Using complexity theory to build interventions that improve health care delivery in primary care

Previous observational research confirms abundant variation in primary care practice. While variation is sometimes viewed as problematic, its presence may also be highly informative in uncovering ways to enhance health care delivery when it represents unique adaptations to the values and needs of people within the practice and interactions with the local community and health care system. We describe a theoretical perspective for use in developing interventions to improve care that acknowledges the uniqueness of primary care practices and encourages flexibility in the form of intervention implementation, while maintaining fidelity to its essential functions.     

Local treatment of Pseudomonas infection of the ear. A small clinical study

Infections of the middle and external ear caused by the problem-micro-organism Pseudomonas aeruginosa can be cured by local therapy with Ciprofloxacin and Tutofusin very quickly and without any complications. Drum ruptures caused by ear secretions close up again spontaneously. Tympanon tubes can be left in situ. Function disturbances of the middle and internal ear clear up and the functions return to normal.     

Effect of the white blood count on the clinical management of the febrile infant

BACKGROUND. The white blood count is commonly used in the evaluation of the febrile infant without a focal source of infection. This study describes the physician's use of diagnostic tests in this clinical situation and also evaluates the effect of an elevated white blood count (WBC) on diagnostic test ordering and patient management. METHODS. A case scenario describing a febrile infant was mailed to all 294 pediatric, family, general, and emergency physician members of the Academy of Medicine of Cleveland. Questions about test ordering and case management were asked, both before and after the patient's WBC was known. Physicians were randomly assigned to receive a case scenario with either a normal or an elevated WBC. RESULTS. Of the 294 physicians contracted, 196 (67%) returned usable questionnaires. Physicians ordered an average of 1.4 tests in the initial management of the case, for an average cost of $82. Emergency physicians ordered more tests than other physicians (2.4 vs 1.2 tests, P = .001). Once the WBC was known, physicians in the high WBC group ordered more additional tests than the normal WBC group (0.89 vs 0.33 tests, P less than .001), and were more likely to change to a more aggressive therapeutic management strategy (P less than .001). CONCLUSIONS. The cost of physician-ordered laboratory testing is significant for the clinical scenario of a febrile infant without a localizing source. An elevated WBC affects physician management by causing more tests to be ordered and by influencing some physicians to choose more aggressive management strategies.     

The effect of harmaline on intestinal sodium transport and on sodium-dependentd-glucose transport in brush-border membrane vesicles from rabbit jejunum

Harmaline inhibition of sodium uptake and of sodium-dependentd-glucose transport was investigated using brush-border membrane vesicles from frozen rabbit jejunum. Under sodium-gradient conditions, initiald-glucose uptake (20 s) was inhibited by harmaline at concentrations above 0.5 mM, but at lower harmaline concentrationsd-glucose uptake was stimulated by 10–15%. When a similar potassium gradient was used, harmaline had no effect. At concentrations upt to 2 mM, harmaline did not alter the equilibrium uptake ofd-glucose ord-mannitol. After pre-equlibration with sodium (25 mM),d-glucose uptake was inhibited at harmaline concentrations ranging from 0.1 to 2 mM. Sodium (10 mM) uptake was also inhibited by harmaline. Increasing the sodium concentration reduced the inhibitory effect of harmaline on tracer sodium uptake as well as on sodium-dependentd-glucose uptake. Similar to phlorizin, harmaline (1 mM) was able to prevent glucose-induced sodium influx across the brush-border membrane.Sodium uptake into brush-border membrane vesicles seems to be inhibited at lower harmaline concentrations than sodium-dependentd-glucose uptake. At high (2 mM) inhibitor concentrations, however, sodium-dependent glucose uptake is more strongly inhibited than sodium uptake. These results suggest that harmaline inhibits both sodium and sodium-dependent transport across intestinal brush-border membranes by interacting with specific sodium-binding sites.     

Defensin deficiency, intestinal microbes, and the clinical phenotypes of Crohn's disease

Crohn's disease is a chronic, inflammatory disease of the intestinal mucosa. Although intestinal bacteria are implicated in disease pathogenesis, the etiology is still unclear. The main location of disease is the small intestine (ileum) and the colon. Ileal disease has been linked to a mutation in the NOD2 gene. Defensins are antimicrobial peptides and in the ileum, are mainly expressed in Paneth cells, epithelial cells that also express NOD2. In the colon, defensins are expressed by enterocytes or metaplastic Paneth cells. Crohn's disease patients with ileal involvement, compared with controls or Crohn's patients without ileal involvement, have diminished expression of ileal Paneth cell defensins. This decrease is even more pronounced in Crohn's patients displaying a NOD2 mutation. In contrast, Crohn's disease of the colon is characterized by an impaired induction of beta-defensins in enterocytes. The colonic expression of the constitutive beta-defensin 1 is also decreased in the inflamed colonic mucosa, but this decrease is less specific to Crohn's disease, as it can also be found in ulcerative colitis patients. In conclusion, the regional localizations of Crohn's disease, ileal or colonic disease, can be linked to different defensin profiles. Crohn's disease of the ileum is associated with diminished defensin expression in Paneth cells. Crohn's disease of the colon is associated with diminished beta-defensin expression in enterocytes. Thus, it can be speculated that decreased defensin levels lead to a weakened intestinal barrier function to intestinal microbes and might be crucial in the pathophysiology of Crohn's disease.