Search tips
Search criteria 


Logo of canvetjReference to the Publisher site.Journal Web siteJournal Web siteHow to Submit
Can Vet J. 2010 May; 51(5): 527–529.
PMCID: PMC2857436

Language: English | French

A case of splenic torsion with progressive anemia and thrombocytopenia


A 4-year-old male, castrated Saint Bernard was evaluated for acute onset of lethargy and collapse. Moderately severe anemia and splenomegaly were noted. Immune mediated hemolytic anemia was initially suspected. Abdominal ultrasound demonstrated an absence of splenic blood flow. Splenic torsion was confirmed on exploratory laparotomy and a splenectomy was performed.


Un cas de torsion splénique avec anémie progressive et thrombopénie. Un Saint-Bernard mâle âgé de 4 ans a été évalué pour l’apparition aiguë de léthargie et de collapsus. Une anémie et une splénomégalie modérément graves ont été observées. L’anémie hémolytique à médiation immunitaire a été initialement suspectée. Une échographie abdominale a démontré l’absence d’écoulement sanguin splénique. La torsion splénique a été confirmée par une laparotomie exploratoire et une splénoctomie a été réalisée.

(Traduit par Isabelle Vallières)

Case description

A 4-year-old male, castrated Saint Bernard weighing 31 kg was referred to a private emergency/specialty veterinary hospital for evaluation of acute onset of lethargy and collapse. Lethargy was first noted the night prior to presentation. The patient collapsed on a walk the next morning, and his owner noted pale mucous membranes. Following collapse, the dog was promptly presented to the referring veterinarian for evaluation. A packed cell volume and total solids (PCV/TS) demonstrated a moderately severe anemia (PCV 23%; reference range: 37% to 55% and TS 60 g/L; reference range: 55 to 75 g/L). A brief abdominal ultrasound performed by the referring veterinarian revealed marked splenomegaly. A complete blood (cell) count (CBC) indicated anemia (hematocrit 22.7%; reference range: 37% to 55%) and a mild thrombocytopenia (142 × 109/L; reference range: 175 to 500 × 109/L). A manual differential was not performed. A biochemistry and electrolyte panel was unremarkable. A crystalloid bolus (1 L of 0.9% saline, IV) was administered and the patient was referred for additional evaluation and treatment.

Upon presentation to the referral hospital that evening, the patient was lethargic and depressed but alert. A sinus tachycardia (160 beats per min) with bounding femoral pulses and mild hyperthermia (39.6°C; reference range: 38.4°C to 39.4°C) were noted. Mucous membranes were tacky and the capillary refill time was prolonged. The dog was thin and estimated to be 5% dehydrated. An enlarged, firm spleen was palpated; however, the patient’s abdomen did not appear to be painful. Packed cell volume and TS were rechecked and demonstrated severe anemia (16% and 58 g/L, respectively). Moderate hyperglycemia (11.05 mmol/L; reference range: 3.33 to 6.38 mmol/L) and a moderate elevation of blood lactate (3.3 mmol/L; reference range: < 2.5 mmol/L) were noted. Prothrombin time and partial thromboplastin time (PT/PTT) were within normal limits. A venous blood gas and electrolyte panel including ionized calcium measurement (iStat CG8+; Abbott Laboratories, Abbott Park, Illinois, USA) demonstrated normal ionized calcium with no significant blood gas or electrolyte abnormalities. An enzyme-linked immunosorbent assay (ELISA) test (SNAP 4Dx Test Kit; IDEXX Laboratories, Westbrook, Maine, USA) was positive for Anaplasma and Lyme disease, and negative for Ehrlichia and heartworm disease. A gross slide agglutination test was negative. Blood was submitted for a CBC with a complete differential and a cytologic review by a pathologist, Coomb’s test, and Rickettsia rickettsii serology.

Thoracic radiographs were unremarkable. Marked splenomegaly with dorsal displacement of the colon was noted on abdominal radiographs. A brief abdominal ultrasound demonstrated a markedly enlarged spleen with diffusely heterogeneous parenchyma. No abdominal effusion was detected. An ultrasound-guided splenic aspirate was submitted for cytology.

Immune-mediated hemolytic anemia (IMHA) was suspected by the emergency clinician as rapidly progressive anemia was documented with stable total solids and no hemorrhage was evident. Treatment for IMHA was initiated with immunosuppressive dosages of prednisone (0.85 mg/kg, PO, q12h), azathioprine (2.1 mg/kg, PO, q24h), and low-dose aspirin (0.5 mg/kg, PO, q24h). Doxycycline was administered at 5 mg/kg, PO, q12h as empirical treatment for tick-borne disease which could be a possible inciting cause for IMHA. The patient was blood typed (DEA 1.1 positive). A transfusion of 4 units (~120 mL/unit) of packed red blood cells was administered. The post-transfusion PCV was 23%. The blood lactate was noted to normalize following the transfusion.

Results of laboratory tests revealed a CBC of poorly regenerative anemia (hematocrit 17.8%, reticulocytes 40 480/L; reference range: < 60 000/L), moderate thrombocytopenia (129 × 109/L; reference range: 170 to 400 × 109/L), and moderate leukocytosis (26.3 × 109/L; reference range: 4.0 to 15.5 × 109/L) characterized by a mature neutrophilia (22 355/L; reference range: 2060 to 10 600/L) with a regenerative left shift (1315/L; reference range: 0 to 300/L) and a monocytosis (1052/L; reference range: 0 to 840/L). No spherocytes were detected. Rickettsia rickettsii serology and the direct Coomb’s test were negative. Splenic cytology demonstrated reactive lymphoid hyperplasia with no evidence of malignancy.

A thorough abdominal ultrasound detected severe splenomegaly. The spleen appeared to be normally positioned; however, the splenic parenchyma was diffusely heterogeneous with multiple parallel echogenic lines in a coarse, lacy, hypoechoic pattern. Splenic vessels were identified and appeared to be within normal limits, but blood flow was not detected with color flow Doppler. The mesentery surrounding the spleen appeared hyperechoic, consistent with inflammation and/or peritonitis. A small volume of abdominal effusion was detected. Splenic infarct or torsion was suspected due to the lack of blood flow within the spleen; however, splenic thromboembolism secondary to IMHA was also considered. Immunosuppressive therapy was discontinued at this time.

An exploratory laparotomy revealed ~500 mL of serosanguinous fluid within the abdomen. The spleen was markedly enlarged, very firm, and black in color. It was torsed on its pedicle along the sagittal axis. All splenic vessels were thrombosed. No other abnormalities were noted. A splenectomy was performed without detorsing the spleen in order to prevent reperfusion injury.

The patient recovered well from surgery; however, a postoperative coagulation panel demonstrated a mildly prolonged PTT (133 s; reference range: 71 to 102 s). Three units (~120 mL/unit) of fresh-frozen plasma were administered. The patient’s electrocardiogram was monitored continuously via telemetry overnight. Intermittent premature ventricular contractions and occasional paroxysmal ventricular tachycardia were detected. The arrhythmia was not treated as the heart rate and blood pressure remained within normal limits.

On the 3rd day, the patient’s PTT was rechecked and was within normal limits; however, the PCV had dropped to 18%. Two units of packed red blood cells were transfused. The post-transfusion PCV was 26%. The PCV remained stable following the 2nd blood transfusion. Upon rechecking a CBC with differential, the thrombocytopenia and neutrophilia with inflammatory shift were noted to have improved. The platelet count was assessed to be adequate and a very mild regenerative left shift was noted to persist. An increased regenerative response was reported with respect to the anemia (reticulocytes 81 200/L).

The patient proceeded to recover without complications; he was discharged from hospital 48 h following the splenectomy.


In the present case, a splenic torsion resulted in clinical signs and laboratory changes that were similar to those seen in dogs with IMHA and immune-mediated thrombocytopenia (ITP). With canine IMHA, common laboratory abnormalities may include mild to severe regenerative anemia with spherocytes, positive slide agglutination, and a positive Coomb’s test. An inflammatory leukogram characterized by a mature neutrophilia and occasionally a left shift may be seen associated with increased marrow release during the strong regenerative erythroid response, cytokine-stimulated myeloid hyperplasia, neutrophil demargination, and decreased migration into poorly perfused necrotic tissues. Hyperbilirubinemia due to intravascular hemolysis can also be seen in association with IMHA (1).

The anemia in this case was likely the result of sequestration of red blood cells within the torsed spleen. The inflammatory leukogram was suspected to have represented inflammation associated with the poorly perfused splenic parenchyma, a localized peritonitis secondary to the torsion, and possibly an increased release of neutrophils from the bone marrow during the regenerative erythroid response. Although not a feature of this case, hyperbilirubinemia can also be seen in association with splenic torsion; however, the underlying pathophysiology is not well understood (2).

In the present case, the thrombocytopenia and prolonged clotting times were likely the consequence of disseminated intravascular coagulation (DIC), which can occur secondary to splenic torsion (2,3). Dogs with IMHA typically do not demonstrate prolonged clotting times unless there is concurrent DIC. Previous reports indicate that 50% to 70% of dogs with IMHA have concomitant ITP leading to a thrombocytopenia (1).

Radiographic evidence of splenomegaly with loss of serosal detail and gastrointestinal displacement may suggest the presence of splenic torsion (46). Intrasplenic gas may be present secondary to splenic thrombosis causing breakdown of oxygenated hemoglobin resulting in free oxygen or carbon dioxide released from necrotic tissues undergoing anaerobic metabolism (6). Abdominal radiographs in this case demonstrated splenomegaly with dorsal displacement of the colon. This is a non-specific finding which may suggest splenic torsion, splenic neoplasia, or IMHA (1,6). Ultrasonographic evidence of splenomegaly is also considered non-specific; however, diffuse splenic hypoechogenicity with linear echodensities separating large anechoic areas giving the spleen a coarse ‘lacy’ appearance in association with lack of splenic blood flow visualized by color Doppler is highly suggestive of splenic torsion (2,3,58). In the present case, abdominal ultrasound findings were consistent with splenic torsion.

The pathogenesis associated with splenic torsion remains undetermined; however, large breed, deep-chested dogs appear to be at an increased risk with males being affected more frequently than females (9,10). Splenic torsion occurs when the tail of the spleen rotates around the pedicle. The pedicle is weakly anchored by the gastrosplenic and splenicocolic ligaments making the normal spleen relatively mobile (8,11). Torsion results in mechanical compression of the splenic veins and causes vascular congestion. Occlusion of the splenic arteries results in the formation of thromboemboli and infarction of the spleen (8). One theory proposes that repeated episodes of gastric dilatation, or partial gastric dilatation and volvulus (GDV), may stretch the gastrosplenic and splenocolic ligaments sufficiently to allow splenic hypermobility. Congenital absence or malformation of the splenic ligaments may predispose to development of splenic torsion (6). It is also believed that splenic torsion may occur secondary to splenic congestion which frequently occurs with gastric dilatation and volvulus (3,6,11).

Treatment for splenic torsion includes supportive therapy and splenectomy. As noted in this case, rapid ventricular arrhythmias occur commonly in association with splenectomy. Similar arrhythmias can be seen with splenic torsion alone; however, the pathogenesis is not well understood. Ventricular tachyarrhythmias may be asymptomatic and require no intervention; however, they can progress to be fatal. It is recommended that post-operative splenectomy patients are monitored with continuous electrocardiography to assess the frequency and extent of tachyarrhythmias (12). As used in this case, telemetry can be a valuable tool for monitoring the post-operative patient. Treatment may be considered based on assessment of clinical hemodynamic effects of the arrhythmias. Gastropexy should be considered as GDV has been reported to occur following surgical treatment due to the excess space created in the cranial abdomen (2,3,6). The prognosis with surgical correction is good and a 79% survival rate has been reported (5,6).

In conclusion, splenic torsion should be a differential for any case that has a progressive anemia with stable total solids. Lack of blood flow through the splenic vasculature and a heterogeneous, coarse ‘lacy’ appearance to the spleen on abdominal ultrasound is highly suggestive of splenic torsion (1,3,58). Splenectomy is the treatment of choice. The prognosis is good if diagnosed and treated early in the disease process (5,6). CVJ


Ms. Schnier will receive 50 free copies of her article courtesy of The Canadian Veterinary Journal.

Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ( gro.vmca-amvc@nothguorbh) for additional copies or permission to use this material elsewhere.


1. Balch A, Mackin A. Canine immune-mediated hemolytic anemia: Pathophysiology, clinical signs, and diagnosis. Compend Contin Educ Pract Vet. 2007;29:217–224. [PubMed]
2. What is your diagnosis? J Small Anim Pract. 1999;40:294–296. [PubMed]
3. Neath PJ, Brockman DJ, Saunders HM. Retrospective analysis of 19 cases of isolated torsion of the splenic pedicle in dogs. J Small Anim Pract. 1997;38:387–392. [PubMed]
4. King R, Pack LA. Splenic torsion in a dog. J Am Vet Med Assoc. 2002;220:973–974. [PubMed]
5. Jaeger GH, Maher E, Simmons T. What is your diagnosis? Splenic torsion. J Am Vet Med Assoc. 2006;229:501–502. [PubMed]
6. Konde LJ, Wrigley RH, Lebel JL, et al. Sonographic and radiographic changes associated with splenic torsion in the dog. Vet Radiol Ultrasound. 1989;30:41–45.
7. Saunders HM, Neath PJ, Brockman DJ. B-mode and Doppler ultrasound imaging of the spleen with splenic torsion: A retrospective evaluation. Vet Radiol Ultrasound. 1998;39:349–353. [PubMed]
8. Goldsmid SE, Davis P, Pechman R. Successful derotation of a splenic torsion in a racing greyhound. J Small Anim Pract. 1994;35:112–115.
9. Mai W. The hilar perivenous hyperechoic triangle as a sign of acute splenic torsion in dogs. Vet Radio Ultrasound. 2006;47:487–491. [PubMed]
10. Weber NA. Chronic primary splenic torsion with peritoneal adhesions in a dog: Case report and literature review. J Am Anim Hosp Assoc. 2000;36:390–394. [PubMed]
11. Marino DE, Matthiesen DT, Fox PR, Lesser MB, Stamoulis ME. Ventricular arrhythmias in dogs undergoing splenectomy: A prospective study. Vet Surg. 1994;23:101–106. [PubMed]

Articles from The Canadian Veterinary Journal are provided here courtesy of Canadian Veterinary Medical Association