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Fenoldopam, a vasodilating agent, may represent a potential therapeutic opportunity to increase renal perfusion in those conditions where renal hemodynamics are severely impaired by vascular sub-occlusion, as, indeed, is the case in thrombotic microangiopathies. The renal resistance index (RRI) was measured, on and off fenoldopam, in 27 children with STEC-HUS. A 12% decrease in RRI was observed on fenoldopam compared to off treatment without changes in the systemic hemodynamics and with no side effects. If confirmed in larger series, fenoldopam may become an important addition to supportive care to reduce ischemic damage in STEC-HUS and improve long-term outcomes.

We report on the case of a 7-year-old boy with Shiga toxin-producing Escherichia coli-related hemolytic uremic syndrome (STEC-HUS), initially presenting with abdominal pain as the only clinical feature and thus requiring differential diagnosis with a surgical emergency. Diagnosis of STEC-HUS was made with the appearance of bloody diarrhea and renal function impairment, and the clinical picture rapidly progressed to multiorgan failure. Relatively late and severe central nervous system (CNS) involvement was present, characterized by subacute encephalitis progressing to coma, which became apparent when the acute phase of thrombotic microangiopathy was resolving. Therefore, neurologic manifestations were thought to be related to reperfusion damage to the CNS and high-dose IV steroid pulse therapy was empirically administered. Following this therapeutic scheme, neurologic involvement resolved with no sequelae. This case offers several points of discussion on the clinical presentation and the diagnostic approach to STEC-HUS, on the related neurologic complications, and on a novel approach to their management.

An innovative international rotation in integrative rehabilitation medicine was implemented as part of the physical medicine and rehabilitation residency program at the Medical College of Wisconsin. Rotation objectives were to introduce medical knowledge of integrative medicine treatments into physical medicine and rehabilitation practice and to initiate collaboration with international academic partners. Residents were approved based on their academic record, completion of prerequisites, and personal statement. During a 4-wk rotation located in Italy, residents developed an integrative treatment strategy for each patient using conventional medical care and other therapeutic options, including acupuncture, biofeedback, aquatic therapy, yoga, and others. Postrotation assessment included evaluations by Italian team and patients, residents' evidence-based presentations, and postrotation self-reflection. Participating residents reported high achievement in clinical performance, improved application of integrative medicine, broader appreciation of cultural diversity in patient care, and increased personal and professional development. This reciprocal program model serves as an example for other programs interested in implementing similar international rotations.

OBJECTIVE:Noninvasive continuous positive airway pressure (nCPAP) is applied through different interfaces to treat mild acute respiratory failure (ARF) in infants. Recently a new pediatric helmet was introduced in clinical practice to deliver nCPAP. The objective of this study was to compare the feasibility of the delivery of nCPAP by the pediatric helmet with delivery by a conventional facial mask in infants with ARF.PATIENTS AND METHODS:We conducted a single-center physiologic, randomized, controlled study with a crossover design on 20 consecutive infants with ARF. All patients received nCPAP by helmet and facial mask in random order for 90 minutes. In infants in both trials, nCPAP treatment was preceded by periods of unassisted spontaneous breathing through a Venturi mask. The primary end point was the feasibility of nCPAP administered with the 2 interfaces (helmet and facial mask). Feasibility was evaluated by the number of trial failures defined as the occurrence of 1 of the following: intolerance to the interface; persistent air leak; gas-exchange derangement; or major adverse events. nCPAP application time, number of patients who required sedation, and the type of complications with each interface were also recorded. The secondary end point was gas-exchange improvement.RESULTS:Feasibility of nCPAP delivery was enhanced by the helmet compared with the mask, as indicated by a lower number of trial failures (P < .001), less patient intolerance (P < .001), longer application time (P < .001), and reduced need for patient sedation (P < .001). For both delivery methods, no major patient complications occurred.CONCLUSIONS:The results of this current study revealed that the helmet is a feasible alternative to the facial mask for delivery of nCPAP to infants with mild ARF.

Aims and methods: The present study evaluated time-related changes in platelet monoamine oxidase B (MAO-B) activity in an Italian cohort of alcohol-dependent subjects ( n = 98) during early abstinence, and the effect of potential confounding factors, such as gender and smoking status, on the temporal trend of the enzyme activity. Results: While still under the influence of ethanol (time point T1), the mean value of platelet MAO-B activity in alcoholics was 6.4 ± 3.1 nmol/mg of protein/h. This increa sed by >40% (to 9.3 ± 4.4 nmol/mg of protein/h) after 8 days of withdrawal (T2), and remained stable thereafter (T3 and T4: 15 and 2 2 days of abstinence, respectively). In a cohort of 138 healthy subjects, MAO activity levels averaged 9.9 ± 0.9 nmol/mg of protei n/h. In the group of alcoholic patients, alcohol intake cessation was confirmed by the progressive decrease of serum % carbohydrate-def icient transferrin (CDT), which was pathologically above the reference limits (6%) at T1 (7.8 ± 3.3%), declined to 6.6 ± 2.1% at T2 and reached physiological values at T3 and T4. In a subgroup of cirrhotic alcoholics, %CDT did not decrease over time, while MAO ac tivity rose after the first week of abstinence, without further change at T3 and T4. During early withdrawal, neither gender nor tobac co smoking affected the temporal pattern of MAO activity. Conclusions: MAO-B can be regarded as a state marker of alcohol consumption. The temporal pattern of platelet MAO-B activity may be used for the diagnostic assessment of alcoholism and early abstinence, r egard- less of gender and smoking status.

Context. Neuropathic pain is common, disabling, and often difficult to treat. Objectives. To compare guideline-based drug management with Scrambler therapy, a patient-specific electrocutaneous nerve stimulation device. Methods. A clinical trial with patients randomized to either guideline-based pharmacological treatment or Scrambler therapy for a cycle of 10 daily sessions was performed. Patients were matched by type of pain including postsurgical neuropathic pain, postherpetic neuralgia, or spinal canal stenosis. Primary outcome was change in visual analogue scale (VAS) pain scores at one month; secondary outcomes included VAS pain scores at two and three months, pain medication use, and allodynia. Results. Fifty-two patients were randomized. The mean VAS pain score before treatment was 8.1 points (control) and 8.0 points (Scrambler). At one month, the meanVASscorewasreducedfrom8.1to5.8(� 28%)inthecontrolgroup,andfrom 8 to 0.7 points (� 91%) in the Scrambler group (P< 0.0001). At two and three months, the mean pain scores in the control group were 5.7 and 5.9 points, respectively, and 1.4 and 2 points in the Scrambler group, respectively (P< 0.0001). More relapses were seen in polyradicular pain than monoradicular pain, but retreatmentandmaintenancetherapygaverelief.Noadverseeffectswereobserved. Conclusion. In this pilot randomized trial, Scrambler therapy appeared to relieve chronic neuropathic pain better than guideline-based drug management. J Pain Symptom Manage 2012;43:87e95. 2012 U.S. Cancer Pain

Cardiac dysfunction including arrhythmias and myocardial ischemia have often been reported in carbon monoxide poisoning; scattered punctiform hemorrhages throughout the heart have been documented in autopsy samples. An appropriate diagnostic approach is crucial to assess carbon monoxide cardiac damage. This evaluation may be confounded by several factors, including the absence of overt symptoms and of specific ischemic changes in the electrocardiogram. In experimental studies, laboratory animals can develop cardiac changes similar to those seen in humans and therefore proved to be useful models to study the effects and the mechanisms of cardiac damage due to carbon monoxide. These investigations, as well as others performed in vitro, provide support for a direct action of carbon monoxide on the heart, in addition to systemic hypoxia produced by carboxyhemoglobin formation. This review focuses on the diagnostic aspects of carbon monoxide cardiotoxicity. Experimental results obtained in animals and in vitro models are also discussed.

Cardiovascular disorders including myocardial ischemia and heart failure have been described in both laboratory animals and humans following carbon monoxide poisoning. Carbon monoxide cardiotoxicity may be clinically occult and often remains undiagnosed because of the lack of overt symptoms and specific ischemic changes in the electrocardiogram. Routine myocardial necrosis markers have low diagnostic efficiency, particularly in patients with concomitant skeletal muscle necrosis or multiple organ failure complicating carbon monoxide poisoning. Carbon monoxide-induced cardiotoxicity has been investigated rarely in children.This paper describes carbon monoxide poisoning in a 12-year-old child who suffered from occult cardiac damage despite mild symptoms and low carboxy hemoglobin concentrations. Myocardial and mitral valve dysfunctions were observed, suggesting an ischemia-like syndrome. Cardiac damage was completely reversible within 1 month.This case report supports that a prolonged carbon monoxide exposure can cause cardiac damage in children even in the absence of specific symptoms, cerebral failure and high carboxyhemoglobin concentrations.

Ciguatera poisoning causes mainly gastrointestinal and neurological effects of variable severity. However, symptoms of peripheral neuropathy with paresthesias and paradoxical disturbance of thermal sensation are the hallmark. Electrophysiological studies are often normal, except in severe cases. We report four people who developed mild ciguatera poisoning after barracuda ingestion. Electrophysiological studies documented normocalcemic latent tetany. These findings are consistent with ciguatoxin's mechanism of toxicity, which involves inactivation of voltage-gated Na + channels and eventually increases nerve membrane excitability.

Cerebellar granule cells (CGCs) are a sensitive target for methylmercury (MeHg) neurotoxicity. In vitro exposure of primary cultures of rat CGCs to MeHg resulted in a time- and concentration-dependent cell death. Within 1 hr exposure, MeHg at 5-10 microM caused impairment of mitochondrial activity, de-energization of mitochondria and plasma membrane lysis, resulting in necrotic cell death. Lower MeHg concentrations (0.5-1 microM) did not compromise cell viability, mitochondrial membrane potential and function at early time points. Later, however, the cells progressively underwent apoptosis and 100% cell death was reached by 18 hr treatment. Neuronal network fragmentation and microtubule depolymerization were detected as early as within 1.5 hr of MeHg (1 microM) exposure, long before the occurrence of nuclear condensation (6-9 hr). Neurite damage worsened with longer exposure time and proceeded to the complete dissolution of microtubules and neuronal processes (18 hr). Microtubule stabilization by taxol did not prevent MeHg-induced delayed apoptosis. Similarly ineffective were the caspase inhibitors z-VAD-fluoromethylketone and z-DEVD-chloromethylketone, the L-type calcium channel inhibitor nifedipine, the calcium chelator EGTA and BAPTA, and the NMDA receptor antagonist MK-801. On the other hand, insulin-like growth factor-I partially rescued CGCs from MeHg-triggered apoptosis. Altogether these results provide evidence that the intensity of MeHg insult is decisive in the time of onset and the mode of neuronal death that follows, i.e., necrosis vs. apoptosis, and suggest that cytoskeletal breakdown and deprivation of neurotrophic support play a role in MeHg delayed toxicity.