- Email: [email protected]
Liver Lobe Torsion in a Domestic Ferret (Mustela putorius furo)
Author’s Accepted Manuscript LIVER LOBE TORSION IN A DOMESTIC FERRET (MUSTELA PUTORIUS FURO) Laura Vilalta, Yvonne Espada, Natalia Majó, Jaime Martorell www.sasjournal.com
PII: DOI: Reference:
S1557-5063(16)30081-7 http://dx.doi.org/10.1053/j.jepm.2016.06.008 JEPM684
To appear in: Journal of Exotic Pet Medicine Cite this article as: Laura Vilalta, Yvonne Espada, Natalia Majó and Jaime Martorell, LIVER LOBE TORSION IN A DOMESTIC FERRET ( MUSTELA PUTORIUS FURO) , Journal of Exotic Pet Medicine, http://dx.doi.org/10.1053/j.jepm.2016.06.008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
AEMV Forum
Liver Lobe Torsion in a Domestic Ferret (Mustela Putorius Furo) Laura Vilalta, DVM, Yvonne Espada, DVM, PhD, Natalia Majó, DVM, PhD, Dip. ECVP, Jaime Martorell, DVM, PhD, Dip.ECZM (Small Mammal) From the Fundació Hospital Clínic Veterinari (Vilalta, Espanda, Martorell), Departament de Medicina i Cirurgia Animal (Espada, Moartorell), Departament de Medicina i Sanitat Animals (Majó), Facultat de Veterinària, Universitat Autònoma de Barcelona, Barcelona, Spain Address correspondence to Laura Vilalta Solé, DVM, Fundació Hospital Clínic Veterinari, Facultat de Veterinaria, Universitat Autònoma de Barcelona, 08193 Bellaterra (Cedanyola del Valles), Barcelona, Spain. Email address: [email protected]. Tel: 004407784288071
Abstract A 6-year-old female domestic ferret presented with a 3-day history of lethargy and anorexia. Clinical examination revealed severe jaundice, painful abdominal palpation and a mass in the left cranial abdomen. Hematologic diagnostic tests of the patient revealed a regenerative anemia, severe neutrophilic and monocytic leukoctytosis, increased alanine aminotransferase (ALT) and total bilirubin, and decreased albumin and glucose concentration. Liver lobe torsion was identified through radiographic and ultrasonographic imaging. Post-mortem examination confirmed a left lateral liver lobe torsion, and a generalized hepatic lipidosis. Liver lobe torsion is a rare condition with few reported cases in veterinary medicine. Liver lobe torsion should be considered as a differential disease diagnosis in ferrets presenting with acute abdomen.
Key words: Ferret; liver lobe torsion; acute abdomen; jaundice; abdominal mass
Liver lobe torsion (LLT) is a rare condition in veterinary medicine reported in dogs1-4, cats4,5, pigs6, horses7, otters8, and rabbits9-14. Sporadic reports exist describing LLT in humans, most of which involve the accessory liver lobes (Reidels’s lobe).7 Liver lobe torsionLT leads to occlusion of the venous return prior to occlusion of the arterial supply, which causes acute congestion within the affected liver lobe (LL), and subsequent necrosis, effusion, hemoabdomen, and shock.10,11 Clinical signs are often non-specific, and can include lethargy, abdominal distension, anorexia, and vomiting. If untreated, LLT may result in acute collapse and sudden death.1 This case report describes the clinical disease signs, and laboratory, radiologic and ultrasonographic diagnostic results associated with LLT in a ferret.
CASE HISTORY A 6-year-old 850 gram spayed female domestic albino ferret was evaluated for a 3-day history of lethargy and anorexia. On physical examination, the ferret was depressed, mildly dehydrated, and dyspneic, and mucous membranes appeared jaundiced (Fig. 1). Auscultation revealed decreased lung sounds of left hemi-thorax. The abdomen was tense and painful, and a mass was palpated in the cranial left abdomen. Initial treatment included oxygen, shock fluid therapy (intravenous bolus of 10 ml/kg crystalloid solution [LactatoRingerVet,Braun, Spain], and 3 ml/kg of 6% Hydroxyethyl starch solution [Isoes
6%, Braun, Germany]), and buprenorphine (0.03mg/kg, intravenously, Buprex® 0.3mg injectable; Schering-Plough S.A., Madrid, Spain). A complete blood count (CBC) revealed a normocytic normochronic regenerative anemia, thrombocytopenia and marked neutrophilic and monocytic leukocytosis. Serum biochemical analysis showed increases in total bilirubin, alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, and phosphorus concentration, and decreases in albumin, glucose, and potassium levels. Coagulation profile showed prolongation of prothrombin time (PT) and activated partial thromboplastin time (APTT) (Tables 1and 2). Radiographic images indicated the presence of an enlarged liver, especially on the left side, and diffuse loss of serosal detail in the cranial and ventral abdomen. A large soft tissue opacity was evident in the left hemithorax, and the cranial mediastinum was enlarged (Fig. 2). Abdominal ultrasonography confirmed severe hepatomegaly affecting the left lateral liver lobe.left lobes. The hepatic parenchyma was heterogenous with multiple echogenic areas. Color Doppler evaluation showed decreased blood flow to the left lateral hepatic lobe (Fig. 3). There was a mild amount of anechoic peritoneal effusion and an increased echogenicity of the mesentery and omentum. Ultrasonographic findings were most consistent with hepatic mass or LLT. Fine needle aspiration (FNA) of the affected liver lobe revealed neutrophilic inflammation, and FNA of the thoracic mass was inconclusive. The owner declined an exploratory laparatomy or further diagnostic testing, and due to poor prognosis euthanasia was performed. Post-mortem findings included severe jaundice of all the mucous membranes, skin, and sclera. The liver was enlarged in size, with a torsed, dark colored left lateral liver lobe (Fig. 4). The remaining liver tissue was yellowish with a lobular
pattern (Fig. 5). A white soft mass, consistent with adipose tissue was observed in the cranial mediastinum. Histological examination of the excised liver lobe showed severe, diffuse hepatic coagulative necrosis with marked vascular congestion (Fig. 6) while the nontorsed liver tissue showed a diffuse cytoplasmatic vacuolization of the hepatocytes, and intrahepatic and intracanalicular cholestasis (Fig. 7). The cranial mediastinum was confirmed to be mature adipose tissue. Histopathology was consistent with left lateral LLT and concurrent diffuse hepatic lipidosis.
DISCUSSION The liver of the ferret is relatively large, with a 4.3% liver-weight/body-weight ratio, compared with 3.4% ratio in dogs. The ferret liver is divided into left and right lobes; each one is subdivided in lateral and medial lobules, and caudate and quadrate lobes. The left lateral is the largest liver lobe in the ferret and is attached to the diaphragm by the left triangular ligament.15 Liver lobe torsion is a rare condition based on an extensive literature search underreported in the ferret. Manifestations of this condition in other species may be acute or chronic, and range from non-specific clinical signs (e.g., anorexia, lethargy), to severe acute abdomen, collapse, and sudden death.1-5,7,10,12,14 The most common clinical signs in dogs and cats with LLT are abdominal pain, abdominal distention, lethargy, anorexia, vomiting, and diarrhea.1-4 The most common clinical signs in rabbits with LLT are abdominal pain, lethargy, anorexia, decreased fecal production, and crouched or hunched body position.9,11,12. Physical examination findings in most species are nonspecific, and include weakness, pyrexia, painful abdominal palpation, and
abdominal distension. Jaundice is not a common clinical condition associated with LLT in dogs and cats with LLT, but has been reported in rabbits.9 Despite the fact that the underlying cause of LLT is unknown in dogs and cats, it has been hypothesized that congenital absence of supporting ligaments or laxity secondary to trauma or dilation of other abdominal organs may be contributing factors.1,3,7 In dogs, gastric dilation-volvulus or gastric surgeries may increase the risk of LLT.2,9 Liver lobe torsion in dogs can also occur secondary to a variations in hepatic shape and size resulting from anatomic differences among individual liver lobes, or secondary to diseases that alter lobe architecture, such as neoplasia, infection, or parasitic infestation; or secondary to diaphragmatic hernia.7,10,11 Torsion of the left lateral lobe is most commonly reported in dogs and cats, and is attributed to its larger size, greater mobility, and anatomic separation from the other lobes.1,3,5 In contrast, torsion of the caudate liver lobe is most commonly reported in rabbits, theoretically due to small circular shape and narrow attachment at the hilus.11-14 A recent retrospective review in rabbits showed that the caudate lobe was affected in 62.5% of cases LLT.10,12 As in this case, the most common hematologic abnormalities in dogs and cats with LLT are anemia10-12, leukocytosis with mature neutrophilia1,2, and thrombocytopenia10,12. Potential causes of regenerative anemia include hemorrhage into the affected LL, erythrocyte fragmentation and peritoneal hemorrhagic effusion. Venous obstruction, passive congestion, increased hydrostatic pressure or coagulopathies can be responsible for the serosanguineous effusion associated with most LLT cases. The hepatic congestion, inflammation, and necrosis that appear after occlusion of hepatic
vessels during LLT, are possible explanations for the leukocytic neutrophilia diagnosed in this case.1,16 Common biochemical findings include moderate to markedly increased liver enzyme levels indicative of hepatocelular necrosis and enzyme leakage.2,7,12 Increased bilirrubin is not noted in dogs and cats1-5, but is a condition commonly described in horses7 and in some cases in rabbits9. Abdominal radiographs in most species often reveal a mass within the cranial abdomen and loss of serosal detail compatible with peritoneal effusion, as observed in this case. Ultrasonographic findings consistent with LLT include abnormally large hepatic lobe size with round lobar margins, a heterogeneous appearance of liver parenchyma, as a result of ischemia and necrosis, and peritoneal effusion. Color flow Doppler assessment of the hepatic vessels often reveal a decreased blood flow within the affected lobes, and support the diagnosis of LLT.2,7 Nevertheless, LLT can be difficult to diagnose with radiographic and abdominal ultrasound imaging alone, particularly in early disease stages, and computed tomography or exploratory laparatomy may be necessary to obtain a definitive diagnosis.10 Prompt diagnosis and surgical correction of LLT are recommended; however, signs are often non-specific, which can result in delayed treatment. Resection of the affected LL is the treatment of choice for LLT.5 Techniques to resolve LLT through surgical correction include ligation of the affected lobe with suture, stainless steel ligation clips (solely or in combination), stapling devices, and/or electro thermal bipolar vascular sealing devices.2,7,11 Repositioning of the torsed lobed into proper anatomic alignment during surgical manipulation is not recommended due to the possibility of bacterial toxin release and ischemic reperfusion injury.11 Intraoperative hemorrhage is a potentially life-threatening
complication.7 Despite treatment recommendations, some rabbits with LLT have survived only with supportive care measures (e.g., subcutaneous fluids, analgesic medication, antimicrobial therapy, supplemental feeding, prokinetic agents).10-13 Hepatectomy appears to have a good prognosis; however, in dogs, postoperative complications such as anemia, hemoperitoneum, arrhythmia, or an increasing hypoalbuminemic condition have been described.2,4 Histological examination and aerobic and anaerobic bacterial culture of excised LL tissue may be useful to help determine ideal postoperative treatment and prognosis.11 Histological changes associated with LLT include diffuse hepatocellular coagulative necrosis and acute or chronic inflammation.14 In the present case, severe hepatic lipidosis was identified and may have been associated with the severe jaundice. Marked accumulation of mediastinal and pericardial adipose tissue displaced and partially compressed the left cranial lung lobes. An underlying cause of the LLT was not identified in this case and there was no evidence of liver neoplasia, infection, or parasitism on post-mortem examination. In summary, LLT should be considered as a differential disease diagnosis in ferrets with abdominal pain, anorexia, lethargy, and jaundice.
REFERENCES 1. Massari F, Verganti S, Secchiero B, et al: Torsion of quadrate and right middle liver lobes and gallbladder in a German Shepherd dog. Aust Vet J 90:44-47, 2012 2. Schwartz SG, Mitchell SL, Keating JH, et al: Liver lobe torsion in dogs: 13 cases (1995-2004). J Am Vet Assoc 228:242-247, 2006
3. von Pfiel DJ, Jutkowith LA, Hauptman L: Left lateral and left middle liver lobe torsion in a Saint Bernard puppy. J Am Anim Hosp Assoc 42:381385, 2006 4. Swann HM, Brown DC: Hepatic lobe torsion in 3 dogs and a cat. Vet Surg 30:482-486, 2001 5. Haider G, Dokic Z, Petritsch B, et al: Left lateral liver lobe torsion in a cat with moderate pectus excavatum. J Feline Med Surg 25:1-3, 2015 6. Morin M, Sauvageau R, Phaneuf JB, et al: Torsion of abdominal organs in sows: a report of 36 cases. Can Vet J 25:440-442, 1984 7. Tennent-Brown BS, Mudge MC, Hardy J, et al: Liver lobe torsion in six horses. J Am Vet Med Assoc 241:615-620, 2012 8. Warns-Petit ES: Liver lobe torsion in an oriental small-clawed otter (Aonyx cinerea) .Vet Rec 148:212-213, 2001 9. Wenger S, Barrett EL, Pearson GR, et al: Liver lobe torsion in three adult rabbits. J Small Anim Pract 50:301-305, 2009 10. Graham L, Basseches L: Liver lobe torsion in pet rabbits: clinical consequences, diagnosis, and treatment. Vet Clin North Am Exot Anim Pract 17:195-202, 2014 11. Stanke NJ, Graham JE, Orcutt C.J, et al: Successful outcome of hepatectomy as treatment for liver lobe torsion in four domestic rabbits. J Am Vet Med Assoc 238:1176-1183, 2011 12. Graham JE, Orcutt JC, Casale SA, et al: Liver lobe torsion in rabbits: 16 cases (2007 to 2012). J Exot Pet Med 23:258-265, 2014
13. Taylor HR, Staff CD: Clinical techniques: Successful management of liver lobe torsion in a domestic rabbit (Oryctolagus cuniculus) by surgical lobectomy. J Exot Pet Med 16:175-178, 2007 14. Weisbroth SH: Torsion of the caudate lobe of the liver in the domestic rabbit (Oryctolagus). Vet Pathol 12:13-15, 1975 15. Evans H, Quoc NA: Anatomy of the ferret, in Fox JG, Marini RM (ed): Biology and Diseases of the Ferret (ed 3). Ames, IA, Wiley Blackwell. pp 47-49, 2014
Table 1. Hematological findings in a ferret with liver lobe torsion. Parameter Case Reference range * Hematocrit (%) 28 36-51 Hemoglobin (g/dl) 9.6 12-17.4 Red blood cells (x106/µl) 6.02 6.8-12.2 MCV (fl) 49.1 42.6-51 MCH (pg) 15.9 13.7-16 MCHC (g/dl) 32.4 30.3-34.9 Platelets (x103 µl) 90 297-910 Reticulocytes ( x/ µl) 118594 1-14 White blood cells ( x/ µl) 32340 2500-15400 Neutrophils ( x/ µl) 22314 300-12659 Lymphocytes (x/ µl) 5498 625-14630 Monocytes ( x/ µl) 4528 50-1263 Eosinophils ( x/ µl) 0 0-1386 Basophils ( x/ µl) 0 0-447 MCH, mean corpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume. * Quesenberry KE, Carpenter JW: Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. (ed 3). St. Louis, MO: Elsevier/Saunders, 2012
Table 2. Biochemical findings in a ferret with liver lobe torsion. Parameter Case Reference range* Gluc (mg/dL) 57 94-207 BUN (mg/dL) ˃130 10-45 Crea (mg/dL) 1.8 0.4-0.9 Phos (mg/dL) ˃16.1 4-9.1 Ca (mg/dL) 7.3 8-11.8 TP (g/dL) 5.3 5.1-7.8 Alb (g/dL) 2.2 2.6-3.8 Glob (g/dL) 3.1 1.8-3.1 ALT (IU/L) ˃1000 82-289 ALKP (IU/L 71 9-84 GGT (IU/L) 5 0.2-14 TBil (mg/dL) 9.3 0.1-1 CHOL 100 64-296 (mg/dL) Na (mmol/L) 161 140-170 K (mmol/L) ˂1.5 3.9-5.9 Cl (mmol/L) 141 108-119 Coagulation profile in a ferret with liver lobe torsion. Parameter Case Reference range PT (sec) 36 10.6-11.6 APTT (sec) 226 18.6-22.1 Alb, albumin; ALKP, alkaline phosphatise; ALT, alanine aminotransferase; BUN, blood urea nitrogen; Ca, calcium; CHOL, cholesterol; Cl, chloride; Crea, creatinine; GGT, gamma-glutamyl transpeptidase; Glob, globulins; Glu, glucose; K, potassium; Na, sodium; Phos, phosphorus; PT, prothrombin time; APTT, activated partial thromboplastin time; TBil, total bilirubin; TP, total protein. * Quesenberry KE, Carpenter JW: Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. (ed 3). St. Louis, MO: Elsevier/Saunders, 2012
FIGURE LEGENDS Figure 1. Gross appearance of a ferret with liver lobe torsion. Note severe jaundice of all mucous membranes, skin, and sclera. Figure 2. Right and ventrodorsal radiographs of the thorax and abdomen of a ferret with liver lobe torsion. A: Right lateral view. Increase radiopacity in cranial abdomen (arrows), and diffuse loss of serosal detail. B: Ventrodorsal view. Hepatomegaly, especially in the left lobes (arrows), and cranial mediastinum enlargement (head arrows). Figure 3. Abdominal ultrasound of a ferret with liver lobe torsion. Liver ultrasound revealed left lateral liver lobe torsion (arrows). The hepatic parenchyma was heterogeneous with multiple echogenic areas. Figure 4. Gross examination at necropsy of a ferret with liver lobe torsion. Note severe jaundice and an enlarged, dark and torsed left lateral liver lobe in the abdominal cavity, and a white soft tissue mass in the cranial mediastinum. Figure 5. Gross examination of the liver of a ferret with liver lobe torsion. Note left lateral liver lobe torsion and marked pale discoloration of the remaining hepatic parenchyma (hepatic lipidosis). Figure 6. Microscopic examination of the liver of a ferret with liver lobe torsion. (A) Microscopic examination showing severe distension and congestion of the hepatic sinusoids. (B) Microscopic examination at higher magnification exhibiting marked atrophy of the hepatic cords. H&E stain. Figure 7. Microscopic examination of the liver of a ferret with liver lobe torsion. (A) Microscopic examination of the remaining hepatic parenchyma showing diffuse hepatic lipidosis. (B) Microscopic examination at higher magnification of
the hepatocytes with intracytoplasmic lipid vacuoles, and intrahepatic and intracanaluclar cholestasis (arrows). H&E stain.
PII: DOI: Reference:
S1557-5063(16)30081-7 http://dx.doi.org/10.1053/j.jepm.2016.06.008 JEPM684
To appear in: Journal of Exotic Pet Medicine Cite this article as: Laura Vilalta, Yvonne Espada, Natalia Majó and Jaime Martorell, LIVER LOBE TORSION IN A DOMESTIC FERRET ( MUSTELA PUTORIUS FURO) , Journal of Exotic Pet Medicine, http://dx.doi.org/10.1053/j.jepm.2016.06.008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
AEMV Forum
Liver Lobe Torsion in a Domestic Ferret (Mustela Putorius Furo) Laura Vilalta, DVM, Yvonne Espada, DVM, PhD, Natalia Majó, DVM, PhD, Dip. ECVP, Jaime Martorell, DVM, PhD, Dip.ECZM (Small Mammal) From the Fundació Hospital Clínic Veterinari (Vilalta, Espanda, Martorell), Departament de Medicina i Cirurgia Animal (Espada, Moartorell), Departament de Medicina i Sanitat Animals (Majó), Facultat de Veterinària, Universitat Autònoma de Barcelona, Barcelona, Spain Address correspondence to Laura Vilalta Solé, DVM, Fundació Hospital Clínic Veterinari, Facultat de Veterinaria, Universitat Autònoma de Barcelona, 08193 Bellaterra (Cedanyola del Valles), Barcelona, Spain. Email address: [email protected]. Tel: 004407784288071
Abstract A 6-year-old female domestic ferret presented with a 3-day history of lethargy and anorexia. Clinical examination revealed severe jaundice, painful abdominal palpation and a mass in the left cranial abdomen. Hematologic diagnostic tests of the patient revealed a regenerative anemia, severe neutrophilic and monocytic leukoctytosis, increased alanine aminotransferase (ALT) and total bilirubin, and decreased albumin and glucose concentration. Liver lobe torsion was identified through radiographic and ultrasonographic imaging. Post-mortem examination confirmed a left lateral liver lobe torsion, and a generalized hepatic lipidosis. Liver lobe torsion is a rare condition with few reported cases in veterinary medicine. Liver lobe torsion should be considered as a differential disease diagnosis in ferrets presenting with acute abdomen.
Key words: Ferret; liver lobe torsion; acute abdomen; jaundice; abdominal mass
Liver lobe torsion (LLT) is a rare condition in veterinary medicine reported in dogs1-4, cats4,5, pigs6, horses7, otters8, and rabbits9-14. Sporadic reports exist describing LLT in humans, most of which involve the accessory liver lobes (Reidels’s lobe).7 Liver lobe torsionLT leads to occlusion of the venous return prior to occlusion of the arterial supply, which causes acute congestion within the affected liver lobe (LL), and subsequent necrosis, effusion, hemoabdomen, and shock.10,11 Clinical signs are often non-specific, and can include lethargy, abdominal distension, anorexia, and vomiting. If untreated, LLT may result in acute collapse and sudden death.1 This case report describes the clinical disease signs, and laboratory, radiologic and ultrasonographic diagnostic results associated with LLT in a ferret.
CASE HISTORY A 6-year-old 850 gram spayed female domestic albino ferret was evaluated for a 3-day history of lethargy and anorexia. On physical examination, the ferret was depressed, mildly dehydrated, and dyspneic, and mucous membranes appeared jaundiced (Fig. 1). Auscultation revealed decreased lung sounds of left hemi-thorax. The abdomen was tense and painful, and a mass was palpated in the cranial left abdomen. Initial treatment included oxygen, shock fluid therapy (intravenous bolus of 10 ml/kg crystalloid solution [LactatoRingerVet,Braun, Spain], and 3 ml/kg of 6% Hydroxyethyl starch solution [Isoes
6%, Braun, Germany]), and buprenorphine (0.03mg/kg, intravenously, Buprex® 0.3mg injectable; Schering-Plough S.A., Madrid, Spain). A complete blood count (CBC) revealed a normocytic normochronic regenerative anemia, thrombocytopenia and marked neutrophilic and monocytic leukocytosis. Serum biochemical analysis showed increases in total bilirubin, alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, and phosphorus concentration, and decreases in albumin, glucose, and potassium levels. Coagulation profile showed prolongation of prothrombin time (PT) and activated partial thromboplastin time (APTT) (Tables 1and 2). Radiographic images indicated the presence of an enlarged liver, especially on the left side, and diffuse loss of serosal detail in the cranial and ventral abdomen. A large soft tissue opacity was evident in the left hemithorax, and the cranial mediastinum was enlarged (Fig. 2). Abdominal ultrasonography confirmed severe hepatomegaly affecting the left lateral liver lobe.left lobes. The hepatic parenchyma was heterogenous with multiple echogenic areas. Color Doppler evaluation showed decreased blood flow to the left lateral hepatic lobe (Fig. 3). There was a mild amount of anechoic peritoneal effusion and an increased echogenicity of the mesentery and omentum. Ultrasonographic findings were most consistent with hepatic mass or LLT. Fine needle aspiration (FNA) of the affected liver lobe revealed neutrophilic inflammation, and FNA of the thoracic mass was inconclusive. The owner declined an exploratory laparatomy or further diagnostic testing, and due to poor prognosis euthanasia was performed. Post-mortem findings included severe jaundice of all the mucous membranes, skin, and sclera. The liver was enlarged in size, with a torsed, dark colored left lateral liver lobe (Fig. 4). The remaining liver tissue was yellowish with a lobular
pattern (Fig. 5). A white soft mass, consistent with adipose tissue was observed in the cranial mediastinum. Histological examination of the excised liver lobe showed severe, diffuse hepatic coagulative necrosis with marked vascular congestion (Fig. 6) while the nontorsed liver tissue showed a diffuse cytoplasmatic vacuolization of the hepatocytes, and intrahepatic and intracanalicular cholestasis (Fig. 7). The cranial mediastinum was confirmed to be mature adipose tissue. Histopathology was consistent with left lateral LLT and concurrent diffuse hepatic lipidosis.
DISCUSSION The liver of the ferret is relatively large, with a 4.3% liver-weight/body-weight ratio, compared with 3.4% ratio in dogs. The ferret liver is divided into left and right lobes; each one is subdivided in lateral and medial lobules, and caudate and quadrate lobes. The left lateral is the largest liver lobe in the ferret and is attached to the diaphragm by the left triangular ligament.15 Liver lobe torsion is a rare condition based on an extensive literature search underreported in the ferret. Manifestations of this condition in other species may be acute or chronic, and range from non-specific clinical signs (e.g., anorexia, lethargy), to severe acute abdomen, collapse, and sudden death.1-5,7,10,12,14 The most common clinical signs in dogs and cats with LLT are abdominal pain, abdominal distention, lethargy, anorexia, vomiting, and diarrhea.1-4 The most common clinical signs in rabbits with LLT are abdominal pain, lethargy, anorexia, decreased fecal production, and crouched or hunched body position.9,11,12. Physical examination findings in most species are nonspecific, and include weakness, pyrexia, painful abdominal palpation, and
abdominal distension. Jaundice is not a common clinical condition associated with LLT in dogs and cats with LLT, but has been reported in rabbits.9 Despite the fact that the underlying cause of LLT is unknown in dogs and cats, it has been hypothesized that congenital absence of supporting ligaments or laxity secondary to trauma or dilation of other abdominal organs may be contributing factors.1,3,7 In dogs, gastric dilation-volvulus or gastric surgeries may increase the risk of LLT.2,9 Liver lobe torsion in dogs can also occur secondary to a variations in hepatic shape and size resulting from anatomic differences among individual liver lobes, or secondary to diseases that alter lobe architecture, such as neoplasia, infection, or parasitic infestation; or secondary to diaphragmatic hernia.7,10,11 Torsion of the left lateral lobe is most commonly reported in dogs and cats, and is attributed to its larger size, greater mobility, and anatomic separation from the other lobes.1,3,5 In contrast, torsion of the caudate liver lobe is most commonly reported in rabbits, theoretically due to small circular shape and narrow attachment at the hilus.11-14 A recent retrospective review in rabbits showed that the caudate lobe was affected in 62.5% of cases LLT.10,12 As in this case, the most common hematologic abnormalities in dogs and cats with LLT are anemia10-12, leukocytosis with mature neutrophilia1,2, and thrombocytopenia10,12. Potential causes of regenerative anemia include hemorrhage into the affected LL, erythrocyte fragmentation and peritoneal hemorrhagic effusion. Venous obstruction, passive congestion, increased hydrostatic pressure or coagulopathies can be responsible for the serosanguineous effusion associated with most LLT cases. The hepatic congestion, inflammation, and necrosis that appear after occlusion of hepatic
vessels during LLT, are possible explanations for the leukocytic neutrophilia diagnosed in this case.1,16 Common biochemical findings include moderate to markedly increased liver enzyme levels indicative of hepatocelular necrosis and enzyme leakage.2,7,12 Increased bilirrubin is not noted in dogs and cats1-5, but is a condition commonly described in horses7 and in some cases in rabbits9. Abdominal radiographs in most species often reveal a mass within the cranial abdomen and loss of serosal detail compatible with peritoneal effusion, as observed in this case. Ultrasonographic findings consistent with LLT include abnormally large hepatic lobe size with round lobar margins, a heterogeneous appearance of liver parenchyma, as a result of ischemia and necrosis, and peritoneal effusion. Color flow Doppler assessment of the hepatic vessels often reveal a decreased blood flow within the affected lobes, and support the diagnosis of LLT.2,7 Nevertheless, LLT can be difficult to diagnose with radiographic and abdominal ultrasound imaging alone, particularly in early disease stages, and computed tomography or exploratory laparatomy may be necessary to obtain a definitive diagnosis.10 Prompt diagnosis and surgical correction of LLT are recommended; however, signs are often non-specific, which can result in delayed treatment. Resection of the affected LL is the treatment of choice for LLT.5 Techniques to resolve LLT through surgical correction include ligation of the affected lobe with suture, stainless steel ligation clips (solely or in combination), stapling devices, and/or electro thermal bipolar vascular sealing devices.2,7,11 Repositioning of the torsed lobed into proper anatomic alignment during surgical manipulation is not recommended due to the possibility of bacterial toxin release and ischemic reperfusion injury.11 Intraoperative hemorrhage is a potentially life-threatening
complication.7 Despite treatment recommendations, some rabbits with LLT have survived only with supportive care measures (e.g., subcutaneous fluids, analgesic medication, antimicrobial therapy, supplemental feeding, prokinetic agents).10-13 Hepatectomy appears to have a good prognosis; however, in dogs, postoperative complications such as anemia, hemoperitoneum, arrhythmia, or an increasing hypoalbuminemic condition have been described.2,4 Histological examination and aerobic and anaerobic bacterial culture of excised LL tissue may be useful to help determine ideal postoperative treatment and prognosis.11 Histological changes associated with LLT include diffuse hepatocellular coagulative necrosis and acute or chronic inflammation.14 In the present case, severe hepatic lipidosis was identified and may have been associated with the severe jaundice. Marked accumulation of mediastinal and pericardial adipose tissue displaced and partially compressed the left cranial lung lobes. An underlying cause of the LLT was not identified in this case and there was no evidence of liver neoplasia, infection, or parasitism on post-mortem examination. In summary, LLT should be considered as a differential disease diagnosis in ferrets with abdominal pain, anorexia, lethargy, and jaundice.
REFERENCES 1. Massari F, Verganti S, Secchiero B, et al: Torsion of quadrate and right middle liver lobes and gallbladder in a German Shepherd dog. Aust Vet J 90:44-47, 2012 2. Schwartz SG, Mitchell SL, Keating JH, et al: Liver lobe torsion in dogs: 13 cases (1995-2004). J Am Vet Assoc 228:242-247, 2006
3. von Pfiel DJ, Jutkowith LA, Hauptman L: Left lateral and left middle liver lobe torsion in a Saint Bernard puppy. J Am Anim Hosp Assoc 42:381385, 2006 4. Swann HM, Brown DC: Hepatic lobe torsion in 3 dogs and a cat. Vet Surg 30:482-486, 2001 5. Haider G, Dokic Z, Petritsch B, et al: Left lateral liver lobe torsion in a cat with moderate pectus excavatum. J Feline Med Surg 25:1-3, 2015 6. Morin M, Sauvageau R, Phaneuf JB, et al: Torsion of abdominal organs in sows: a report of 36 cases. Can Vet J 25:440-442, 1984 7. Tennent-Brown BS, Mudge MC, Hardy J, et al: Liver lobe torsion in six horses. J Am Vet Med Assoc 241:615-620, 2012 8. Warns-Petit ES: Liver lobe torsion in an oriental small-clawed otter (Aonyx cinerea) .Vet Rec 148:212-213, 2001 9. Wenger S, Barrett EL, Pearson GR, et al: Liver lobe torsion in three adult rabbits. J Small Anim Pract 50:301-305, 2009 10. Graham L, Basseches L: Liver lobe torsion in pet rabbits: clinical consequences, diagnosis, and treatment. Vet Clin North Am Exot Anim Pract 17:195-202, 2014 11. Stanke NJ, Graham JE, Orcutt C.J, et al: Successful outcome of hepatectomy as treatment for liver lobe torsion in four domestic rabbits. J Am Vet Med Assoc 238:1176-1183, 2011 12. Graham JE, Orcutt JC, Casale SA, et al: Liver lobe torsion in rabbits: 16 cases (2007 to 2012). J Exot Pet Med 23:258-265, 2014
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Table 1. Hematological findings in a ferret with liver lobe torsion. Parameter Case Reference range * Hematocrit (%) 28 36-51 Hemoglobin (g/dl) 9.6 12-17.4 Red blood cells (x106/µl) 6.02 6.8-12.2 MCV (fl) 49.1 42.6-51 MCH (pg) 15.9 13.7-16 MCHC (g/dl) 32.4 30.3-34.9 Platelets (x103 µl) 90 297-910 Reticulocytes ( x/ µl) 118594 1-14 White blood cells ( x/ µl) 32340 2500-15400 Neutrophils ( x/ µl) 22314 300-12659 Lymphocytes (x/ µl) 5498 625-14630 Monocytes ( x/ µl) 4528 50-1263 Eosinophils ( x/ µl) 0 0-1386 Basophils ( x/ µl) 0 0-447 MCH, mean corpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume. * Quesenberry KE, Carpenter JW: Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. (ed 3). St. Louis, MO: Elsevier/Saunders, 2012
Table 2. Biochemical findings in a ferret with liver lobe torsion. Parameter Case Reference range* Gluc (mg/dL) 57 94-207 BUN (mg/dL) ˃130 10-45 Crea (mg/dL) 1.8 0.4-0.9 Phos (mg/dL) ˃16.1 4-9.1 Ca (mg/dL) 7.3 8-11.8 TP (g/dL) 5.3 5.1-7.8 Alb (g/dL) 2.2 2.6-3.8 Glob (g/dL) 3.1 1.8-3.1 ALT (IU/L) ˃1000 82-289 ALKP (IU/L 71 9-84 GGT (IU/L) 5 0.2-14 TBil (mg/dL) 9.3 0.1-1 CHOL 100 64-296 (mg/dL) Na (mmol/L) 161 140-170 K (mmol/L) ˂1.5 3.9-5.9 Cl (mmol/L) 141 108-119 Coagulation profile in a ferret with liver lobe torsion. Parameter Case Reference range PT (sec) 36 10.6-11.6 APTT (sec) 226 18.6-22.1 Alb, albumin; ALKP, alkaline phosphatise; ALT, alanine aminotransferase; BUN, blood urea nitrogen; Ca, calcium; CHOL, cholesterol; Cl, chloride; Crea, creatinine; GGT, gamma-glutamyl transpeptidase; Glob, globulins; Glu, glucose; K, potassium; Na, sodium; Phos, phosphorus; PT, prothrombin time; APTT, activated partial thromboplastin time; TBil, total bilirubin; TP, total protein. * Quesenberry KE, Carpenter JW: Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. (ed 3). St. Louis, MO: Elsevier/Saunders, 2012
FIGURE LEGENDS Figure 1. Gross appearance of a ferret with liver lobe torsion. Note severe jaundice of all mucous membranes, skin, and sclera. Figure 2. Right and ventrodorsal radiographs of the thorax and abdomen of a ferret with liver lobe torsion. A: Right lateral view. Increase radiopacity in cranial abdomen (arrows), and diffuse loss of serosal detail. B: Ventrodorsal view. Hepatomegaly, especially in the left lobes (arrows), and cranial mediastinum enlargement (head arrows). Figure 3. Abdominal ultrasound of a ferret with liver lobe torsion. Liver ultrasound revealed left lateral liver lobe torsion (arrows). The hepatic parenchyma was heterogeneous with multiple echogenic areas. Figure 4. Gross examination at necropsy of a ferret with liver lobe torsion. Note severe jaundice and an enlarged, dark and torsed left lateral liver lobe in the abdominal cavity, and a white soft tissue mass in the cranial mediastinum. Figure 5. Gross examination of the liver of a ferret with liver lobe torsion. Note left lateral liver lobe torsion and marked pale discoloration of the remaining hepatic parenchyma (hepatic lipidosis). Figure 6. Microscopic examination of the liver of a ferret with liver lobe torsion. (A) Microscopic examination showing severe distension and congestion of the hepatic sinusoids. (B) Microscopic examination at higher magnification exhibiting marked atrophy of the hepatic cords. H&E stain. Figure 7. Microscopic examination of the liver of a ferret with liver lobe torsion. (A) Microscopic examination of the remaining hepatic parenchyma showing diffuse hepatic lipidosis. (B) Microscopic examination at higher magnification of
the hepatocytes with intracytoplasmic lipid vacuoles, and intrahepatic and intracanaluclar cholestasis (arrows). H&E stain.