline phosphatase (ALP) was 18.12 μkat/L; reference range, 0.02–2.37 SI units].
On thoracic radiographs, sternal lymphadenopathy was suspected. Hepatomegaly and decreased serosal detail were identified on abdominal radiographs. Abdominal ultrasound with color-flow Doppler analysis was performed. Hepatomegaly with normal echogenicity and echotexture was identified. The spleen was shifted into the right cranial abdominal quadrant, was hypoechoic, with lacey echotexture and a linear hyperechoic band of tissue dividing two portions of the organ (Figure 1). Color-flow Doppler revealed complete lack of arterial and venous blood flow to the spleen (Figure 2). The mesentery adjacent to the spleen was focally hyperechoic.
Citation: Journal of the American Animal Hospital Association 51, 3; 10.5326/JAAHA-MS-6129
Citation: Journal of the American Animal Hospital Association 51, 3; 10.5326/JAAHA-MS-6129
Based on those findings, either a splenic torsion or splenic infarct with necrosis was suspected. The dog was hospitalized in the intensive care unit and administered IV fluidsa in preparation for surgery. In order to further evaluate the nonregenerative anemia, an iron panel was performed. Iron concentration was 49.4 μmol/L (reference range, 15.75–42.6 SI units), total iron binding capacity was 51.19 μg/dL (reference range, 44.03–80.55 SI units), and ferritin was 13,453 pmol/L (reference range, 179.76–1,797.6 SI units), which was consistent with adequate iron reserves.
The following morning, the dog was anesthetized for an exploratory laparotomy. The spleen was grossly abnormal and identified based on anatomic location. The parenchyma was light colored, rounded, and very soft with numerous omental adhesions. Complete torsion of the splenic vascular pedicle was observed. A routine splenectomy was performed and the organ was submitted for histopathological evaluation. The liver was mildly enlarged with rounded edges and biopsies were obtained. A moderate amount of opaque peritoneal effusion was present, and a sample was obtained and submitted for aerobic and anaerobic cultures. No other abnormalities were observed. A prophylactic gastropexy was performed. The dog recovered without incident and was discharged 2 days later with cephalexinb (22 mg/kg PO q 12 hr), tramadolc (6 mg/kg PO q 8 hr), and a 10 day tapering course of prednisone.d The owner was also instructed to discontinue azothiaprine.
Histopathological evaluation of the spleen revealed complete parenchymal necrosis. The omentum was adhered to the splenic capsule by granulation tissue. Multifocal necrosis and mineralization was present in the adjacent adipose tissue. Those findings were consistent with chronic splenic infarction. Histopathology of the liver biopsies was consistent with moderate, multifocal, random, hepatic lipidosis. Aerobic bacterial culture of the abdominal fluid yielded a Salmonella spp. with a wide susceptibility profile, including susceptibility to a first-generation cephalosporin and fluoroquinolone. Anaerobic culture yielded no bacterial growth.
The dog presented for re-evaluation 5 days after surgery. The dog was reportedly doing well at home, was more energetic, and had an improved appetite. Physical exam was largely unchanged, and the surgical incision and cutaneous ulcer both appeared to be healing well. Blood work at that time revealed a persistent leukocytosis (36.4 × 109 cells/L) and neutrophilia (32.4 × 109 cells/L) with the presence of bands (0.4 × 109 cells/L). The severity of the anemia was unchanged (hematocrit was 26%); however, the anemia appeared regenerative (reticulocyte count was 172.6 × 109 cells/L and % reticulocytes was 5.2%). ALT (34.27 μkat/L) and ALP (29.98 μkat/L) were both increased from preoperative values, presumptively due to surgical trauma. Based on culture results, the cephalexin was discontinued and an 8 wk course of ciprofloxacine (10 mg/kg PO q 12 hr) was instituted because a fluoroquinolone was considered to be more appropriate for treatment of Salmonella spp. infection.
Re-evaluation with the primary care veterinarian 2 wk later revealed a persistent leukocytosis (44.8 × 109 cells/L) and neutrophilia (37.1 × 109 cells/L) and an improved regenerative anemia (hematocrit was 31.3%, reticulocyte count was 104 × 109 cells/L, and % reticulocytes was 2.4%). ALP (8.13 μkat/L) concentration had decreased dramatically, likely due to cessation of steroid therapy; ALT (17.67 μkat/L) had also decreased to preoperative levels. Because of concern for persistent hepatocellular injury, a combination of s-adenosylmethionine and silymarinf was instituted as a hepatoprotective agent.
Two months postsplenectomy, the dog presented for re-evaluation at the KSU-VHC. General physical exam revealed complete healing of the cutaneous ulcer as well as improved body condition, normal muscle distribution, and resolution of abdominal distention. The coat was much fuller than previously observed. The anemia, leukocytosis, and liver enzyme elevations had completely resolved. No long-term complications of either the splenic torsion or therapy were observed.
Case 2
A 5 yr old castrated male French bulldog was presented to the internal medicine service at the KSU-VHC with a 2 wk history of mild abdominal pain, dyschezia, and intermittent anorexia. The dog was initially evaluated by an emergency clinic for evaluation of an episode of diarrhea followed by a reported lack of defecation for a 3–4 day period, vocalization when attempting to lie down, reluctance to jump, and a “tucked” appearance to his abdomen when walking. The emergency clinician diagnosed an anal gland abscess and dietary indiscretion and prescribed amoxicillin trihydrate/clavulanate potassium (19.2 mg/kg PO q 12 hr).
The following day, the dog was presented to the primary care veterinarian for evaluation of continued abdominal discomfort and anorexia. Abnormal examination findings included stertorous breathing; a healing anal gland abscess; and a palpable, firm, nonpainful, midabdominal mass. No gastrointestinal parasites were identified on fecal flotation. A mass effect was suspected in the middle left abdomen quadrant on abdominal radiographs. Famotidine (0.4 mg/kg PO q 12 hr), metronidazole (19.2 mg/kg PO q 12 hr), tramadol (3.8 mg/kg PO q 12 hr), and a bland diet were prescribed. The patient re-presented to the primary care veterinarian 4 days later with persistent abdominal discomfort, reluctance to lie down, and dyschezia. No significant abnormalities were found on blood work, and the dog was not anemic at that time (hematocrit was 55.31%; reference range, 37–55%). Splenomegaly was identified on repeat abdominal radiographs and the dog was referred to the KSU-VHC for further evaluation and treatment.
Two weeks after clinical signs were first noted, the patient presented to KSU-VHC. The dog was bright, alert, and responsive with normal vital parameters. Stertor was noted when the dog was panting, and a nonpainful, midabdominal mass was appreciated on palpation. Six months previously, the patient was diagnosed with an elongated soft palate and the referring veterinarian performed a staphylectomy at that time.
At the time of referral, the packed cell volume was 52% and total protein was 80 g/dL, which were both within their respective references ranges. Abdominal radiographs revealed decreased serosal detail and a midabdominal mass (Figure 3). Based on location, a splenic mass was strongly suspected. On abdominal ultrasound, the spleen was malpositioned in a circular orientation and was markedly enlarged with rounded margins. Splenic echogenicity was mildly coarse but the echotexture was diffusely homogenous (Figure 4). Additionally, small volume peritoneal effusion and mild renal cortical changes were noted. Color-flow Doppler revealed partially reduced splenic blood flow. No evidence of pathology was identified on cytology of splenic aspirates. Based on those findings, either a splenic torsion or splenitis was suspected, with splenic neoplasia as a less likely differential diagnosis.
Citation: Journal of the American Animal Hospital Association 51, 3; 10.5326/JAAHA-MS-6129
Citation: Journal of the American Animal Hospital Association 51, 3; 10.5326/JAAHA-MS-6129
The next day, anesthesia, abdominal exploratory, and splenectomy were performed. The torsed spleen was notably enlarged necessitating splenic exteriorization and removal prior to completion of surgical exploration. The entire spleen was submitted for histopathology together with two enlarged mesenteric lymph nodes found following splenectomy. On upper airway evaluation, a persistently elongated soft palate was discovered and a routine staphylectomy was performed. The patient recovered uneventfully in the intensive care unit and was discharged 2 days following surgery with tramadol (4.8 mg/kg PO q 8 hr).c
Histological evaluation of the spleen revealed severe congestion with fibrosis and siderotic plaques. Areas of fibrosis were considered consistent with splenic torsion as suspected in the history. The adjacent mesenteric lymph nodes were considered reactive. Four months postoperatively, owners reported that the dog was doing well, with complete resolution of prior abdominal clinical signs and only mild stertor.
Discussion
Splenic torsion is an uncommon disease in dogs, representing <1% of all cases of splenic diseases in one histological survey.4 Large-breed dogs are most often affected, with Great Danes and German shepherd dogs being overrepresented; however, splenic torsion can occur in small breed dogs.1–3 A predisposition in male dogs has also been suggested.1 The underlying etiology of splenic torsions is unknown; however, an association with gastric dilation/volvulus has been reported.5 It is suspected that intermittent twisting of the stomach stretches and induces laxity of the gastrosplenic ligaments allowing free movement of the spleen and predisposing to torsion. The acute form of splenic torsion presents as a rapid deterioration of clinical condition including collapse, severe abdominal pain, and signs consistent with hypovolemic shock (i.e., tachycardia, hypotension, poor perfusion parameters), similar to the presentation of gastric dilation/volvulus.
The clinical presentation of chronic splenic torsion is more insidious and can include lethargy, anorexia, vomiting, anemia, and elevation in liver enzymes.1,6 Additionally, presentation can be variable. The lethargy, inappetence, and anemia of the dog described in case 1 were most likely caused by chronic blood loss/sequestration and inflammation. That dog did not have any signs specifically attributable to abdominal disease. In contrast, the dog described in case 2 had abdominal discomfort and a palpable abdominal mass, but was not anemic. Given the vague and variable nature of clinical findings, chronic splenic torsion can be easily misdiagnosed or overlooked.
Misdiagnosis of chronic splenic torsion for IMHA has been previously reported.7 Anemia due to IMHA is typically regenerative, and other classic features of IMHA such as hyperbilirubinemia and a positive Coombs' test are supportive of a diagnosis. Those additional features were lacking in case 1, although the Coombs' test could have been falsely negative due to prednisone therapy. In case 1, a regenerative anemia was initially present; however, as the course of disease progressed, the anemia became nonregenerative. Adequate serum iron concentration ruled out iron deficiency as a contributing factor. Thus, the anemia became nonregenerative as a result of the inflammatory reaction elicited by splenic necrosis and local peritonitis. That was supported by the elevation in ferritin, an acute phase protein, and a persistent inflammatory leukogram.
The duration of clinical signs associated with chronic splenic torsion was previously reported as lasting 1–28 days. In case 1, the dog experienced clinical signs for >4 mo prior to diagnosis. Ultrasound performed at the primary care veterinarian's office within 1 wk of onset of clinical signs revealed splenomegaly. Although splenomegaly can be associated with IMHA and the exact date torsion unknown, it is suspected that the splenic torsion was the underlying cause of disease during the entire 4 mo period and not a secondary process. The duration of clinical signs in case 2 was more consistent with previous reports. Although the splenic torsion was not initially diagnosed by the emergency clinician, intra-abdominal (specifically, splenic pathology) were strongly suspected by the primary care doctor early on. That dog had persistent abdominal discomfort prompting aggressive imaging (sequential abdominal radiographs and abdominal ultrasound at a referral facility), which expedited diagnosis.
B-mode and Doppler abdominal ultrasound are very important tools in the diagnosis of splenic torsion. Classically, torsed spleens are enlarged and hypoechoic, oftentimes with multiple linear hyperechoic foci, giving it a lacy appearance. The splenic veins are often enlarged, sometimes with hyperechogenicities within the lumen, suggesting venous thrombosis.2,8 Splenic malpositioning, as seen in case 2, has also been described with a C-shaped appearance and suggests a >180° torsion around the splenic pedicle.3 Doppler ultrasound may demonstrate either decreased or absent venous blood flow within the spleen, and complete occlusion may result in absent arterial blood flow as well. Those findings strongly suggest splenic infarction.2
Conclusion
Several important points regarding splenic torsion and anemia in dogs are highlighted by the cases presented herein. Although splenic torsion may present acutely, some cases may also present for signs of chronic illness. Anemia may or may not be present and clinical signs may be vague. Abdominal ultrasonography, including Doppler evaluation is useful to identify splenic torsion and the long-term prognosis for surgically treated chronic splenic torsion may be good.
B-mode ultrasound image of the spleen of a 5 yr old spayed female standard poodle (case 1). The hypoechoic parenchyma with lacey echotexture was consistent with splenic torsion. A linear hyperechoic band of tissue (arrow) divided two portions of the spleen likely represents torsed splenic capsule and/or mesentery.
Color-flow Doppler ultrasound image of the spleen of a 5 yr old spayed female standard poodle (case 1). Complete lack of arterial and venous blood flow was consistent with splenic torsion or infarction.
Lateral (A) and ventrodorsal (B) abdominal radiographs in a 5 yr old castrated male French bulldog (case 2) with splenic torsion. Decreased serosal detail and a midabdominal mass with lack of normal visualized spleen were consistent with the diagnosis.
B-mode ultrasound image of the spleen of the 5 yr old castrated male French bulldog described in case 2. A C-shaped splenic malpositioning (arrow) and coarse echogenicity are consistent with the diagnosis of splenic torsion.
Contributor Notes
M. Sherwood's updates credentials are DVM, MS.
M. Sherwood's present affiliation is VCA Oso Creek Animal Hospital and Emergency Center, Corpus Christi, Texas.
