Managing the premenstrual syndrome

The definition, classification, proposed etiologies, diagnosis, and treatment of the premenstrual syndrome (PMS) are discussed, and guidelines for the clinical management of PMS are presented. PMS encompasses a cluster of physical and psychosocial symptoms that recur during each menstrual cycle. Proposed etiologies for the syndrome include a hormonal imbalance between estrogen and progesterone, pyridoxine hydrochloride deficiency, hypoglycemia, excess prostaglandin production, and increased aldosterone concentrations in the luteal phase of the menstrual cycle. Diagnosis of PMS is usually based on a patient's history of recurrent symptoms accompanied by a seven-day, symptom-free period in the first half of the menstrual cycle. Management of PMS is complicated by the difficulty in diagnosing the syndrome and its unclear etiology. If possible, conservative nonpharmacologic treatment should be tried initially; suggested measures include modifications in diet, exercise, substance use, stress factors, rest patterns, and social support. Pharmacologic treatment should be considered when conservative therapies are ineffective or when PMS symptoms are more severe. Although most therapies are empirical, treatment with progesterone, pyridoxine, bromocriptine, or diuretics might prove beneficial. Once the decision is made to initiate drug therapy, the treatment regimen should be individualized and based on the patient's PMS symptom complex. The clinical management of PMS is complicated by the lack of well-designed clinical investigations of proposed treatments. Future research should be directed toward evaluating the efficacy of proposed therapeutic regimens.     

Using a dense PTFE membrane without primary closure to achieve bone and tissue regeneration.

The most common types of barrier membranes used for bone or tissue regeneration are made of expanded-polytetrafluoroethylene (e-PTFE) or resorbable materials, such as collagen. Both the e-PTFE and resorbable membranes require primary soft tissue coverage. This article explores the use of a dense-polytetrafluoroethylene (d-PTFE) membrane, which does not require primary soft tissue coverage. The advantages of d-PTFE in contrast to the other more commonly used types of barrier membranes and the clinical significance of these advantages for implant surgical and restorative treatment are discussed.     

Successful replantation of amputated nose and auricle

Amputations of the nose and of the auricle present difficult management problems. Application of simple reattachment techniques, followed by aggressive medical therapy which consists of cooling, anticoagulation, antibiotic coverage, and multiple stab incisions in the amputated tissues, have resulted in the successful replantation of major portions of an amputated nose and an amputated auricle with satisfactory cosmetic results.     

Firearms in the home and child safety

One hundred fifty families who were seen in the pediatric outpatient clinics at The University of Texas Medical Branch, Galveston, were surveyed to learn about firearm possession in the home and its hazards to children. Thirty-eight percent of these families kept at least one gun in their home. Fifty-five percent of this group reported that the gun was loaded at all times, and 10% reported that the gun was kept loaded, unlocked, and within the reach of a child. We identified demographic characteristics of at-risk families and considered national statistics for gun safety. It was concluded that household firearms pose a significant risk to children and that intervention by physicians could help reduce this public health problem.     

Caring for patients with traumatic injuries of the thoracic aorta.

Trauma is a major cause of mortality and morbidity in the United States, with blunt traumatic injuries of the thoracic aorta continuing to occur despite the increased use of seatbelts and airbags. Emerging from crash analysis are effective interventions and provides increased awareness of the occult nature of these types of injuries. This article describes those interventions that healthcare providers must embed throughout the continuum of care for patients experiencing thoracic aortic injuries. Outcomes will be dependent upon the healthcare provider's knowledge of the physics of the event and the urgency of the diagnosis, as well as the ability to assess and manage all the variables involved. Current procedural issues are delineated and case studies are used to illustrate the processes of care needed by these patients.     

Pathways for the bioactivation of aliphatic nitriles to free cyanide in mice

Reports from several laboratories agree that many, but not all, aliphatic nitriles undergo hepatic biotransformation in mice and rats to release free cyanide, but the mechanisms at work in these reactions remain in doubt. We have used primarily n-butyronitrile, propionitrile, and their respective alpha-carbon-hydroxylated homologs, propionaldehyde cyanohydrin and lactonitrile, to examine this question in mice. Pretreatment of mice with the hepatic microsomal enzyme inducers, pregnenolone-16 alpha-carbonitrile, troleandomycin, and isosafrole, or with the cytochrome P-450-depleting agent, cobaltous chloride, did not influence the mortality of mice given single doses of nitriles. Repeated injections of aspirin or sodium salicylate in water failed to protect mice against death by the nitriles. Dimethyl sulfoxide, however, was effective in reducing mortality after nitrile administration. Repeated injections of 4-methylpyrazole or disulfiram protected mice against death after nitriles. Most of the treatment regimens successful against the nitriles also protected against death due to the cyanohydrins. The cyanohydrins were more acutely toxic than their parent nitriles, produced death much more rapidly, and resulted in the same toxic signs, suggesting that they are intermediates in the bioactivation pathway leading to free cyanide. The cyanohydrins appeared to serve as weak substrates for yeast alcohol dehydrogenase, however, incubation of them with either yeast or horse liver alcohol dehydrogenase did not increase the rate of cyanide release over that in incubations where the enzymes were absent. The slow rate of cyanide release due to spontaneous hydrolysis interfered with the determinations of alcohol dehydrogenase activity, but it cannot account for the rapid action and high toxicity of the cyanohydrins in vivo, or for the efficacy of the treatment regimens which protected against death. It appears unlikely that prostaglandin synthetase or alcohol dehydrogenase are importantly involved in nitrile bioactivation. The same active process, however, appears to be responsible both for alpha-carbon hydroxylation and for the subsequent degradation of the resulting cyanohydrins to release free cyanide. It is far more efficient in mediating the latter reaction than the former.