Cannulation of the Internal Mammary Vein With a Single-Lumen Infusion Catheter in a Patient With Portal Hypertension: A Case Report.

We present a central venous catheter misplacement case. A left internal jugular vein percutaneous introducer was inserted for fluid resuscitation with a single-lumen infusion catheter placed through the lumen for medication infusions. Placement was performed under ultrasound guidance, with confirmation of the wire within the venous lumen. Radiographs suggested that the introducer had perforated the innominate vein. Contrast was injected through the single-lumen infusion catheter and showed cannulation of the left internal mammary vein. The link between portal hypertension and increased risk of central line misplacement as well as diagnosis and potential methods to avoid this rare complication are discussed.

Evidence of augmented central pain processing in idiopathic chronic low back pain.

OBJECTIVE: For many individuals with chronic low back pain (CLBP), there is no identifiable cause. In other idiopathic chronic pain conditions, sensory testing and functional magnetic resonance imaging (fMRI) have identified the occurrence of generalized increased pain sensitivity, hyperalgesia, and altered brain processing, suggesting central augmentation of pain processing in such conditions. We compared the results of both of these methods as applied to patients with idiopathic CLBP (n = 11), patients with widespread pain (fibromyalgia; n = 16), and healthy control subjects (n = 11). METHODS: Patients with CLBP had low back pain persisting for at least 12 months that was unexplained by MRI/radiographic changes. Experimental pain testing was performed at a neutral site (thumbnail) to assess the pressure-pain threshold in all subjects. For fMRI studies, stimuli of equal pressure (2 kg) and of equal subjective pain intensity (slightly intense pain) were applied to this same site. RESULTS: Despite low numbers of tender points in the CLBP group, experimental pain testing revealed hyperalgesia in this group as well as in the fibromyalgia group; the pressure required to produce slightly intense pain was significantly higher in the controls (5.6 kg) than in the patients with CLBP (3.9 kg) (P = 0.03) or the patients with fibromyalgia (3.5 kg) (P = 0.006). When equal amounts of pressure were applied to the 3 groups, fMRI detected 5 common regions of neuronal activation in pain-related cortical areas in the CLBP and fibromyalgia groups (in the contralateral primary and secondary [S2] somatosensory cortices, inferior parietal lobule, cerebellum, and ipsilateral S2). This same stimulus resulted in only a single activation in controls (in the contralateral S2 somatosensory cortex). When subjects in the 3 groups received stimuli that evoked subjectively equal pain, fMRI revealed common neuronal activations in all 3 groups. CONCLUSION: At equal levels of pressure, patients with CLBP or fibromyalgia experienced significantly more pain and showed more extensive, common patterns of neuronal activation in pain-related cortical areas. When stimuli that elicited equally painful responses were applied (requiring significantly lower pressure in both patient groups as compared with the control group), neuronal activations were similar among the 3 groups. These findings are consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP.

Evoked pain measures in fibromyalgia.

Fibromyalgia is defined by widespread pain and tenderness at a minimum of 11 of 18 defined tender points. Current evidence indicates that tender points are not unique to fibromyalgia and are simply regions in the body where all people are more tender. Tenderness (i.e. sensitivity to pressure) is widespread in fibromyalgia rather than being confined to tender points, and patients are also more sensitive to heat, cold and electrical stimulation. Using the number of painful tender points as a measure of tenderness is clinically expedient but is theoretically vulnerable to bias and is influenced by subjective distress. Other means of assessing tenderness (e.g. pressure dolorimeter devices, or more elaborate psychophysical methods) demonstrate the same increased pain sensitivity in fibromyalgia that is noted with tender point assessments, but these measures are relatively independent of biasing factors or distress. Fibromyalgia is one of only a few syndromes defined by the presence of both spontaneous (i.e. clinical) and evoked (i.e. experimental) pain. While the issues associated with the evaluation of spontaneous pain are shared with all chronic pain syndromes, the issues associated with the evaluation of evoked pain sensitivity are specific to fibromyalgia and related musculoskeletal disorders. This chapter focuses on the evaluation of altered pain sensitivity in fibromyalgia. It describes current measurement methodology, briefly reviews studies of sensitivity to experimentally evoked painful and non-painful sensations, analyses the factors assessed by different measurement methodologies, and concludes with recommendations for future diagnostic criteria and measurement methods.