Care related pain in hospitalized patients: A cross‐sectional study

Context: Care‐related pain includes pain occurring during transportation, movement, diagnostic imaging, physical examination, or treatment. Its prevalence has never been assessed in a large adult inpatient population. Objective: To identify the procedures likely to induce or increase pain in hospital patients, attempting to separate the most painful from those reported as most frequently inducing pain. Design: A single‐day cross‐sectional survey conducted in two large French teaching hospitals, including all hospitalized patients, free of communication problems. One third was randomly selected and interviewed about the painful episodes that had occurred or were associated with the procedures performed during the previous two weeks. Patients were interviewed using a structured questionnaire. Results: Six‐hundred‐eighty‐four patients were randomly selected. Six‐hundred‐seventy‐one painful events were reported in 55% of the patients, with an average of 1.8events/patient. Fifty‐two percent of the painful events were associated with procedures performed by non‐medical staff; 38% of the painful episodes occurred during procedures involving vascular puncture and 24% during patients’ mobilization. In 57% of painful procedures, pain was rated as severe or extremely severe. The most painful procedures were invasive procedures, other than vascular and non vascular punctures (74% of severe and extremely severe painful episodes). Maximum pain intensity was rated higher for procedures that were repeated than for those experienced only once (62% versus 53%, p=0.02). Conclusion: This survey gives new insight into our daily practice. Proper management of care‐related pain should be a major concern of all hospital staff to improve the quality of our health care.     

Granulocyte-macrophage colony-stimulating factor: signals for its mRNA accumulation

Granulocyte-monocyte colony-stimulating factor (GM-CSF) is an important hematopoietic growth factor. Mesenchymal cells produce abundant GM-CSF in response to tumor necrosis factor alpha (TNF). We wished to determine (1) what cellular pathways enhanced levels of GM-CSF mRNA, and (2) if TNF used any of these pathways. Modulation in levels of GM- CSF mRNA in human fibroblasts (WI-38) was studied by using Northern blot analysis. Markedly increased levels of GM-CSF mRNA occurred in these cells after exposure to sodium fluoride (NaF) and the effect of NaF was slightly enhanced by aluminum chloride; these results suggest that accumulation of GM-CSF mRNA can occur by activating a G-binding protein. Stimulators of protein kinase C dramatically increased levels of GM-CSF mRNA; however, blockade of protein kinase C activity did not attenuate accumulation of GM-CSF mRNA stimulated by TNF and NaF. Exposure to ouabain increased levels of GM-CSF mRNA and this effect was prominently enhanced in the presence of low concentrations of extracellular K+ and was almost abolished in high concentrations of extracellular K+. A monovalent ionophore (monensin) also increased levels of GM-CSF mRNA. Both ouabain and monensin can increase intracellular Ca++ concentration (Cai++) through Na+-Ca++ exchange. A calcium channel blocker (diltiazem) blocked the increased levels of GM- CSF mRNA mediated by ouabain, but could not block the stimulation mediated by TNF alpha. Ca++ ionophores also increased levels of GM-CSF mRNA and rapidly increased levels of Cai++. TNF did not increase Cai++ and, moreover, was able to stimulate accumulation of GM-CSF mRNA in the absence of extracellular Ca++. Taken together, we have found that several different cellular pathways can lead to prominent accumulation of GM-CSF mRNA in mesenchymal cells including (1) activation of protein kinase C, (2) increase in Cai++, and (3) stimulation of G-binding protein. Our studies show that TNF appears to increase levels of GM-CSF mRNA independent of protein kinase C activity or levels of Cai++.     

Relapse cell population differs from acute onset clone as shown by absence of the initially activated N-ras oncogene in a patient with acute myelomonocytic leukemia

We have conducted a follow-up study of a patient with myelomonocytic leukemia exhibiting an N-ras mutation (Gln61----Lys61) using the polymerase chain reaction method and synthetic oligonucleotide hybridization probes. This method allowed us to detect as little as 3% of N-ras-mutated cells within a population. When the patient went into clinical remission, the mutation became undetectable. When a relapse occurred, the blasts did not carry the N-ras mutation. Analysis of M13 cloned amplified N-ras sequences from relapse DNA revealed exclusively the wild type allele of the N-ras gene. These findings suggest that the relapse cell population is derived from a different clone than the acute phase population. Furthermore, the data argue that N-ras mutation is not an initiating lesion in this case of acute myelomonocytic leukemia (AMML).     

Quantification of blood flow with dynamic MR imaging and presaturation bolus tracking

A technique is described for rapid imaging of blood flow and dynamic measurement of its velocity. The method is a combination of bolus tracking and low-flip-angle gradient-echo cine angiography. This method provides precise determination of velocity with high temporal resolution in a single measurement. Unlike what occurs in phase imaging techniques, flow is displayed directly, eliminating potential errors that result from non-flow-related sources of phase shifts. Manipulation of raw data sets is avoided. Results obtained from a flow phantom, healthy volunteers, and a patient with an aortic aneurysm demonstrate the capability of the technique to track flow at low and high velocities and to differentiate flowing blood from thrombus. Because of its conceptual simplicity, rapidity, and lack of susceptibility to extraneous phase shifts, this technique may prove ideal for in vivo flow measurement and evaluation of flow patterns.