Introduction
Splenic torsion can present in both acute and chronic forms ranging from acute collapse, abdominal pain, and shock to chronic weakness and hematuria.1 Diagnosis can be challenging, but early surgical management is recommended to reduce patient morbidity and mortality.1
Spherocytosis can be seen in numerous conditions including immune-mediated hemolytic anemia (IMHA),2 posttransfusion,3 envenomations (viper bite4,5 and honeybee5), acetaminophen6 and zinc7 intoxication, disorders associated with erythrocyte fragmentation (hemangiosarcoma,8 hemolytic uremic syndrome,9 and endocarditis10), hypersplenism,11 pyruvate kinase deficiency,12 and dyserythropoiesis.13 Perhaps most commonly, spherocytosis is well recognized as a component in the diagnostic criteria for IMHA.2
A previous retrospective case series1 of 102 dogs with primary splenic torsion documented a high prevalence of anemia and thrombocytopenia but did not state the presence of spherocytosis in any patients, and a prior case report14 has suggested the absence of spherocytosis helps distinguish between IMHA and splenic torsion.
This case series aimed to describe the presentation, diagnostics, treatment, and outcome of 4 cases with concurrent splenic torsion and spherocytosis.
Methods
This was a retrospective case series. The electronic medical records of the Queen Mother Hospital for Animals were searched using a computerized search of all patients presenting to the hospital between 2007 and 2021. Cases were identified using search terms in the clinical notes (eg, splenic AND torsion, spherocyt*).
Dogs were eligible for inclusion if they had a final diagnosis of splenic torsion confirmed with exploratory laparotomy by board-certified surgeons or a supervised resident-in-training and spherocytosis documented on blood smear review by a board-certified clinical pathologist or supervised resident-in-training. Data extracted from clinical records included signalment, historical and physical examination findings, clinicopathologic data, imaging findings, management strategies, and outcome.
Statistical analysis
Results are presented as medians and ranges. Calculations were made with available spreadsheet software (SPSS Statistics, version 26; IBM Corp). Due to the small sample size, no statistical associations were assessed between patients.
Results
A total of 18 dogs with splenic torsion were highlighted by the search terms. Fourteen dogs were excluded due to a lack of spherocytosis on review of the blood smear report. The population included 3 males and 1 female, all neutered but of different breeds (Boxer, Great Dane, Weimaraner, and Chow Chow). The median age was 5 years (range, 3 to 7 years).
Clinical signs
All cases presented as referrals with a history of lethargy. Additional complaints included hyporexia (patients 1, 2, and 3), exercise intolerance (patients 2 and 3), collapse (patient 2), and pigmenturia (patient 4). Patient 3 had an acute non–weight-bearing lameness of the right pelvic limb noted 3 days prior to presentation. Patient 4 had been started on prednisolone (2 mg/kg) and clopidogrel (37.5 mg) PO due to concern regarding IMHA prior to referral; however, the Coombs and in-saline agglutination test results were negative, making IMHA less likely.
Physical examination documented a mass effect and pain associated with the ventral midabdomen in 3 patients (patients 2, 3, and 4). Tachycardia was documented in 2 patients (patients 2 and 4), and femoral pulses were absent bilaterally in patient 3. Patient 2 was nonambulatory and laterally recumbent with appropriate mentation. Findings from the physical examination were considered normal in patient 1.
Clinical pathologic findings
Hematological and biochemical assessments were performed in all 4 patients. Hematology results (Table 1) included neutrophilia (patients 1, 2, 3, and 4; range, 15.86 X 109 to 57.25 X 109/L; reference interval [RI], 3.0 X 109 to 11.5 X 109/L), mild to moderate anemia (patients 1, 2, and 4; Hct range, 21.9% to 32.2%; RI, 37.0% to 55.0%), monocytosis (patients 2, 3, and 4; range, 3.13 X 109 to 8.07 X 109/L; RI, 0.15 X 109 to 1.50 X 109/L), and thrombocytopenia (patient 3; 128 X 109/L; RI, 150 X 109 to 900 X 109/L). Blood smear evaluation documented spherocytosis in all 4 patients (Figure 1). Spherocytosis was described as occasional (patient 1), rare (patient 2), low number (patient 3), and 1+ (patient 4). At the authors’ institution, occasional, rare, and low are consistent with < 1+ spherocytes, or < 1 to 10 spherocytes per hpf. Additional findings included mild to moderate (1+ to 2+) polychromasia (patients 1, 3, and 4), mild to moderate (1+ to 2+) anisocytosis (patients 3 and 4), mild to moderate (1+ to 2+) acanthocytosis (patients 1 and 2), moderate (2+) keratocytosis (patient 1), mild (1+) schistocytosis (patient 2), and mild to moderate (1+ to 2+) echinocytosis (patients 1 and 2).
Summary of hematological analysis in 4 dogs with splenic torsion.
| Test | Patient 1 | Patient 2 | Patient 3 | Patient 4 | Reference range | Unit |
|---|---|---|---|---|---|---|
| WBC conc | 20.6a | 28.4a | 73.4a | 45.9a | 6.0–17.1 | 109/L |
| Neutrophil conc | 15.9a | 24.4a | 57.3a | 41.3a | 3.0–11.5 | 109/L |
| Band neutrophil conc | — | — | 4.4 | — | 0–0.3 | 109/L |
| Lymphocyte conc | 2.3 | 0.9a | 3.7 | 1.4 | 1.0–4.8 | 109/L |
| Monocyte conc | 1.9a | 3.1a | 8.1a | 3.2a | 0.1–1.5 | 109/L |
| Eosinophil conc | 0.6 | 0.0 | 0.0 | 0.0 | 0–1.3 | 109/L |
| RBC conc | 4.27a | 4.49a | 5.44a | 3.21a | 5.50–8.50 | 109/L |
| Nucleated RBCs | — | — | 15a | — | < 1 | Per 100 WBCs |
| Hemoglobin conc | 10.6a | 10.5a | 11.9a | 6.8a | 12.0–18.0 | g/dL |
| Hct | 32.2a | 31.4a | 37.8a | 22.2a | 37.0–55.0 | % |
| Absolute reticulocyte conc | — | — | — | 423 | — | 109/L |
| MCV | 75.3 | 69.9 | 69.6 | 69.1 | 60.0–77.0 | fL |
| MCH | 24.7a | 23.3 | 22.0 | 21.3 | 19.5–24.5 | pg |
| MCHC | 32.8 | 33.3 | 31.5a | 30.8a | 32.0–36.0 | g/dL |
| Red cell distribution width | 15.6 | 12.0a | 16.1 | 17.1 | 12.9–18.3 | % |
| Platelet conc | 858 | 170 | 128a | 178 | 150–900 | 109/L |
| Morphological comments | 1+ to 2+ polychromasia; | 1+ polychromasia; | 2+ anisocytosis; | 3+ anisocytosis; | — | — |
| occ spherocytosis; | 1+ acanthocytosis; | 2+ polychromasia; | 2+ to 3+ | |||
| 2+ echinocytosis; | occ schistocytosis; | low numbers | polychromasia; | |||
| 2+ keratocytosis; | occ keratocytosis; | of spherocytes | 1+ spherocytosis | |||
| 2+ acanthocytosis | rare spherocytosis; | |||||
| 3+ echinocytosis |
Conc = Concentration. Occ = Occasional.
aValues with a superscript are abnormal findings.
Blood smear image from a dog with splenic torsion. Note the rare spherocyte (black arrow) with a circular outline, smaller diameter (compared to other erythrocytes), and dark staining (due to the thickness of spherical vs disc-shaped cells). Modified Wright stain, 100X objective.
Citation: Journal of the American Veterinary Medical Association 262, 9; 10.2460/javma.24.03.0148
Biochemical assessment revealed elevated creatine kinase activity (patients 2 and 4; range, 1,400 to 2,946 U/L; RI, 61 to 394 U/L), mild hyperkalemia (patients 1 and 4; range, 5.60 to 5.85 mmol/L; RI, 4.10 to 5.30 mmol/L), hypercholesterolemia (patients 3 and 4; 7.95 to 11.30 mmol/L; RI, 3.30 to 8.90 mmol/L), elevated ALT activity (patient 3; 392 U/L; RI, 13 to 88 U/L), hyperbilirubinemia (patient 4; 13.7 µmol/L; RI, 0.1 to 4.2 µmol/L), elevated ALP activity, (patient 4; 250 U/L; RI, 0 to 130 U/L), and elevated C-reactive protein concentration (patient 4; 80 mg/L; RI, < 30 mg/L). Urinalysis was performed in patients 2 and 4, documenting 2+ bilirubinuria and > 3+ hematuria in both, and 3+ proteinuria in patient 4.
Preoperative coagulation testing was performed in patient 3. Prothrombin time (PT) and activated partial thromboplastin time (aPTT) were within the reference interval. Thromboelastography with kaolin activation documented a shortened reaction time (3.8 minutes; RI, 4.0 to 8.0 minutes), a shortened kinetics (K) time (1.2 minutes; RI, 2.0 to 4.0 minutes), increased α angle (70.8°; RI, 40.0° to 67.0°), and a normal maximum amplitude (57.6 mm; RI, 46.0 to 64.0 mm) compatible with hypercoagulability.
Imaging findings
Point-of-care ultrasound examination was performed in all 4 patients and documented free abdominal fluid and splenomegaly with a “starry sky” appearance (Figure 2) in patient 4.
A—Point-of-care ultrasound at the left paralumbar view using an 8.5-MHz curvilinear probe. Image taken with probe placed in longitudinal orientation with marker directed toward the head. B—Color Doppler has been placed over the splenic vein.
Citation: Journal of the American Veterinary Medical Association 262, 9; 10.2460/javma.24.03.0148
All 4 patients had abdominal imaging performed and interpreted by a board-certified or specialist-in-training radiologist and included radiography (patient 1), ultrasound (patients 1, 3, and 4), and CT (patient 2). Abdominal radiography documented splenomegaly (patient 1). Ultrasonographic findings included diffuse hypoechoic splenomegaly and absence of blood flow in the splenic vein and splenic parenchyma on color Doppler in all patients. Additional ultrasonographic findings included a coarse, “lacy” texture to the splenic parenchyma (patients 1 and 4), abnormal hyperechogenicity of the mesenteric fat surrounding the spleen (patient 4), and bunching of the splenic vessels (patient 4). Computed tomography findings in patient 2 included a poorly contrast-enhancing, enlarged spleen with abnormal orientation. The splenic vessels were noted to twist and converge in the midabdomen, and the surrounding peritoneal fat had a streaky increase in attenuation. Evidence of thromboembolic disease was present in patient 2 (CT evidence of left renal infarction and an intrahepatic thrombus) and patient 4 (femoral arterial thrombus on Doppler ultrasound).
Management
Exploratory laparotomy was performed under general anesthesia and documented a complete splenic torsion in all patients. A splenectomy was performed without derotation (patients 1, 2, and 3) and with derotation (patient 4). Derotation was required in patient 4 due to involvement of the pancreas, and a partial pancreatectomy was performed. Intraoperative hemorrhage was documented in patient 4. Histopathological findings were also consistent with splenic torsion without evidence of neoplasia in all 4 cases.
Outcome
Patients 1 and 2 recovered well from general anesthesia and were discharged within 48 hours with carprofen (patient 1) and tramadol (patient 2). Both cases were lost to follow-up.
Patient 3 received postoperative anticoagulation with low–molecular-weight heparin (dalteparin) at 150 IU/kg SC. The day following surgery, patient 3 developed a sudden cardiorespiratory arrest, suspected to be secondary to thromboembolic disease. Cardiopulmonary resuscitation was not attempted.
Patient 4 had a poor recovery from anesthesia and remained persistently tachycardic. Tranexamic acid (20 mg/kg) was administered IV, and the patient received a blood-type–appropriate packed RBC transfusion (15 mL/kg, IV). Repeated point-of-care ultrasound documented free abdominal fluid in 4 out of 4 sites on the abdominal focused assessment with sonography for trauma,15 and a worsening anemia (Hct, 17.0%; RI, 37.0% to 55.0%) was noted. Prothrombin time and aPTT were both markedly prolonged (PT, > 100 seconds; PT RI, 11 to 14 seconds; aPTT, > 350 seconds; aPTT RI, 72 to 102 seconds). A fresh frozen plasma transfusion was administered (10 mL/kg, IV). The patient developed sudden stupor, loss of gag reflex requiring endotracheal intubation, and suffered a cardiopulmonary arrest, suspected to be due to intracranial hemorrhage. Cardiopulmonary resuscitation was not attempted.
Discussion
In this case series, we highlighted the first reported cases of spherocytosis associated with splenic torsion.
All 4 of our cases presented with vague, nonspecific clinical signs of lethargy and hyporexia, and although physical examination documented abdominal pain and/or a mass effect in 3 out of 4 cases, a diagnosis of splenic torsion was not immediately apparent.
Clinical pathological abnormalities were present in all patients in this case series. Only 3 out of 4 cases had evidence of anemia on initial hematological examination, which varied from poorly to strongly regenerative. Blood film examination documented several erythrocyte morphology changes consistent with fragmentation injury including spherocytosis, schistocytosis, and acanthocytosis.
The American College of Veterinary Internal Medicine’s consensus statement for the diagnosis of IMHA suggests that, following the identification of anemia, ≥ 2 signs of immune-mediated destruction (ie, prominent spherocytosis, positive in-saline agglutination test result, positive direct antigen test/Coombs test result) and ≥ 1 sign of hemolysis (eg, hyperbilirubinemia, significant bilirubinuria, hemoglobinemia, hemoglobinuria, or erythrocyte ghost cells) are needed to definitively diagnose IMHA.2 Partially meeting these criteria is recommended to be, at best, supportive of IMHA, but further tests are recommended to rule out additional causes of anemia.2 Quantifying spherocytosis in relation to the number of spherocytes per hpf at 100X oil emulsion has been used to assess diagnostic accuracy in IMHA.16 Presence of ≥ 5 spherocytes/hpf has greater specificity but lower sensitivity for IMHA than ≥ 3 per hpf,16 and as such, the American College of Veterinary Internal Medicine’s consensus statement for the diagnosis of IMHA recommends a minimum of ≥ 5 spherocytes/hpf as supportive of a diagnosis, but that ≥ 3 to 4 per hpf may be supportive if another cause of spherocytosis is not found.2 These thresholds are similar to the criteria for 1+ spherocytosis in a widely used semiquantitative grading system.17 All cases in this series were described as below the 1+ spherocytosis quantification. Appropriate quantification of spherocytosis may help to reduce the risk of an erroneous diagnosis of IMHA and commencement of immunosuppressive therapy. This is particularly important when excluding a diagnosis of IMHA, as presence of spherocytes can support the diagnosis of IMHA despite a lack of positive in-saline agglutination or Coombs test results.2
The mechanism of spherocytosis in the dogs with splenic torsion is likely to be microangiopathic fragmentation damage, given the concurrent presence of other shear injury products, such as schistocytes, keratocytes, and acanthocytes in these cases. However, spherocyte fragmentation may be seen independently of microangiopathic damage and can be due to both immune-mediated and non–immune-mediated disease.18 Spherocytosis has been documented in 5% of patients with splenic neoplasia, potentially supporting a microangiopathic anemia and fragmentation injury in splenic disease.19 Spherocytosis has also been seen in hemolytic uremic syndrome, supporting fragmentation injury as a contributing mechanism.9 Additionally, anemia has been documented in 30 out of 59 dogs with lung lobe torsion20 and 2 out of 12 dogs with liver lobe torsion.21 Although clinicopathologic assessment of blood smears was not documented in either of these studies, it is possible that microangiopathic damage and fragmentation injury may contribute to anemia in visceral organ torsion. Unfortunately, in this study, both patients that survived to discharge were lost to follow-up, and so inferences cannot be made about the resolution of the spherocytosis postsplenectomy. Alternatively, spherocytosis may have been present in this study due to a reduction in the normal physiologic clearance of spherocytes by the spleen due to altered splenic function in torsion. Given the marked contrast in treatment options for various causes of anemias with concurrent spherocytosis, it is important to consider alternative diagnoses to IMHA prior to commencing treatment. In cases where low numbers of spherocytes are documented, along with other morphological changes consistent with shear injury, clinicians should consider non–immune-mediated conditions and assess the patient for risks of microangiopathic damage.
Various imaging modalities have been assessed for the diagnosis of splenic torsion, including radiography,22 B-mode and Doppler ultrasound,23 and CT.24 Although CT is considered the gold standard for the diagnosis of splenic torsion in people,25 CT is not readily available in primary care practice. In contrast, ultrasound is widely available to most practitioners. Ultrasonographic findings of splenic torsion include splenomegaly, splenic IV thrombosis, absent or minimal intrasplenic blood flow on color Doppler, diffuse hypoechogenic splenic parenchyma with lacy echogenic separations (“starry sky” pattern), and a hilar perivenous hyperechoic triangle.1,23,26 Point-of-care ultrasound is a growing field of veterinary medicine, and various protocols are described in depth elsewhere.15,27 The abdominal focused assessment with sonography for trauma protocol is generally followed at the authors’ institution and includes assessment of the splenorenal site.15 In 1 case in this series, point-of-care ultrasound documented free abdominal fluid and splenomegaly with a “starry sky” appearance as previously reported,22 which prompted rapid further evaluation by a board-certified radiologist.
Splenectomy is the treatment of choice for splenic torsion, and outcome is favorable if treated early in the disease course, with a reported mortality rate of 8.8%; intraoperative hemorrhage is associated with a worse prognosis.1 Chronic splenic torsion can lead to shock, ventricular arrhythmias, and disorders of coagulation.28
Two out of 4 cases suffered cardiopulmonary arrest in hospital, suspected to be due to dysregulation of coagulation. Splenic torsion has been previously reported to be associated with suspected disseminated intravascular coagulation,29,30 although the diagnosis of disseminated intravascular coagulation remains challenging, with various scoring systems recommended.31 Unfortunately, extensive coagulation testing was not performed in all patients in this case series. Patient 3 had imaging evidence of thromboembolic disease and hypercoagulability on thromboelastography with normal PT and aPTT. Patient 4 had prolonged clotting times postoperatively and had an acute neurological deterioration, raising concern over a cerebrovascular event, although this was not confirmed postmortem and it is unclear whether the prolongation in clotting times developed pre-, intra-, or postoperatively. However, these cases show that both hyper- and hypocoagulable states can be seen in splenic torsion, and the clinician should consider the potential alterations in coagulation in the perioperative period.
The current case series was limited by its retrospective nature, and each patient was investigated and treated based on clinician preferences and patient clinical status. An additional limitation was the impact of medication received prior to referral. For example, patient 4 was started on an immunosuppressive dose of prednisolone prior to transport. The Coombs test has a reported sensitivity of 61% to 82%.16,32 The impact of previous immunosuppressive therapy on positive Coombs test results is not known, although antibody-positive erythrocytes are reduced following therapy when assessed via flow cytometry.33 Another limitation was the lack of reticulocyte counts in all patients. At the authors’ institution, reticulocyte counts are only performed when the PCV is < 30% or if clinicians specifically request it. The varied case descriptions and treatment plans in this series presented a realistic overview of how each case of splenic torsion is unique and can be challenging for the clinician to initially diagnose using routine hematological and biochemical tests.
This case series was the first to describe concurrent splenic torsion and spherocytosis and highlighted the need for consideration of nonimmunologic causes of spherocytosis, as well as reinforced the necessity of confirmatory testing in patients with suspected IMHA to reduce the likelihood of misdiagnosis.
Acknowledgments
None reported.
Disclosures
The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.
Funding
The authors have nothing to disclose.
ORCID
D. Beeston https://orcid.org/0000-0001-7230-1441
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