Osteomyelitis: detection with US

To evaluate the role of ultrasound (US) in the detection of osteomyelitis, the authors prospectively studied 48 patients clinically suspected of having osteomyelitis. A sonographic diagnosis was made if fluid was seen directly in contact with bone, without intervening soft tissues. Twelve of the 48 patients were subsequently found to have osteomyelitis. In 10 of them, US demonstrated abnormal fluid adjacent to the bone. This fluid was thought to represent an inflammatory exudate dissecting in a subperiosteal and/or extraperiosteal location. Eight of the 48 patients had soft-tissue fluid collections. The rest of the patients either had no abnormalities or had cellulitis. The authors conclude that US can be useful in the detection of osteomyelitis.     

Thromboxane synthesis inhibition reverses group B Streptococcus-induced pulmonary hypertension

Group B Streptococcus (GBS) sepsis in humans may cause the persistent pulmonary hypertension syndrome. Infusions of GBS in animals elevate pulmonary artery pressure (PAP) and resistance and are associated with elevated thromboxane levels. We investigated the hemodynamic effects of the specific thromboxane synthesis inhibitor, dazmegrel, in a piglet model of GBS-induced pulmonary hypertension. PAP rose from 22 +/- 6 to 42 +/- 11 (SD) mm Hg during infusion of heat-killed GBS; pulmonary vascular resistance increased from 1440 +/- 400 to 4000 +/- 1040 dyne X sec/cm5. No significant changes in cardiac output, mean arterial pressure, or left atrial pressure were noted. Treatment with 1 mg/kg of dazmegrel resulted in a rapid return of PAP and resistance to control values. No other hemodynamic effects of either bacteria or drug were observed despite continued infusion of GBS.     

Consumer views of pressure sores: a preliminary survey

AIM: To obtain consumer views about pressure sore development, particularly in A&E departments. METHOD: The local Patient and Carers Association received a freepost survey in the form of a simple fixed choice questionnaire. RESULTS: Fewer than half the questionnaires were returned. Relatively few respondents were aware that pressure sores could be avoided, and few were aware that prolonged bed rest or lying on a hospital trolley could increase the risk. CONCLUSION: The survey raised more questions than it managed to answer. More research is needed into the views of patients and carers before they can be involved in healthcare planning.     

Intervention studies to reduce the prevalence and incidence of pressure sores: a literature review

Much has been written about the prevention of pressure sores. However, electronic and manual searches located only 10 studies within the literature in the UK that described interventions able to reduce either their incidence or prevalence. All the studies located contained serious methodological flaws. Apparent success in reducing the number or severity of pressure sores could have resulted because staff involved in data collection were aware that the study was being undertaken and thus took more interest in pressure area care. From the review findings it is apparent that there is a dearth of research evidence upon which to base practice in the sphere of pressure sore prevention and further research is urgently required.     

Studies on the mechanism of bacterial resistance to complement-mediated killing. II. C8 and C9 release C5b67 from the surface of salmonella minnesota S218 because the terminal complex does not insert into the bacterial outer membrane

The mechanism for consumption of terminal complement components and release of bound components from the surface of serum-resistant salmonella minnesota S218 was studied. Consumption of C8 and C9 by S218 occurred through interaction with C5b67 on the bacterial surface because C8 and C9 were consumed when added to S218 organisms previously incubated in C8-deficient serum and washed to remove all C5b67 on the bacterial surface because C8 and C9 were consumed when added to S218 organisms previously incubated in C8- deficient serum and washed to remove al but cell bound C5b67. Rapid release of (125)I C5 and (125)I C7 from the membrane of S218 was dependent on binding of C8 because (125)I C5 and (125)I C7 deposition in C8D serum was stable and was twofold higher in C8D than in PNHA, and addition of purified C8 or C8 and C9 to S218 previously incubated in C8D serum caused rapid release of (125)I C5 and (125)I C7 from the organism. Analysis by sucrose density gradient ultracentrifugation of the fluid phase from the reaction of S218 and 10 percent PNHS revealed a peak consistent with SC5b-9, in which the C9:C7 ratio was 3.3:1, but the NaDOC extracted bound C5b-9 complex sedimented as a broad peak with C9:C7 of less than 1.2:1. Progressive elution of C5b67 and C5b-9 from S218 but not serum-sensitive S. minnesota Re595 was observed with incubation in buffers of increasing ionic strength. Greater than 90 percent of the bound counts of (125)I C5 or (125)I C9 were released from S218 by incubation in 0.1 percent trypsin, but only 57 percent of (125)I C9 were released by treatment of Re595 with trypsin. These results are consistent with the concept that C5b-9 forms on the surface of the serum-sensitive S. minnesota S218 in normal human serum, but the formed complex is released and is not bactericidal for S218 because it fails to insert into hydrophobic outer membrane domains.     

Cervicogenic headache

Eleven female patients with cervicogenic headache (mean age, 43 years; range, 25-59 years) have been examined with the pupillometer. The pupillary diameter was examined in the basal state (that is, the status before pharmacologic stimulation) and after topically administered tyramine (2%), phenylephrine (1%), and hydroxyamphetamine (1%). A total of 51 tests were performed, 35 in the asymptomatic period and 16 during pain attacks. In a control group consisting of 26 age-matched women a total of 39 tests were carried out. Before pharmacologic stimulation (that is, in the "basal state") the pupils were smaller in the asymptomatic (pain-free) period than during pain attacks in the patients and also as compared with that of control individuals. The anisocoria (the difference in pupillary size in the same individual) observed was not significantly different between the patient group and control individuals either in the basal state (before pharmacologic stimulation) or after pharmacologic stimulation. The mydriasis resulting from the instillation of the three sympathicomimetic drugs was symmetrical in both controls and patients both during and between the pain attacks. This finding is in clear contrast to what is found in cluster headache, in which there is a "Horner-like" syndrome on the symptomatic side. These two headaches thus seem to differ essentially with regard to this variable.