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Aim To develop an understanding of how nurses provide spiritual care to terminally ill patients in order to develop best practice. Background Patients approaching the end of life (EoL) can experience suffering physically, emotionally, socially and spiritually. Nurses are responsible for assessing these needs and providing holistic care, yet are given little implementable, evidence-based guidance regarding spiritual care. Nurses internationally continue to express inadequacy in assessing and addressing the spiritual domain, resulting in spiritual care being neglected or relegated to the pastoral team. Design Systematic literature review, following PRISMA guidelines. Methods Nineteen electronic databases were systematically searched and papers screened. Quality was appraised using the Critical Appraisal Skills Programme qualitative checklist, and deductive thematic analysis, with a priori themes, was conducted. Results Eleven studies provided a tripartite understanding of spiritual caregiving within the a priori themes: Nursing Spirit (a spiritual holistic ethos); the Soul of Care (the nurse-patient relationship); and the Body of Care (nurse care delivery). Ten of the studies involved palliative care nurses. Conclusion Nurses who provide spiritual care operate from an integrated holistic worldview, which develops from personal spirituality, life experience and professional practice of working with the dying. This worldview, when combined with advanced communication skills, shapes a relational way of spiritual caregiving that extends warmth, love and acceptance, thus enabling a patient's spiritual needs to surface and be resolved. Relevance to clinical practice Quality spiritual caregiving requires time for nurses to develop: the personal, spiritual and professional skills that enable spiritual needs to be identified and redressed; nurse-patient relationships that allow patients to disclose and co-process these needs. Supportive work environments underpin such care. Further research is required to define spiritual care across all settings, outside of hospice, and to develop guidance for those involved in EoL care delivery.

Acute oral toxicity studies with Brown FK gave LD50 values greater than 2 g/kg and 8 g/kg in mice and rats respectively. The values for intraperitoneal injection were 1·5–2 g/kg in mice and 0·75–1·15 g/kg in rats. When repeated daily oral doses ranging from 0·1 to 2 g/kg were given to rats, a precipitate weight loss and a vacuolar myopathy of the heart and skeletal muscles accompanied by lipofuscin formation occurred with doses of 0·5 g/kg and over. At the highest dose employed (2 g/kg) there was also hepatic centrilobular necrosis and renal tubular degeneration. Pretreatment with antibiotics reduced the incidence of muscle lesions. Repeated intraperitoneal injection did not have any effect on the heart or skeletal muscle. Only two of the six components of Brown FK, compound I (2,4-diamino-5-(p-sulphophenylazo)toluene) and compound II (1,3-diamino-4-(p-sulphophenylazo)benzene), were found to produce muscle damage after repeated oral doses of 0·5 g/kg. Comparable doses of mixtures containing the other components as well as I or II were considerably less toxic. After daily oral doses of 1 g/kg, muscle lesions were found in rats, rabbits and guinea-pigs, but none were seen in mice or hamsters. The results suggest that the intestinal microflora is responsible for the breakdown of the components of Brown FK to toxic products. Variations between species and between animals of the same species may be due to qualitative and quantitative differences in the intestinal microbial population.

Administration of two or three massive (1 g/kg) oral doses of Brown FK to rats induced a myopathy in cardiac and skeletal muscles characterized by multiple vacuoles about 1–2 μ in diameter. Ultrastructurally, these were shown to consist of areas of fibrillolysis, affecting initially the A-band. Histochemically, the myopathy was accompanied by a moderate increase in acid-phosphatase activity and by a loss of phosphorylase activity. Subsequently, complete lysis of the affected fibres ensued. In the heart, lysis was followed by macrophage invasion and fibroblastic proliferation, and in skeletal muscle, by regeneration. The occurrence of lipofuscin in muscle fibres and in macrophages was scanty and erratic. When Brown FK was given in the diet at a level of 2%, fibrillolysis and an increase in the number and electron-density of lysosomes was observed ultrastructurally during wk 2–3 of the test. These changes were accompanied by a marked elevation of histochemically-demonstrable acid phosphatase. Progressive deposition of lipofuscin was the principal pathological feature during wk 3–12. Initial damage to the A- and I-bands in both cardiac and skeletal muscle distinguishes the Brown FK myopathy from that known to be produced by high doses of corticosteroids, thyroxine, chloroquine or plasmocid, from ischaemic damage and from muscle damage resulting from deprivation of potassium, calcium or magnesium. The lysosomal changes and accumulation of lipofuscin are suggestive of primary lysosomal damage which may be responsible, at least in part, for the pathological effects observed.