Incidence of inferior vena cava thrombosis detected by transthoracic echocardiography in the immediate postoperative period after adult cardiac and general surgery.

Venous thromboembolism is an important complication after general and cardiac surgery. Using transthoracic echocardiography, this study assessed the incidence of inferior vena cava (IVC) thrombosis among a total of 395 and 289 cardiac surgical and major surgical patients in the immediate postoperative period after cardiac and major surgery, respectively. All transthoracic echocardiography was performed by a specialist intensivist within 24 hours after surgery with special emphasis on using the subcostal view in the supine position to visualise the IVC. Of the 395 cardiac surgical patients studied, the IVC was successfully visualised using the subcostal view in 315 patients (79.8%) and eight of these patients (2.5%) had a partially obstructive thrombosis in the IVC. In 250 out of 289 (85%) general surgical patients, the IVC was also clearly visualised, but only one patient (0.4%) had an IVC thrombosis (2.5 vs 0.4%, P <0.05). In summary, visualisation of the IVC was feasible in most patients in the immediate postoperative period after both adult cardiac and major surgery. IVC thrombosis appeared to be more common after adult cardiac surgery than general surgery. A large prospective cohort study is needed to define the risk factors for IVC thrombus and whether early thromboprophylaxis can reduce the incidence of IVC thrombus after adult cardiac surgery.

Ultrasound-guided combined intermediate and deep cervical plexus nerve block for regional anaesthesia in oral and maxillofacial surgery.

OBJECTIVES: We examined the application of an ultrasound-guided combined intermediate and deep cervical plexus nerve block for regional anaesthesia in patients undergoing oral and maxillofacial surgery. METHODS: A total of 19 patients receiving ultrasound-guided combined intermediate and deep cervical plexus anaesthesia followed by neck surgery were examined prospectively. The sternocleidomastoid and the levator of the scapula muscles as well as the cervical transverse processes were used as easily depicted ultrasound landmarks for the injection of local anaesthetics. Under ultrasound guidance, a needle was advanced in the fascial band between the sternocleidomastoid and the levator of the scapula muscles and 15 ml of ropivacaine 0.75% was injected. Afterwards, the needle was advanced between the levator of the scapula and the hyperechoic contour of the cervical transverse processes and a further 15 ml of ropivacaine 0.75% was injected. The sensory block of the cervical nerve plexus, the analgesic efficacy of the block within 24 h after injection and potential block-related complications were assessed. RESULTS: All patients showed a complete cervical plexus nerve block. No patient required analgesics within the first 24 h after anaesthesia. Two cases of blood aspiration were recorded. No further cervical plexus block-related complications were observed. CONCLUSIONS: Ultrasound-guided combined intermediate and deep cervical plexus block is a feasible, effective and safe method for oral and maxillofacial surgical procedures.

Cardiovascular ultrasound in detecting central venous catheter thrombosis in the intensive care unit: splenectomy and antiphospholipid syndrome.

Venous thrombosis of the upper extremities is becoming increasingly prevalent in the intensive care unit as a result of chronic in-dwelling central venous catheters. We report two rare cases in which combined transoesophageal echocardiography and vascular ultrasound examination aided in the identification of catheter-related thrombosis in two patients suffering from splenectomy-induced thrombocytosis and antiphospholipid syndrome respectively.

Clonidine changes lidocaine free concentrations in rat myocardium without affecting heart function measured by echocardiography.

Lidocaine is a local anaesthetic widely used in regional and epidural anaesthesia. Clonidine a alpha2-adrenergic agonist is an antihypertensive agent, regulating the production of catecholamines (epinephrine and norepinephrine) and added to local anesthetic infusions in order to improve postoperative analgesia. The aim of the study was to investigate the influence of clonidine co-administration on the binding of 14C lidocaine to rat serum and heart tissue protein as well as its pharmacodynamic effects in the heart. Four groups of Wistar rats (n=7) were used; Groups I and II received 4 mg/kg lidocaine i.m. Groups III and IV received lidocaine and 1 microg/kg clonidine i.m. In group I and III fifteen minutes and in groups II and IV thirty minutes after the initial treatment, ultrasound examination of heart function (heart rate, diameter of left ventricle in systole and diastole, ejection fraction) was performed. The animals were then sacrificed in all groups. Lidocaine free fraction in serum and heart was evaluated via ultrafiltration. The kinetics of lidocaine was altered by clonidine co-administration probably by mechanisms related to protein binding alterations. However, the pharmacokinetic interactions were not accompanied by changes of pharmacodynamic parameters including those of heart function as measured by echocardiography.

Ischemic preconditioning fails to confer additional protection against ischemia-reperfusion injury in the hypothyroid rat heart.

There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfusion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts (P<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts (P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts.