Neurologic injury in cardiac surgery: aortic atherosclerosis emerges as the single most important risk factor

With older and sicker patients undergoing cardiac surgery, neurologic injury has emerged as an increasingly important cause of rising costs, morbidity and mortality. Several studies investigating the relationship between atherosclerotic aortic disease and subsequent adverse clinical outcomes have demonstrated that the single most important risk factor for neurologic injury following cardiac surgery is the presence of aortic atheromatous disease. The results of these studies suggest that atheroemboli are correlated with neurologic injury following cardiac surgery. Surgical techniques to avoid and prevent particulate debris during cardiac surgery may be a major step in preventing severe neurologic injury.     

Differential effects of systemically administered ketamine and lidocaine on dynamic and static hyperalgesia induced by intradermal capsaicin in humans

We have examined the effect of systemic administration of ketamine and lidocaine on brush-evoked (dynamic) pain and punctate-evoked (static) hyperalgesia induced by capsaicin. In a randomized, double-blind, placebo-controlled, crossover study, we studied 12 volunteers in three experiments. Capsaicin 100 micrograms was injected intradermally on the volar forearm followed by an i.v. infusion of ketamine (bolus 0.1 mg kg- 1 over 10 min followed by infusion of 7 micrograms kg-1 min-1), lidocaine 5 mg kg-1 or saline for 50 min. Infusion started 15 min after injection of capsaicin. The following were measured: spontaneous pain, pain evoked by punctate and brush stimuli (VAS), and areas of brush- evoked and punctate-evoked hyperalgesia. Ketamine reduced both the area of brush-evoked and punctate-evoked hyperalgesia significantly and it tended to reduce brush-evoked pain. Lidocaine reduced the area of punctate-evoked hyperalgesia significantly. It tended to reduce VAS scores of spontaneous pain but had no effect on evoked pain. The differential effects of ketamine and lidocaine on static and dynamic hyperalgesia suggest that the two types of hyperalgesia are mediated by separate mechanisms and have a distinct pharmacology.      

Resolution of cirrhosis in autoimmune hepatitis with corticosteroid therapy

Successful therapy for liver diseases, including autoimmune hepatitis, primary biliary cirrhosis, and hepatitis C, has been associated with a reduction in hepatic fibrosis. Recently, a study of needle liver biopsy specimens documented resolution of cirrhosis in a small group of patients with autoimmune hepatitis who responded to corticosteroid therapy. We describe a woman with autoimmune hepatitis who had cirrhosis on a wedge biopsy of the liver in 1985 and who attained a biochemical response with immunosuppressive therapy. A repeat wedge liver biopsy performed 14 years later was normal, providing unequivocal evidence that cirrhosis can reverse completely in autoimmune hepatitis.     

Lamotrigine for central poststroke pain: a randomized controlled trial

OBJECTIVE: Central poststroke pain (CPSP) is usually difficult to treat. Amitriptyline, the only oral preparation shown to be effective in a randomized controlled trial, is often associated with a range of side effects related to the many mechanisms of actions of tricyclic antidepressants. We investigated the effect of lamotrigine, a drug that reduces neuronal hyperexcitability, on poststroke pain. METHODS: Thirty consecutive patients with CPSP (median age 59 years, range 37 to 77; median pain duration 2.0 years, range 0.3 to 12) from two centers participated in a randomized, double-blind, placebo-controlled cross-over study. The study consisted of two 8-week treatment periods separated by 2 weeks of wash-out. The primary endpoint was the median value of the mean daily pain score during the last week of treatment while treated with 200 mg/d lamotrigine. Secondary endpoints were median pain scores while on lamotrigine 25 mg/d, 50 mg/d, and 100 mg/d; a global pain score; assessment of evoked pain; areas of spontaneous pain; and allodynia/dysesthesia. RESULTS: Lamotrigine 200 mg/d reduced the median pain score to 5, compared to 7 during placebo (p = 0.01) in the intent-to-treat population of 27 patients. No significant effect was obtained at lower doses. Twelve patients (44%) responded to the treatment. There was a uniform tendency to reduction of all secondary outcome measures, but lamotrigine only had significant effects on some of the secondary outcome measures. Lamotrigine was well tolerated with few and transient side effects. Two mild rashes occurred during lamotrigine treatment, one causing withdrawal from study. CONCLUSIONS: Oral lamotrigine 200 mg daily is a well tolerated and moderately effective treatment for central poststroke pain. Lamotrigine may be an alternative to tricyclic antidepressants in the treatment of CPSP.     

Utility of fiberoptic bronchoscopy before bronchial artery embolization for massive hemoptysis

OBJECTIVE: We wanted to investigate the utility of performing fiberoptic bronchoscopy before bronchial artery embolization in patients with massive hemoptysis. MATERIALS AND METHODS: We retrospectively reviewed the cases of all patients with hemoptysis who had presented at either of two local hospitals, one county hospital and one community hospital, between 1988 and 2000 and who had undergone fiberoptic bronchoscopy before bronchial arteriography. All data were abstracted using a standardized coding form, and radiographs were independently reviewed by two of the authors. RESULTS: Twenty-nine patients meeting the inclusion criteria were identified; one patient was excluded because of missing radiographs. The remaining 28 patients consisted of 19 men and nine women, with an average age of 54.6 years (age range, 16-91 years). The clinically determined diagnoses of their symptoms were tuberculous bronchiectasis (n = 14; 50.0%); bronchogenic carcinoma (n = 4; 14.3%); active tuberculosis (n = 2; 7.1%); nontuberculous bronchiectasis (n = 2; 7.1%); active coccidioidomycosis, pancreaticobronchial fistula, arteriovenous malformation, and tetralogy of fallot (n =1 each; 3.6% each); and unknown cause (n = 2; 7.1%). The bleeding site determined through bronchoscopy was consistent with that determined through radiographs in 23 patients (82.1%); all had either unilateral disease (n = 15), bilateral disease with unilateral cavities (n = 5), or a preponderance of disease on one side (n = 3). Bronchoscopy was an essential tool in determining the bleeding site in only three patients (10.7%), all of whom had bronchiectasis without localizing features visible on chest radiographs. In the remaining two patients (7.1%), bronchoscopic findings were indeterminate, but radiographs were helpful. CONCLUSION: Fiberoptic bronchoscopy before bronchial artery embolization is unnecessary in patients with hemoptysis of known causation if the site of bleeding can be determined from radiographs and no bronchoscopic airways management is needed.     

Management of anaphylactic shock evaluated using a full-scale anaesthesia simulator

BACKGROUND: The diagnosis of an anaphylactic reaction during anaesthesia is not the first consideration for the anaesthetist and might be missed. The aim of this study was to describe anaesthetists' management of an anaphylactic reaction concerning diagnosing, treatment and application of anaesthesia crisis resource management (ACRM) in a full-scale anaesthesia simulator. METHODS: Forty-two anaesthetists in teams of two attended training sessions with a critical incident of anaphylactic shock in a full-scale simulator. Trained observers from the study group evaluated the medical treatment according to a treatment sequence developed from the literature and graded the ACRM performance on a five-point scale where 1 is bad and 5 is best. RESULTS: None of the teams made the correct diagnosis within 10 min and treatment according to the treatment sequence was not initiated. Only 6/21 teams considered the right diagnosis but first after hints from the instructor 15 min after the start of the incident. Evaluation of the use of the total ACRM concept (that is the use of all of the ACRM expressions seen in a total connection: called general impression) gave a median value of 2.0 with a range of (1-3). CONCLUSION: Anaphylactic shock was difficult to diagnose and no structured plans were used for the treatment in the simulated incident in this study.     

Acute pain induces insulin resistance in humans

BACKGROUND: Painful trauma results in a disturbed metabolic state with impaired insulin sensitivity, which is related to the magnitude of the trauma. The authors explored whether pain per se influences hepatic and extrahepatic actions of insulin. METHODS: Ten healthy male volunteers underwent two randomly sequenced hyperinsulinemic-euglycemic (insulin infusion rate, 0.6 mU x kg(-1) x min(-1) for 180 min) clamp studies 4 weeks apart. Self-controlled painful electrical stimulation was applied to the abdominal skin for 30 min, to a pain intensity of 8 on a visual analog scale of 0-10, just before the clamp procedure (study P). In the other study, no pain was inflicted (study C). RESULTS: Pain reduced whole-body insulin-stimulated glucose uptake from 6.37+/-1.87 mg x kg(-1) x min(-1) (mean +/- SD) in study C to 4.97+/-1.38 mg x kg(-1) x min(-1) in study P (P < 0.01) because of a decrease in nonoxidative glucose disposal, as determined by indirect calorimetry (2.47+/-0.88 mg x kg(-1) x min(-1) in study P vs. 3.41+/-1.03 mg x kg(-1) x min(-1) in study C; P < 0.05). Differences in glucose oxidation rates were not statistically significant. The suppression of isotopically determined endogenous glucose output during hyperinsulinemia tended to be decreased after pain (1.67+/-0.48 mg x kg(-1) x min(-1) in study P vs. 2.04+/-0.45 mg x kg(-1) x min(-1) in study C; P = 0.06). Pain elicited a twofold to threefold increase in serum cortisol (P < 0.01), plasma epinephrine (P < 0.05), and serum free fatty acids (P < 0.05). Similarly, circulating concentrations of glucagon and growth hormone tended to increase during pain. CONCLUSIONS: Acute severe pain decreases insulin sensitivity, primarily by affecting nonoxidative glucose metabolism. It is conceivable that the counterregulatory hormonal response plays an important role. This may indicate that pain relief in stress states is important for maintenance of normal glucose metabolism.     

Lipopolysaccharides do not alter metabolic disturbances in hippocampal slices of fetal guinea pigs after oxygen-glucose deprivation

The aim of the present study was to clarify whether endotoxins [lipopolysaccharides (LPS)] have a toxic effect on fetal brain tissue after cerebral ischemia, while excluding their effect on the cardiovascular system. Experiments were therefore performed on hippocampal slices prepared from mature fetal guinea pigs. In particular, we studied the influence of LPS on nitric oxide production, energy metabolism, and protein synthesis after oxygen-glucose deprivation (OGD). Incubating hippocampal slices in LPS (4 mg/L) for as long as 12 h did not alter cGMP tissue concentrations significantly. However, 10 min after OGD of 40-min duration, cGMP tissue concentrations were substantially increased in relation to controls, and this increase was almost completely blocked by the application of 100 microM N:(omega)-nitro-L-arginine, indicating that nitric oxide synthase was activated after OGD in fetal brain tissue. Again, LPS did not have any effect on cGMP tissue concentrations after OGD. Furthermore, addition of LPS altered neither protein synthesis nor energy metabolism measured 12 h after OGD. We therefore conclude that, apart from their well-known influence on the cardiovascular system, LPS do not alter metabolic disturbances in hippocampal slices of fetal guinea pigs 12 h after OGD. A direct toxic effect of LPS on immature brain tissue within this interval does not therefore seem to be very likely. However, delayed activation of LPS-sensitive pathways that may be involved in cell death, or damage limited to a small subgroup of cells such as oligodendrocyte progenitors, cannot be fully excluded.