Spontaneous left medial liver lobe torsion and left lateral lobe infarction in a rottweiler

Abstract

The abdominal ultrasonogram of a dog admitted for acute onset of collapse revealed an abnormally displaced left medial liver lobe with no blood flow. Surgical and histological findings confirmed the ultrasonographic diagnosis of left liver lobe torsion. Ultrasonographic findings were useful and probably sufficient for a correct diagnosis.

A5-year-old, 37.1 kg, neutered male, rottweiler was presented to Canada West Veterinary Specialists and Critical Care Hospital (CWVS & CCH) for further evaluation after the acute onset of collapse, pale mucous membranes, vomiting, and lethargy. Prior to referral, the dog had vomited and been listless for 24 h. Referral radiographs showed a small heart, indicating hypovolemia. Poor abdominal detail and dorsal displacement of the mildly distended, partially gas-filled, stomach suggested a ventral abdominal mass effect and peritoneal effusion.

Upon presentation, the dog was quiet, but distressed, with an increased respiratory effort. The rectal temperature was 38.6°C, heart rate 140 beats/min (reference range: 70 to 120 beats/min, and indirect systolic blood pressure was 95 mmHg (reference range: 110 to 150 mmHg). The dog’s pulses were weak, but no pulse deficits were present. The hematocrit was 34 L/L (reference range: 39 to 56 L/L). An elevated white blood cell count 35.5 × 10⁹ cells/L (reference range: 4.0 to 15.0 × 10⁹ cells/L), characterized by neutrophilia of 31.94 × 10⁹ cells/L (reference range: 2.8 to 10.56 × 10⁹ cells/L) with slight toxic change, was present. A lymphopenia of 0.36 × 10⁹ cells/L (reference range: 0.96 to 4.8 × 10⁹ cells/L), a monocytosis of 3.2 × 10⁹ cells/L (reference range: 0.00 to 0.980 × 10⁹ cells/L), and a reticulocyte count less than 1% was found. The leukogram changes were interpretated as indicating severe acute inflammation, with stress. There was also a nonregenerative anemia from either acute blood loss or chronic disease. The major biochemical changes included elevated liver enzymes; alkaline phosphatase 427 U/L (reference range: 4 to 113 U/L), alanine aminotransferase 4121 U/L (reference range: 0 to 113 U/L), amylase 2466 U/L (reference range: 206 to 1250 U/L), lipase 1441.6 U/L (reference range: 40 to 560 U/L), indicating cholestasis, hepatocellular injury, and secondary pancreatic disease. The total bilirubin was not available because the sample had hemolyzed. The urinalysis (free catch sample) showed bilirubinuria, 3+; urine specific gravity, 1.018; bacterial rods; and proteinuria of 1 g/L. There was also elevation of blood urea nitrogen 14.3 mmol/L (reference range: 2.5 to 9.2 mmol/L) and creatinine 166.1 μmol/L (reference range: 68 to 141 μmol/L).

Two grossly abnormal liver lobes were apparent ultrasonographically (Figure 1). The left medial liver lobe was found to be abnormally displaced, with caudal malangulation. It was swollen and hypoechoic (dark), especially towards its distal margins where the diameter was over 5 cm on cross-section. Complete thrombosis through the hepatic and portal veins was clearly indicated by marked distension of the hepatic veins with uniform hyperechoic tissue. There was no blood flow within the lobe, as determined by Doppler examination. The left lateral lobe showed marked swelling and markedly decreased to completely absent blood flow in areas. The lobar images were interpreted as a vascular accident due to torsion of the left lateral and left medial liver lobes. There was a small amount of echogenic peritoneal effusion, typical of hemorrhage.

Figure 1.

Caudal malangulation of the left medial liver lobe, with severe vascular thrombosis and diffuse hypoechoic swelling of parenchyma.

The venous blood gas analysis revealed the following: pH 7.42 (reference range: 7.33 to 7.38), pCO₂ 32.6 mmHg (reference range: 38 to 46 mmHg), HCO₃ 21.5 mmol/L (reference range: 16 to 24 mmol/L), and base excess −3 mEq/L (reference range: −4 to +4 mEq/L), which indicated a mild respiratory alkalosis, likely due to tachypnea from pain. A coagulation profile revealed a normal prothrombin time of 16 s (reference range: 12 to 17 s) and an activated partial thromboplastin time of 106 s (reference range: 71 to 102 s). The patient was blood typed as dog erythrocyte antigen 1.1 negative. Donor’s blood was cross-matched with the recipient’s packed red blood cells and found to be compatible. Prior to anesthesia and surgery, the dog received 2 boluses of isotonic balanced electrolyte solution (Normosol-R; Abbott Laboratories, North Chicago, Illinois, USA), 22 mL/kg BW, IV, and 5 mL/kg BW, IV, which helped to reduce his heart rate to 110 beats/min, and indirect systolic blood pressure to 105 mmHg, and to increase the amplitude of the pulse. The patient was premedicated with hydromorphone (Hydromorphone hydrochloride 10 mg/mL; Sandoz Canada, Boucherville, Quebec), 0.05 mg/kg BW, IV. Anesthesia was induced with propofol (Propofol injectable 10 mg/mL; Novapharm, Toronto, Ontario), 2.5 mg/kg BW, IV, and diazepam (Diazepam injection USP; Sandoz Canada), 0.2 mg/kg BW, IV, and maintained with 1.5% to 2% isoflurane (Isoflo, Abbott Laboratories) in oxygen at 1 L/min.

A standard ventral midline incision from the xiphoid process to the pubis was made and 600 mL of bloody peritoneal effusion (packed cell volume 0.2 L/L) was removed. The left medial liver lobe, which was torsed approximately 180 degrees in a clockwise direction (Figure 2), had a firm consistency and appeared dark red with areas of edema. The left lateral liver lobe was similar in color to the medial lobe and had multiple areas that were very dark blue-black, presumed to be infarctions. Both the left lateral and the medial liver lobes were easily movable and the spleen was small. The left lateral liver lobe was resected first, using a suturing device (Autosuture TA 60 3.5 mm disposable stapler; Tyco Healthcare, Norwalk, Connecticut, USA). This allowed good access to the twisted left medial liver lobe. The left medial liver lobe was resected in a similar fashion. The peritoneal and abdominal cavities were closed routinely, using #1 polydioxanone (PDS II, Ethicon; Somerville, New Jersey, USA), 2-0 polydioxanone (PDS II, Ethicon), and 3-0 nylon (Ethilon, Ethicon). Intraoperatively, the dog experienced a period of hypotension that responded to the administration of pentastarch (Pentaspan; DuPont, Mississauga, Ontario), 0.8 mL/kg BW, IV, over 1 h. Balanced electrolyte solution (Normosol-R) was administrated at 10 mL/kg/h, IV; this was subsequently increased to 22 mL/kg/h. One unit of packed red blood cells was given intraoperatively. The patient developed persistent ventricular tachycardia with a heart rate of 150 beats/min, indirect systolic blood pressure of 95 mmHg, and pulse deficits at 5 h following surgery and was treated with 2 boluses of lidocaine (Lidocaine HCl 2%; Vetoquinol Canada, Lavaltrie, Quebec), 2 mg/kg BW, IV, q1h. This treatment was successful in converting the rhythm to sinus rhythm. A continuous rate infusion (CRI) of lidocaine, 50 μg/kg BW/min was initiated and continued for 19 h, at which time the ventricular tachycardia had resolved and the treatment was discontinued. Shortly thereafter, ventricular premature complexes in couplets and triplets, and runs of ventricular tachycardia occurred intermittently; however, there was no effect on the blood pressure and no other hemodynamic instability was noticed. The patient was administered sotalol hydrochloride (Betapace AF; Bayer Healthcare Pharmaceutical, Wayne, New Jersey, USA), 1.14 mg/kg BW, PO, q12h, in case a maintenance therapy for arrhythmias was required. However, the sotalol was discontinued after the patient had received a total of 3 doses, as the intermittent ventricular premature complexes had subsided.

Figure 2.

Intraoperative image showing the parietal surface of the left lateral liver lobe in its normal orientation. Note that the visceral surface of the left medial lobe is facing ventrally due to a 180 degrees clockwise torsion (noted with arrow). The cranial aspect of the patient is at the top of the photograph.

An abdominal ultrasonograph was taken 24 h postoperatively. Portal vein blood flow velocity was normal, varying between 13 to 15 cm/s. The blood flow to the other liver lobes was also normal. Repeated blood panels on days 2, 5, 14, and 21, postoperatively, showed gradual but significant improvement in liver enzymes and renal parameters. Three weeks postoperatively, the alkaline phosphatase was mildly elevated at 125 U/L and the alanine aminotransferase was normal. The dog continued to produce dilute urine with a specific gravity of 1.011.

Histologically, both liver lobes revealed diffuse and marked congestion. This was characterized by prominent dilation of the sinusoids with compression of the adjacent hepatocellular cords. The hepatocytes were diffusely hypereosinophilic and there were variable degrees of nuclear pyknosis, suggestive of coagulation necrosis. Multifocally, a thin line of hepatocytes in the periportal regions were unaffected. A small amount of bile was present in cholangioles. The changes in the left medial liver lobe were more pronounced than those in the left lateral liver lobe. Lining the zone of necrosis, there was a thin band of neutrophils. Fibrin exudation onto the hepatic capsule was a feature. The changes were consistent with venous infarction and liver lobe torsion. The aerobic and anaerobic cultures obtained from the liver revealed a growth of Staphylococcus intermedius, which was sensitive to the majority of the antibiotics tested, except amoxicillin.

Torsions of the liver lobes are exceedingly rare in dogs but should be included in the differential diagnoses for acute abdominal pain with elevated liver enzymes or radiographic evidence of gas in the hepatic parenchyma (1–4). Most commonly, the left division of the liver (left lateral and left medial lobes) is affected in large breed dogs (2,5). Torsion of a liver lobe from any division results in strangulation of vessels of the torsed lobe, which leads to infarction and necrosis (6). Etiology of liver lobe torsion is still unknown, although several different factors have been proposed (5). It has been speculated previously that chronic gastric dilatation in large breed dogs may put pressure on the liver lobes and cause stretching or weakening of the supporting structures (7). Other theorized causes include liver masses, trauma, or vigorous jumping, which may cause separation of the liver capsule allowing greater freedom of movement (2,3,8). These events may also expose the liver vasculature at its pedicle, which could act as a weak spot by increasing laxity at the base of the liver lobe. This increased laxity could allow the liver lobe to move freely about its axis and, by means of a pendulum-like effect, potentiate liver lobe torsion (3,7). Weakness or aplasia of hepatogastric or left triangular ligaments are also among the considered causes (2,3,5). Ultrasonography and color flow Doppler might be helpful in detecting decreased or minimal blood flow to the twisted liver lobe (5,9). Liver lobe torsion and subsequent hemoabdomen is a surgical emergency and should be dealt with immediately, otherwise death can occur due to hypovolemic shock and hemorrhage (1).

In the previously reported cases, single liver lobe torsion or, in 1 case, double lobe torsions, have been documented (1–5,7–9). None of the previously reported cases had infarction of an adjacent liver lobe, as we saw in this case. This was clearly identified preoperatively by Doppler examination of the liver. This underlines the importance of evaluating adjacent liver lobes when dealing with liver lobe torsion. It has been recommended not to untwist the liver lobe before resection to prevent release of bacterial toxins (8). There is also a risk of releasing emboli (thrombi) and bacteria into the circulation that could compromise the patient (7). The extent of the liver torsion varied from 180 degrees to 360 degrees in the 5 previously reported cases (2,3,7–9). The direction of left medial liver lobe torsion was clockwise in our case, but it can be in either a clockwise or a counterclockwise direction, as reported in torsion of the papillary process of the caudate lobe and the quadrate lobe (8,9). Torsion of the liver results in passive congestion, ischemic necrosis, and subsequent hepatic rupture and peritonitis (1,4). Staphylococcus intermedius was isolated from the liver in our case, but in the previously reported cases, Clostridium spp. and/or Bacillus spp., Klebsiella pneumoniae, Pasteurella spp., Escherichia coli, and gram-negative nonfermenting rods had been isolated (5,7). Staphylococcus intermedius has been reported to be a normal intestinal flora in healthy humans; it is also one of the most common bacteria isolated from hepatic abscesses in dogs (10–12). In our patient, S. intermedius may have gained access to the liver by translocation from the gastrointestinal tract. We do not know if this occurred prior to the torsion or played a role in causing the torsion. In 1 study, aerobic bacteria, such as a S. intermedius, a Eubacterium sp., a Pasteurella sp., and a nonhemolytic Streptococcus sp., were isolated from the liver of clinically healthy dogs (13). No apparent cause of the torsion was found at surgery. There was no history of bloating, trauma, or vigorous exercise prior to the illness. The mild gastric distention with air, seen on referral radiographs, may have been due to gastric dilation, which is thought to be a causative factor for liver torsion. We speculate that the source of hemorrhagic peritoneal effusion in our case could have been due to venous obstruction from the torsion. The arterial portion of the blood flow could have remained partially intact and, due to impaired venous return, led to rupture of capillaries, serous transudation, and diapedesis of red cells. CVJ