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Does Personhood Begin at Conception?
Published in Christopher Kaczor, The Ethics of Abortion, 2023
Even if comatose patients are considered living human beings, it would not necessarily follow, in one sense, that this human being has the same right to life as you or I. Such a human being has a right to life equal to you or me in the sense that he or she has a right not to be intentionally killed. But it does not follow from an equal right not to be intentionally killed that each person has an equal right to receive the same medical treatments. In other words, some treatments that would be appropriate to give to someone in a temporary coma may not be appropriate to give to the person in a permanent coma because though such treatments might be of tremendous benefit to the person in the temporary coma, they may be of relatively little benefit to the person in a permanent coma. What treatments should be given is a matter of prudential judgment and should take into account both the burdens and the benefits of treatment. Assessing the burdens and benefits of treatment may be importantly different in cases of temporary versus permanent comas. In this imprecise sense of a right to life, the right to life of those in a permanent coma differs significantly from the right to life of those who will recover from comas. In Kantian terms, our imperfect duties to benefit others are not exactly alike but must take into account various circumstances even though our perfect duties not to intentionally harm others are alike for all human beings.
Disorders of Consciousness, Disability Rights, and Triage During the Covid-19 Pandemic
Published in Joel Michael Reynolds, Christine Wieseler, The Disability Bioethics Reader, 2022
Let us begin with coma, which is an eyes-closed state of unconsciousness. A coma after traumatic brain injury can last a week or two and can be a precursor to brain death or recovery. Comas can also be induced and prolonged with sedative medication, a therapeutic strategy sometimes used to promote recovery after brain trauma.
Carbamylphosphate synthetase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
The clinical abnormalities of CPS1D are indistinguishable from those of OTCD (Chapter 26). Usually, the infant is normal at birth and may do well for a short period, often until feedings begin. Then failure to feed well and lethargy develop. There may be grunting or rapid respiration, hypotonia or hypertonia, convulsions, and hypothermia. Sometimes initial abdominal symptoms (vomiting, disturbed transport) may be so prominent that abdominal disease is suspected and investigated (Figure 27.2) [12]. Symptoms are rapidly progressive to deep coma, in which there is a complete unresponsiveness to stimuli. We have compared this state to surgical anesthesia. Apnea supervenes and the infant survives only with assisted ventilation. The history often reveals that siblings died very early in life. Compared to distal urea cycle disorders (argininosuccinate synthetase deficiency and argininosuccinate lyase deficiency; see Figure 25.1), subjects with CPS1D and OTCD present earlier – mostly between 24 and 72 hours of age – and with a higher initial peak-blood ammonia level (PBAL) [13].
Behavioral intervention approaches for people with disorders of consciousness: a scoping review
Published in Disability and Rehabilitation, 2022
Giulio E. Lancioni, Nirbhay N. Singh, Mark F. O’Reilly, Jeff Sigafoos, Lorenzo Desideri
Supplementary search strategies to identify relevant articles were also employed. First, the references of the 35 articles selected as well as the references of recent review and opinion articles were inspected. Second, a Google Scholar “cited by” search was conducted using the initially identified 35 articles. Third, a search alert in Google Scholar using the terms “minimally conscious state”, “disorder of consciousness”, “vegetative state”, “unresponsive wakefulness”, “coma”, and “comatose” was activated in order to ensure that relevant literature published while this paper was being written could be identified and included in the review. The aforementioned strategies led to the finding of five extra articles that all authors agreed to be relevant for the review, so that 40 articles were finally included (see Figure 1). The inclusion of new articles was completed in May 2021.
A different challenge with Benadryl: adolescent diphenhydramine ingestions reported to National Poison Database System, 2007–2020
Published in Clinical Toxicology, 2022
Michael A. Darracq, Stephen L. Thornton
Table 4 describes the reported frequencies of seizures, coma, and cardiovascular complications amongst adolescent diphenhydramine ingestions. Cardiac complications, seizure, and coma were reported in 6.1%, 4.1%, and 0.6% of cases, respectively. Cardiac complications, seizures, and coma were more commonly associated with intentional ingestions (7.3% [95% CI: 7–7.6], 4.9% [95% CI: 4.7–5.1], and 0.7% [95% CI: 0.6–0.8) as compared to unintentional ingestions (0.9% [95% CI: 0.7–1], 0.8% [95% CI: 0.6–1], and 0.1% [95% CI: 0–0.2). Amongst ingestions due to an intentional reason, cardiac complications, and seizures were more commonly associated with suspected suicide (8.5% [95% CI: 8.2–8.8], 5.5% [95% CI: 5.2–5.8], and 0.9% [95% CI: 0.8–1]) as compared to unknown (5.6% [95% CI: 4.6–6.6], 4.5% [95% CI: 3.6–5.4], and 0.5% [95% CI: 0.2–0.8]) misuse (1.5% [95% CI: 1.1–1.9], 0.9% [95% CI: 0.5–1.2], and 0.1% [95% CI: 0–0.2]) or abuse (5.1% [95% CI: 4.4–5.8], 4.3% [95% CI: 3.7–4.9], and 0.2% [95% CI: 0.1–0.3]. Cardiac complications, seizures, and coma were however more infrequently reported amongst all of the subgroups as compared with other clinical effects. Table 5 describes the five most common clinical effects reported for each category of reason for exposure.
Chameleons, red herrings, and false localizing signs in neurocritical care
Published in British Journal of Neurosurgery, 2022
Boyi Li, Tolga Sursal, Christian Bowers, Chad Cole, Chirag Gandhi, Meic Schmidt, Stephan Mayer, Fawaz Al-Mufti
Acute hypercapnia can have many etiologies, commonly including acute respiratory distress syndrome (ARDS). Acute hypercapnia can cause severe renal and cardiovascular consequences.90 As a FLS, acute hypercapnia may be a sign of increased ICP, which increases the diffusion rate of CO2 across the blood brain barrier causing a sharp drop in CSF pH; this in turn inhibits post-synaptic glutamate receptors.80 The most prominent clinical symptom is drowsiness advancing into coma; other symptoms include headaches, confusion, papilledema, tremor of outstretched hands, and seizures.80 Lumbar puncture can be done in patients with acute hypercapnia presenting with such symptoms to diagnose increased ICP. Acute hypercapnia has been associated with increased ICU mortality; therefore, prompt and careful diagnosis is critical.91