Surgical Attenuation Research Articles

Cis-Atracurium in dogs with and without porto-systemic shunts

ObjectiveTo evaluate the non-depolarizing neuromuscular blocking drug cis-atracurium in dogs with porto-systemic shunts, and to compare it in clinically normal animals. AnimalsThirteen dogs of mixed breed and sex, aged between 3 and 31 months old, weighing 2.2–25.5 kg, with ASA physical status II–IV, and undergoing surgical attenuation of porto-systemic shunt. A control group of 11 bitches of mixed breed, between 8 and 60 months old, and weighing 4.5–41.0 kg, all ASA physical status I, undergoing routine ovarohysterectomy were also studied. Materials and methodsPre-anaesthetic medication was an opioid analgesic, given either alone or in combination with acepromazine. Following induction of general anaesthesia with intravenous (IV) propofol and oro-tracheal intubation, anaesthesia was maintained using isoflurane in either oxygen or oxygen and nitrous oxide. Ventilation was controlled. The train of four (TOF) technique was used to monitor neuromuscular blockade. An initial dose of 0.1 mg kg−1cis-atracurium was given IV and additional doses of 0.03 mg kg−1cis-atracurium were administered when at least one twitch of the TOF was present. ResultsExcept for one dog that was killed during surgery because its anomaly was inoperable, all animals recovered satisfactorily from anaesthesia and surgery. In dogs with porto-systemic shunt, onset of neuromuscular blockade was 3.1 ± 1.1 minutes (mean ± SD) and in control dogs was 3.4 ± 0.7 minutes (not significantly different). Neuromuscular blockade lasted 34 ± 13 minutes in dogs with porto-systemic shunt and 29 ± 17 minutes in control dogs (not significantly different). ConclusionsThe presence of porto-systemic shunt did not affect the rate of onset or duration of action of cis-atracurium. Clinical relevancecis-Atracurium may have a use in veterinary anaesthesia for producing neuromuscular blockade in dogs with hepatic insufficiency, including those with porto-systemic shunt.

Ultrasonographic assessment of hemodynamic changes in the portal vein during surgical attenuation of congenital extrahepatic portosystemic shunts in dogs.

To determine portal hemodynamic changes associated with surgical shunt ligation and establish ultrasonographic criteria for determining the optimal degree of shunt narrowing and predicting outcome. Case series. 17 dogs, each with a single congenital extrahepatic portosystemic shunt. Pre- and postligation flow velocities and flow directions were determined by Doppler ultrasonography intraoperatively in the shunt and in the portal vein cranial and caudal to the shunt origin. Outcome was evaluated 1 month after surgery by measuring blood ammonia concentration and performing abdominal ultrasonography. Hepatofugal flow was detected in 9 of 17 dogs before shunt attenuation in the portal segment that was between the shunt origin and the entering point of the gastroduodenal vein. If hepatofugal flow became hepatopetal after shunt ligation, hyperammonemia resolved. Hepatofugal portal flow was caused by blood that flowed from the gastroduodenal vein toward the shunt. Shunt attenuation converted hepatofugal flow to hepatopetal in the shunt in 12 of 17 dogs. Chronic portal hypertension developed or perioperative death occurred when the portal congestion index caudal to the shunt origin increased by > 3.6 times. After hepatopetal flow in the cranial portal vein and the shunt is established, further shunt narrowing is contraindicated. Increase of the portal congestion index caudal to the shunt > 3.5 times should be avoided. Poor outcome because of severe hypoplasia of the portal branches can be expected if the flow direction remains hepatofugal after shunt occlusion cranial to the shunt origin.

Anatomy of the patent ductus venosus in the cat

The biplanar mesenteric vein portovenograms of 10 cats with left divisional intrahepatic portosystemic shunts consistent with a patent ductus venosus (PDV) were reviewed. A corrosion cast of the hepatic portal vasculature was made post mortem from one individual that died post operatively following surgical attenuation of the shunting vessel. On the basis of the combined surgical, post mortem and imaging data, these left divisional shunts were found to have consistent anatomy, each having a straight vessel which drained into a venous ampulla before draining into the caudal vena cava at the level of the diaphragm. The left phrenic vein and left hepatic vein both entered the ampulla independently of the shunting vessel. The anatomical similarity between these findings in the cat and the PDV in the dog suggest that it is appropriate to describe this particular portosystemic shunt as a PDV.

Neurological dysfunction in dogs following attenuation of congenital extrahepatic portosystemic shunts.

Eleven of 89 dogs (12 per cent) developed neurological signs within six days of surgical attenuation of a congenital extrahepatic portosystemic shunt. Neurological signs were not associated with hepatic encephalopathy or hypoglycaemia. Signs varied in severity from non-progressive ataxia (three dogs) to generalised motor seizures (four dogs), progressing to status epilepticus (three dogs). In a further four cases, ataxia and disorientation were treated vigorously with anticonvulsant medication, presumably preventing the development of seizures. Two dogs that developed status epilepticus died or were eventually euthanased. All other animals survived, although some had persistent neurological deficits. Postligation neurological complications were not prevented by gradual shunt attenuation. Prophylactic treatment with phenobarbitone (5 to 10 mg/kg preoperatively, followed by 3 to 5 mg/kg every 12 hours for three weeks) did not significantly reduce the incidence of neurological sequelae (2/31 [6 per cent] dogs with phenobarbitone vs 9/58 [16 per cent] without phenobarbitone; P = 0.2). However, no animal receiving phenobarbitone experienced generalised motor seizures or status epilepticus. In conclusion, these observations suggest that postligation neurological syndrome comprises a spectrum of neurological signs of variable severity. Perioperative treatment with phenobarbitone may not reduce the risk of neurological sequelae, but may reduce their severity.

Outcomes after extrahepatic portosystemic shunt ligation in 49 dogs.

To evaluate outcomes after attenuation of extrahepatic portosystemic shunts in dogs using surgical silk. Retrospective study. Case records were reviewed for degree of surgical attenuation, experience of the primary surgeon, perioperative mortality and problems related to persistent portosystemic shunting or shunt ligation. Presence of portosystemic shunting after surgery was evaluated by ammonia tolerance testing, measurement of postprandial serum bile acid, plasma urea and cholesterol concentrations and liver enzyme activity. The influence of age, postocclusion portal pressure, primary surgeon, degree of attenuation and postoperative biochemical findings on the occurrence of postoperative problems was assessed. The mortality rate was 2.1%. Shunt attenuation was complete in 34% and partial in 66% of dogs. Portal hypertension necessitating ligature removal was encountered in only one dog. Five dogs experienced neurological abnormalities (seizures or ataxia), possibly as a manifestation of 'postligation seizure syndrome'. Postoperative liver function was normal in 78% of dogs, including 70% with partial shunt attenuation. Experience of the surgeon was related positively to outcome after partial attenuation (P = 0.002). Postoperative biochemical evidence of abnormal liver function was the most sensitive predictor of recurrence of clinical signs referable to persistent portosystemic shunting. In the hands of an experienced surgeon, surgical attenuation of single extrahepatic shunts was safe and effective, even in animals with partial attenuation. Most dogs with biochemical evidence of persistent shunting suffer relapse of clinical signs within 18 months of surgery. Postligation neurological syndromes of variable intensity may be more common than previously thought.

Surgical treatment of intrahepatic portosystemic shunts in 45 dogs

The surgical attenuation of an intrahepatic portosystemic shunt in 45 dogs is described. Twenty-nine (64 per cent) had left divisional shunts consistent with a patent ductus venosus (PDv), 15 (33...

Portosystemic communications: follow-up of 32 cases.

A multicentre retrospective study of dogs that underwent surgical attenuation of portosystemic communications (PSC) was conducted. These dogs were followed from three months after surgery to evaluate the long term effect of surgery on their life span, disease-free interval, and owner assessment of postoperative quality of life of the dogs. Seventy-five per cent of the dogs in this study had no long term postoperative recurrence of clinical signs. Of the 25 per cent of dogs that showed recurrent clinical signs, all but one had partial attenuation of the PSC. The location of the PSC was the only factor that correlated with whether the dogs were still alive. All owners were pleased with the postoperative quality of life of their dogs.

Generalized motor seizures after portosystemic shunt ligation in dogs: Five cases (1981-1988)

Summary Severe generalized motor seizures developed in 5 dogs between 13 hours and 3 days after surgical attenuation of a single extrahepatic portosystemic shunt. Three dogs died, and a fourth was euthanatized because of poor prognosis for recovery. The fifth dog, although improved, was still not clinicall ynormal 15 months after surgery. An intra-orextracranial cause for the seizures could not be identified in any of these dogs. Postmortem examination results in 3 dogs were similar to findings previously reported in dogs with portosystemic shunts, but which did not undergo surgical shunt ligation. Of the 5 dogs, 4 were >18 months old, which may indicate that older dogs are more likely to develop seizures after shunt ligation than are younger dogs.