Surgical treatment of scapulohumeral subluxation in an alpaca (Vicugna pacos) using osteotomy of the acromion, open reduction and extracapsular tension sutures.

CASE HISTORY AND CLINICAL FINDINGS: A 3.3-year-old male alpaca, weighing 60 kg was referred for investigation of a severe left forelimb lameness of 4 weeks duration. A scapulohumeral subluxation had been diagnosed radiographically by the referring veterinarian. CLINICAL FINDINGS AND DIAGNOSIS: Based on clinical, ultrasonographic and radiographic findings the diagnosis of cranio-lateral subluxation of the left humeral head was confirmed. In addition, a full thickness lesion (approximately 1×1 cm) of the articular cartilage on the caudomedial aspect of the humeral head was diagnosed by arthroscopy. TREATMENT AND OUTCOME: Treatment included open reduction with internal fixation. Severe muscle contraction and local tissue fibrosis around the scapulohumeral joint (SHJ) required osteotomy of the acromion 3 cm proximal to the distal acromial edge, to allow adequate access. Internal stabilisation was achieved by placing tension band sutures between one cortical screw in the scapular neck and two cortical screws, with washers, craniolaterally on the greater tubercle of the humerus. Post-surgery, a carpal flexion sling was applied with the carpus maintained in 70° flexion for 4 weeks to avoid postoperative weight-bearing. An exercise programme was started 8 days after surgery and continued for 12 weeks. The alpaca had an uneventful postsurgical recovery and showed no lameness after 8 weeks. The long-term outcome was excellent; 21 months after surgery the alpaca was sound and the range of movement of the left SHJ was equal to the right SHJ. CLINICAL RELEVANCE: Even in this chronic case of subluxation of the SHJ of 4 weeks duration, surgical treatment using osteotomy of the acromion, open reduction and internal fixation with extracapsular scapulohumeral tension sutures resulted in an excellent long-term outcome in this alpaca, despite the presence of a cartilage lesion.

[Perioperative use of fluidwarmers reduces hypothermia in cats]. / Der Einsatz von Infusionswärmepumpen vermindert perioperative Hypothermie bei Katzen.

OBJECTIVE: Perioperative hypothermia is a common problem that must not be underestimated. There are plenty of methods to prevent or reduce heat loss during anaesthesia. The aim of this study was to evaluate the influence of warmed intravenous (IV) infusions to the perioperative decrease of body temperature of anaesthetized cats. MATERIAL AND METHODS: In this randomly designed study 30 cats undergoing surgical procedures were anaesthetized with a standardized anaesthesia protocol. Fifteen cats received IV infusions with room temperature; the IV infusion of the other 15 cats was constantly warmed to 38-39°C using a fluid warming device. The development of body temperature within the first 60 minutes of anaesthesia of both groups was compared and analysed. Additionally the influence of the room temperature on the body temperature and the influence of body temperature at the end of anaesthesia on the recovery period were evaluated. RESULTS: After 60 minutes of anaesthesia cats receiving warmed IV infusions had a significant higher body temperature than cats receiving IV infusions with room temperature. Room temperatures lower than 26°C had a significant influence on the development of perioperative hypothermia. The evaluation of the recovery period showed a significant correlation between low body temperature at the end of anaesthesia and prolonged time until extubation on the one hand and postoperative shivering on the other hand. CONCLUSION AND CLINICAL RELEVANCE: The present study shows that warmed IV infusions have a significant influence on the reduction of perioperative heat loss in cats. Nevertheless other additional methods to prevent heat loss are necessary to keep the patient in a normothermic range. Room temperatures play an essential role in decreasing hypothermia and should be at least 26°C. Low body temperature at the end of anaesthesia prolongs the recovery periode and enhances postoperative shivering.

Effects of sevoflurane on cognitive deficit, motor function, and histopathology after cerebral ischemia in rats.

BACKGROUND: The volatile anesthetic sevoflurane exhibits neuroprotective properties when assessed for motor function and histopathology after cerebral ischemia in rats. Damage of hippocampal neurons after ischemia relates to a number of cognitive deficits that are not revealed by testing animals for motor function. Therefore, the present study evaluates cognitive and behavioral function as well as hippocampal damage in rats subjected to cerebral ischemia under sevoflurane compared with fentanyl/nitrous oxide (N(2)O)/O(2) anesthesia. METHODS: Thirty-four rats were trained for 10 days using a hole-board test to detect changes in cognitive and behavioral function. Rats were randomly assigned to the following groups: (A) sham/fentanyl/N(2)O/O(2) (n=7); (B) ischemia/fentanyl/N(2)O/O(2) (n=10); (C) sham/2.0 vol% sevoflurane in O(2)/air (n=7); and (D) ischemia/2.0 vol% sevoflurane in O(2)/air (n=10). Cerebral ischemia was produced by unilateral common carotid artery occlusion combined with hemorrhagic hypotension (mean arterial blood pressure 40 mmHg for 45 min). Temperature, arterial blood gases, and pH were maintained constant. Cerebral blood flow was measured using laser-Doppler flowmetry. After surgery, cognitive and behavioral function was re-evaluated for 10 days. On day 11, the brains were removed for histopathologic evaluation (hematoxylin/eosin-staining). RESULTS: Cognitive testing revealed deficits in declarative and working memory in ischemic rats anesthetized with fentanyl/N(2)O. Rats anesthetized with sevoflurane during ischemia showed a significantly better outcome. Hippocampal damage was significantly worse with fentanyl/N(2)O. CONCLUSION: The present data add to previous investigations showing that sevoflurane prevents a deficit in cognitive function and histopathological damage induced by cerebral ischemia in rats.

Long-term effects of hypothermia on neuronal cell death and the concentration of apoptotic proteins after incomplete cerebral ischemia and reperfusion in rats.

BACKGROUND: The present study investigates the long-term effects of postischemic hypothermia on neuronal cell damage and concentration changes of apoptotic proteins after cerebral ischemia. METHODS: Sixty-four Sprague-Dawley rats were anesthetized, intubated and ventilated with 2.0 Vol% isoflurane and 70% N2O/O2. After preparation the animals were randomly assigned to the following groups: group 1 (n = 32, fentanyl-N2O/normothermia 37.5 degrees C), and group 2 (n = 32, fentanyl-N2O/hypothermia 34.0 degrees C. Ischemia (45 min) was induced by common carotid artery occlusion plus hemorrhagic hypotension (MAP = 40 mmHg). Arterial blood gases and pH were maintained constant. After 1, 3, 7, or 28 days (each n = 8) the brains were removed, frozen and cut. Neuronal damage was assessed by analyzing Bax, Bcl-2, p53, and Mdm-2 proteins, activated caspases-3-positive and eosinophilic cells. A third group (n = 8) of untreated animals served as naive controls. RESULTS: In hypothermic animals, Bax concentration was decreased by 50-70% over time compared to normothermia. On days 1 and 3, Bcl-2 was increased by 50% with hypothermia. The amount of activated caspase-3-positive cells in the ischemic hemisphere was 0.5% in the hypothermic and 1-2% in the normothermic animals. Of the hippocampal cells, 10-25% were eosinophilic in both groups over time. CONCLUSION: The present data show that hypothermia prevents an ischemia-induced increase of the pro-apoptotic protein Bax for as long as 28 days and increases the concentration of the antiapoptotic protein Bcl-2 up to 3 days compared to normothermic animals. Therefore, after cerebral ischemia, hypothermia has the sustained neuroprotective potential to shift apoptosis-related proteins towards neuronal cell survival.

Anaesthesia with midazolam/medetomidine/fentanyl in chinchillas (Chinchilla lanigera) compared to anaesthesia with xylazine/ketamine and medetomidine/ketamine.

We studied four different drug regimes for anaesthetic management in chinchillas and evaluated and compared their cardiovascular and respiratory effects. In this randomized, cross-over experimental study, seven adult chinchillas, five females, two males [515 +/- 70 (SD) g] were randomly assigned to one of the following groups: group 1 [midazolam, medetomidine and fentanyl (MMF), flumazenil, atipamezole and naloxone (FAN); MMF-FAN] received 1.0 mg/kg midazolam, 0.05 mg/kg medetomidine and 0.02 mg/kg fentanyl i.m., and for reversal 0.1 mg/kg flumazenil, 0.5 mg/kg atipamezole and 0.05 mg/kg naloxone s.c. after 45 min; group 2 (MMF) 1.0 mg/kg midazolam, 0.05 mg/kg medetomidine and 0.02 mg/kg fentanyl i.m.; group 3 [xylazine/ketamine (X/K)] 2.0 mg/kg xylazine and 40.0 mg/kg ketamine i.m.; and group 4 [medetomidine/ketamine (M/K)] 0.06 mg/kg medetomidine and 5.0 mg/kg ketamine i.m. Reflexes were judged to determine anaesthetic stages and planes. Anaesthesia with X/K and M/K was associated with a prolonged surgical tolerance and recovery period. By reversing MMF, recovery period was significantly shortened (5 +/- 1.3 min versus 40 +/- 10.3 min in MMF without FAN, 73 +/- 15.0 min in X/K, and 31 +/- 8.5 min in M/K). Without reversal, MMF produced anaesthesia lasting 109 +/- 16.3 min. All combinations decreased respiratory and heart rate but compared with X/K and M/K, respiratory and cardiovascular complications were less in the MMF groups. Focussing on the clinical relevance of the tested combinations, completely reversible anaesthesia showed two major advantages: anaesthesia can be antagonized in case of emergency and routinely shortens recovery. In small animals particularly these advantages lead to less complications and discomfort and thus often can be lifesaving. As all analgesic components (medetomidine and fentanyl) are reversed, postoperative analgesia should be provided before reversal of anaesthesia.

Sevoflurane and propofol influence the expression of apoptosis-regulating proteins after cerebral ischaemia and reperfusion in rats.

BACKGROUND AND OBJECTIVE: Sevoflurane and propofol reduce the extent of necrosis and improve neurological outcome in rodent models of cerebral ischaemia and reperfusion. However, the effects of these anaesthetics on programmed cell death (apoptosis) are unclear. The present study investigates whether sevoflurane and propofol affect the expression of apoptosis-regulating proteins after cerebral ischaemia in rats. METHODS: Thirty-two fasted male Sprague-Dawley rats were tracheally intubated and the lungs were ventilated (isoflurane and N2O/O2 anaesthesia). After surgical preparation, the animals were randomly assigned to one of the following groups: control (n = 8): fentanyl intravenous (10 microg kg(-1) bolus and 25 microg kg(-1) h(-1) infusion) with N2O/O2; sevoflurane (n = 8): 2.0% sevoflurane (end-tidal concentration) and O2/air; propofol (n = 8): 0.8-1.0 mg kg(-1) min(-1) propofol intravenous and O2/air; sham-operated (n = 8): 25 microg kg(-1) h(-1) fentanyl intravenous and N2O/O2, no cerebral ischaemia. Ischaemia (30 min) was induced by unilateral common carotid artery occlusion plus haemorrhagic hypotension to a mean arterial pressure of 30-35 mmHg. Four hours after cerebral ischaemia the brains were removed and the expression of apoptosis-regulating proteins (Bax, Bcl-2, p53, Mdm-2) was determined using immunofluorescence and Western-blot analyses. RESULTS: The expression of the pro-apoptotic protein Bax was greater in control animals than in sevoflurane or propofol anaesthetized rats and than in sham-operated animals. The concentrations of Bcl-2, p53 and Mdm-2 were not changed 4 h after cerebral ischaemia. CONCLUSIONS: In addition to the anti-necrotic effects of sevoflurane and propofol, these anaesthetics also reduce the concentration of the apoptosis-inducing protein Bax as early as 4 h after ischaemia.