Avsnitt
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A few random thoughts on the trial of Lucy Letby, open justice, freedom of information and censorship.
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Show notes: https://docs.google.com/document/d/1vhPDBPBbYwU4VekCs1HKGd0T7ZVKh1-qp42DqmO8bKU/edit?usp=sharing
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Saknas det avsnitt?
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Analysis of the clinical baloney of the case of Baby L
Tattle life Link: https://tattle.life/wiki/lucy-letby-case-10/#prosecution-opening-statement-child-l
Show notes: https://docs.google.com/document/d/1ILJApDGuJhL2lD8E1r7FyZR1rVt6zkj-SmIqlgTja9I/edit?usp=sharing
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Episode 35 is a quick review of the recent book Unmasking Lucy Letby, with a little science thrown in, which is more than can be said for the book.
Show Notes: https://docs.google.com/document/d/1vdALlJDrm5Bkd8P1WRSDSUDM6ia4xQzbrkBjgljY38I/edit?usp=sharing
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Dr Jayaram's inconsistent story about Baby K, for me is not credible. Letby was retried for the attempted murder, perhaps to save Jayaram's blushes. His public claim that the only reason that preterm babies dislodge ET tubes is not true.
https://feed.podbean.com/1962strat/feed.xml
Show notes: https://docs.google.com/document/d/1N92i69K4HSdzqi2KwE5s5PN5Wmc7C-5rDwgV--tUPU8/edit?tab=t.0
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In a long episode we analyse the basic medical science that can easily explain the collapse of Baby J.
Tattle Life Link: https://tattle.life/wiki/lucy-letby-case-9/#child-j
Show notes link: https://docs.google.com/document/d/116CV35WDmiXb4f1zNDIChiLNB0FMockTY01ZJosAQuM/edit?usp=sharing
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A lack of coordinated care is all too common in medical practice and is evident in this case. There are perfectly acceptable medical reasons for the collapses and death of Baby I, that are far removed from the fantastical and baseless conclusion of the cheif witness in this trial.
Link to Tattle life Wiki: https://tattle.life/wiki/lucy-letby-case-8/#child-i
Link to show notes: https://docs.google.com/document/d/1HT1AqoMvVBDxoWekK_Q5Hs2F94b_nwrQ3P7fp4960AU/edit?usp=sharing
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An introduction to the circumstance of the death of Baby I, where so called expert witnesses boil almost three months of progressive deterioration of a critically ill preterm neonate, into four single events. They do so in defiance of our knowledge of the cumulative effects of disease and its relationship to mortality and the extremely high mortality of neonates born after premature rupture of membranes at or before 21 weeks gestation.
https://tattle.life/wiki/lucy-letby-case-8/#child-i
Very premature rupture of membranes (PPROM) at 21 weeks gestation has significant effects on neonatal mortality and morbidity.
The survival rate for neonates born after PPROM at less than 24 weeks gestation is generally low. Studies indicate that survival with rupture of membranes at less than 21 weeks of gestation is rare. The survival rate to discharge can be highe with expectant management with one study claiming that 26% of babies survived to discharge from hospital when PPROM occurred before 23 weeks gestation.
Neonates who survive PPROM at such early gestational ages often experience severe morbidity. Studies have shown that among survivors, a high percentage experience severe morbidities such as intraventricular hemorrhage, retinopathy of prematurity, bronchopulmonary dysplasia, and necrotizing enterocolitis. For instance, one study reported that 77.8% of survivors experienced severe morbidity at the time of discharge.
The duration of the latency period (time between onset of PPROM and birth) is a critical factor. Longer latency periods are associated with better survival rates and fewer severe morbidities. For example, a study found that later gestational age at PPROM and longer latency periods were significantly associated with survival without severe morbidities, but these studies do not include premature rupture of membranes occurring at 21 weeks gestation.
The gestational age at birth also plays a crucial role. Babies born at more advanced gestational ages tend to have better outcomes. For instance, one study found that survivors were born at more advanced gestational ages compared to non-survivors.
In summary, PPROM at 21 weeks gestation is associated with high neonatal mortality and morbidity rates.
Citations:
Neonatal outcomes in women with preterm premature rupture of membranes at periviable gestational age
Preterm Premature Rupture of Membranes Between 14 and 24 Weeks of Gestation Outcomes With Expectant Management
Preterm infant outcomes in relation to the gestational age of onset and duration of prelabour rupture of membranes: a retrospective cohort study
Preterm prelabour rupture of membranes before 23 weeks’ gestation: prospective observational study
Prognosis of preterm premature rupture of membranes between 20 and 24 weeks of gestation: A retrospective cohort study
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In episode 30, we take a brief look at the chaotic care of Baby H. The NNU, with 13 babies and only four nurses, is a clear example of systemic failures. Every identified failing in the RCPCH report is in play, yet the blame is malignantly shifted to Letby. The behaviour towards patients in this example is shockingl. The standard of practice is abysmal, and the integrity of the prosecution is non-existent.
https://tattle.life/wiki/lucy-letby-case-8/#mother
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In the final part of the analysis of Baby the expert witnesses conveniently miss other episodes of "projectile" vomiting, not caused by injecting air ( or something else) into the stomach.
Tattle Life WiKI: https://tattle.life/wiki/lucy-letby-case-7/
Show notes: https://docs.google.com/document/d/1X98yb_nMiRE0FyBVSnWMXOAi0U3VIRCObFj9Q0wj2F4/edit?usp=sharing
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The addition and removal of insulin from preterm neonates is still largely a mystery and varies significantly from one baby to the next. Some institutions use experimental mathematical models to estimate insulin requirements. The calculations needed are hugely complex and subject to error and assumption. But not for the experts in the Letby trial.
One immunoassay for insulin and C-peptide is insufficient to prove exogenous insulin poisoning. Here are the key reasons:
1. Traditional immunoassays can have cross-reactivity with non-target compounds and may not be able to differentiate between endogenous insulin and recombinant pharmaceutical analogues[1][2][4].
2. Immunoassays are unreliable for postmortem specimens due to interferences with hemolyzed samples and are generally unsuitable for forensic purposes[1][2].
3. Accurate diagnosis requires measuring insulin, C-peptide, and proinsulin and interpreting these in context with each other. A single immunoassay cannot provide the comprehensive data needed for a definitive diagnosis[2][5].
4. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is now considered the definitive method for measuring insulin, C-peptide, and proinsulin, especially in forensic investigations, due to its ability to discriminate between various synthetic analogues[1][2].
Therefore, relying solely on one immunoassay for insulin and C-peptide is insufficient to prove exogenous insulin poisoning. A combination of tests, including LC-MS/MS, and a thorough clinical and forensic investigation are necessary to diagnose accurately.
Citations:[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6507008/
[2] https://jlpm.amegroups.org/article/view/5995/html
[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556768/
[4] https://www.sciencedirect.com/science/article/abs/pii/S0009912015002787
[5] https://onlinelibrary.wiley.com/doi/full/10.1002/pdi.875
Tattle Life link: https://tattle.life/wiki/lucy-letby-case-6/#professor-peter-hindmarsh
Show notes link: https://docs.google.com/document/d/1yK22YKISPEIS_enWH_HEdsTBseTqrPJKYUwOIiTODeg/edit?usp=sharing
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In Episode 27, we move on with the case of Baby F and argue that the single immunoassay test used to construct the story that Baby F was poisoned should have been inadmissible as evidence and grounds for appeal. In the absence of a defence witness, the lawyer's ignorance of the nuances of medicine devastated Letby.
RSS feed: https://feed.podbean.com/1962strat/feed.xml
Tattle Life link: https://tattle.life/wiki/lucy-letby-case-6/
Link to show notes: https://docs.google.com/document/d/1HgBpAGPgiqD5FjVxAgmMVexY1dTJTJOLsGDeT4n1K9s/edit?usp=sharing
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This episode examines the complexities of maintaining adequate glucose levels in preterm neonates. The expert witnesses in the Lucy Letby trial reduced these real-world challenges to primary school simplicity and offered only one outlandishly improbable possibility. This will contrast with the next episode, where we explain the flaws in the expert evidence in the case of Baby F.
Reference to the article discussed:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753077/pdf/nihms755707.pdf
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Not only was the evidence against Lucy Letby in the Baby F case circumstantial, but the circumstances were a menu of assumptions. How on earth is this just?
Show notes: https://docs.google.com/document/d/1a90Z6DiIYQGxrpwka1jkDBYi9UCgUWNyPE0ockfhXqI/edit?usp=sharing
Tattle Life Wiki: https://tattle.life/wiki/lucy-letby-case-6/
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The ultimate stable baby at the CoCH. Thirty weeks gestation, actively bleeding from the gut, has lost at least 25% of total blood volume, is on 100 oxygen and is still "a stable baby".
Tattle Life Wiki: https://tattle.life/wiki/lucy-letby-case-5/
Show notes.
https://docs.google.com/document/d/1MeX2ipz0PRKCGQC1mLb3kmg6DkKSNbadwK36tpagTKs/edit?usp=sharing
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In this episode, we continue with the expert witnesses in Baby E's case. Without post-mortem findings, it's open season for the imagination, bizarre claims abound, and the defence remains in the trenches.
Tattle Life Wiki: https://tattle.life/wiki/lucy-letby-case-5/
Link to detailed show notes
https://docs.proton.me/u/0/doc?mode=open&volumeId=nQGA2CWSuKl6zOCuObFrpj6OeqaqusHoARmBS4bl5n2lrVzNZDYAqOOdHe9vH8dqcz0u5l_pBrbmwCurC2ZWCQ%3D%3D&parentLinkId=ihkEGwDzluWqaim1zWuhrKyUrikwAw4Npj5jEI-5yDDhRa_jUq-0KhMgwMfL1MNQGLjLHF01lZcZU4f3edULBg%3D%3D&linkId=C3Odrqhs9belrlvrQxrr40tjb9v_Yny2CPBLdFDEqYVrP-Ob1p_u265KGWLkAgq3SqAlSAwxc7k6MwZdSx6mNA%3D%3D
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Without an autopsy every opinion of the expert witnesses is mere speculation, some of it quite extraordinary and inappropriate for professional people.
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The Death of Baby D
or details and citations refer to
https://docs.google.com/document/d/1Lql0NRpwxHhksnw0HmQAew1SbCGQMuheL_fBlDQ0nUk/edit?usp=sharing -
A personal description of the fate of Baby D who arguably developed pneumonia while still in utero. A baby with findings of acadaemia while in ICU,a circumstance often lethal to newborns and which occurred long before Letby's involvement.
A blood pH between 7.194 and 7.173 in a 2-day-old term neonate with pneumonia is concerning and potentially dangerous, as it indicates significant metabolic acidosis.
1. Normal blood pH range: The normal arterial blood pH range for neonates is 7.35-7.45[1]. A pH below 7.35 is considered acidosis.
2. Severity of acidosis: The pH values of 7.194 and 7.173 are well below the normal range, indicating moderate to severe acidosis[2]. This level of acidosis can have serious implications for the newborn's health.
3. Causes and implications:
- Pneumonia in neonates can lead to respiratory acidosis due to impaired gas exchange and CO2 retention[3].
- Metabolic acidosis may also occur due to sepsis, tissue hypoxia, or poor perfusion associated with severe pneumonia[4].
- Acidosis of this severity can negatively impact various organ systems, including the cardiovascular, respiratory, and central nervous systems[5].
4. Potential complications:
- Severe acidosis can lead to myocardial dysfunction, decreased cardiac output, and hypotension[4].
- It may also cause pulmonary vasoconstriction, potentially worsening respiratory distress[4].
- Neurological complications such as intraventricular hemorrhage are associated with severe acidosis in neonates[6].
5. Need for intervention:
- A pH this low requires immediate medical attention and intervention to correct the underlying cause and manage the acidosis[2].
- Treatment may include respiratory support, antibiotics for pneumonia, fluid management, and in some cases, cautious use of buffer solutions like sodium bicarbonate[7].
6. Monitoring and follow-up:
- Close monitoring of blood gases, electrolytes, and clinical status is crucial[2].
- Serial measurements are important to track the response to treatment and guide further management.
A blood pH between 7.194 and 7.173 in a 2-day-old neonate with pneumonia is dangerous and requires urgent medical intervention. The acidosis needs to be addressed promptly to prevent potential complications and improve outcomes.
Citations:
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8558493/
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869402/
[3] https://onlinelibrary.wiley.com/doi/full/10.1111/apa.16127
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10662854/
[5] https://www.safercare.vic.gov.au/best-practice-improvement/clinical-guidance/neonatal/blood-gas-interpretation-for-neonates
[6] https://onlinelibrary.wiley.com/doi/full/10.1111/ppe.12663
[7] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4533247/
[8] https://www.medicalnewstoday.com/articles/ph-of-blood
[9] https://www.cochrane.org/CD003215/NEONATAL_base-administration-or-fluid-bolus-for-preventing-morbidity-and-mortality-in-preterm-infants-with-metabolic-acidosis - Visa fler
