Throughout March and April 2020, debate raged about how best to allocate limited intensive care unit (ICU) resources in the face of a growing COVID-19 pandemic. The debate was dominated by utility-based arguments for saving the most lives or life-years. These arguments were tempered by equity-based concerns that triage based solely on prognosis would exacerbate existing health inequities, leaving disadvantaged patients worse off. Central to this debate was the assumption that ICU admission is a valuable but scarce resource in the pandemic context.In this paper, we argue that the concern about achieving equity in ICU triage is problematic for two reasons. First, ICU can be futile and prolong or exacerbate suffering rather than ameliorate it. This may be especially true in patients with COVID-19 with emerging data showing that most who receive access to a ventilator will still die. There is no value in admitting patients with poor prognostic indicators to ICU to meet an equity target when intensive critical care is contrary to their best interests. Second, the focus on ICU admission shifts focus away from important aspects of COVID-19 care where there is greater opportunity for mitigating suffering and enhancing equitable care.We propose that the focus on equity concerns during the pandemic should broaden to include providing all people who need it with access to the highest possible standard of end-of-life care. This requires attention to culturally safe care in the following interlinked areas: palliative care, communication and decision support and advanced care planning.
Debate on the potential and uses of human stem cells tends to be conducted by two constituencies—ethicists and scientists. On many occasions there is little communication between the two, with the result that ethical debate is not informed as well as it might be by scientific insights. The aim of this paper is to highlight those scientific insights that may be of relevance for ethical debate.Environmental factors play a significant role in identifying stem cells and their various subtypes. Research related to the role of the microenvironment has led to emphasis upon “plasticity”, which denotes the ability of one type of stem cell to undergo a transition to cells from other lineages. This could increase the value given to adult stem cells, in comparison with embryonic stem cell research. Any such conclusion should be treated with caution, however, since optimism of this order is not borne out by current research.The role of the environment is also important in distinguishing between the terms totipotency and pluripotency. We argue that blastocysts (early embryos) and embryonic stem cells are only totipotent if they can develop within an appropriate environment. In the absence of this, they are merely pluripotent. Hence, blastocysts in the laboratory are potentially totipotent, in contrast to their counterparts within the human body which are actually totipotent. This may have implications for ethical debate, suggesting as it does that arguments based on potential for life may be of limited relevance.
Parkinson's Disease (PD) is an age-related, disabling neurodegenerative disorder. Although sufferers usually respond to dopamine agonists for extended periods, the disease remains progressive and adverse drug effects can compromise effective long term treatment. Cell-based therapies have been the subject of much hype and optimism with regard to PD. Proof of principle was provided in the 1980s with fetal tissue transplantation trials demonstrating successful graft survival. Embryonic stem cells and reprogrammed or transdifferentiated somatic cells may provide alternative sources of tissue with the potential to overcome the material shortages and technical difficulties that have hindered fetal neural transplants. This article will review the state of the science for cell based therapies and examine the ethical issues that societies must negotiate regarding their clinical use.
A 21-year-old female had recurrent presentations to the emergency department with myalgia, vomiting, abdominal pain and subsequently developed generalized seizures. She was volume depleted with a plasma sodium of 125 mmol/L (reference interval: 135-145) and she had fluctuating hypertension. Acute porphyria was suspected and confirmed with raised urine porphobilinogen/creatinine ratio of 12:4 μmol/mmoL (reference interval < 1:5) and she was treated with intravenous haem arginate. Urinary porphyrin/creatinine ratio was 673 nmol/mmoL (reference interval <35) and faecal porphyrins 2430 μmol/kg dry weight (reference interval: <200) were markedly elevated, with raised faecal CIII:CI ratio, consistent with acute coproporphyria. Diagnosis was confirmed by the demonstration of a novel missense variant in the coproporphyrinogen oxidase gene c.863T > G (p.Leu288Trp) predicted to be deleterious and which segregated with three other affected family members. Although CT head was normal, magnetic resonance imaging scan revealed symmetrical signal abnormalities and swelling in the parietal and occipital lobes consistent with posterior reversible encephalopathy. Over several days, her seizures ceased and sodium and blood pressure normalized. The aetiology of the acute porphyric attack was likely multifactorial with contributions from a recent viral illness and caloric deprivation. No drug precipitant was identified. We postulate that untreated hypertension played a key role in the development of posterior reversible encephalopathy. Early clinical suspicion and urine porphobilinogen testing are the key components in preventing morbidity and mortality in acute porphyrias.
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