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Why Did Prof Sally Kinsey Testify That Babies Did Not Have Antiphospholipid Syndrome?

Updated: Oct 11

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The babies' clinical notes say they did (antiphospholipid syndrome would have explained the babies' symptoms, rashes, etc)

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Update on reporting restrictions: I have not sought legal advice about what the reimposition of reporting restrictions means for what I can write in relation to Lucy's case but I have spoken to someone who knows about these things. The test is whether a published report poses a "substantial risk of serious prejudice." The trial to which the reporting restrictions pertain is a year or so away (it hasn't even started!) Also, this article is about Prof Sally Kinsey whose testimony had nothing to do with Child K (the case being retried).

Professor Sally Kinsey was one of seven prosecution medical experts in Lucy's trial. She is a paediatric haematologist and practices at Leeds Teaching Hospitals NHS Trust ( ).

Professor Sally Kinsey testified in relation to Children (twins) A and B ( ), E ( ), F ( ), and N ( ). The Chester Standard article about her 29 November testimony in relation to Children A, B and E, "BLOOD abnormalities were not the cause of the collapse of three babies allegedly attacked by nurse Lucy Letby, a court has heard", can be found here: .

Professor Sally Kinsey testified in relation to Children A and B that the mother's antiphospholipid syndrome, an autoimmune disease, had not passed to either of her children (see below).

Professor Sally Kinsey appears to have dismissed clinical notes that said both Child A and Child B had antiphospholipid syndrome (see below).

Below are extracts from mainstream media articles about Prof Kinsey's testimony, information about antiphospholipid syndrome, and information about Prof Kinsey herself that is in the public domain. The parts that pertain specifically to antiphospholipid syndrome are in red (and underlined). Other parts that may be of relevance are underlined. Make of it what you will. Suffice to say that there appear to be questions as to why Prof Kinsey's testimony was contrary to the clinical notes, why she testified about air embolus when she she was not qualified to do so, and why issues such as the long line inserted by Dr Harkness being too close to the heart, lack of fluids for several hours, possible sepsis (sepsis was ruled out by Dr Dewi Evans), effects of resuscitation, etc, were discounted/not considered relevant.

As a general point about expert witnesses, they are there to guide jurors in matters beyond their understanding. They are supposed to be independent, with an attempt made before the trial to reach agreement between prosecution and defence experts. It appears that in Lucy's case, none of the prosecution's experts' written testimony was rebutted by the defence team's medical expert, Michael Hall. As a neonatologist he would not have been qualified to rebut the evidence of the prosecution's radiologist, endocrinologist, biochemist, haematologist, and pathologist but it is not clear why he did not do a better job of rebutting the testimony of the two paediatricians (perhaps it was because their testimony in relation to air embolism, rashes, collapses etc was endorsed by the other experts). So, given that a) the only experts the jurors heard from were the prosecution's experts and b) they are in no position to dispute it, it is no wonder they found Lucy guilty on 14 counts. What is perhaps surprising is that in the other seven counts where there was prosecution expert testimony (there was no expert testimony in relation to count 14/Child K), jurors either returned not guilty verdicts (two counts) or were not able to return verdicts (five counts). There is no clear pattern between these seven counts and the experts involved. Perhaps others can discern patterns in relation to other witnesses, agreed facts?

Child A testimony by Prof Sally Kinsey

Her first report is dated March 4, 2020, relating to Child A. The court hears the conditions that Child A and Child B's mother had before her birth, and the decision to deliver the twins by C-section in June 2015. The events of Child A's treatment at the Countess of Chester Hospital neonatal unit, subsequent collapse and death, are relayed in court. Child A's blood count was considered 'normal' for his age. She said she had considered whether Child A's mother's auto-immune disease could have been a significant factor in the death of Child A. Said auto-immune disease was a rare condition (affecting about 50 in 100,000 people) which affected the mother, which can cause increased blood clotting. It is "well recognised" that pregnancy can cause issues, which can cause nutritional problems for babies in the womb, and a C-section can be required "to save the life of the mother and the child". The court hears it can cause premature birth and blood clotting for the mother. Nicholas Johnson KC, for the prosecution, asks: "Did the...syndrome pass on to [Child A or Child B]?" Professor Kinsey: "No, that is not the case."

Mr Johnson says there was concern the condition had passed from mother to son, but says Professor Kinsey is sure it did not. "It didn't," Professor Kinsey replies. Prof Kinsey says, for the conclusion of air embolus for Child A, the doctors' descriptions of skin discolourations on the baby had "cemented" her concerns. She adds it is very "rare" and has not seen it in her experience, but she says she has read it from literature, and the skin discolourations are a "stark" feature. Prof Kinsey says she is sure the cause of Child A's death does not have a haematological origin.

Child B testimony by Prof Sally Kinsey

The case of Child B, a baby girl, is now being discussed. The events of Child B's treatment at the neonatal unit and her collapse are relayed to the court. The jury is being shown clinical records which have previously been shown as part of the sequence of events and from doctor/nurse witnesses. Prof Kinsey confirms she had noted what was written for Child B's skin discolouration on June 10 - the 'purple blotching'. For all the blood results Prof Kinsey had seen, she said they were 'normal' for her age and the time the tests were taken. There was, like Child A, no passing on of the mother's auto-immune disease to Child B, she adds. The question of air embolus is raised. She said she had made similar observations to Child A. The professor says there was no haematological evidence that could have caused Child B's collapse, and wanted to draw attention to the skin discolouration in the area around the chin, which she said was most likely a 'rash' caused when medical staff were trying to administer air.

Cross Examination of Prof Sally Kinsey by Ben Myers KC

Ben Myers KC, for Letby's defence, is now asking Prof Kinsey questions. He says his questions are more concerned on the nature of an air embolus. Mr Myers asks about the principle of experts giving evidence, and their areas of expertise. He refers to Prof Kinsey's expertise in haematology and certain paediatric specialisms, and her reports. They include focus on cancers and blood disorders. Mr Myers: "Air embolus does not feature in your expertise, does it?" Prof Kinsey: "No." Mr Myers refers to the diagrams of gas exchange, which are 'standard images' in the way gas exchange works in the body. Mr Myers: "In no way are they designed to explain an air embolus." Prof Kinsey: "They were produced to explain the gas exchange and circulation." Mr Myers: "What you are doing in your evidence is to take that understanding of circulation and gas exchange and use it to explain how an air embolus is displayed." Prof Kinsey: "Yes." Mr Myers says Prof Kinsey has, at times, commented on the issue of air embolus in her reports for Childs A, B and E. Prof Kinsey: "Only in the changes to the colour of the skin, very impactful." Mr Myers refers to the summary/opinion for Child A, and whether there was any haematological significance for Child A. He says that is not in dispute. He refers to the conclusion, which he says relies on comment from [medical experts] Dr Dewi Evans and Dr Sandie Bohin, and the description from [Countess of Chester Hospital consultant] Dr Ravi Jayaram of the skin discolouration for Child A. Mr Myers refers to the 1989 medical journal review: "mentioning a particular case - 'blanching and migrating areas of cutaneous pallor were noted in several cases and, in one of our own cases, we noted bright pink vessels against a generally cyanosed...background." Prof Kinsey confirms she is drawing a parallel between the 1989 journal review and what had been observed by doctors and nurses. She tells the court she was "shocked" by Dr Jayaram's description of skin discolouration for Child A, which she said came before she had considered the possibility of air embolus. She said she knew this is what air embolus was like, and knew from her own education, before seeing that description matched what was said in the 1989 medical journal review. Mr Myers says Dr Jayaram's clinical note - 'legs noted to look very white and pale before cardiac arrest' does not contain the full details from her report. Dr Jayaram did not add anything further to the skin discolouration observation in the report to the coroner, Mr Myers adds. Mr Myers: "The description you read came from his statement [to police] two and a half years later." Prof Kinsey agrees. Mr Myers refers to the case of Child B, and the summary/opinion Prof Kinsey made in her report. He says, for air embolus, Prof Kinsey again draws parallels between the 1989 medical journal and the skin discoluration observations seen for Child B. The clinical note of 'widespread purple discolouration with white patches' for Child B, made at the time, is shown to the court, along with a subsequent 'improvement in skin perfusion'. A doctor's note on June 10, shown to the court: 'suddenly purple blotching of body all over...upon my arrival purple blotching...[later] purple discolouration almost resolved'. Lucy Letby's note on June 10 is also shown to the court: 'Cyanosed in appearance...colour changed rapidly to purple blotchiness with white patches'. Mr Myers: "In none of those is there any description of a bright pink or red feature?" Prof Kinsey: "No." Prof Kinsey's report, dated November 1, 2022, is referred to. Mr Myers says Prof Kinsey was asked to give further consideration as to how an air embolism worked. She says she was asked to give further explanation on the features of an air embolism. She said she was not an expert in such mechanisms, but has provided an explanation. Mr Myers says the report notes there is very little medical literature in relation to air emboli. Mr Myers: "You have used your knowledge of blood and circulation to assist this?" Prof Kinsey: "Yes." Mr Myers says part of the limited medical literature relates to decompression in deep-sea divers, colloquially known as 'the bends', and that in those circumstances, nitrogen bubbles would be in the circulation longer than oxygen bubbles. He asks Prof Kinsey if that is the case. Prof Kinsey: "I don't know the answer to that question." Mr Myers says the research paper in question [for 'the bends'] dealt with four overweight deep-sea diving adults. Prof Kinsey: "Yes, there were many limitations to their findings. Mr Myers said the results were "very specific based to the people [in that study]." Mr Myers asks if the symptoms of decompression sickness would always result in skin discolouration. Prof Kinsey said it would not. Mr Myers asks if that can be applied to babies - if an air embolus could always lead to skin discolouration observations. Prof Kinsey said it would not. Prof Kinsey says the problem with decompression syndrome, in comparison to air embolus in infants, is the bubbles get larger as the deep-sea diver returns to the surface. Mr Myers says that is another limitation of the available medical literature for air emboli. Prof Kinsey says the reason that study was used in her report was that skin discolouration had been an observation in that study, as it had been in cases of air embolus. Prof Kinsey says the scale of the air embolus problem would depend on the size of the air bubble and the type of vessel that it is in. Upon a question from the judge, Prof Kinsey says she has never encountered any discussion about nitrogen bubbles in the system, other than in deep-sea divers. She says the biggest factors for any air embolus would be the size of the air bubble and the vessel that it is in. What was not a factor in her discussions was the quantities that made up the air [ie what amount was nitrogen, what amount was oxygen, carbon dioxide, etc].

Child A witness box testimony by Lucy on 5th May 2023 (

The focus turns to the case of Child A, born on June, 7, 2015, twin of Child B. Child A died the following day. Mr Myers is retelling the notes for Child A's birth. Child A, a baby boy, was born with antiphospholipid syndrome. He died the following day. Mr Myers refers to nursing notes, referring to the UVC line being in the wrong position on June 8 for Child A. It was reinserted but was still in the wrong position. A long line was inserted. Care was handed over to Lucy Letby at 8pm. Mr Myers refers to retrospective nursing notes written by Lucy Letby on the morning of June 9. The notes include: 'Instructed line not to be used by registrar. [Child A] noted to be jittery, was due to have blood gas and blood sugar taken. 'At 20.20 [Child A's] hands and feets noted to be white. Centrally pale and poor perfusion. [Child A] became apnoeic. Reg in the nursery. [Child A] making nil respiratory effort...' Child A later died. Lucy Letby says that, around the time of this taking place, she had moved to Ash House in June 2015. She said she was "still in the process of moving an unpacking" at the time of Child A's events. She says she had received a text message that morning asking her to work that night's shift. A text message from Yvonne Griffiths from 9.21am on June 8, 2015 is shown to the court asking Lucy Letby to work that night. Letby tells the court she was "frequently" asked to come in and cover neonatal unit shifts at short notice, saying she was very "flexible". Letby tells the court the first she knew she was going to be caring for Child A, in nursery room 1 was when she arrived for the handover at 7.30pm. She recalls there was "a lot of activity" in the nursery, with Dr David Harkness doing a line procedure and nurse Melanie Taylor sorting fluids for Child A. She explained Child A had been without fluids for a few hours. An intensive care chart is shown for Child A - after 4pm on June 9, the 'cannula tissued' which meant Child A's fluids had stopped, the court is told. A clinical note is shown to the court about the UVC and long line insertions. Letby says she was told by Dr Harkness and nurse Taylor the long line was suitable for use to administer 10% glucose. A collective handover had taken place prior to Letby arriving at the nursery, lasting about 20 minutes. Letby tells the court when fluids are administered via a long line, one of the two nurses present has to be sterilised, and in this case that was nurse Melanie Taylor, handling the bag, cleaning the long line, attaching the bag to the long line 'port' on Child A's left arm and making sure the line was 'flushed'. Letby was, she says, the 'dirty nurse' (ie unsterilised) for this procedure. Letby say she turned her attention to hanging the bag on to the drip stand cotside and programming the pump. Letby says the "usual practice" is for the line to be flushed with sodium chloride prior to fluid administration. She says she did not observe if that took place. The 10% dextrose solution is shown from a fluid prescription chart as beginning at 8.05pm. Letby says Melanie Taylor went over to a computer to start writing up notes. Letby said she was doing some checks - on cotside equipment, suction points, emergency equipment. She says Dr Harkness at this point was doing a procedure on twin Child B at this point. Letby says she observed Child A to be "jittery". Letby says "jittery" was an abnormal finding for Child A. It was "an involuntary jerking of the limbs". She says she remembered it was "noticeable". Child A's monitor sounded and his "colour changed". Letby says the alarm sounded, but she did not know what it indicated at the time. She says she noted Child A' "hands and feet were white". She went over to Child A, who was not breathing, so they went to Neopuff him. Letby and nurse Taylor disconnected the 10% dextrose, on Dr Harkness's advice. Referring to 'centrally pale', Letby says that refers to Child A being pale in the abdomen and torso. Child A was apnoeic - "not breathing". Nurse Caroline Bennion was also in nursery room 1, and had been during handover, the court hears. Letby says she began the 'usual procedure' of administering Neopuff to Child A. Child A's heart stopped and a 'crash call' was put out. Letby says that is an emergency line for doctors to arrive urgently. Dr Ravi Jayaram arrived immediately and another nurse arrived shortly afterwards. Letby says she cannot recall the resuscitation efforts, and says it was "an unexpected, huge shock", saying she had just gone through the doors and "then this was happening". Child A died shortly before 9pm. Letby says she, as designated nurse, arranged hand and foot prints for Child A as part of the hospital's 'bereavement checklist' which the court heard about on Tuesday. A nursing colleague helped assist in the hand and footprints, as that was a two-staff procedure. A baptism was offered to Child A during resuscitation, and Child A and Child B were baptised together. The court hears this was part of the practice. Letby said she felt after Child A, the bag of fluids and the long line "should be retained". She says she labelled the bag as "at the time...we should be checking everything in relation to the line and fluids" as it could be "tested" afterwards. She says she did not know what happened to the bag afterwards. Letby said, in reaction to Child A's death, she was "stunned, in complete felt like we had walked through the door into this awful situation - that was the first time I met [Child A] and [Child A's] parents". A nursing colleague messaged Letby on June 9, praising her for how she handled the sitation with Child A: "...You did fab." Letby responded: "...Appreciate you saying that & Thanks for letting me do it but supporting me so well x" Letby says the network of support among colleagues in messaging each other outside of work was "something we all did". Mr Myers asks why Letby searched for the mum of Child A on June 9 at 9.58am. Letby says "it was just curiosity" that she wanted to see the people behind that "awful" event, and the parents "were on my mind". She says it was a "pattern of behaviour" she had, as she searched the name as part of a "quick succession" of name searches in a short period of time. Letby says there was a debrief after Child A had died, a few days later, led by Dr Jayaram, which discussed if there was anything to learn from the event. Letby said it was "more clinically based" rather than emotional support. She said the event "affected her" emotionally, and denies causing Child A any deliberate harm. Letby says, of that night: "You never forget something like that".

Child A cross examination of Lucy Letby on 18th May 2023 (

Mr Johnson asks about the case of Child A. Letby says she did have independent memory of Child A. "Before [Child A], had you ever known a child to die unexpectedly within 24 hours of birth?" LL: "I can't recall - I'm not sure." Letby says she can recall "two or three" baby deaths prior at the Countess of Chester Hospital, and "several" at her placement in Liverpool Women's Hospital. Mr Johnson says Letby had previously told police it was "two" at Liverpool. Letby says her memory would have been clearer back then. Letby says it was discussed at the time Child A's antiphospholipid syndrome could have been a contributing factor at the time. Letby tells the court "in part", staffing levels were a contributing part in Child A's death, due to a lack of fluids for four hours and issues with the UVC line. She says they were "contributing factors", and put Child A "at increased risk of collapse". "I can't tell you how [Child A] died, but there were contributing factors that were missed." Letby says the issues with Child A's lines "made him more vulnerable", with one of the lines "not being connected to anything". Letby is asked why she didn't record this on a 'Datix form'. LL: "It was discussed amongst staff at the time...I didn't feel the need to do a Datix, it had been raised verbally with two senior staff, one Dr Jayaram, one a senior nursing staff." She adds: "I don't know why [Child A] died." Letby says if the cause of death was established as air embolous, then it would have come from the person connecting the fluids, "which wasn't me". Mr Johnson: "Do you accept you were by [Child A] at the time he collapsed?" LL: "I accept that I was in his cot space, checking equipment, yes...I was in his close vicinity." NJ: "Could you reach out and touch him?" LL: "I could touch his incubator - the incubator was closed." NJ: "Could you touch his lines?" LL: "No." Letby says "there's no way of knowing" from the signatures, who administered the medication between the two nurses, Letby or nurse Melanie Taylor. Dr David Harkness recalled to the court: "There was a very unusual patchiness of the skin, which I have never seen before, and only seen since in cases at the Countess of Chester Hospital." Letby disagrees with that skin colour description for Child A. She agrees with Dr Harkness that Child A had "mottling", with "purple and white patches". Letby says she cannot recall any blotchiness. "I didn't see it - if he says he saw it...that's for him to justify. "It's not something I saw. "I was present and I did not see those." Dr Ravi Jayaram said Child A was "pale, very pale", and referred to "unusual patches of discolouration." Letby: "I don't agree with the description of discolouration, I agree he was pale." Letby disagrees with the description of Child A being blue, with pink patches 'flitting around'. An 'experienced nurse of 20 years', who the court hears was a friend of Letby, said: "I've never seen a baby look that way before - he looked very ill." Letby agrees Child A looked ill. She disagrees with the nurse's statement of the discolouration, or the blotchiness on Child A's skin. "I agree he was white with what looked like purple markings." Letby agrees with the statement that the colouring "came on very suddenly". Mr Johnson refers to Letby's police interview, in which Letby was asked to interpret what she had seen on Child A. Letby explained to police mottling was 'blotchy, red markings on the skin' "Like, reddy-purple". Child A was "centrally pale". In police interview, Letby was asked about what she saw on Child A. She said: "I think from memory it [the mottling] was more on the side the line was in...I think it was his left." Letby tells the court she felt Child A was "more pale than mottled". She says it was "unusual" for Child A to be pale and to have discolouration on the side", but there was "nothing unusual" about the type of discolouration itself. Mr Johnson asks about the bag being kept for testing. Letby says she cannot recall if she followed it up if the bag was tested. She had handed it over to the shift leader. Letby is asked if she accepts Child A did not have a normal respiratory problem. Letby agrees. Mr Johnson asks if Letby has ever seen an arrhythmia in a neonate. Letby: "No, I don't think so, no." Mr Johnson says air bubbles were found in Child A afterwards. "Did you inject [Child A] with air?" "No." Mr Johnson asks if Letby was "keen" to get back to room 1 after this event. Letby says from her experience at Liverpool Women's, she was taught to get back and carry on as soon as possible. Letby had been asked what the dangers of air embolus were, and she had not known. "Were you playing daft?" "No - every nurse knows the dangers." Letby said she did not know how an air embolous would progress, but knew the ultimate risk was death. The trial is now resuming. Nicholas Johnson KC says there is one thing he overlooked from the morning's evidence. He asks Lucy Letby why she said "blotchiness" rather than "mottling" in part of her police statement. "I think they are interchangeable," Letby tells the court.

Child B witness box testimony by Lucy on 5th May 2023 ( )

Mr Myers turns to the case of Child B, Child A's twin sister. Child B was born on June 7, 2015, weighing 1,669g. Mr Myers says Child B was born with antiphospholipid syndrome, as noted on a clinical note. Mr Myers notes that, at birth, Child B was 'blue and floppy, poor tone, HR approx 50.' Resuscitation efforts were required, with a series of inflation breaths. Intubation was successful after a couple of attempts, and Child B stabilised on the evening of June 7. Mr Myers refers to nursing notes written retrospectively on the morning June 10. Child B had desaturated to 75% 'shortly before midnight', with Child B's CPAP prongs pushed out of nose. 'Prongs and head reposition. Took a little while and O2 to recover. HR remained stable.' '0030. Sudden desaturation to 50%. Cyanosed in appearance. Centrally shut down, limp, apnoeic. CMV via Neopuff commenced and chest movement seen...' 'Became bradycardiac to 80s. Successfully intuinated...and HR improved quickly. 0.9% saline bolus given and colour started to improve almost as quickly as it had deteriorated. Started to breathe for self...' Lucy Letby says she does not have much recollection of the night shift for June 9-10, in respect of Child B. A diagram shows Letby was in nursery room 3 for that night shift, looking after two babies. Letby says without that diagram, she would not have recalled who was doing what from that night. Mr Myers asks how Letby would know if a nurse needed assistance in a non-emergency situation. Letby says they would come and ask. Letby says CPAP prongs can be dislodged "very easily" and it happened "frequently" in babies. Before 12.30am, Letby says she believed she carried out a blood gas test on Child B, at about 12.15am. A fluid chart is shown to the court. She says at 10pm on June 9, lipids were administered. A blood gas chart is shown with a reading at 12.16am, with Lucy Letby's signature initials. She says it was "usual practice" that two nurses would be involved in the blood gas test, and she says she had no other involvement with Child B in the run-up to her deterioration. Letby is asked about a morphine bolus administered to Child B, as referred to in police interviews, when establishing contact with the baby. Mr Myers says, to be clear about the timing of this morphine bolus, a prescription is shown to the court, with the 'time started' being 1.10am. The court hears this is 40 minutes after the collapse. Letby says she cannot recall, "with any clarity", events in the build-up to Child B's collapse. She says she knows there was a deterioration "fairly soon" after the blood gas test. She said both she and a nursing colleague were in nursery 1 when Child B's colour changed - "becoming quite mottled", "dark", "all over". She says the nursing colleague alerted her to the deterioration. Letby is asked if she had seen that mottling before. Letby said it was not unusual but it was a concern, in light of Child A's death the night before. Child A was "pale" but Child B had "purple mottling". She says she and the nursing colleague were joined by a doctor at that point. Letby said she was asked to get the unit camera from the manager's office to take a picture of the mottling. She says on her return, Child B had stabilised and returned to normal colouring, and there was no mottling to photograph. She said she had the camera with her, and she had returned to the nursery "very quickly". Letby says she believes she administered some of the prescribed drugs for Child B after the collapse. A blood gas test taken at 12.51am is signed by Letby. She says as it is a two-nurse procedure, the signature does not indicate whether that was also the nurse who took the initial blood sample. Letby says following Child B's collapse, other doctors came to the nursery room, but she cannot recall who. She says presumably the designated nurse would have communicated with the family following the collapse. An observation chart shows Letby took observations for child B at 1am. She says this was "not unusual" for nurses to do this, especially if the designated nurse was busy elsewhere. The court hears this could be if that designated nurse is speaking with the parents.

Child A defence closing on 27 June ( )

The respiration rate chart for Child A is shown, with what Mr Myers says is "escalating up to the point of collapse", and is in a yellow bracket (ie elevated above normal). He says [medical expert] Dr Sandie Bohin would not accept that, saying it was stable. Mr Myers says the defence wonder how much attention was paid to Child A, with Melanie Taylor looking after two babies. Mr Myers says Child A received no fluids for four hours, and Dr Bohin agrees it was "sub-optimal". He says the long line was "in the wrong place" for Child A. He said the records show it was not correctly sited. He refers to an x-ray review on June 8: 'Long be pulled back'. Dr David Harkness put in 9.20pm he was unable to move the long line as he had been called to another patient. Mr Myers says Dr Harkness had a review with colleagues the following day and they agreed it was in a 'perfect place'. Mr Myers cross-examined Dr Bohin on the long line position, which she reported was 'not in the best position'. He says Dr Bohin didn't mention it in her evidence. Mr Myers says the line 'was too close to the heart', and fluids were put down it, and Child A had a fatal collapse within 20 minutes of that. He says Dr Harkness removed the line as soon as the collapse happened.

Antiphospholipid Syndrome ( )

Antiphospholipid syndrome occurs when the immune system mistakenly attacks some of the normal proteins in the blood, causing abnormal clotting. This condition is quite rare; most family doctors will never see anyone with this condition. Therefore, it is vitally important for your child to be immediately assessed by a pediatric rheumatologist if it is suspected that he or she might have antiphospholipid syndrome. Antiphospholipid syndrome can cause blood clots to form in the arteries or veins of the fingers, toes, legs, kidneys, lungs or brain. Blood clots in the brain can cause stroke, which is a serious symptom of this condition. A heart attack, lung clot or pulmonary embolism (PE) may also be caused by this condition. Other less common symptoms of antiphospholipid syndrome include:

  • Neurological effects. This condition can cause restricted blood flow to the brain, which can lead to chronic headaches, migraines, dementia and seizures.

  • Rash. A red rash with a lacy, net-like pattern—called livedo reticularis—can develop.

  • Cardiovascular disease. Clotting caused by this condition can damage the heart valves.

  • Bleeding. In some children with the condition, the blood platelet count is low.

Diagnosis of Antiphospholipid Syndrome

If your child’s rheumatologist suspects that he or she may have antiphospholipid syndrome, a series of blood tests will be conducted over the course of several weeks. The doctor will analyze your child’s blood for the presence of at least one of the following antibodies:

  • Lupus anticoagulant

  • Anti-cardiolipin

  • Beta-2 glycoprotein I

In order to make a definitive diagnosis of antiphospholipid syndrome, at least one of these antibodies must be present in your child’s blood in at least two separate blood tests conducted 12 weeks apart. Your child’s doctor will begin to treat the condition as soon as it is recognized, which is sometimes before the definitive diagnosis at 12 weeks.


There is no cure for this condition, but your child’s doctor will use various medicines in order to reduce the risk of blood clots. The medicines used may include:

  • Heparin. Usually, the doctor will give your child an injection of the blood thinner heparin combined with a pill that also thins the blood, such as warfarin. Blood thinners—also known as anticoagulants—reduce the chance of clotting.

  • Warfarin. After your child takes blood thinners in both injection and pill form for several days, the doctor may discontinue the heparin and continue the warfarin, potentially for the rest of your child's life.

  • Aspirin. In some cases, the doctor may recommend your child also take a low-dose aspirin each day.

  • Immunosuppressants. Your child’s doctor may prescribe immunosuppressant medications in order to reduce the body’s production of the harmful autoantibodies.

If your child is taking anticoagulants, there are some safety measures that he or she can take to reduce the chance of bleeding. It is recommended that he or she:

  • Avoid contact sports or other activities that could lead to bodily trauma or bruising

  • Use a soft toothbrush and waxed floss

  • Take extra care when using knives, scissors and other sharp objects

Blood clots related to this condition will be greatly reduced if your child takes the prescribed medicines and follows the lifestyle modifications recommended by the doctor.

Key Points to Remember

  • Antiphospholipid syndrome is a clotting disorder that is caused by an overactive immune system.

  • Left untreated, the condition can cause blood clots in major organs or structures that can lead to tissue damage like stroke or pulmonary embolus.

  • Your child’s doctor will run a series of blood tests over a 12-week time period in order to accurately diagnose the condition.

  • There is no cure for antiphospholipid syndrome, but the related blood clotting can be controlled with blood thinners and immunosuppressant medicines.

Antiphospholipid Syndrome ( )

Disease Overview

Antiphospholipid syndrome (APS) is a rare autoimmune disorder characterized by recurring blood clots (thromboses). Blood clots can form in any blood vessel of the body. The specific symptoms and severity of APS vary greatly from person to person depending upon the exact location of a blood clot and the organ system affected. APS may occur as an isolated disorder (primary antiphospholipid syndrome) or may occur along with another autoimmune disorder such as systemic lupus erythematosus (secondary antiphospholipid syndrome). APS is characterized by the presence of antiphospholipid antibodies in the body. Antibodies are specialized proteins produced by the body’s immune system to fight infection. In individuals with APS, certain antibodies mistakenly attack healthy tissue. In APS, antibodies mistakenly attack certain proteins that bind to phospholipids, which are fat molecules that are involved in the proper function of cell membranes. Phospholipids are found throughout the body. The reason these antibodies attack these proteins and the process by which they cause blood clots to form is not known.

Signs & Symptoms

The specific symptoms associated with antiphospholipid syndrome are related to the presence and location of blood clots. Blood clots can form in any blood vessel of the body. Clots are twice as likely to form in vessels that carry blood to the heart (veins) as in vessels that carry blood away from the heart (arteries). Any organ system of the body can become involved. The lower limbs, lungs and brain are affected most often. APS also causes significant complications during pregnancy. The severity of APS varies, ranging from minor blood clots that cause few problems to an extremely rare form (catastrophic APS) in which multiple clots form throughout the body. However, in most cases, blood clots will only develop at one site. When blood clots affect the flow of blood to the brain a variety of issues can development including serious complications such as stroke or stroke-like episodes known as transient ischemic attacks. Less frequently, seizures or unusual shaking or involuntary muscle movements (chorea) may occur. Blood clots in large, deep veins are referred to as deep vein thrombosis (DVT). The most common site of DVT is the legs, which can become painful and swollen. In some cases, a piece of the blood clot may break off, travel in the bloodstream, and become lodged in the lungs. This is referred to as pulmonary embolism. Pulmonary embolism may cause breathlessness, a sudden pain the chest, exhaustion, high blood pressure of the pulmonary arteries, or sudden death. Skin rashes and other skin diseases may occur in people with APS. These include blotchy reddish patches of discolored skin, a condition known as livedo reticularis. In some cases, sores (ulcers) may form on the legs. Lack of blood flow to the extremities can cause loss of living tissue (necrotic gangrene), especially in the fingers or toes. Additional abnormalities that may occur in individuals with APS include clot-like deposits on the valves of the heart (valvular heart disease) which can permanently damage the valves. For example, a potential complication is mitral valve regurgitation (MVR). In MVR, the mitral valve does not shut properly allowing blood to flow backward into the heart. Affected individuals may also experience chest pain (angina) and the possibility of a heart attack (myocardial infarction) at an early age but these problems are not thought to be related to valvular heart disease. Some affected individuals can develop low levels of blood platelets (thrombocytopenia). Thrombocytopenia associated with antiphospholipid antibodies is usually mild and only rarely causes easy or excessive bruising and prolong bleeding episodes. Affected individuals are also at risk for autoimmune hemolytic anemia, a condition characterized by the premature destruction of red blood cells by the immune system. Some individuals have reported symptoms that resemble multiple sclerosis including numbness or a sensation of pins and needles, vision abnormalities such as double vision, and difficulty walking, but it is not known if these problems are related to APS. Some data show an association of APS with cognitive dysfunction, but the mechanism is not known. In women, APS can cause complications during pregnancy including repeated miscarriages, fetal growth delays (intrauterine growth retardation), and preeclampsia. Preeclampsia is a condition characterized by high blood pressure, swelling and protein in the urine. Symptoms associated with preeclampsia vary greatly, but may include headaches, changes in vision, abdominal pain, nausea and vomiting.


Catastrophic antiphospholipid syndrome, also known as CAPS or Asherson’s syndrome, is an extremely rare variant of APS in which multiple blood clots affect various organ systems of the body potentially causing life-threatening multi-organ failure. The specific presentation, progression and organs involved vary from person to person. CAPS may develop in a person with primary or secondary APS or in individuals without a previous diagnosis of APS. In some cases, infection, trauma, or surgery appears to trigger the condition.


Antiphospholipid syndrome is an autoimmune disorder of unknown cause. Autoimmune disorders are caused when the body natural defenses (antibodies, lymphocytes, etc.) against invading organisms attack perfectly healthy tissue. Researchers believe that multiple factors including genetic and environmental factors play a role in the development of APS. In rare cases, APS has run in families suggesting that a genetic predisposition to developing the disorder may exist. The antibodies that are present in APS are known as antiphospholipid antibodies. These antibodies were originally thought to attack phospholipids, fatty molecules that are a normal part of cell membranes found throughout the body. However, researchers now know that these antibodies mostly target certain blood proteins that bind to phospholipids. The two most common proteins affected are beta-2-glycoprotein I and prothrombin. The exact mechanism by which these antiphospholipid antibodies eventually lead to the development of blood clots is not known.

Affected populations

APS affects males and females, but a large percentage of primary APS patients are women with recurrent pregnancy loss. Some estimates suggest that 1 in 5 cases of recurrent miscarriages or deep vein thromboses are due to APS. As many as one-third of cases of stroke in people under 50 years of age may be due to APS. Secondary APS occurs mainly in lupus, and about 90% of lupus patients are female.

Disorders with Similar Symptoms

Symptoms of the following disorders can be similar to those of antiphospholipid syndrome. Comparisons may be useful for a differential diagnosis. Several rare genetic disorders are characterized by the formation of blood clots (thromboses). These disorders may be collectively referred as the thrombophilias and include protein C deficiency, protein S deficiency, antithrombin III deficiency, and factor V Leiden. (For more information on these disorders, contact the National Alliance for Thrombosis and Thrombophilia.) Some individuals with APS may be misdiagnosed as having multiple sclerosis (MS) because of the development of similar neurological symptoms. Multiple sclerosis is a chronic disease of the brain and spinal cord (central nervous system) that may be progressive, relapsing and remitting, or stable. The pathology of MS consists of small lesions called plaques that may form randomly throughout the brain and spinal cord. These patches prevent proper transmission of nervous system signals and thus result in a variety of symptoms including eye abnormalities, impairment of speech, and numbness or tingling sensation in the limbs and difficulty walking. The exact cause of multiple sclerosis is unknown. (For more information on this disorder choose “Multiple Sclerosis” as your search term in the Rare Disease Database.) Lupus (systemic lupus erythematosus) is a chronic, inflammatory autoimmune disorder that can affect various organ systems. In autoimmune disorders, the body’s own immune system mistakenly attacks healthy cells and tissues causing inflammation and malfunction of various organ systems. In lupus, the organ systems most often involved include the skin, kidneys, blood and joints. Many different symptoms are associated with lupus, and most affected individuals do not experience all of the symptoms. The initial symptoms may include arthritis, skin rashes, fatigue, fever, pleurisy, and weight loss. In some cases, lupus may be a mild disorder affecting only a few organ systems. In other cases, it may result in serious complications.


A diagnosis of antiphospholipid syndrome is made based upon a thorough clinical evaluation, a detailed patient history, identification of characteristic physical findings (at least one blood clot or clinical finding), and a variety of tests including simple blood tests. The most common blood tests used to detect antiphospholipid antibodies are anticardiolipin antibody immunoassays (which, despite the name, detect mainly antibodies to beta-2-glycoprotein I), anti-beta-2-glycoprotein antibody immunoassays, and lupus anticoagulant tests (coagulation assays that detect subsets of anti-beta-2-glycoprotein I antibodies and anti-prothrombin antibodies). Positive tests should be repeated because antiphospholipid antibodies can be present in short intervals (transiently) due to other reasons such as infection or drug use. Borderline negative tests may need to be repeated because individuals with APS have initially tested negative for the antiphospholipid antibodies.

Standard Therapies - Treatment

Individuals with APS who do not have symptoms may not require treatment. Some individuals may undergo preventative (prophylaxis) therapy to avoid blood clots from forming. For many individuals, daily treatment with aspirin (which thin the bloods and prevents blood clots) may be all that is needed. Individuals with a history of thrombosis may be treated with drugs that preventing clotting by thinning the blood. These drugs are often referred to as anticoagulants and may include heparin and warfarin (Coumadin). New oral blood thinners (dabigatran, rivaroxaban, and apixaban) have recently been approved to treat other blood clotting conditions. Studies are needed to determine whether these drugs are appropriate for preventing recurrent blood clots in patients with APS. Individuals with repeated thrombotic events may require lifelong anticoagulant therapy. Importantly, affected individuals are strongly encouraged to avoid or reduce risk factors that increase the risk of a blood clot forming. Such risks include smoking, the use of oral contraceptives, high blood pressure (hypertension), or diabetes. During pregnancy, women at a high risk for pregnancy loss are treated with heparin, sometimes in combination with low dose aspirin. In some cases, heart valve damage may be severe and require surgical replacement.

Sally Kinsey's Companies House entry ( )

Sally Elizabeth KINSEY

Total number of appointments 3

Date of birth: November 1958

THE CANDLELIGHTERS TRUST (03020552) Company status: Active

Correspondence address: 8 Woodhouse Square, Leeds, England, LS3 1AD Role: RESIGNED Director

Appointed on: 10 February 1995

Resigned on: 10 January 2018 Nationality: British

Country of residence: England

Occupation: Paediatric Haematologist

Candlelighters Trust: and

Prof Kinsey's resignation coincides with the start of her involvement in the Letby investigation.

BSH ENTERPRISES LIMITED (02677826) Company status: Active

Correspondence address: Sea Moor Farm, Brown Bank Lane Silsden, Keighley, West Yorkshire, BD20 0NN Role: RESIGNED Director

Appointed on: 19 September 2000

Resigned on: 22 January 2002 Nationality: British

Occupation: Physician

British Society for Haematology:

THE KINSEY PARTNERSHIP LIMITED (04850975) Company status: Active

Correspondence address: 21 Victoria Avenue, Apartment 1, Harrogate, England, HG1 5RD Role: ACTIVE Secretary

Appointed on: 30 July 2003 Nationality: British

According to , "Kinsey are specialist providers of high performance quality brands to the most prestigious golf establishments worldwide and corporate clients".

From :

A Harrogate business has set up a company in Ireland ahead of Brexit in case trade talks “go horribly wrong”. David Kinsey, owner of The Kinsey Partnership which distributes golf clothing and headwear worldwide, said he was confident his business will survive any outcome of Brexit. It comes as today is the last day of crunch talks between the UK and European Union over a post-Brexit trade deal. Mr Kinsey said he felt the outcome of the talks were “up the air”, but added that he would want to see a deal reached. He said: “I would like to see a smooth, easy transition like most would. I personally think everybody wants us to get a deal. I am sure all the nations in Europe want us to get a trade deal.” The Kinsey Partnership imports and exports golf goods to shops and golf resorts in countries like Ireland, Sweden and the United Arab Emirates. Mr Kinsey said, while he cannot plan ahead due to the uncertainty of the trade talks, he had set up a company in Ireland as a contingency. “I’m in a position where I have set up a company in Ireland, just in case that is something we need in case things go horribly wrong and we can ship and import into Ireland if we have to.” While the Brexit talks has caused uncertainty for trade, Mr Kinsey said coronavirus has caused the company bigger problems due to a shutdown on people playing golf. He said the virus has been a “much bigger issue” on stock and trade.

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