Community nursing. Room for a view.
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Biomedical subjects
Publications and source records attributed to A Norman.
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OBJECTIVE: To evaluate the medical impact of reactive pharmacy intervention. DESIGN: Analysis of all interventions during 28 days by all 35 pharmacists in hospitals in Nottingham. SETTING: All (six) hospitals in the Nottingham health authority (a teaching district), representing 2530 mainly acute beds, 781 mental illness beds, and 633 mainly health care of the elderly beds. PATIENTS: Hospital inpatients and outpatients. INTERVENTIONS: Recording of every important intervention made by pharmacists to prescriptions for both inpatients and outpatients when they perceived inadequacies of drug prescription or administration, including characterisation of the problem, coding of outcome, recording of time taken to initiate and resolve intervention, and grade of prescribing doctor. The problems were independently assessed for their potential to cause medical harm. RESULTS: 769 Interventions (about 2.9% of prescriptions) were made, of which 60 concerned prescriptions rated as having a major potential for medical harm. The commonest problems concerned dosage, which was wrong in 280 prescriptions (102 for antibiotics) and not stated in 50 (one for antibiotics), especially those associated with a major potential for medical harm (32 prescriptions). These concerned sedatives; analgesics; cardiovascular drugs or diuretics; and iron, vitamin, or mineral preparations. Also common were overprolonged prescription of antibiotics (48 prescriptions), confusion of drug names (nine), and inadvertent coprescription of excessive quantities of aspirin or paracetamol in plain and compound preparations (seven). The pharmacist's recommendation was accepted in 639 instances (86%), and the prescription was altered in 575, leading to an appreciable (246 cases) or minor (231 cases) improvement. Interventions had little effect on costs; 427/646 had no effect and 130 produced savings less than 50p. Pharmacy intervention (730/769 interventions) occupied on average 41 minutes per pharmacist per week. CONCLUSIONS: Most reactive pharmacy interventions concerned prescribing errors with a limited potential for medical harm, but a small number of detected errors with a major potential for medical harm; cost savings were not appreciable.
Many tumors in the brain and in other tissues can be delineated precisely in images obtained with a CT scanner. After the scan is obtained the patient is taken to another room for radiation therapy and is positioned in the beam with the aid of external markers, simulators or stereotactic devices. This procedure is time consuming and subject to error when precise localization of the beam is desired. The CT scanner itself, with the addition of a collimator, is capable of delivering radiation therapy with great precision without the need for external markers. The patient can be scanned and treated on the same table, the isocenter of the beam can be placed precisely in the center of the lesion, the beam can be restricted to just those planes in which the lesion appears several arcs can be obtained by simply tilting the gantry, and the position of the patient in the beam can be monitored continuously during therapy. We describe here the properties of the CTX, the CT scanner modified for therapy.
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The effect of antacids on the systemic absorption of oral norfloxacin was evaluated in 12 healthy volunteers. Subjects were given each treatment in a balanced sequence at 7-day intervals. Treatments included 400 mg of norfloxacin alone, 400 mg of norfloxacin 5 min after aluminum-magnesium hydroxide (Maalox), Maalox 2 h after 400 mg of norfloxacin, and 400 mg of norfloxacin 5 min after calcium carbonate (Titralac). Blood and urine samples were collected at predetermined time intervals for 24 and 48 h, respectively. Norfloxacin concentrations in plasma and urine were determined by high-pressure liquid chromatography. The area under the plasma concentration-versus-time curve from time zero to infinity and urinary recovery were used to compare the relative bioavailability of norfloxacin with antacids with that of norfloxacin alone. Norfloxacin bioavailability was markedly reduced when subjects received antacid pretreatment. When norfloxacin was given 5 min after Maalox and Titralac, the bioavailabilities were 9.02 and 37.5%, respectively, relative to that for 400 mg of norfloxacin alone. When Maalox was given 2 h after norfloxacin, maximal concentrations of norfloxacin in plasma occurred between 1 and 1.5 h postdose, and absorption was reduced to a lesser extent, with a relative bioavailability of 81.31%. Norfloxacin concentrations in urine were also reduced as a result of antacid administration. Antacids containing aluminum and magnesium salts and calcium carbonate should be avoided by patients taking norfloxacin.
Vascularly perfused duodenal loops from normal vitamin D-replete chicks were used to obtain insight with regards to the possible mechanism(s) by which 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] rapidly stimulates intestinal Ca2+ transport (transcaltachia). The phorbol ester, 12-o-tetradecanoyl phorbol-13 acetate (TPA) (100 nM), and the adenylate cyclase activator, forskolin (10 microM), were found to stimulate Ca2+ transport from the lumen to the vascular effluent to the same extent that physiological levels of 1,25(OH)2D3 achieve. The effects of both substances exhibited concentration dependence. Similarly to 1,25(OH)2D3, addition of either TPA or forskolin to the lumenal compartment of normal chicks or vascular perfusion of duodena from vitamin D-deficient chicks failed to stimulate Ca2+ transport. Also and analogously to 1,25(OH)2-D3, TPA and forskolin-enhanced duodenal Ca2+ transport was abolished by the Ca2(+)-channel antagonists nifedipine (1 microM) and verapamil (30 microM). In addition, the protein kinase C inhibitor, staurosporine, totally abolished the rise in Ca2+ transport caused by 130 pM 1,25(OH)2D3. The synthetic peptide IP20, a well characterized cAMP-dependent protein kinase inhibitor, was also effective in suppressing 1,25(OH)2D3-dependent stimulation of duodenal Ca2+ transport. Collectively these results suggest that protein kinase C and cAMP-dependent protein kinase mediate 1,25(OH)2D3 activation of basal lateral membrane Ca2(+)-channels as an early effect in the transcaltachic response.
Periosteal chondroma is a slow-growing benign cartilaginous tumor of limited size arising within or under the periosteum, which, through constant pressure, induces cortical erosion and periosteal reaction. Ten new cases of periosteal chondroma are reported. All were treated by marginal or intralesional excision. No local recurrence was seen following this treatment. These patients demonstrated the clinical, roentgenographic, and pathologic features of this benign entity, which aid diagnosis, thereby avoiding overtreatment.
Two different methods for evaluating platelet antibody were used to study 12 normal subjects and 24 patients consisting primarily of intravenous drug users (IVDUs) who were positive for human immunodeficiency virus (HIV). Total platelet-associated immunoglobulin G (IgG) and immunoglobulin M (IgM) were measured by enzyme-lined immunosorbent assay on platelet lysate, and platelet surface-associated IgG and IgM were measured by semiquantitative flow cytometry. IgG and IgM values showed significant correlations between the two measurement methods. Mean platelet surface IgG and total IgG were 3.6 and 4.3 times greater, respectively, in IVDUs than in controls, and platelet IgM was also significantly higher in IVDUs than in controls as measured by both techniques. Although mean platelet immunoglobulin levels were higher in the IVDUs with thrombocytopenia than in IVDUs with normal platelet counts, these differences did not achieve significance. These data show that platelet IgG and IgM levels are increased in IVDU-associated HIV infection and suggest that these increases are not confined to patients manifesting thrombocytopenia. The herein described platelet surface antibody and total platelet antibody measurements appear to be equally useful in studying this patient population. Specific details for generating platelet-associated immunofluorescence units are discussed.
We present four adults with tuberculous granulomas of bone. In three patients the granuloma involved the end of a long bone. The vertebral body and the right pedicle of the 10th thoracic vertebra were involved in the fourth patient. In all four the adjacent joint or the disk space was spared; hence the lesions mimicked bone neoplasms. Sclerotic changes, periosteal reaction and sequestration were present in three patients. Three of the four patients were not white. Since histologic specimens may not reveal mycobacteria, radiologists should alert orthopedic surgeons to the need to obtain material for culture at the time of biopsy of lesions that might be unusual manifestations of skeletal tuberculosis.
The similarity in clinical features of X-linked Becker muscular dystrophy (BMD) and the autosomal recessive limb-girdle (LGD) type of adult muscular dystrophy makes differential diagnosis of the isolated male case difficult. DNA probes complementary (cDNA) to the Duchenne/Becker muscular dystrophy gene product, dystrophin, can detect molecular deletions in 60-70% of affected subjects. Thirty-three patients with BMD or LGD (thirty isolated and three with an affected brother) were screened with a panel of cDNA probes for the whole dystrophin gene. Deletions were found in thirteen of eighteen (72%) patients with a diagnosis of BMD. Deletions were also found in four of the fifteen (27%) patients previously thought to have LGD, who were therefore reclassified as having BMD. All male patients with progressive muscular dystrophy of limb-girdle pattern should be routinely screened with these cDNA probes as a useful adjunct to their clinical diagnosis since the results have important implications for genetic counselling of affected families.
Manifesting carriers of Duchenne and Becker muscular dystrophy are uncommon but well described. Such patients are of particular importance with regard to the differential diagnosis from autosomal recessive limb-girdle muscular dystrophy. All mothers of affected males known to the Genetic Register of Muscular Dystrophy Families in Wales were contacted, and 167 out of a possible 190 were examined. It was estimated from pedigree and creatine kinase analysis that 119 out of the 167 were carriers of the Duchenne/Becker gene. Three manifesting carriers were identified, giving the proportion affected as 3/119 = 2.5%. We estimate the prevalence of manifesting carriers to be 1 in 100,000 of the female population, a figure comparable to the prevalence of autosomal recessive limb-girdle muscular dystrophy. During the period of the survey, several other women with similar clinical findings but without an appropriate family history were seen. We strongly suspect that some of these are also manifesting carriers of the Duchenne/Becker gene.
A study involving 25 health male volunteers was conducted to evaluate the effect of lomefloxacin on the pharmacokinetics of theophylline. The mean age was 22.4 +/- 3.0 years, and the mean weight was 77.3 +/- 7.7 kg. A single 6-mg/kg aminophylline dose was given intravenously on study days 1 and 15. The subjects received a 400-mg lomefloxacin dose (four 100-mg capsules) on study days 9 through 15. No treatment was given on study days 2 through 8. Thirteen blood samples were collected within 24 h after each aminophylline dose. Theophylline concentrations in serum were measured by enzyme immunoassay (EMIT). The mean aminophylline dose was 437 +/- 36 mg, equivalent to 344 mg of theophylline. Multiple doses of lomefloxacin had no effect on the area under the concentration-time curve from 0 h to infinity, maximal concentration, or clearance of theophylline from serum. There was a slight increase in the theophylline half-life from 6.72 +/- 1.63 to 7.02 +/- 1.37 h after lomefloxacin dosing (P = 0.04); however, the change was clinically insignificant. No change in theophylline dose is required when lomefloxacin therapy is instituted in a patient receiving theophylline.
Thirty asymptomatic ankles were studied with high-resolution surface coil magnetic resonance (MR) imaging to identify normal structures. Several normal variants were demonstrated, including (a) Cortical irregularity of the posterior tibiotalar joint (should not be mistaken for osteonecrosis) in 27 of 30 cases; (b) normal posterior talofibular ligament with irregular and frayed superior edge simulating a tear in 13 of 30 cases; (c) normal navicular insertion of the posterior tibial tendon with heterogeneous signal intensity in 14 of 30 cases; (d) deltoid ligament inhomogeneity in seven of ten cases; and (e) fluid in the shared peroneal tendons sheath (may be confused with a longitudinal tendon tear) in three of 30 cases. Ankle imaging with the use of MR is still a relatively new procedure. Further investigation is needed to better define normal anatomy and normal variants.
Radiographs of symptomatic joints were retrospectively evaluated in 24 patients with inflammatory arthritis and human immunodeficiency virus (HIV) infection. Clinically, 20 patients had a seronegative arthritis including Reiter syndrome (54%), psoriatic arthritis (17%), and undifferentiated forms of spondyloarthropathy (13%). These patients were indistinguishable radiographically from patients with typical seronegative disorders except for the predominance of lower-extremity abnormalities. Four patients (17%) had a rheumatoidlike arthritis defined as acute symmetric polyarthritis (ASP). With the exception of extensive proliferative periostitis, ASP simulated classic rheumatoid arthritis. HIV-associated arthritis was manifest during various stages of HIV infection. It preceded acquired immunodeficiency syndrome in 64% of patients with stage IV HIV infection. Awareness of the coexistence of HIV infection in patients with the above-mentioned arthritides is important, since immunosuppressive therapy, commonly used in the treatment of arthritis, can have detrimental effects in patients with HIV infection.
[24-14C] glycochenodeoxycholate-3-sulphate (GCDC-3S) was given intravenously to seven patients with liver cirrhosis and the elimination of the isotope from blood and the isotope excretion in urine and faeces followed. The bile acid conjugates in serum and urine were separated by HPLC and the change in specific activity in isolated conjugates determined. [24-14C] GCDC-3S was rapidly eliminated either by urinary excretion or faecal excretion and the half-life of the labelled conjugates varied between 76-198 min. No deamination or desulphation of the isotope occurred prior to urinary excretion. Only small amounts of GCDC-3S excreted in bile were absorbed from the intestine, as no isotope was recovered in other bile acid conjugates in serum.
Twenty-two histologically proven cortical metastases in 11 patients with bronchogenic carcinoma (10 squamous cell and one adenocarcinoma) were studied. The intracortical foci could be classified according to four distinctive patterns of bone destruction: small focal intracortical lesions ("cookie-bite" or "cookie-cutter" pattern); large osteolytic lesions; saucerized intracortical lesions with well-defined periosteal reaction; and lesions with predominant cortical destruction extending into the soft tissue as well as the medullary cavity. All lesions were located in the femoral bones.
In 36 women with unexplained primary recurrent abortion, 13 with secondary unexpained recurrent abortion, 25 with primary unexplained infertility, 7 with secondary unexplained infertility and two groups of control women, autoantibodies to soluble cellular antigens were measured by Western blotting to a disaggregated HeLa cell antigen preparation, by counter immunoelectrophoresis and by indirect immunofluorescence. Using Western blotting the women with primary infertility and those with secondary recurrent abortion had a significantly higher prevalence of autoantibodies (P less than 0.01 in each case). This was not shown using the other methods. It is possible that these antibodies could be causally related to the pathology of the conditions studied.
We have defined variants (V) resistant to 6-thioguanine (TG) by their ability to divide at least once during a 72-h incubation in a medium containing 0.2 mM TG. We blocked cytokinesis by adding cytochalasin B (CB) after 30 h in culture. The cells that had undergone nuclear division were identified by their content of 2 or more nuclei. The long incubation period allowed slow growing V to be counted. As a result we scored an order of magnitude more V than have been reported in assays using the conventional 30-40 h culture times. In the gamma-ray dose range of 0-0.5 Gy we scored 80 V per 1000 surviving lymphocytes per Gy--a result some two orders of magnitude larger than has been reported previously.