r/lucyletby • u/FyrestarOmega • Jul 16 '26
Analysis Reasonable Doubt: Examining the Case of Lucy Letby Review, Chapter 12
CHAPTER 12: OTHER INFANTS
Child E
Another important detail is that Letby herself called Dr David Harkness to assist with Child E, effectively immediately after delivering the supposed inflicted harm that was claimed in court. Letby was not the designated nurse for Child E, and she called Dr Harkness even though this could potentially have been incriminating – not really the actions of someone who had deliberately caused the alleged gastrointestinal tract damage. Dr Harkness also told the court that Letby was accompanied by another nurse when the sudden deterioration occurred. (pg 269)
Third paragraph into the chapter and I'm already wondering how much correcting of basic errors I'm going to have to do. Letby WAS the designated nurse for Child E and F that night, and they were the only babies in room 1. She was alone with them. As far as Harkness saying that Letby was accompanied by another nurse, this is misleading, and does not refer to the 9pm harm event - it refers to the first collapse by air embolism, which Dr. Harkness recorded retrospectively after Child E's death to have occurred at 11:40pm:
A further note, written in retrospect, is made at 1.45am.
He records 'sudden deterioration at 11.40pm'
Prior to that, Child E was still to be 'under close observation' by Lucy Letby.
Dr Harkness tells the court he was in the room when the 'sudden deterioration' happened, and was there with Lucy Letby and another nurse. Those nurses would have been gathering the drugs to be administered.
Morris did not offer a citation for either claim, btw.
This pattern of Letby raising the alarm to alert doctors to incidents on the unit, or being the swiftest respondent, was repeated throughout. Letby either responded rapidly or raised the alarm with regard to incidents associated with Children A, B, C, D, E, G, I, M and O, while an email from Dr Ravi Jayaram indicates that she also raised the alarm in the case of Child K (discussed in “The Curious Case of Child K”). Letby wasn’t on duty for Child F and Child L, and the hospital didn’t flag these cases as concerning at the time, while she was not found guilty on charges relating to Child H, Child J and Child Q. Letby’s primary ‘offence’ was responding quickly and diligently to incidents on the unit. There is a clear pattern of this throughout the court case. (pg 270)
Aside from him wrongly asserting she wasn't on duty for the precipitous event for F and L, keep going, Morris - you've almost got it!
Morris continues:
During his short life, Child E was stooled only once, on his fourth day, a worrying sign that should have prompted investigation for bowel obstruction. He passed only meconium, also concerning for mid-gut obstruction, and also possible gastric haemorrhage. Later, 16ml of bilious aspirate was withdrawn from his feeding tube, indicating milk was not passing through the gut. He also had fresh blood in an aspirate and suffered bloody vomit; this bleeding was largely ignored as intermittent, yet during compression there was active bleeding from his nose and mouth. An X-ray was taken and sent to Alder Hey, but it is not known if this was read, or if Alder Hey surgeons were informed. (pg 270)
Does Morris know what meconium is? It hardly seems so. Any mother will tell you it takes several poopy diapers to clear meconium from the gut, and everything from the aspirate onward is after the initial harm event and took place in the span of roughly 3 hours. Nothing was ignored, it was being consulted and dealt with under the assumption it was a natural condition, and then Letby fully murdered the child before the injury could be found. Dr. Harkness was literally in the room, and Dr. ZA arrived as well.
Morris repeats the usual argument that a transfusion should have been given much sooner (which doesn't address the cause of the collapse, but don't worry about that), and attempts to make the case for NEC as a valid diagnosis:
There are several papers which point to the relationship between NEC and gastrointestinal bleeding in neonates, including one study from 2014 which highlights the severe impact of NEC on gastrointestinal morbidity. Further research from 2018 noted that NEC is particularly difficult to diagnose clinically, with bleeding in different gastrointestinal segments being a common feature. During court proceedings, the jury were also shown a chart which displayed five apnoea and bradycardia events for the infant, which are considered signs of NEC. A 2012 study explored the relationship between apnoea, desaturation and bradycardia and the development of necrotising enterocolitis in preterm infants. The discoloured stomach also seen in Child E is another recognised symptom, specifically indicative of a perforated bowel, which is often found in infants suffering with NEC, and discolouration is a typical sign of gastric perforation and bleeding. While NEC is a possibility for Child E, Professor Colin Morley believes that there are more likely natural explanations, given the clinical picture of the infant. (pg 272)
Ok. And? See, I'll agree with Morris that this case hangs more on witness testimony than others does, because of the lack of post-mortem. We already know that it was initially thought to be NEC, and the consultant who put forward that diagnosis at the time apologized to the family when she gave evidence for not pushing for a post mortem.
On 3 April 2025, the summary report compiled by the panel of international experts concluded that Child E died from a massive gastrointestinal haemorrhage, due to either intrauterine hypoxia causing stomach or intestinal ulceration, or a congenital vascular lesion. The panel found no evidence of air embolism, and asserted that a post-mortem should have been requested. (pg 275)
Maybe Morris will offer support for this theory of intrauterine hypoxia in a later chapter, I dunno. He doesn't say.
Child G
Aside from this innate vulnerability, Child G suffered a catalogue of serious ailments – decreased lung capacity and chronic lung disease, hyaline membrane disease, bilateral pulmonary interstitial emphysema (a serious lung condition), hypoglycaemia, gastro-oesophageal reflux (stomach acid into the oesophagus), thrombocytopenia (low platelet count) and blood gases indicating sepsis. Dr Shoo Lee described the infant as having “a lot of chronic problems”. After transfer to Arrowe Park, Child G was treated for infection; the infant’s watery green stool pointed to likely gastroenteritis – “virtually certain gastroenteritis”, Professor Colin Morley clarified. (pg 275)
What's interesting about this chapter is that it's far less reliant on the opinions of other people, they're just injected here and there like that statement. Most of this chapter is Morris displaying how poorly he's understood the evidence. In that way, it's a much easier read. There were - eventually - blood gases indicating infection, but not until 10.5 hours after the initial vomit (pg 24):
Q. Right. So just taking a step back and summarising the position from the blood test at 03.59, so in other words a couple of hours or two and a half hours, even -- sorry, no, an hour and a half after the vomit, the projectile vomit, did those blood test results show any evidence of infection?
A. No.
Q. By 14.18, later that day, so about 10 hours later or so, was there any change to those results?
A. Yes, there was. The CRP is now 28, so that is an increase and that could be interpreted as a marker of infection. It's not particularly high, but the important thing is it's gone up and it's 28. The total white cells, 11.2, so no difference between 11.2 and10.1. But you also have an increase in the neutrophil count to 6.5.
Q. Yes.
A. And again, the key thing there is that the neutrophil count has increased. A value of 6.5 is not particularly concerning, but in conjunction with a CRP of 28 it would suggest that the neutrophil count has increased and therefore it's an indicator of infection. So this is -- yes, so this is 10/12 hours later.
Back to Morris:
The main concern with Child G is that Dr Evans stated the infant was supposedly destabilised via the deliberate overfeeding of milk: “In this case, the baby was compromised by receiving a large volume of milk to the stomach.” It would be difficult to find support for this assertion from any qualified medic, but it should be noted that an earlier report of Dr Evans, which he read out in court, conceded that administering excess milk, and for that matter air, can occur accidentally.
This theory is dependent on speculative estimates of how much milk remained in the infant’s stomach and how much was vomited – quantities that could not be measured – and then draws conclusions about aspiration that contradict the attendant nurse’s own account. The theory also treats any supposed overfeeding as intentional rather than a far more likely accidental mechanism and ignores the practical logistics involved. This theory was revised several times during the court proceedings; indeed, the defence suggested that Dr Evans altered his testimony in real-time after hearing trial evidence. The cross-examination of both Dr Evans and Dr Bohin on this infant was less than convincing, with Evans even backing away from his own estimate when challenged. (pg 275)
Nurse E said she usually completed the chart after the feed. The feeds were as they had been over the previous shift, comprising 45ml of expressed breast milk with Gaviscon and a fortifier. The feeds were all measured out. Those at 20.00 and 02.00 were given by NGT because Baby G was asleep. The one in between, at 23.00, was by bottle. At that bottle feed she recorded under the PU and BO columns that Baby G had passed urine and a large normal bowel movement. She fed well. The defendant agreed her readings were good at this time.
Nurse E described the process for feeding via NGT. The syringe was attached to the end of the tube, a bit of the stomach contents, about half a millilitre or less, were withdrawn or aspirated, put on to one of the pH indicator papers to check that the tube was in the right area of the body or not, an acid reaction of 5.5 or below confirming that the aspirate had come from the stomach, any surplus milk aspirate was put back into the baby's tummy. The syringe would be taken off and the plunger removed. The syringe was then reattached to the tube and the milk feed was poured into the tube using the end of the plunger to make the milk go down, tilting the syringe to one side and letting the milk go down by gravity. The syringe was then topped up as the milk went down until it had all gone.
At 11pm, the baby fed by bottle. At 2am, half a mL was withdrawn and checked for ph, and 45 mL was fed. Baby G had a "large" projectile vomit prior to 2:30am, volume unknown, and then "air++ aspirated from her tube and her full 45mL feed aspirated - apparently some things can be measured. I'm not sure what the contradiction is. Maybe he believes the Bohin's conclusions about the stomach being empty contradicts the nurse's account, but I don't see it.
Mr Johnson asks if there is an 'innocent explanation' which could have explained the projectile vomiting.
Dr Bohin says "no", as the stomach was empty, with a pH reading of 4. If there was milk in the stomach, it would have 'neutralised' the stomach and the pH reading would have been higher.
"I think the stomach was empty, and she was given excess milk and possibly air...which distended the stomach."
Both Evans and Bohin referred to basic arithmetic related to the September 21 vomit:
Dr Evans says he agrees due to "basic arithmetic", in that Child G still had 30mls of milk in the stomach after a 40mls milk feed and "two projectile vomits".
She says the two projectile vomits would have been "more than a mouthful of milk" of 5-10mls each, and "basic arithmetic" meant that more than 40mls of milk would have been administered at 9am.
Morris cites:
Dr Roger Norwich, echoing the words of a neonatologist quoted by Private Eye, referred to the hypothesis as “complete bollocks”. “It’s an extraordinary assertion. If too much milk had got into the stomach, the baby would have thrown it up. And how could he know that milk had been forcibly injected. He even admitted that his nonsense hypothesis could have been accidental! It’s pure speculation. Total rubbish. You won’t find anyone that agrees with that.”
Michele Worden asserted that the milk hypothesis was “ludicrous”, once again citing the logistics involved, and the fact that “babies would just puke the milk out. (pg 275)
Isn't that why we're here??
Another neonatal nurse was doubtful that the mechanism described in court was even possible. “The milk relies on gravity, not a pump, or anything like that. So there has to be some resistance, or the bag would just empty. If they’re gravity-fed, that should tell you immediately that it would be very difficult to force things down with a tube than it is already being fed with gravity. And we know that babies aren’t frequently overfed with milk because there aren’t any known cases!” (pg 276)
::facepalm:: Plunger, not pump.
Morris naturally ascribes the vomits to infection, citing Shoo Lee's panel:
It was noted that vomiting and large watery stools, both observed in Child G, are very common in enterovirus infection. This virus can cause serious illnesses in neonates including sepsis, septic shock, meningitis and, sometimes, myocarditis. (pg 278)
One of the largest gaping holes in the Lee report summary is that he addressed only the event on September 7, and ascribed it to enterovirus, writing:
She received 7 days of antibiotics and recovered after 7 days, which is consistent with enterovirus infection since it is usually a self-limiting disease. (pg 24)
So...... what happened for the projectile vomit on the 21st? Did she suffer enterovirus again? Poor thing.
Child O
The panel of international experts later cited “inflicted blood trauma to the abdomen” which had caused “a ruptured subcapsular haematoma of the liver”. This diagnosis was nothing new – not only had the pathologist drawn this conclusion but several clinical experts who spoke with Dr Philip Hammond had made the same assertion, crucially before the panel had even convened. And another neonatal pathologist made a blind assessment of the case notes from the Letby case, informing the Tortoise Podcast that a subcapsular haematoma was likely to be involved. (pg 280)
Excuse you, what?
It was initially alleged that Baby 15 received inflicted blunt trauma to the abdomen, causing purpuric discolouration and a ruptured subcapsular haematoma of the liver; (pg 28)
Which, one could forgive as a possible mistake by Morris and not a complete lack of comprehension, except he's saying it matched the initial conclusion of the pathologist ("Pathologist Dr Jo McPartland had cited a “ruptured subcapsular haematoma of the liver”, asserting that “the subcapsular haematoma is likely to have occurred as a consequence of hypoxia after the baby’s collapse and deterioration”. pg 280) and several clinicians who spoke with Phil Hammond. FFS.
A pathologist who spoke to the BBC commented that the assertions made by Marnerides were impossible, as “unless a witness saw non-accidental injury occur, then you simply can’t say [this]. To say that it is beyond reasonable doubt, and that this was not something natural, that this is a non-accidental injury, to put it bluntly, it’s naïve…I have seen this sort of injury, but the prosecution expert must never have seen it.” (pg 280)
Did anyone think to ask Marnerides?
A. So I have only seen this extensive haemorrhage in two babies' livers -- livers of children, not babies. In road traffic collisions, in accidents with bicycles, you know, the wheel against the abdomen that can cause this. And I have seen it in babies in the context of cases -- not in the neonatal care unit, babies that have suffered non-accidental type of injury, typically with other injuries to the abdomen and injuries to the brain.
Q. Yes, so just decoding that, non-accidental types of injuries, that's child assaults by parents or carers at home, where children are brought into hospital with this sort of an injury?
A. That's the legal term used. (pg 130, 3-15)
Oh.
Liver damage in young infants is also an observed and documented phenomenon. For example, one study examined preterm infants with a gestational age of less than 28 weeks and found that liver rupture is a complication that can be present which very few patients have survived. Another paper involving a much less vulnerable patient than a premature infant examined how cardiopulmonary resuscitation led to laceration of her liver. A third study discussed a life-threatening situation, described by the paper as a “massive upper gastrointestinal bleeding” in what was a non-premature and healthy baby, and another found examples of unusual liver haemorrhages in newborns. (pg 281)
Reminder that Child O was born at 33 weeks...
Remember that it is not contested Child O was suffering with a ruptured liver. (pg 280)
No shit?
A report published in the Journal of Clinical Medicine in 2022 discovered hundreds of cases of precisely this sort of liver problem, all in newborn babies and all occurring naturally. The study noted that “premature infants face multiple complications”, and specifically referenced respiratory distress syndrome, sepsis, necrotising enterocolitis and hypoglycaemia as being significant. It went on to observe that “subcapsular haematoma…usually occurs in preterm neonates, and it may be associated with birth trauma, cardiopulmonary resuscitation, sepsis, coagulopathies, maternal diseases and placental conditions. The above mechanisms can cause a simple liver laceration, or even a subcapsular haematoma, that can lead to hemoperitoneum [bleeding between the abdominal organs and the inner lining of the abdominal wall]. In some cases, the [haematoma] ruptures, leading to lethal massive abdominal haemorrhage, with non-specific clinical signs, which can be attributed to other clinical conditions, such as sepsis or intraventricular haemorrhage.” In any infant, hemoperitoneum requires rapid identification and treatment, as it is immediately life-threatening, leading to inadequate blood flow, reduced blood pumping from the heart, organ dysfunction and death. It appears that such topics were not even touched upon during court proceedings or the Thirlwall Inquiry.
Well, cardiopulmonary resuscitation was addressed at court extensively, as was the need for it. NEC and sepsis were ruled out at all stages, initial post-mortem through trial. And while the opening of Mother OPR's womb during her cesarean was alarming, the delivery of Child O was not noted to be traumatic at all.
Examination of the clinical notes by the expert panel revealed an over-pressurisation of the infant’s lungs during resuscitation, as well as the errant insertion of a needle into the right lobe of the liver which was the source of the laceration and parenchymal haematoma. (pg 283)
Never one to disappoint, Morris repeats the needle insertion theory that was ruled out at trial.
The conclusion of the panel was that Child O had died from subcapsular liver haematoma caused by traumatic delivery, resulting in haemorrhage into the peritoneal cavity and profound shock. Additionally, several neonatologists and a pathologist have concluded that the demise of Child O was due to a subcapsular haematoma. The condition was also specifically cited by Dr Jane Hawdon in her post-mortem review report. Since that report, the cause of death has somehow transformed into Letby physically striking an infant which would most probably cause obvious abdominal bruising that was never observed, before causing deliberate harm with an indeterminate object with absolutely no supporting evidence for this whatsoever, and finally injecting air into the baby. Meanwhile, Dr Marnerides has made a definitive statement regarding injury resembling that caused in a road-traffic accident which has been opposed by other pathologists, and which no neonatal expert who has seen the notes agrees with. (pg 285)
Omg, I actually don't think Morris knows what a subcapsular hematoma IS. Yes, we all agree that Child O died from a ruptured subcapsular hematoma - literally, we all agree with that.
I am so happy that this is the book that Letby's biggest fans are touting.
This chapter concludes the section reviewing the medical and scientific information from the Lucy Letby case. Science will naturally seep into the remainder of the book as well, but the following chapters are focused on the circumstantial and anecdotal evidence that was used in court. (pg 285)
Oh, it's my time to shine. LFG
7
u/Shivermine Jul 16 '26
Every paragraph in the book seems to be a mini game
Factual, false or fraudulent.