Preoperative percutaneous portal vein embolization: evaluation of adverse events in 188 patients

PURPOSE: To retrospectively assess the frequency of adverse events related to percutaneous preoperative portal vein embolization (PPVE). MATERIALS AND METHODS: Institutional review board did not require its approval or patient informed consent for this study. The adverse events that occurred during PPVE or until planned hepatic surgery was performed or cancelled were retrospectively obtained from clinical, imaging, and laboratory data files in 188 patients (109 male and 79 female patients; mean age, 60 years; range, 16-78 years). Liver resection was planned for metastases (n = 137), hepatocarcinoma (n = 31), cholangiocarcinoma (n = 15), fibrolamellar hepatoma (n = 1), and benign disease (n = 4). PPVE was performed with a single-lumen 5-F catheter and a contralateral approach with n-butyl cyanoacrylate mixed with iodized oil as the main embolic agent. The rate of complications in patients with cirrhosis was compared with that in patients without cirrhosis by using the chi(2) test. RESULTS: Adverse events occurred in 24 (12.8%) of 188 patients, including 12 complications and 12 incidental imaging findings. Complications included thrombosis of the portal vein feeding the future remnant liver (n = 1); migration of emboli in the portal vein feeding the future remnant liver, which necessitated angioplasty (n = 2); hemoperitoneum (n = 1); rupture of a metastasis in the gallbladder (n = 1); transitory hemobilia (n = 1); and transient liver failure (n = 6). Incidental findings were migration of small emboli in nontargeted portal branches (n = 10) and subcapsular hematoma (n = 2). Among the 187 patients in whom PPVE was technically successful, there was a significant difference (P < .001) between the occurrence of liver failure after PPVE in patients with cirrhosis (five of 30) and those without (one of 157). Sixteen liver resections were cancelled due to cancer progression (n = 12), insufficient hypertrophy of the nonembolized liver (n = 3), and complete portal thrombosis (n = 1). CONCLUSION: PPVE is a safe adjuvant technique for hypertrophy of the initially insufficient liver reserve. Post-PPVE transient liver failure is more common in patients with cirrhosis than in those without cirrhosis.     

Conservative treatment of placenta percreta: a safe alternative

Placenta percreta was diagnosed antenatally in two patients in the same university medical school and conservative treatment was planned. Both uterine arteries were embolized. In one patient, embolization preceded cesarean section and in the other, embolization was done immediately after operation. In each case, the placenta was left in situ and disappeared 5-6 months after delivery.     

Effect of methylphenidate on vital signs and adverse effects in adults with traumatic brain injury

OBJECTIVE: To study methylphenidate's adverse effects and impact on vital signs within the adult traumatic brain injury population. DESIGN: Thirty-five adults with traumatic brain injury enrolled in a double-blind, placebo-controlled, 6-wk crossover study of methylphenidate, given in a dose of 0.3 mg/kg/dose, twice a day. Vital signs were taken by trained clinicians and research assistants. Participants filled out weekly questionnaires pertaining to the adverse effects. RESULTS: Poor appetite was the only adverse effect related to methylphenidate. Other adverse effects commonly associated with methylphenidate, such as insomnia, rapid heart rate, and anxiety, were not found to be significantly related to the medication. The average rise in mean arterial pressure on methylphenidate was 2.5 mm. Methylphenidate showed a stronger impact on pulse, with an average increase of 7 beats/min. Baseline vital signs did not predict the degree of increase on methylphenidate. CONCLUSION: Methylphenidate appears to be safe for the adult population with traumatic brain injury. However, because a few individuals experienced significant changes in vital signs and adverse effects, all patients should be monitored.     

The agents used for sedation in neurointensive care unit

Sedation and analgesia can be routinely prescribed in head injury patients. The goals of such sedation are three: brain protection, prevention and treatment of intracranial hypertension and therapeutic facilitation. In such situation, the use of sedative and analgesic therapy should respect the rate of cerebral blood flow/cerebral oxygen consumption coupling while preserving cerebral perfusion pressure and decreasing the intracranial pressure. This treatment should have an analgesic and myorelaxing action with short and predictable time of action. The ideal sedation agent with all these properties does not exist. Only the combination of several different pharmacological classes of compounds may reach this goal. Benzodiazepines are the most frequently used agents. In most of the cases they are associated with analgesic agents such as opioid or ketamine. Opioids may be the basic analgesic agents because they do not produce brain haemodynamic modifications if arterial pressure is maintained. Among them, sufentanil, thanks to its pharmacokinetics properties, remains the most prescribed opioid. However, in the future, remifentanil that presents a fast elimination may be more frequently used for neurological follow up of patients. Ketamine whose use is subject of debate, has the main advantage of maintaining haemodynamic status. Ketamine has no side effects on brain haemodynamic when used with propofol or midazolam. Taking into account their deleting effect on haemodynamic status and immune system, barbituric are no longer used as long term sedative agents. However, their use is still recommended in the cases of refractory intracranial hypertension. Propofol remains the ideal sedative agent because of its short duration action but its use is limited by its cost. Its use may be recommended for short time sedations with or without an opioid drug. The curare use should be restrain to refractory intracranial hypertension to usual treatments and happening during stimulation.     

Decreased TNF-alpha and NK activity in obsessive-compulsive disorder

BACKGROUND: Accumulating evidence points towards the involvement of autoimmune mechanisms in the pathophysiology of some subgroups of obsessive-compulsive disorder (OCD). This study was carried out to investigate whether obsessive-compulsive disorder is associated with altered activity of the immune system, and whether these changes are related to particular clinical characteristics. METHODS: Ex vivo production of TNF-alpha, IL-4, IL-6, IL-10, and IFN-gamma in whole blood cultures, and NK-cell activity and peripheral blood NK cell-, monocytes-, T-cell-, and B-cell- percentages were measured in 50 medication-free outpatients with OCD and 25 controls. RESULTS: In OCD patients, we found a significant decrease in production of TNF-alpha (p < 0.0001) and NK-activity (p = 0.002) in comparison with controls. No significant differences were observed in the other immune variables. Patients with first-degree relatives with OCD had significant lower NK-activity than patients who had no relatives with OCD (p = 0.02), and patients with a childhood onset of OCD had significantly lower number of NK-cells than patients with a late onset (p= 0.003). CONCLUSIONS: Changes in TNF-alpha and NK activity suggest a potential role of altered immune function in the pathophysiology of obsessive-compulsive disorder.