Changes in muscle strength and pain in response to surgical repair of posterior abdominal wall disruption followed by rehabilitation.

BACKGROUND: Posterior abdominal wall deficiency (PAWD) is a tear in the external oblique aponeurosis or the conjoint tendon causing a posterior wall defect at the medial end of the inguinal canal. It is often known as sportsman's hernia and is believed to be caused by repetitive stress. OBJECTIVE: To assess lower limb and abdominal muscle strength of patients with PAWD before intervention compared with matched controls; to evaluate any changes following surgical repair and rehabilitation. METHODS: Sixteen subjects were assessed using a questionnaire, isokinetic testing of the lower limb strength, and pressure biofeedback testing of the abdominals. After surgery and a six week rehabilitation programme, the subjects were re-evaluated. A control group were assessed using the same procedure. RESULTS: Quadriceps and hamstrings strength was not affected by this condition. A deficit hip muscle strength was found on the affected limb before surgery, which was significant for the hip flexors (p = 0.05). Before surgery, 87% of the patients compared with 20% of the controls failed the abdominal obliques test. Both the injured and non-injured sides had improved significantly in strength after surgery and rehabilitation. The strength of the abdominal obliques showed the most significant improvement over the course of the rehabilitation programme. CONCLUSIONS: Lower limb muscle strength may have been reduced as the result of disuse atrophy or pain inhibition. Abdominal oblique strength was deficient in the injured patients and this compromises rotational control of the pelvis. More sensitive investigations (such as electromyography) are needed to assess the link between abdominal oblique function and groin injury.

Emergency admissions for upper gastrointestinal disease and their relation to NSAID use.

BACKGROUND: There are considerable variations in estimates of the number of emergency upper gastrointestinal admissions per annum which are attributable to nonsteroidal anti-inflammatory drug (NSAID) use. AIM: To obtain a more accurate estimate of the number of these emergency admissions per annum in UK. METHODS: A retrospective survey of the case notes of all emergency admissions for upper gastrointestinal disease ('Cases') to two English District General Hospitals with a combined catchment population of 550,000. Records of all community deaths attributed to upper gastrointestinal diagnoses (with the same ICD codes) were also surveyed. Matched controls were identified from emergency admissions not caused by upper gastrointestinal diagnoses. The proportions of patients taking NSAIDs on admission to hospital (or at the time of death at home) and the outcome following admission to hospital were analysed. RESULTS: 620 emergency upper gastrointestinal admissions were identified and matched with 460 controls. Cases were more likely to be NSAID users than Controls (31% vs. 16%, OR 2.4, 95% CI: 1.8, 3.3: P < 0.001). Case NSAID use was higher in females and with increasing age. As severity of mode of presentation worsened, the probability of NSAID use increased (e.g. OR relative to controls for peptic pain 1.9, for perforation 5.9). Blood transfusion requirements were significantly higher (P < 0.0001) in Cases taking NSAIDs, although NSAID use did not influence mortality. Extrapolation from these data indicate that there are 65,000 emergency upper gastrointestinal admissions per annum in UK; 12,000 of these admissions (including 2230 deaths) are attributable to NSAID use. A further 330 attributable deaths occur in the community. CONCLUSIONS: There is a strong association between NSAID use and propensity for upper gastrointestinal emergency admission; NSAID use is associated with significant morbidity and mortality each year in UK.

Considerations for nonsteroidal anti-inflammatory drug therapy: safety.

Although therapeutically beneficial, nonsteroidal anti-inflammatory drugs are associated with serious gastrointestinal side effects, including ulceration, hemorrhage, and perforation. Endoscopic studies indicate that up to 30% of chronic NSAID users will develop gastroduodenal ulceration. Various case-control studies have reported an association between ulcer-related complications or deaths and NSAID use. An imprecise correlation has been found to exist between the presence of NSAID-induced gastrointestinal damage and symptoms, such as dyspepsia and pain. It is now thought that the major deleterious effects of NSAIDs on the gastrointestinal tract are related to the ability of systemically absorbed NSAIDs to alter gastric and duodenal defense mechanisms, primarily via inhibition of mucosal prostaglandin synthesis. Although various therapeutic agents have been investigated for their ability to prevent NSAID-induced ulcers, only the prostaglandin analogue misoprostol has been shown to significantly reduce the incidence of both gastric and duodenal ulcers in NSAID users. Recently, the Misoprostol Ulcer Complications Outcomes Safety Assessment trial demonstrated that misoprostol also reduces the most serious complications of NSAID-induced ulcers, namely bleeding, perforation, and gastric outlet obstruction.

Non-steroidal anti-inflammatory drugs and life threatening complications of peptic ulceration.

Two hundred and thirty five consecutive patients with a life threatening complication of peptic ulceration, who either died or required emergency surgery, have been studied over a 36 month period. Seventy eight of these high risk patients died; 25 at home, 19 in hospital without surgery and 34 postoperatively. Ninety eight patients had bleeding ulcers, 132 perforated ulcers and five had both bleeding and perforated ulcers. One hundred and forty one of these 235 patients (60%) were taking a non-steroidal anti-inflammatory drugs (NSAID) and the individual agents have been listed. The overall incidence of NSAID use in a hospital control group was 9.9%. The first sign of an ulcer was a life threatening complication in 58.2% of patients taking a NSAID. Nearly 80% of all ulcer related deaths occurred in patients using an anti-inflammatory agent. Patients using these drugs were older, with more pre-existing medical conditions and had larger ulcers than those not taking NSAIDs. The mortality associated with a peptic ulcer complication in patients taking a NSAID was more than twice that in patients with no such drug history. There appears to be a relationship between the development of a life threatening complication of peptic ulceration and NSAID ingestion. Much of the associated mortality and morbidity may be potentially avoidable.