Left Lateral and Left Middle Liver Lobe Torsion in a Saint Bernard Puppy

Introduction

Hepatic lobe torsion is a rare condition that has been reported in dogs, cats, pigs, rabbits, horses, and humans.^1–17 Signs associated with liver lobe torsion are variable and may include abdominal pain, anemia, anorexia, abdominal effusion, and fever.^1–8 Different etiologies for this condition have been described or suggested; they include trauma, stretching or aplasia of the hepatic ligaments, distinct lobulation of the liver, entrapment of the liver by the hepatogastric ligament, torsion secondary to gastric dilatation volvulus or other gastric surgeries, and hepatic neoplasia.^1–7,18 In one review of liver lobe torsion in the dog, the left lateral lobe was most commonly affected (48%, 11 cases), followed by the caudate lobe (22%, five cases), the right lateral lobe (17%, four cases), the right medial lobe (4%, one case), and the entire liver (4%, one case).⁷ Double liver lobe torsion is an extremely rare condition and was reported in only one case from 1959.⁶ In that report, torsion of the left lateral lobe and papillary process of the caudate liver lobe was described in a puppy, secondary to congenital aplasia of the left triangular ligament.⁶

The purpose of this report is to describe torsion of both the left lateral and left medial lobes in a young dog. No underlying cause for these abnormalities could be determined.

Case Report

A 5-month-old, 36-kg, male Saint Bernard was referred for acute weakness, collapse, and abdominal discomfort. The dog had experienced lethargy, inappetence, and soft stools for 2 days prior to examination and had vomited twice in the 24 hours prior to referral. Initial diagnostic tests performed by the referring veterinarian included a fecal flotation and an in-house parvovirus test, both of which were negative, and abdominal radiographs that showed loss of serosal detail. A complete blood count (CBC) revealed marked anemia, leukocytosis, and thrombocytopenia [see Table]. A serum biochemical panel was unremarkable except for a mildly elevated blood urea nitrogen (BUN) [see Table].

Physical examination findings at the time of presentation included lethargy, pale mucous membranes, prolonged capillary refill time (3 seconds), moderate dehydration, tachypnea (96 breaths per minute), tachycardia (200 beats per minute), weak pulse quality, fever (39.6°C; 103.3°F), and a distended, painful abdomen. A fluid wave was present on abdominal palpation, and a firm structure could be palpated in the cranial abdomen.

Packed cell volume (PCV) and total solids on admission were 14% and 5.1 g/dL, respectively (normal 43% to 59% and 5.5 to 7.4 g/dL, respectively). A venous blood gas analysis revealed respiratory alkalosis [see Table]. Abdominocentesis yielded a nonclotting, sanguinous fluid with a PCV and total solids of 21% and 5 g/dL, respectively. Cytological examination showed large numbers of erythrocytes, occasional nondegenerate neutrophils, and occasional macrophages, consistent with hemorrhagic effusion. Initial treatment included the intravenous (IV) administration of lactated Ringer’s solution^a (90 mL/kg) and one unit (350 mL) of packed red blood cells (RBCs).

A CBC revealed normocytic, normochromic, nonregenerative anemia; thrombocytopenia; leukocytosis; neutrophilia; and lymphopenia [see Table]. Elevations in BUN, alkaline phosphatase, total bilirubin, and creatine kinase, as well as hypoproteinemia and hypoalbuminemia, were detected on a biochemical panel. Mild elevations in calcium and phosphorus were considered normal for a puppy [see Table]. A urinalysis was unremarkable except for isosthenuria (specific gravity 1.009). A coagulation profile revealed prolongation of prothrombin time and activated partial thromboplastin time, decreased fibrinogen, and positive d-dimers consistent with disseminated intravascular coagulation (DIC) [see Table]. The dog was blood typed as dog erythrocyte antigen 1.1 positive.

Abdominal ultrasonography revealed a moderate amount of hypoechogenic peritoneal effusion. A large, hypoechoic mass was identified on the left lateral aspect of the midabdomen. There were hyperechoic parallel lines within the mass [Figure 1]. No evidence of blood flow was seen within the mass on Doppler examination. The lateral aspect of the left lateral liver lobe was hypoechoic, with hyperechoic speckles scattered throughout the stroma [Figure 2], and it lacked blood flow on Doppler examination. These findings were interpreted as splenic torsion and possible thrombosis of a portion of the left lateral liver lobe.

An exploratory celiotomy was performed for diagnostic and therapeutic purposes. Prior to surgery, the dog received one unit of fresh-frozen plasma (275 mL) over a 2-hour period. Anesthesia was induced using a 50:50 mixture of diazepam^b (5 mg/mL) and ketamine^c (100 mg/mL) at a dose of 0.1 mL/kg IV to effect. Anesthesia was maintained with isoflurane^d (1.5% to 2%) in oxygen (0.4 L per minute). Lactated Ringer’s solution^a was also given at 20 mL/kg per hour IV, and oxymorphone^e (0.1 mg/kg IV) was administered at the beginning of surgery. A standard ventral midline approach to the abdomen was made, and 2.5 L of serosanguinous effusion was suctioned from the abdominal cavity. Both the left lateral and left middle liver lobes were torsed approximately 180° around their pedicles [Figure 3]. Both lobes were dark red to black in color [Figure 4]. They were easily movable, and there was no gross evidence of infection or neoplasia. Without untwisting the lobes, resection was performed using stapling equipment.^f No bleeding occurred at the resection site after the lobes were removed. A thorough abdominal exploration revealed no other abnormalities. The abdominal cavity was flushed with 4 L of warm, sterile saline solution. The liver lobectomy sites were again checked for bleeding, and the abdomen was closed in a routine manner. Packed cell volume and total protein immediately after surgery were 18% and 5.0 g/dL, respectively.

Postoperative treatment consisted of hydromorphone^g (0.1 mg/kg IV q 4 hours), midazolam^h (0.2 mg/kg IV q 4 hours as needed), a second unit of fresh-frozen plasma, a second unit of packed RBCs, and lactated Ringer’s solution^a supplemented with 20 mEq/L potassium chloride.ⁱ Indirect blood pressure monitoring was performed every 4 hours using a Doppler flow probe^j for 12 hours after surgery, and pressure remained between 100 and 120 mm Hg. A second coagulation profile, taken 1 day after surgery, showed mild improvement in the dog’s coagulation status [see Table]. The dog improved clinically and was discharged 44 hours after surgery, with a PCV of 25% and a total serum protein of 5.4 g/dL. Telephone contact with both the owner and referring veterinarian 2 months after surgery revealed that the puppy had completely recovered and was healthy.

Discussion

Clinical signs associated with hepatic torsion are variable and may be consistent with shock.^1–5,7,8,18 The dog in this report presented with signs consistent with hypovolemic shock. Radiographs of the abdomen may show a mass-effect in the cranial abdomen and loss of serosal detail, as seen in this case. Pneumoperitoneum or a gas-filled mass in the cranial abdomen may also be seen as a result of hepatic abscessation.^1,4 Ultrasonographic examination of liver lobe torsions may reveal a mass of mixed echogenicity as a result of ischemia and necrosis, and the findings in this case were similar.¹⁸ As in this report, it has been found in previous cases that it can be difficult to diagnose hepatic lobe torsion with diagnostic imaging alone.^4,18

In the dog of this study, liver lobe torsion was initially not high on the list of differential diagnoses, as the condition is not commonly reported in young dogs. The preliminary diagnosis of splenic torsion was made from the sonographic appearance of the mass on the left side of the abdomen and the inability to identify a normal spleen. A final diagnosis of liver lobe torsion was reached only at the time of surgery, which was consistent with previous reports where diagnosis was made only at surgery or necropsy.^{1–5,7,8,10–12,15,18}

Computed tomography and magnetic resonance imaging are noninvasive options that could have been considered to better visualize the lesion. However, as emergency surgery was dictated by the dog’s clinical status, these techniques were not explored. Rapid surgical intervention is generally recommended in the treatment of liver lobe torsion in order to prevent massive hemorrhage into the abdominal cavity, DIC, and possible bacterial hepatitis leading to peritonitis.^2–4 The dog in this case was diagnosed with DIC, and treatment for DIC principally includes elimination of the inciting cause, restoration of effective circulating volume, and possibly administration of fresh-frozen plasma and/or heparin. In the dog of this report, it was felt that the risk of bleeding outweighed the possible benefits of heparinization, so DIC was addressed through restoration of effective circulating volume, removal of the inciting cause, and plasma transfusions. A coagulation profile, taken 1 day after surgery, showed improvement in coagulation parameters. A second platelet count was not taken postoperatively because of the improvement in the clinical signs and the financial constraints of the owner.

It is recommended that resected liver lobes be submitted for histopathological examination to rule out underlying conditions.⁷ In the dog of this report, the resected lobes were not submitted for histopathological examination because of financial constraints. Neoplasia was considered to be an unlikely explanation for the liver lobe torsion in this 5-month-old puppy, as there was no gross evidence of neoplasia in any liver lobe. The histopathological findings most commonly reported in dogs with liver lobe torsion include necrosis, hepatic atrophy, and intense accumulations of neutrophils in the affected tissue.⁷

Conclusion

Torsion of the left lateral and middle liver lobes was found in a 5-month-old, male Saint Bernard puppy. Clinical signs associated with the liver lobe torsion included lethargy, inappetence, abdominal pain, vomiting, and soft stools. Hypovolemic shock, hemoabdomen, an abdominal mass, and signs of DIC were diagnosed. Immediate stabilization, resection of the affected liver lobes, and adequate postoperative care provided a successful outcome. Although liver lobe torsion has been reported primarily in mature dogs, this report illustrates that regardless of age, torsion of one or more liver lobes should be considered as a differential diagnosis in young dogs presenting with abdominal pain, hemoabdomen, and signs of DIC.