Smith v Sheridan

This is a clinical negligence case arising out of the circumstances of the claimant’s birth on 11^th May 1999. The claimant sues through his Father and Litigation Friend, Jonathan Smith. The defendant was the Consultant Obstetrician responsible for the care and management of the claimant’s mother’s pregnancy and the delivery of the claimant. This is the trial of liability and causation only as ordered by Master Yoxall on 29^th September 2003:

“As to whether or not the defendant is liable to the claimant by reason of the matters alleged in the Particulars of Claim and, if so, whether or not any of the injuries pleaded were caused thereby; and if any such injuries were so caused, the extent of the same”.

The claimant was delivered by the defendant on 11^th May 1999 by caesarean section. This was a first pregnancy in the claimant’s mother after operative intervention for infertility. It was known that the claimant was lying in the breech position (buttocks first instead of head first) and the operative delivery was planned specifically to avoid the complications of a vaginal breech delivery which carries a significant risk of injury to mother and baby.

The delivery of the claimant up to and including his mouth took place without complication. At that point there is no dispute that the claimant was wriggling and passing urine. It is the claimant’s case that this is a clear indication of foetal well being up to this point.

The defendant then encountered difficulty with the delivery of the rest of the claimant’s head. To overcome this difficulty the defendant applied Wrigley’s forceps and pulled. The first pull had no effect. The defendant widened the uterine incision and pulled again. This is described in the operation notes made by the defendant himself as a “hard pull”.

The claimant’s head was then delivered but he was described as “flat” at birth, meaning that he was displaying no signs of life. The claimant’s Apgar scores at delivery appear to have been nought. Apgar is a crude means of scoring from nought to two in five categories: respiratory effort, heart rate, colour, muscle tone and response to stimuli. Hence a full Apgar score is 10. At one minute the claimant’s score was only 2, dropping to 1 at 10 minutes and rising to 3 at 15 minutes. At delivery, the claimant had been immediately transferred for resuscitation but this was not effective until about 17 minutes of life. Thereafter the claimant went on to develop classical signs of an acute hypoxic ischaemic insult.

On 14^th May the claimant underwent magnetic resonance imaging. This demonstrated widespread intracranial haemorrhage and ischaemic damage. The claimant is left severely brain damaged.

It is the claimant’s case that the defendant correctly chose to proceed by way of operation rather than vaginal delivery as this was a breech delivery. It is the claimant’s case that when delivering a baby by means of caesarean section it is mandatory to make an opening large enough to deliver the whole of the baby, including the head. This should be effected without the need for any mechanical force with the baby being lifted out of the uterus. The main complaint is the failure of the defendant to make an adequate opening for the delivery. The first incision was a horizontal one in the lower segment of the uterus. This was of insufficient size. The defendant sought to extend the incision laterally using scissors but he still encountered difficulty. At this stage, the claimant contends, the defendant ought to have extended the incision vertically (with a so-called inverted “T” incision or similar). This would have had the effect of enlarging the opening sufficiently to avoid any trauma to the baby’s head or brain.

Having failed to make an incision large enough, the defendant then delivered the head with forceps and a “hard pull”. The claimant maintains this “hard pull” was excessive and caused the tearing of the veins in the brain, leading to the bleeding and all the subsequent events ending in severe and permanent brain damage.

As to causation, the claimant’s case is as follows. The negligent manner of delivery caused tearing of the veins in the claimant’s brain. This led to bleeding in the brain. This caused the baby to be born “flat”. There was then a significant delay in resuscitation which caused a prolonged period of hypoxia. This hypoxia caused disseminated intravascular coagulopathy (DIC), a well known clotting disorder associated with interruption of the oxygen supply. The DIC caused the bleeding which was already present to extend or be exacerbated, setting up a vicious cycle of bleed/inability to clot/bleed. All of the above damage flowed from the defendant’s sub-standard care in the delivery.

The defendant does not accept that he caused any damage to the claimant. He maintains that his secondary uterine incision was as large as could reasonably be performed without risking serious damage to the claimant’s mother; that it would not have been safe to perform an inverted “T” incision as the claimant’s head was caught under the upper part of the horizontal incision; that he did not use the Wrigley’s forceps inappropriately or with excessive force or traction.

It is the defendant’s case, through his experts, that this is simply one of those cases of intracranial haemorrhage of unknown aetiology, following a normal and unremarkable delivery. Alternatively, the defendant maintains that the claimant was before the delivery already suffering from a bleeding disorder, such that his delivery without any negligence on the defendant’s part precipitated his intracranial haemorrhage. Two alternative mechanisms, it is said, may exist. First, this was a rare case of neonatal alloimmune thrombocytopenia (NAIT), where antibodies are transferred from the mother and prevent the baby from producing platelets in the normal way, or the claimant’s mother suffered a sub-clinical uterine infection ante-natally, which caused the claimant to suffer DIC.

It is agreed that the claimant suffered DIC. In essence, it is the sequence of events which the defendant puts in issue; rather than DIC being the consequence of the cerebral haemorrhage and hypoxia and acidosis (the claimant’s case), DIC was pre-existing and itself caused the cerebral haemorrhage (the defendant’s case).

The claimant’s parents volunteered themselves for blood tests along with the claimant, the expectation being that the proposed tests would resolve the issue of the pre-existing clotting disorder NAIT one way or another. The results of the tests were negative. Contrary to expectation, however, this did not dispose of the argument. The relevant experts for the defendant still maintained that the cause of the claimant’s problems was the pre-existing clotting disorder NAIT caused by maternal anti-bodies. One of the defendant’s experts, Professor Bennett, put forward the theory of pre-existing infection of such severity as to cause DIC prior to delivery. Although the most common types of NAIT have been excluded by such testing, no testing has been performed for rarer types of NAIT (the so-called “private antigens”), of which there were between 3 and 5 cases per year. Thus, it is the defendant’s case that NAIT has not been excluded, and that the clinical and haematological course is typical of a case of NAIT.

The principal issues may be summarised as follows:

A number of important matters are agreed in the joint statements of the various experts:

The factual evidence consisted of the evidence of Mr. and Mrs. Smith the claimant’s parents, and the defendant as well as Dr. Heather Parry, a Consultant in anaesthetics, Angela Hatt and Julie Martin, both midwives. I heard first from Abigail Smith, the claimant’s mother. Her two witness statements were taken as read. In February 1998 she had had surgery to unblock her fallopian tubes. That treatment was carried out by the defendant at the Bushey BUPA Hospital. Later that year, Mrs. Smith found that she was six weeks pregnant with an expected date of delivery of 24^th May 1999. The antenatal care was provided by the defendant, again under BUPA. She and the defendant had a good relationship. There were no complications during her pregnancy save that the baby was a breech presentation and a caesarean section would be needed. On the Friday before Jake was born, Mrs. Smith had some leakage. She saw the defendant on Saturday the 8^th May and he said that everything was fine. The leaking feeling had stopped by the following day. When Mrs. Smith went into work on Tuesday the 11^th May, she had a show at about 11.00 a.m. She telephoned the defendant who said that she should come in to the hospital. She and Mr. Smith arrived at the Watford Hospital at 12- 12.30 p.m. The defendant did not seem his normal self; he seemed panicky and preoccupied. She was put on the monitor and told that everything was fine. She was given an epidural by the anaesthetist. She was then taken to the operation room. In the theatre, a screen was put up which blocked her view of everything except for her husband on her right and a nurse on her left. She could not see the defendant who was standing next to her husband. After the incision, she and her husband were excited and laughing but then everything seemed to take too long. She was reassured by a nurse. When Jake was delivered, she knew that something was wrong because there was no cry from the baby. The defendant then stitched her up. He was very sombre. He kept saying that everything was alright. Later she was wheeled down in her bed with her husband to see Jake on an incubator. He was in a terrible state. He was fitting and drugs were being pumped into him.

In her second witness statement Mrs. Smith refers to a fall that she had whilst she was pregnant with Jake. The fall was probably on Friday the 30^th April 1999 but it could have been a week or two before that. Mrs. Smith had stumbled and fallen but she broke her fall with her hands and her “bump” did not come into contact with the road surface. Her only injuries were to graze the palm of her right hand and jar her right elbow. She telephoned the defendant and went to see him at the BUPA hospital. The defendant carried out a vaginal examination and said that everything was fine.

Mrs. Smith referred in her second witness statement to the birth of her second son, Max, who was born on 5^th May 2004 at the Princess Alexandra Hospital. He was seven weeks premature, he was also a breech baby and was delivered by emergency caesarean section. The obstetrician knew the history of Jake’s delivery, but he did not know about the compensation claim which she and her husband were bringing or that they had been told that the defendant should have used an inverted “T” incision to deliver Jake. Max appeared to be born easily and Mrs. Smith was not aware of any problems. The obstetrician did not use forceps at all. After Max was born, the doctor wrapped him up and gave him to Mr. and Mrs. Smith. He then sewed Mrs. Smith up. Whilst he was doing so, the doctor said something about the shape of Mrs. Smith’s uterus and that he had performed a “T” cut to get the baby out. It is to be noted that in operation notes written up by the obstetrician who delivered Max there appears the following:

“Well formed lower segment. Transverse lower segment incision. Breech extraction after coming head TRAPPED uterus INELASTIC L. segment incision extended to INVERTED T INCISION…… ”.

Mrs. Smith was cross-examined. There were people around in the theatre. She agreed that the defendant was not panicky.

The claimant’s father, Mr. Jonathan Smith, gave evidence. He made three witness statements. As far as he and his wife were aware, the only problem was that this was a breech presentation. The defendant therefore planned to proceed by way of an elective caesarean section. Mr. Smith was present at the birth. The baby’s legs came out, followed by his bottom. He urinated. The defendant could not get the head out. He made a further incision and put something under the baby’s head to give further leverage. It did not look like a traditional forceps but seemed to serve a similar purpose. After using this instrument for two minutes, he got the baby out. The defendant cut the cord and gave Jake to the midwife. Jake was then taken to the resuscitation unit. There were two paediatricians there and about ten medical staff were present in all. Everything seemed to be fine until they heard someone say that the baby’s heart had stopped. At about this time his wife was being stitched up by the defendant.

In his second witness statement, Mr. Smith said that when they arrived at the hospital on 11^th May, the defendant seemed panicky. In the theatre the defendant cut into Mrs. Smith and put his hand in. The staff in the theatre then started to look a bit worried. He thought that it took the defendant over 30 seconds (that was a very rough guess), just to get the baby’s legs out. Then the bottom followed and Jake urinated. Jake was not coming out further. Mr. Smith had the feeling that things were not as they were supposed to be. The atmosphere changed. The defendant put forceps in and the room went quiet. He was pulling with no effect. A couple of students started crying. The defendant then asked for something; Mr. Smith assumed that it was something to extend the cut. The defendant was then using the forceps again, in a rocky motion. He was panicky, not self assured. He levered the forceps up and down. He was pulling as well, but he levered the forceps as if he was trying to get underneath Jake, at least four times. The delivery of Jake’s head seemed to take a long time. Mr. Smith assumed that the time he was given as two minutes was correct. Jake’s head came out. He was a red/blue colour and not moving. Everyone was in a state of shock. The defendant gave Jake to the nurse at Mr. Smith’s side and had to tell her to take him to the table for resuscitation.

In his third witness statement, Mr. Smith referred to his wife’s fall in late April 1999 and to the birth on 5^th May 2004 of their younger son, Max. In his evidence in chief, Mr. Smith added that when Jake’s body had been delivered he saw Jake urinating. He then got the feeling that things were not quite as they should be. He saw something like forceps and then the defendant cut again. He thought that the defendant had the forceps and there was a rocking motion as the defendant gave a good pull. On the second occasion it was a stronger pull. It seemed longer than two minutes.

Mr. Smith was cross-examined. This was the first time he had seen a baby delivered. His first witness statement was made in order to obtain legal advice. He had written down on the back of a newspaper (which he no longer had) what happened. He included mention then of a rocking motion. That was not mentioned in his first witness statement. There was a slight rocking motion as the defendant pulled. He could not remember in what direction the rocking motion was. Jake came out and urinated on the defendant and gasped for air. Richard used his hand but the head did not come out. He used the instrumentation and still the head did not come out. The defendant went in again with forceps in a rocking motion and the baby came out. The defendant extracted Jake’s head after he used the forceps. The witness saw a rocking motion. It was not a fluid movement. The defendant experienced more difficulty than the witness was expecting and more than he expected. Mr. Smith said in his second statement that the defendant levered the forceps up and down. The leverage was three or four times and then Jake came out. The defendant was trying to pull him out. There was leverage. He did not agree that everything was fine until he heard someone say that Jake’s heart had stopped. Mr. Smith was hoping that Jake would be alright. He did have cause for concern when the defendant was trying to get Jake’s head out because he knew that things were not running to plan. As to the defendant being panicky, he was not as assured as when we started out. In re-examination, Mr. Smith said that there was a very slight rocking motion as the defendant pulled so that he could get the head out. The witness demonstrated a slight rocking and said that there was a strong pull and Jake came out.

The defendant gave evidence. He qualified at Guy’s Hospital Medical School in 1979 with MBBS. He obtained his FRCS in 1985 and his MRCOG also in 1985, being awarded his FRCOG in 1999. He became a Consultant in 1991 and had practised at Watford General Hospital ever since. He was, in 2003, a supervisor of high risk pregnancies and also had his own private case load. He had been performing caesarean sections or breeches, both as a junior and consultant for 20 years.

As an experienced obstetrician, he knew that in a caesarean section with a breech presentation that the uterus contracted after an operative incision and that it was necessary to make an incision large enough to allow for such contraction but not so large as to risk damage to the mother. He confirmed that he certainly believed that if the incision was large enough to deliver the baby’s buttocks and then the trunk, it was likely to be large enough to deliver the after coming head. Mrs. Smith was a private patient whom he had seen some years previously, she having attended him in 1997 because of primary infertility. She underwent successful surgery in February 1998 and was referred to him again in October 1998 with a history of six weeks’ absence of menstruation. An ultra sound examination revealed a pregnancy of eight weeks’ gestation. Mrs. Smith requested private antenatal care and delivery and this was agreed by the defendant who wrote to her G.P. accordingly. There were no problems during pregnancy. Mrs. Smith was a well and happy lady. All her booking investigations were normal. Her initial visit was on 2^nd December 1998 when she was 15 weeks’ gestation. On this occasion there was a mildly reduced platelet count. The test was therefore repeated and found to be at a satisfactory level. The defendant concluded that the claimant did not suffer from ITP (Idiopathic thrombocytopenia purpura). The claimant visited regularly and was seen at 20, 23, 26, 30, 32, 34, 36 and also 37 weeks’ gestation. All visits showed normal foetal growth. Platelet counts were now normal and the defendant identified the foetus as presenting by the breech at 32 weeks’ gestation. Delivery by caesarean section was agreed and this was booked for 14^th May 1999. In the defendant’s opinion an elective caesarean section was the safest option and Mrs. Smith was perfectly happy and agreed with that course of action. Mrs. Smith attended at the private hospital on Saturday the 8^th May 1999 complaining of passing urine frequently. A scan was performed followed by an internal examination by the defendant and there was no evidence of any rupture of the membranes.

On 11^th May 1999 Mrs. Smith was admitted with ruptured membranes. She was reviewed by the defendant who noted that she was complaining of backache and had passed a muceous plug. The defendant was happy that all was well. He performed a vaginal examination which revealed the cervix to be 2 centimetres dilated and it was arranged that Mrs. Smith be delivered by caesarean section that day. Dr. Parry was called to administer the spinal anaesthetic and Mrs. Smith was in theatre within approximately an hour of her arrival. Mrs. Smith was prepared for the operation by the midwife and the epidural was tested by Dr. Parry. It was reported that there were no problems. Mrs. Smith also had a CTG prior to receiving the spinal block which again was reported as being normal.

A caesarean section was performed by the defendant at 13.00 hours. He made the following operation note:

“Low incision above old scar

Routine entry

Bladder reflected down

Transverse uterine incision

Male infant delivered to head by traction

And Lovset’s manoeuvre

Mauriceau-Smellie attempts to head

Mouth delivered – gasping and p urine

Extremely tight head fit

Plus – Wrigley’s applied directly

First pull – no

effect therefore further uterine incision → L with

scissors – hard pull – delivery of flat baby (baby → head interval approximate two minutes

Timed by M/W (midwife)….. ”.

The defendant described the operation as commencing with a low skin incision being made which was a standard incision. A routine lower uterine segment caesarean section was carried out. The defendant delivered the baby’s buttocks and trunk by the Lovset’s manoeuvre. He then performed a standard obstetric manoeuvre called the Mauriceau-Smellie-Veit procedure to deliver the baby’s head. That manoeuvre required a finger to be placed in the baby’s mouth and delivery was attempted in that manner. Using the above procedure, the baby was delivered as far as and including his mouth in about 20 seconds from commencing delivery. However, the rest of the head was a tight fit and he therefore tried to deliver the baby with gentle traction using the Wrigley’s forceps. He was unable to deliver the head using the forceps and gentle traction and he therefore made a further uterine incision to the left with a pair of scissors and delivered the baby’s head soon afterwards. He confirmed the time taken to deliver the body as far as his mouth and delivery of the head was 2 minutes. The baby was flat at delivery, that is, it was not kicking and screaming although that was not uncommon in a breech delivery. The defendant was not concerned at that point as the baby had been wriggling and passing urine during delivery of the trunk. The defendant passed the baby to the midwife who took it the to resuscitaire which is standard procedure for flat babies and resuscitation was begun. The resuscitation and neonatal care of the baby was carried out by the staff of the Watford General Hospital. The defendant continued with the operation with the help of his assistant, Dr. El-Marie Bassan who was an experienced senior house officer. The defendant continued to close up the wound. The defendant could then see that the paediatric team were attempting to resuscitate the baby and the defendant could not understand why it was taking so long. He heard one of the specialists registrars shouting words to the effect “There is no foetal heart”.

The defendant said that he made a low skin incision and lower uterine segment incision of a reasonable, proper and sufficient size to deliver the baby. The incision was large enough to deliver the buttocks and trunk by the Lovset’s manoeuvre and it was reasonable to expect that it would also therefore have been sufficient to deliver the head. His second incision was as large as he could reasonably perform without risking serious damage to the baby’s mother. He believed that it would not have been safe or appropriate or possible to perform a longitudinal or T-cut. The baby’s head was caught immediately under the upper part of this incision and with his body being held upright, it would not have been possible safely to perform this cut without putting the baby considerably at risk. In particular, access to the area in that position would have been almost impossible. The defendant confirmed that he did not use the Wrigley’s forceps inappropriately or with excessive force or traction. He said that the Wrigley’s forceps were the smallest forceps available. They were very short-handled forceps with blades which lock into place. It was impossible to pull hard on these forceps as they were designed simply to ease the lifting of the baby and not as a pulling agent. The defendant had never previously encountered any problem whilst using these forceps. The head was placed in the widest part of the forceps and then the baby was gently lifted out. No problems were encountered on using these forceps during the delivery of the baby.

The defendant added in his evidence in chief that he estimated that he used the Wrigley’s forceps in five to ten per cent of breech caesarean sections. He could not remember ever enlarging an incision before. He demonstrated the use of the Wrigley’s forceps and compared them with Simpson’s forceps, used in mid-cavity vaginal delivery; on these latter forceps there were finger-grips and flanges together with a longer handle.

When he saw Mrs. Smith on 11^th May there was no evidence of spontaneous rupture. Mrs. Smith was having backache and she had a dilating cervix. That was a significant change and there was a risk of her going into labour. He described the operation again. Having made the incision in the uterus, he then used a finger of each hand to widen the incision as he drew his hands apart. The incision was probably some 6-8 inches wide. He did not think that he could have made a wider incision safely. He described the detail of the manoeuvres which he carried out to deliver the baby’s body to the point where he could see the mouth and nose. There was an extremely tight head fit. He had never had to increase an incision before. He applied the Wrigley’s forceps directly; he knew exactly where he was putting them, and doing so safely. He demonstrated that manoeuvre, as well as the use of the forceps with his arm bent, and then being moved away from the baby’s head so that the head was guided out of the uterus. On his first pull with the forceps, the defendant felt resistance, so he increased the width of the incision. He demonstrated how he used a pair of curved scissors to extend the incision by about 2 centimetres, but not in a straight line. He used the limit of the lower segment, so he extended the incision in a curved way. If he had pulled reasonably hard, the baby would probably have come out but there may have been trauma to the mother, that is a tear either into the membrane of the uterus or down into the vagina. As to the vertical T-incision, that was not his practice because the incision needed to be to the uterus with the baby’s head below where the incision was to be made. The defendant thus used the scissors to go laterally. He had never found it appropriate in 20 years to cut down with the baby’s head beneath the area to be cut. The forceps remained in place, held by the uterine structure. The defendant then again applied traction to the forceps. As to the “hard pull”, the defendant did not feel that it was excessively hard. His arm was at 40 degrees using his wrist. It was a harder pull than the first pull. That succeeded in delivering the baby. He did not use any rocking motion. To straighten the head out, you needed to pull down and then up, as he demonstrated. He never considered the second pull to be excessive. He had pulled as hard on many occasions with no ill effect, he then saying “Touch wood”. He considered the forceps to be a cage around the baby’s head and if anything was to “shatter”, as he put it, then it would be the uterus. This was not equivalent to pulling a baby some eight inches down the birth canal; the forces here were not equivalent to that. He was not concerned that it took two minutes to deliver the head from the moment that the baby’s nose and mouth were visible. He was very concerned when he heard that there was no foetal heart. He did not think that trauma had been caused to the baby. He had never seen or heard of trauma to a baby in a caesarean forceps delivery.

The defendant was cross-examined. As far as he knew Mrs. Smith did not have a blood-clotting problem. There was no active infection either. Up to the day of delivery, the defendant did not feel that Mrs. Smith’s membranes had ruptured. He had no recollection of Mrs. Smith’s fall at all. There had been a history of leakage when the bladder was full only and the defendant was confident that it was urine that was leaking and not liquor. On 11^th May Mrs. Smith was not in rip-roaring labour. The defendant wanted to perform the caesarean section on that day. Mrs. Smith’s membranes were still intact. The CTG was reassuringly normal; there was nothing about it that upset the defendant and nothing to show a distressed foetus. The defendant agreed that he had never sought to suggest that this was other than a difficult delivery but the processes he went through were, as he put it, on automatic pilot; the defendant did not feel that he could have done things differently and did not believe that he had traumatised the baby. The defendant agreed that it was mandatory to make an incision of sufficient size to deliver the whole of the baby. One made a standard incision to cover the whole of the lower segment. The defendant had never had to increase an incision. He had written the word “extremely” in the operation note. It was a tight head fit but he did not think it was likely to be difficult if the forceps were applied. You can apply more than gentle traction, the defendant said, but gentle traction was all that he ever did. The uterus was clamping down so the defendant decided to increase the incision with the Wrigley’s forceps staying on.

The defendant was re-examined. He had never seen an intracranial haemorrhage resulting from a breech caesarean section.

Dr. Heather Parry gave evidence. She qualified in 1974 and became a Consultant in anaesthetics in 1984.She recalled that Mrs. Smith was booked for an elective section. She attended Mrs. Smith and the CTG trace needed to be discontinued by the midwife when the epidural block was given. She administered the anaesthetic; all her anaesthetic procedures went smoothly with no problems whatsoever. They went into theatre about 15 minutes after the block was administered. Everything was going smoothly. There were no signs of any problems either before or during delivery. She recalled that it took slightly longer than usual for the defendant to deliver the baby. This would have been no longer than an average time for other obstetricians as the defendant was extremely skilful and worked very quickly. She had no concerns regarding the timing of delivery. The baby was flat when delivered. She recalled the baby gasping prior to final delivery. On delivery the baby was handed to the midwife who then took it over to the resuscitaire. She checked that the mother was satisfactory and within a couple of minutes she went over to intubate and ventilate the baby. The baby was not responding to the efforts made to resuscitate him and more skilled assistance was called for. The senior house officer was giving cardiac massage to the baby. Shortly after that, other registrars and finally the consultant paediatrician arrived. Dr. Parry was by Mrs. Smith’s head, standing. She could see over the screen; she was opposite Mr. Smith.

Dr. Parry was cross-examined. She was only concerned about Mrs. Smith’s contractions in relation to the epidural. This was a perfectly well mother. Her main focus of attention during the operation was, as she put it, “my patient”. After delivery, there were major problems with resuscitation. The baby would normally respond. She decided to intubate the baby to assist in ventilating the lungs. The baby did not respond in the way she expected. Resuscitation continued for a considerable period of time, she believed for some 15-17 minutes. As to the allegation of excessive force, she said that she thought she would have been aware if there were excessive force because she may have had to react by giving a drug to help the placenta to come away quickly. She was very surprised that the baby was unresponsive.

Julie Martin gave evidence. She qualified in 1987 and was a fully registered midwife grade G. She had worked at Watford General Hospital ever since qualification and delivered approximately 30-50 babies a year, then working part-time. She could clearly recall Jake’s birth and following the event made notes as to what happened as she always tried to do following the delivery of a brain damaged baby. She had not kept the notes. The pregnancy up to delivery was completely routine with no problems. Mrs. Smith was seen by the anaesthetist in another room and then brought into theatre. The defendant then performed a caesarean operation. The defendant worked very quickly and efficiently and she could see the entire operation. It was a breech delivery and the body of the baby came out without difficulty. She recalled that there was some slight difficulty with the delivery of the head. She recalled a further incision being made with scissors and then the Wrigley’s forceps being used with the head then coming out with no problem as far as she recalled. She believed that the baby then gasped or attempted to cry. The baby was passing urine and was generally flat. The baby was immediately passed to the resuscitaire by her colleague, Angela Hatt, for oxygen suction and assessment. The witness then assisted in finishing off the operation with the defendant. Some two minutes after the delivery, she recalled Angela Hatt requesting a paediatric registrar or general assistance. She believed that she then asked for a “crash call”. At about the same time Dr. Parry went over and intubated the baby. The first paediatric registrar then arrived after a few minutes followed by further members of the paediatric team. She said that she was the scrub midwife. It was her job to pass to the defendant instruments and swabs and anything he needed. She would be standing next to the defendant’s assistant on Mrs. Smith’s left, near her feet. There just seemed to be a slight delay in extracting the baby’s head; it was a little bit more difficult than usual.

Julie Martin was cross-examined. There was no suggestion of any problems with baby or mother. The witness was asked to look at the defendant’s operation note and she agreed that the order of events were as set out in that note. She agreed that the gasp from the baby and the baby passing urine happened before the Wrigley’s forceps were applied. It was when the head was finally delivered that it was clear that the baby was flat. The witness did not do any specific timings.

Angela Hatt gave evidence. She qualified as a midwife in September 1993, having qualified as a nurse in 1990. She had been at Watford General Hospital for one and a half years and was a grade F midwife. She recalled that Mrs. Smith had been admitted early for an elective caesarean section. She recalled that it was she who admitted Mrs. Smith, taking her temperature, pulse and blood pressure, and carried out the CTG monitoring. All appeared normal and well. She received a history from Mrs. Smith of spontaneous ruptured membranes on 8^th May. It was not a definite rupture of membranes as according to Mrs. Smith no speculum was performed. Mrs. Smith had said that she had had backache since the Sunday. Mrs. Smith had said that she had passed clear liquor. She had also passed a mucoid pluggy substance that morning. The witness catheterised Mrs. Smith once the epidural had been administered. Once in theatre all was proceeding as normal and the operation went well. She believed that there was an extra incision as the baby’s head had been slightly difficult to deliver. The head was delivered with no problems with the use of Wrigley’s forceps. Delivery had been slightly longer than expected. She recalled the defendant placing a finger in the baby’s mouth and the baby either took a suck or gasp. At birth the baby made an initial gasp and a sucking reflex was also noted. The witness transferred the baby to the resuscitaire where the senior house officer was present. She also started the clock at this point. On assessment it was found that the baby was not responding well to tactile stimulation and was not making any effort to breathe. She believed that the paediatrician was taking the baby’s heart-beat and it was recorded as far as she could remember at a rate of 80 beats per minute. (In cross examination she said that that was not correct as this was a flat baby). Intermittent positive pressure ventilation was commenced and the baby was given oxygen via a face funnel immediately once on the resuscitaire. Cardiac chest compression was commenced at approximately one minute by the witness and the paediatrician continued to administer oxygen via a bag and mask. Dr. Parry came over and ventilated the baby at approximately two minutes although the baby was not improving. The witness therefore discussed matters with the paediatrician and they both agreed that the paediatric “crash team” needed to be called. She believed that the crash team called was initiated at approximately two minutes following delivery. The crash team arrived at approximately 3-4 minutes following delivery. Once the crash team personel had arrived they then took over resuscitation of the baby. The witness’s job was being the midwife, receiving the baby and taking it over to the resuscitaire. She was on the opposite side from the defendant, that is on the opposite from Julie Martin. When she started the clock (according to her witness statement this was after transferring the baby to the resuscitaire), she was thinking that this was taking a little longer. It was, she thought, two minutes from the time when the forceps went on and she then said that she could not remember and was going from her witness statement. She had made various notes in the neonatal records at pages 44,45 and 46 in which she had referred to the delivery as being a “difficult breech caesarean section” and “delivery of male infant via difficult breech caesarean section head born by forceps”. She said she had seen a caesarean section for breech presentation before and forceps used in such cases.

Angela Hatt was cross examined. She was not asked to note the time of the start of the operation to its completion or from the start of the deliver of the head. She could not remember seeing the baby wriggling and passing urine. She did remember the defendant placing his finger in the baby’s mouth, then applying the forceps and extending the incision. When the baby was born it was completely flat. There was a clock on the resuscitaire and the thinking would be, “we have a flat baby and its important to see how long it takes to resuscitate the baby”. She could not see that she had made any note of the time from the delivery of the mouth to the delivery of the head. She agreed that something had gone wrong with delivery and the head was not coming out. The only reference in her witness statement to a clock and timing was after the baby was transferred to the resuscitaire. It was put to her that she was well aware that things were not going smoothly; she said that she was quite shocked that the baby was as flat as it was. It was a very quick process. Once the head was delivered, the baby was taken immediately to the resucitaire. It was put to the witness that this was a difficult breech delivery and she was referred to pages 45 and 46 of the neonatal notes where she had used the word “difficult” twice; the witness said that it was not routine. In re-examination the witness was asked whether she could see anything in the course of the operation for her to expect the baby to be so flat; her response was to say “No, not really”. She could see no reason why Jake was worse. As to excessive force, she said that she could not remember. She said, “If I saw it, maybe I could remember it but I don’t remember it”. She had used the word “difficult” at pages 45 and 46 of the notes because she just thought it was not straightforward; it was not routine and was taking just slightly longer than normal.

There was some discussion in the course of the evidence of Mr. and Mrs. Smith as to marks on Jake’s face. These were marks down the middle of Jake’s forehead. Neither Mr. Smith nor Mrs. Smith was suggesting that these were marks from the forceps. It can safely be concluded that such marks have no significance in this case.

The paediatric senior house officer was present at delivery. The paediatric note records: “Difficult extraction of head. Baby gasping before complete delivery”. The time of delivery was recorded as 13.13. When Jake was placed on the resuscitaire, he was noted to be pale, floppy and gasping with a slow heart-rate of less than 60 beats per minute (bpm). Bag and mask resuscitation was commenced. However Jake’s condition did not improve rapidly and at one minute of age the heart-rate was still less than 60 bpm and the baby appeared pale and floppy. External cardiac massage was commenced. The Apgar score at one minute was recorded as two. An urgent call was put out for the paediatric registrar. A tube was inserted into the trachea by the anaesthetist at two minutes of age and ventilation with oxygen was continued. The Apgar score at three minutes was 2. The paediatric registrar arrived at four minutes of age. Jake remained in a very poor condition with a slow heart rate despite continuing resuscitation and cardiac massage. Several doses of adrenaline were administered via the endotracheal tube. The Apgar score at ten minutes of age was recorded as 1. An umbilical venous catheter was inserted and 50 mls of normal saline was administered. The heart-rate rose to above 100 bpm at about 15 minutes of age. Occasional gasps were noted. The baby was transferred to the Special Care Baby Unit at 17 minutes of age.

On arrival at the Baby Unit at 13.30, Jake was noted to be pale with low arterial saturation despite administration of oxygen. A venous blood gas specimen showed a severe metabolic and respiratory acidosis. Jake was noted to be pale with irregular gasping respirations. He was given intravenous infusions of albumin (to improve his circulation) and bicarbonate (to reverse the metabolic acidosis). The drug tolazoline was given down the endotracheal tube in an attempt to improve blood flow into the lungs. His colour improved with this treatment and further bag and mask ventilation. Jake’s problems while in the Baby Unit at Watford were:

Jake’s condition gradually improved over the next few days. He was able to breathe without support and became more responsive. His parents were told that his long-term prognosis was poor and that he would have significant neurological problems with cerebral palsy and probable blindness. He was discharged from Great Ormond Street on 7^th June 1999 to the care of Dr. Smythe at St. Mary’s Hospital, Paddington from where he was discharged home. He was seen by the Child Development Service at St. Mary’s Hospital on 6^th July. He was noted to be feeding well and growing. He was mainly asleep and there were concerns about his hearing and vision. There was ongoing fit activity and his head growth was noted to be poor. His tone had improved but his parents were warned that he would have serious neurological handicaps. At a subsequent neurological assessment in June 2000, Jake was found to have four limb cerebral palsy with mixed dyskinetic and hypotonic features, axial hypotonia and a convergent squint. A subsequent report indicated that there was cerebellar ataxia. There was also evidence of developmental delay. It was apparent that Jake is permanently disabled as a consequence of brain injury.

Dr. Michael Clarke, a Consultant Paediatric Neurologist interviewed Mr. and Mrs. Smith on 15^th September 2001 and examined Jake. His findings are set out in his report of 20^th January 2003.Dr. Clarke found that Jake had neuro-developmental impairments and visual difficulties. At the time of examination Jake was two years 4 months old and his parents listed his difficulties as being unable to walk, speak or feed himself and that Jake had learning difficulties and a squint. In Dr. Clarke’s opinion Jake showed significant delay in all areas of development including cognitive development. It was too early to give a long-term prognosis for Jake. He did not have a progressive neurological disorder. It was probable that Jake would have special educational needs. It was probable that Jake would walk independently. His communication and cognitive abilities would, in Dr. Clarke’s opinion, undoubtedly develop but it was probable that the general developmental delay would persist.

Dr. Clarke gave evidence confirming the contents of his January 2003 report. He produced another report dated 28^th January 2004, setting out his opinion on causation. In his opinion Jake had a disorder of motor function and delay in acquisition of motor skills. It was possible that his motor disorder was evolving and in due course there may be more definite signs of cerebral palsy. Jake had an acquired rather than a congenital neurological disorder. That was because of the asymmetry of the neurological signs, i.e. a right visual field defect indicating left hemisphere dysfunction and decreased movement of the right arm. In addition, the radiological findings were asymmetrical with greater left than right hemisphere involvement. Although Jake did not show the expected neurological outcome of an intrapartum hypoxic ischaemic event, it was Dr. Clarke’s opinion that Jake did not have an antenatal cause to his neurological impairments. Jake did, however, in Dr. Clarke’s opinion suffer birth asphyxia i.e. an hypoxic ischaemic event during the process of delivery. Jake had very severe metabolic acidosis (the biochemical manifestation of asphyxia) the first blood gas results at 13.30 indicated very severe lack of oxygen and hence accumulation of acidic compounds.

Criteria indicating an acute intrapartum hypoxic event sufficient to cause permanent neurological impairment had been defined by MacLennan A et al 1999 BMJ Volume 319pages 1054 – 1059, in “a template for defining a cause of relationship between acute intrapartum events and cerebral palsy”. These criteria included a metabolic acidosis in an early sample of blood with values lower than a certain level. That criterion was fulfilled in this case. The second criterion was early onset of severe or moderate encephalopathy. Encephalopathy meant a neurological illness characterised by abnormal level of consciousness and usually seizures. The significance of early onset of encephalopathy was that it indicated an immediately preceding asphyxial event. By 15.30 hours Jake was having seizures. By far the commonest cause of seizures in the first 24 hours of life was asphyxia. There was an entry at page 60 of the records recording that Jake had Grade III hypoxic ischaemic encephalopathy. That was the most severe category. Neurological sequelae were inevitable. In Dr. Clarke’s opinion Jake most certainly had at least Grade II hypoxic ischaemic encephalopathy in which neurological sequelae occurred in 50% of cases. Jake did not fulfil the third criterion.

In Dr. Clarke’s opinion acute subdural haemorrhage occurred at the time of the caesarean delivery. That led to a fall in haemoglobin and abnormal clotting. The latter was exacerbated by hypoxia following delivery during attempts at resuscitation leading to further subdural, intracerebral and also intraventricular haemorrhage. Failure of blood flow because of compression of cerebral veins by subdural harmorrhage had caused cerebral infarction (loss of brain tissue due to abnormality of blood supply); it was therefore Dr. Clarke’s opinion that acute subdural haemorrhage occurred during delivery and that this was the cause of the cerebral damage and the cause of Jake’s present neurological impairments. Worsening hypoxia worsened with clotting abnormalities (DIC) and in this case the result was increased severity of intracranial haemorrhage. Dr. Clarke was of the opinion that there was no neurological impairment before the caesarean section and delivery.

Dr. Clarke was cross-examined. His reports had been written from a paediatric neurological point of view. This was a very severe subdural bleed. The common presentation would be of a traumatic delivery causing intracranial haemorrhage with blood loss being gradual and increasing thereafter. However, in Dr. Clarke’s view a catastrophic presentation could also happen and was also described in the literature. He had never heard of a catastrophic presentation following a breech caesarean section but, he asked, how would one hear of it and who would wish to publish a case record of it. It was very difficult to get single case reports published. He agreed that Professor Drife’s paper confirmed that such a catastrophic presentation was extremely uncommon. Symptomatic subdural haemorrhage was due to trauma. Professor Drife did not specify which type of haemorrhage he was talking about in apparently saying that half his cases were due to mechanical birth trauma. If a baby had a pre-existing bleeding disorder and there was haemorrhage, then it was not likely to be a subdural haemorrhage; such a haemorrhage would in that situation be the most unlikely. There was, here, severe trauma leading to the catastrophic presentation; that explained the massive blood loss. Dr. Clarke agreed that he had mentioned decompression for the first time in his evidence; it was well demonstrated in the medical literature. He did not know why it was not mentioned in his report. He deferred to his obstetric colleagues on the use of forceps in caesarean section. He did not wish to withdraw his evidence about compression and decompression but relied upon his general proposition that subdural haemorrhage resulted from trauma which could include compression and decompression. If there was no excessive force in the use of the forceps then one was left with subdural haemorrhage the cause of which was not identified. Hypoxia would cause DIC and DIC could cause bleeding. Dr. Clarke agreed that the haemorrhage here could have started as a minor bleed.

Dr. Clarke was re-examined. Asymptomatic subdural haemorrhage gave rise to little damage; there was very little bleeding. Such a haemorrhage was found because scanning techniques had improved. With symptomatic subdural haemorrhage, the time course was quite rapid. In his opinion the subdural haemorrhage here was a major one producing a great deal of bleeding in a very short time, the baby being apparently healthy one minute and then moribund the next.

Dr. Brian Kendall, FRCR, FRCP, FRCS, Consultant Neuroradiologist at The Royal Free Hospital and Honorary Consultant Neuroradiologist at The Hospital for Sick Children and the National Hospital for Neurology and NeuroSurgery, London gave evidence. His report of 9^th March 2004 was taken as read. He said that the subdural bleeding was likely to have been caused by tearing of veins running towards the dural sinuses around the tentorium cerebelli. Impression or occlusion of the veins would predispose the haemorrhagic infarction and intracerebral haemorrhage with secondary extension into the lateral ventricles. He was cross-examined. He did not see any evidence of a brain stem haemorrhage. There was haemorrhage in the thalamus quite low down; it was quite possible that might have caused secondary changes in the brain stem. There was a bit of swelling to the skull; it was not a haematoma. He did not see haemorrhage externally. He did see evidence of swelling in the posterior part of the head. He had never seen a case like this or seen one reported in the literature. He agreed that there was an unusual amount of damage. He had seen subdural bleeding from vaginal deliveries. This was one of the worst ones he had seen. It was certainly very severe. He had seen bleeding after caesarean section. The damage here was much worse than a post-caesarean section and was on a par with post-vaginal delivery. To cause such damage, there had to be some distortion of the skull. It could be a minor distortion. One could get a subdural haemorrhage after caesarean section with no note of trauma and the same was true of vaginal delivery, with no admission of trauma. What constituted too much trauma was not easy. Here there was bleeding in all three compartments of the brain.

Dr. Philip Anslow, FRCR, Consultant Neuroradiologist based at the Radcliffe Infirmary, Oxford gave evidence. His report of 24^th June 2004 was taken as read. He went into very great detail in his report as to the abnormalities to be seen on the cranial ultra sound scan dated 13^th May 1999, the cranial MRI scan dated 14^th May 1999 and the cranial MRI scan dated 13^th September 1999. The radiological features were those of a widespread haemorrhage caused by a traumatic injury (of whatever degree) characterised by supratentorial subdural haematoma, infratentorial subdural haematoma, subarachnoid bleeding, parenchymal bleeding (contusions), and haemorrhagic brain splitting (mainly affecting the thalamus). The pattern of abnormality was undoubtedly a consequence of trauma. However, the extent of the damage was on a par with that seen in cases of “shaken baby syndrome” which was thought to involve severe repeated shearing forces (the shake) and perhaps impact (when huge forces could be generated). The degree of damage seen in this case was therefore so unusual that, in Dr. Anslow’s opinion, a search must be made for some susceptibility in the infant to account for the severity of the injury. There were no radiological features to suggest that Jake had any hypoxic - ischaemic brain damage. It was Dr. Anslow’s view that Jake’s poor condition at birth was a direct consequence of physical injury and subsequent bleeding to his brain from whatever cause. There was no suggestion that Jake’s condition was anything other than normal prior to the caesarean section. There were no reported abnormalities in the CTG. Jake was a well-grown foetus, the fundal height was consistent with dates. The indication for the caesarean was breech presentation and draining liquor, not foetal distress. The delivery was not uneventful. Jake was born with few signs of life and was difficult to resuscitate. Dr. Anslow believed that resuscitation was effective, since there was no evidence of hypoxic-ischaemic damage, and prolonged, because of the mass effect of blood and contusion in the posterior fossa and the direct injury to the brain stem affecting its function. If the Court accepted that trauma best explained the radiological findings, Dr. Anslow asked the question as to how this could have occurred. As he put it, one obvious conclusion was that this was simply a brutal delivery by a careless operator, as alleged by the claimant. In favour of that conclusion, was (i) the operative note which did not imply a completely atraumatic delivery and secondly the radiology supported the notion of bleeding caused by brutal delivery. Against that conclusion, there were in Dr. Anslow’s view a number of points. Firstly, delivery by caesarean section was the least traumatic method of delivery. Dr. Anslow had never seen a case like this or seen one reported in the literature. As he put it, even horrendous vaginal deliveries with multiple instrumentation by inexperienced operators did not cause this pattern of damage. Secondly, although not an obstetrician, Dr. Anslow’s understanding was that Wrigley’s forceps protected the skull from damage during delivery, and did not cause damage. Thirdly, if the forceps somehow caused the brain damage, there should have been severe skin bleeding. Fourthly, as to the parenchymal bleeding, it was difficult to see how this could be caused by non-impact surface trauma. Sixthly, it was hard to see how the uterus was unscathed whilst the brain was so damaged, unless there was a bleeding disorder in the foetus. Seventhly, witnesses of the operation did not note anything untoward.

Dr. Anslow then asked himself what other possible explanation there could be for the damage to the claimant. In his view, the issue of DIC had to be carefully examined. Mrs. Smith said in her witness statement that there was some vaginal leakage from the Friday before Jake was born, on the following Tuesday. It was possible that organisms entering the liquor at that stage could have caused DIC. If so, that would explain the traumatic intracranial features of the case as a consequence of the minor trauma of assisted caesarean section. It would also explain why there was such an abrupt change in Jake’s condition. In Dr. Anslow’s view it had to be that Jake’s brain stem (which controlled breathing and heart rate) was damaged. That could be understood if normal rotational forces had caused acute bleeding into the brain stem in a patient made exquisitely susceptible by prior DIC. Dr. Anslow added in his evidence in chief that Jake deteriorated very acutely. There had to be some explanation for Jake’s failure to respond to resuscitation and it was the lesion in the brain stem which explained that. How could the use of forceps, Dr. Anslow asked, cause bleeding in all three compartments. He had never seen haemorrhages in all three compartments of the brain and haemorrhage inside the brain; it made him think that something else was happening. He did not see the little bit of scalp swelling, which he found, as significant; bleeding was the important thing and there was none here on the scalp.

Dr. Anslow was cross-examined. He said that there was a small issue between Dr. Kendall and himself as to whether there was a brain stem haemorrhage. If he was right, as he put it, the damage was sufficiently close to the brain stem to affect respiration and heart rate. He would defer, he said, to expert opinion that, if there was major damage to the brain stem, that would result in death. As to the timing of events, the nature of the lesions and the mechanics leading to the lesions, there was no dispute between him and Dr. Kendall. He said that he did not deal with the clinical consequences of the collapsed neonates. He agreed that low heart rate could be explained by massive blood loss and hypoxia. He did not accept that “Anslow One” had no relation to Jake. He said that “Anslow One” was another case of a child born with a lot of blood in his head. Subdural haemorrhage was the result of trauma sufficient to tear veins and that led to blood loss. In “Anslow One”, the baby was compromised inutero and was in distress; it did not look normal. That was the only other case which had got so much blood in it. There was no evidence of a massive intracranial bleed in “Anslow One”; the baby there had NAIT. There was no evidence of any subdural haemorrhage in “Anslow One”. No-one disputed that, in the case of Jake, DIC had occurred. DIC was probably triggered by events around resuscitation but Dr. Anslow said that he could not comment as to the onset of that bleeding disorder.

Dr. Andrew Lyon, FRCP, FRCPCH, Consultant Paediatrician since 1984 and Consultant Neonatologist since 1992 at The Simpson Centre for Reproductive Health at The Royal Infirmary of Edinburgh, gave evidence. His report of 19^th December 2001 and his letter of 3^rd November 2004 were taken as read. The clinical and haematological picture presented by Jake while in the Baby Unit at Watford was one of DIC. Hypoxia was a potent stimulus for DIC. Jake suffered intracranial bleeding with subdural, intracerebral and intraventricular haemorrhages. Subdural haemorrhage in the neonatal period was most commonly a traumatic lesion. It occurred when there were tears in veins within the head. Many of the affected veins ran in the membranes which separated the skull into compartments, the falx cerebri separating the two cerebral hemispheres and the tentorium cerebelli separating the cortex from the cerebellum. Tears in those membranes occurred when the brain was subjected to compression and stretching forces during delivery, usually with no evidence of any direct trauma to the skull. As Dr. Lyons said in his letter of 3^rd November 2004, the lack of evidence for a clotting disorder or an infection excluded the likely underlying predisposing factors to bleeding in Jake. Despite the rarity, that left the only explanation of the bleeding as the forces applied to the head during delivery. Subdural haemorrhage occurred as a result of shearing forces applied to the brain during delivery. There was often no trauma to the scalp or face. A “stuck” head delivered with a hard pull could result in such forces on the brain, even during a caesarean section.

The commonest maternal condition that caused low platelets in the foetus and newborn baby and was associated with a significant risk of intracranial bleeding was NAIT. In NAIT, the mother’s platelet count was normal but she carried an antibody which was transferred across the placenta to the baby. If the baby had a different platelet group to the mother, that antibody would destroy the platelets. The risk of bleeding was high because the platelets that were left did not function normally. The maternal platelets here were slightly low but not at a level which would have made Dr. Lyon consider that she had any underlying platelet antibody problem. Jake’s platelet count was low just after birth but that was due to his platelets being used up in a condition called DIC. The clotting studies at the time of admission to the Baby Unit were typical for DIC and in this condition the platelet count would fall rapidly. After the first couple of days, Jake’s platelet counts started to rise back to normal. DIC could cause bleeding from all parts of the body including intracerebral haemorrhage. Hypoxia and infection were common triggers for DIC. Jake had had no subsequent bleeding or clotting problems which would suggest that he did not have a defect in any of his clotting factors. In Dr. Lyon’s opinion, on a balance of probabilities, Jake was normal at the start of the caesarean section. He was well grown and the CTG just before delivery was normal. There was no evidence of infection in the mother or baby that could have accounted for his problems. Jake was a breech presentation in whom there were significant problems in delivering the head despite a caesarean section. During delivery, he suffered a subdural bleed and was compromised at birth. He suffered prolonged hypoxia during resuscitation which resulted in DIC which caused the subdural haemorrhage to extend.

In his evidence in chief, Dr. Lyon said that he did not think that resuscitation was a major contributing factor to the damage to Jake. Dr. Lyon did not take issue with Professor Wyatt who said this is his report:

“The acute pallor and very poor condition of the baby immediately following delivery were a requirement for cardiac massage and the improvement seen following the intravenous infusion of saline, all suggest that massive loss of blood had occurred from the circulation within several minutes of the delivery. The only site where this blood loss could have occurred was the intracranial compartment. Thus, there must have been a very rapid loss of a substantial volume of blood (maybe as much as a third of the circulating blood volume) into the brain tissue and into the subarachnoid and subdural spaces over the duration of a few minutes”.

Dr. Lyon said that Mrs. Smith’s membranes had not ruptured and there was no evidence of any infection. It was also clear from the evidence, that the baby had gasped before the head was delivered. As to NAIT, his clinical experience was that it was uncommon; there were two to three babies per year with NAIT in Edinburgh. Dr. Lyon had never seen a baby with a catastrophic bleed at birth and who had NAIT. The antibody in NAIT persisted for several weeks in the baby. One did not have a recovery in 24-48 hours. It was over several weeks. Subdural bleeding was a result of trauma. An intracerebral bleed may have no associated trauma. With a clotting disorder, one continued to bleed; if one traumatised tissue and it bled, then a clotting disorder meant that one continued to bleed; it did not mean that one bled at a faster rate. Jake went from normal to nearly dead in two to three minutes. He had a large amount of blood in his head. He had a low circulating blood volume. A third was dumped into his head. That must have resulted from a tear in a major vessel. There was no way that a normal clotting system would have stopped that from happening.

As to damage to the brain stem, Dr. Lyon said that he was not sure where Dr. Anslow was coming from. Jake had a low circulating blood volume and was hypoxic. If you then knocked out the brain stem in respect of breathing and heart rate, Jake would have died. Bleeding into all three compartments of the brain stem did not trouble Dr. Lyon. He said there was massive blood loss into the cerebral compartment. That much blood would spread. In the main, a subdural haemorrhage was a traumatic lesion. There was a range of haemorrhage from the asymptomatic to the rapidly lethal syndrome. Jake fell within this latter category although he did not die. Mechanical distortion of the head led or could lead to tension of the dural falx which could cause tears. A clotting disorder did not affect the ability to tear veins; he could think of no mechanism for that. Here, Jake’s recovery was too rapid for NAIT to be involved. Here, the recovery was within 24 hours. Dr. Lyon had not seen a case of any NAIT recovering as quickly as Jake did. As to “Anslow One”, Dr. Lyon could not see how it was relevant. There, the baby had problems and distress; there was no massive subdural haemorrhage; all seemed well. Then subsequently, the baby developed intracerebral haemorrhage (not subdural); “Anslow One” was a good example of what could be expected in a case of NAIT. Dr. Lyon then went through “Anslow One” in a little detail: there, there were signs of quite acute foetal stress; the baby looked funny; the baby was not growing well inutero and could not handle the stress of labour well; the baby showed signs of distress during labour; this was more classical of NAIT i.e. a baby compromised inutero, no bleeds in labour but goes on to bleed later. “Anslow One” did not relate to Jake but showed how NAIT might develop only days after the baby was born. In Dr. Lyon’s view, even if Jake had an underlying clotting problem, then it could not account for the initiation of the massive bleed which took place. There had to be mechanical force which tore a vessel; that did not arise from an underlying clotting problem.

Dr. Lyon was cross-examined. He said that his original view was that the bleed was exacerbated by DIC but, he asked, how did a baby go from normal to nearly dead in a very short time. He agreed with Professor Wyatt that there was a large loss of blood. It was an unusual case. It was not puzzling; one had a mechanism. Dr. Lyon had seen babies damaged following caesarean section but not to this extent. Caesarean section was not necessarily atraumatic. One needed some force that distorted the head. It was for the obstetricians to discuss the degree of force. Subdural bleeding could occur after normal well controlled vaginal delivery, and in a forceps delivery.

Dr. Lyon was re-examined. He had never treated a neonate with pre-existing inutero DIC. Inutero infection could result in any extremely sick baby. The level of platelets between 14.24 on 11^th May and 01.35 on 12^th May presented a picture very unlike NAIT. That was because by 01.35, some 12 hours or so after birth, the platelet count was normal at 178 and there was some recovery from 19 to 56 between 14.24 and 16.05 on 11^th May. That was much more like DIC. In NAIT, the platelets would be low and stay low. The platelet figures did not, in Dr. Lyon’s opinion affect his view that there must have been a large loss of blood very quickly.

Professor John Wyatt, FRCP, FRCPCH, DCH, Professor of Neonatal Paediatrics and Consultant Neonatal Paediatrician gave evidence. His reports were taken as read. He agreed with Dr. Anslow that the two more plausible alternative explanations were (a) severe and unusual mechanical trauma was exerted to the head at the time of delivery of the head using Wrigley’s forceps in an otherwise healthy foetus or (b) there was a pre-existing clotting abnormality present in the foetus prior to the onset of caesarean section which meant that Jake was unusually vulnerable to normal mechanical forces exerted on the head at delivery.

As to alternative (b) the evidence in favour was :

In his evidence in chief, Professor Wyatt said that the most striking thing in Jake’s case was that this was a case of elective caesarean section where the baby was profoundly damaged. Elective caesarean section was very different from vaginal delivery. Elective caesarean section was extraordinarily safe. In his view, the most likely possibility was that ante-natal DIC commenced before delivery or NAIT was present in which platelets were abnormally low. He had been persuaded that the most likely explanation was NAIT which existed before the caesarean section. If it was not NAIT, there were still other rare causes. It may be, he said, that Jake had a unique vulnerability which could be not identified. There seemed to be some abnormality of the uterine muscle in Mrs. Smith; that may explain why the after coming head did not come out easily and why the incision had to be extended. The defendant had performed a hard pull, so there was clearly resistance. In being pulled, the forceps were pulling against the muscles of the womb; if the excessive force was traction, then the tissue most likely to be damaged was the muscle of the womb. Wrigley’s forceps were designed to cradle the head from direct compression. It was agreed that a significant amount of blood was lost as the baby came out, the brain scan showing blood in every compartment of the baby’s brain.

Professor Wyatt was cross-examined. There was clear agreement between Professor Wyatt and Dr. Lyon that Jake was neurologically normal up to the passing of the mouth. Within two minutes from that Jake was very seriously ill.

Professor Wyatt was re-examined. In the end, he said, he believed that this case was more probably one of a vulnerable foetus, although it did not fit neatly into any recognised category. As to “Anslow One”, the baby there was abnormal before delivery; it had growth retardation and distorted features. If it was a case of NAIT, then very widespread damage to the brain could occur without the baby being exposed to severe mechanical forces but it was not a similar case.

Dr. Trevor Baglin, PhD, FRCP, FRCPath, Consultant Haematologist, Addenbrooke’s NHS Trust, Cambridge gave evidence. His report and letters were taken as read. When Jake arrived on the Baby Unit at Watford he had a severe acidosis, secondary to acute hypoxia. His platelet count was 19. In Dr. Baglin’s opinion, Jake was suffering from acute DIC. Haematological treatment was administered and that resulted in complete correction of the abnormal blood test results within 24 hours, followed by a deterioration, but with a lesser degree of coagulopathy. Jake therefore suffered a severe global failure of coagulation in association with severe acidosis and hypoxia. Without platelets, the clotting network could not function and so patients with a reduction in platelet count were at risk of excessive bleeding, either in response to minor trauma or spontaneously. The normal platelet count was about 150 – 450. At platelet counts below 150, there was no increased bleeding tendency until the count fell below about 80. As the count approached 20, spontaneously bruising and minor bleeding occurred. Below 20, bleeding could be severe. In Dr. Baglin’s opinion, Jake’s low platelet count was not attributable to ITP in his mother.

Dr. Baglin then described DIC. That was the name given to an acquired disorder of blood coagulation. It was not a primary diagnosis. It was a complication of an underlying serious illness. Therefore, diagnosis of DIC required (i) a pattern of change in blood coagulation tests, and (ii) in the setting of a disorder known to cause DIC. DIC occurred when there was a breakdown of the steady state of anticoagulation within the system. Consequently there was widespread clotting (thrombosis) and clotting factors and platelets (blood cells required for coagulation) were consumed. As a result of this consumption, the blood eventually became unclottable and so severe bleeding developed. Therefore, there was a paradox of both widespread thrombosis and bleeding. DIC occurred in critically ill patients. In neonates, DIC would result from complications of delivery resulting in hypoxia and acidiosis. In Dr. Baglin’s opinion, this was by far the most likely explanation for the bleeding complications suffered by Jake. Jake suffered birth asphyxia with severe acidosis. He therefore had an underlying illness of a severity that would be expected to produce DIC. The blood coagulation tests indicated a global coagulopathy, such as DIC. The pattern of results was typical of severe DIC. The coagulopathy resolved relatively quickly with correction of the underlying problem. Whilst spontaneous intracranial haemorrhage could result from DIC, it was far more likely that DIC caused prolonged or more severe bleeding rather than being the initiating factor. From his examination of the events and the reports of the other experts, it was Dr. Baglin’s opinion that the primary cause of intracerebral bleeding was most likely trauma at delivery, with bleeding then exacerbated by the development of DIC. Most importantly, in his opinion, the birth asphyxia and the development of DIC were not in keeping with a diagnosis of NAIT. He thought it extremely unlikely that this was a case which involved NAIT or ITP. The DIC was probably caused by hypoxia following the prolonged resuscitation; that was by far the most likely diagnosis. He thought that all experts would agree that Jake was not affected by ITP, that NAIT was extremely unlikely and that DIC, secondary to birth asphyxia with acidosis, was the most likely diagnosis. Dr. Baglin referred to a laboratory report which confirmed that there was no evidence that Jake had NAIT. He regarded the possibility of NAIT due to private antigens as extremely unlikely. If Jake had suffered NAIT at birth and if his younger brother Max had also suffered NAIT, then Dr. Baglin would have expected Max to have had severe thrombocytopenia at birth. He did not and therefore he did not have NAIT. The absence of NAIT in Max reduced the chances that Jake had NAIT.

Dr. Baglin added in his evidence in chief that the speed of deterioration of Jake and the development of DIC made him feel that NAIT was unlikely. He thought there should be tests. The tests were carried out and were negative. Then the private antigen theory came up; that was improbable. There were 3 -5 cases in the U.K. per annum of private antigen NAIT. The delivery of Max reduced the possibility of NAIT in Jake by 50%. Post birth, clinically there was DIC. One could ask about private antigen NAIT, but it was much more likely that NAIT was not present. The platelet count at birth was probably higher than 19; the platelet count must have started at a considerably higher level as the DIC was severe. The clotting screen was recorded as normal by 4.00 a.m. on 12^th May 1999. For the clotting problem to be corrected in that time after one transfusion was a quick resolution so that DIC was of short duration. For NAIT (if it was NAIT) that was a pretty rapid recovery.

Dr. Baglin was cross-examined. Platelets would only drop if there was massive blood loss and dilution by transfusion of fluids. DIC was a secondary event. More commonly it developed over hours but there were cases where DIC could be almost instantaneous. One did see rapid DIC in neonates. There was evidence of DIC when Jake was on the Baby Unit. Congenital blood disorders did not cause torrential blood loss. Less than 50% of NAIT children bled at birth; it was not a typical pattern to bleed at birth. With NAIT, one would not have a massive bleed amounting to the loss of one third of the baby’s blood volume in about two minutes. Babies with a bleeding disorder did not bleed in the majority of cases at the slightest trauma. Jake’s platelets at birth could have been normal. They must have fallen from 150. Jake had DIC to cope with; the DIC process would have started during resuscitation. DIC was a clinical diagnosis; you did not just look at the blood tests. It was true that DIC was not suspected until Jake was some 3 hours old but, in Dr. Baglin’s, view DIC was established and that was because of the long and difficult resuscitation; Dr. Baglin said that DIC was established by 2.00 p.m. In the scenario facing Jake, he would be expected to have DIC. There was DIC and the events associated with it; there was a long and difficult resuscitation. If one looked at the spectrum of events, in Dr. Baglin’s view there was DIC developing early. To say that there was DIC at or shortly after 2.00 p.m. meant looking at the whole picture. The platelet count was 19. There was DIC and no NAIT. There was nothing pre-existing. That was the most probable explanation. With a platelet count of 19, Jake was very much at risk of spontaneous bleeding and it could well have been severe. If the platelets were as low as 20, Jake would be liable to bleed as a result of mild trauma. The platelets were 56 at 16.05 and 31 at 21.30. DIC was then in full flow. Jake had been given 50mls of saline; that was a dilution and the effect wore off. The difference between 19 and 56 could have been the result of all these dilutional factors. Once the baby was born and the cord was clamped, there would be no transfer of antibodies but the destructive element could persist. Not all the antibodies were bound; there were usually free antibodies around.

In re-examination, Dr.Baglin said that, putting the whole thing together, there was no evidence of a pre-existing disorder. He saw disorder following resuscitation. NAIT was an improbability. DIC was a certainty; as to its onset, overall this was severe DIC starting at the time of resuscitation. The rate of bleeding was rapid. If subdural in origin, spontaneous bleeding in patients with bleeding/clotting disorders was slow. For a rapid bleed, one needed an additional factor; if trauma caused the bleeding, then the bleeding would be rapid. All that Dr. Baglin could say was that the rapidity of the bleeding was out of context with a bleeding disorder. It suggested a mechanical bleeding, for example, in surgery or other trauma. Rapid recovery was not impossible with NAIT but it was unusual and all normal NAIT had been excluded. Dr. Baglin saw NAIT by private antigen as very unlikely by a very long way. He had not seen NAIT corrected within 12-14 hours.

Dr. Elizabeth Letsky FRC Path, FRCOG (ad eundem), FRCPCH, Retired Consultant Haematologist at Queen Charlotte’s and Chelsea Hospital for Women gave evidence. Her reports were taken as read. The collapse at delivery and very rapid onset of DIC suggested an ongoing process prior to the caesarean section. It was unusual for DIC to present with such a low platelet count. Established DIC was confirmed by the very high D-dimer count in the second sample. Clinically and haematalogically the most likely diagnosis in this case at the time of delivery was NAIT. NAIT, although rare, was the most common cause of severe thrombocytopenia. NAIT arose when the foetus carried paternally derived platelet antigens, which the mother lacked. She produced antibodies against these antigens which crossed the placenta and bound to both platelet and endothelial (lining of blood vessels) receptors in the foetus. The tests of platelet type carried out on Jake and his parents were performed almost five years after Jake’s birth. Results excluded the most usual causes of NAIT. However, there remained rare “private” antigens, which would not be picked up by those tests. That was because the antibodies usually disappeared from the maternal circulation within weeks of delivery. DIC was always a secondary phenomenon. There were many triggers that could occur inutero. Fetomaternal bleeding, Abruptio Placentae, trauma inutero and infection inutero could all effectively be excluded. In her opinion, the usual screening tests and prophylactic antibiotics virtually excluded infection in Jake although there was a suggestion of earlier rupture of membranes. There was no pre-existing DIC in this case although Dr. Letsky said that she would leave that to her obstetric colleagues. In her opinion, DIC was caused post-birth by shock and acidosis. The very severe thrombocytopenia documented shortly after birth and the established DIC with very high D-dimers and failure to achieve blood clotting in the laboratory, virtually from delivery, suggested that such derangement of haemostasis was ongoing at the time of delivery. The trigger for this remained unclear but the possibility of a fetomaternal bleed (unlikely as the CTG was normal) or NAIT due to a “private” antigen had not been excluded. Those findings suggested that there was a pre-exiting defect in haemostasis rendering the foetus exquisitely vulnerable to even minor trauma at delivery. NAIT was very rare. The fact that Max did not suffer from NAIT did not alter Dr. Letsky’s contention that, on the balance of probabilities, as she put it, the clinical picture would still fit that of Jake developing thrombocytopenia and haemostatic incompetence due to NAIT resulting from a paternal “private” antigen.

Dr. Letsky added in her evidence in chief, “As to the onset of bleeding with NAIT, it was not the speed but the spontaneous nature of the bleeding with minor trauma”. She believed DIC was triggered on the resuscitaire when the heart stopped beating and the baby had to have cardiac massage and intubation but not prior to that. DIC became apparent to two and three quarter hours after delivery. The clinicians then decided to seek a coagulation screen to confirm or refute that. Dr. Letsky said that the clinical reasons which led her to say that this was a case of NAIT were (i) the fact that Jake haemorrhaged and (ii) the platelet count was only 19 within an hour of delivery. She could not think of anything else that would explain the position. DIC probably started at the time of the collapse of Jake. She did not consider that the platelet count would have been normal at birth; it could have been lower than 19 then. In her view, it was very unlikely that Jake could have had a much higher platelet count at birth, taking full account of the saline dilution. In the case of a baby, the platelets were very unlikely to drop from a normal level down to 19 in three quarters of an hour.

Dr. Letsky was cross-examined. The tests carried out excluded 95% of NAIT. She agreed that “we are into super rarity”. Max was completely normal. Max had a 50/50 chance of inheriting the private antigen NAIT, so that was a further point of rarity. She was told that Jake was a breech presentation delivered by caesarean section, that he collapsed at delivery and had a low platelet count recorded within an hour; that was a classical presentation of NAIT. There was a rapid collapse at delivery in a caesarean section and she looked for a possible cause. She believed that DIC was triggered at the point of resuscitation and not before. She agreed that the “private” antigen NAIT was only a possibility which could have been tested for at an earlier stage but there had been a failure at Watford to screen for it.

Mr. Gareth Thomas, LLM, FRCOG, Consultant Obstetrician and Gynaecologist, Trust Deputy Medical Director, Department of Maternity and Gynaecology, The Ipswich Hospital NHS Trust gave evidence. His report was taken as read. It was encumbent upon the surgeon to create sufficient space for delivery in a caesarean section. The initial transverse insertion would usually self extend laterally if extra space was needed for the head to pass through. That appeared not to happen in this case and scissors were required in order to enlarge the incision. Even then there was difficulties. These were overcome with “a hard pull” which was used to complete the delivery. It was Mr. Thomas’s opinion that the difficulties should have been overcome by increasing the size of the uterine opening first with an adequate lateral extension to each side and then, in the event of failure, a vertical relieving incision, sometimes referred to as a “T” incision. As it happened, it this case, there was sufficient space for the surgeon to extend the incision towards the left without damaging blood vessels lying on the lateral wall of the uterus. When it was discovered that extension to the left had still not made an incision of sufficient size, then extension to the right should have been considered. In the event that the incision was still too small, a vertical relieving incision should have been made thus eradicating the need for a hard pull with forceps.

The foetal head was retained unexpectedly by the uterine musculature after the rest of the baby had been delivered. Wrigley’s forceps were applied to the head. Normally these would provide a protective role against rapid moulding and unmoulding of the foetal head but in this case the forceps were used for traction. The first pull was described as having “no effect”, presumably because the uterine incision was not sufficiently large to allow passage of the head. Forceps deliveries could be associated with intracranial bleeding and on a balance of probabilities the subdural haemorrhage shown by the MRI was caused at the time of the traction applied during the forceps delivery. It was likely that the bleeding arose from a tear in one of the veins which lie in the folds of the dura, the material which lies between the inside of the skull and the brain itself. One of the potential causes for such a tear would be excessive traction as evidenced by the description of a “hard pull” and a rocking movement as described by the father, Mr. Smith. On a balance of probabilities, it was this forcible traction which caused the tear. Having enlarged the incision to the left with scissors, the defendant increased the degree of traction to a “hard pull”. Unfortunately, in Mr. Thomas’s opinion, that was the wrong course of action. The reasonable obstetrician would have stopped momentarily in his efforts, taken stock and then, rather than risking foetal trauma by pulling on the head still more, either further enlarged the uterine incision by greater lateral extension or, more likely and more effectively, made a vertical relieving “T” incision from the mid-line of the upper edge of the uterine incision. Such an incision would be confined to the lower segment or the very lower reaches of the upper segment. There was no evidence that it weakened the uterine wall and it did not imply a repeat caesarean section in subsequent pregnancies. The incision had the same effect on the circumference of the transverse lower segment incision as that of an episiotomy on the vaginal entrance during a vaginal delivery – each centimetre of incision provided almost 2 centimetres of circumference. It was Mr. Thomas’s opinion that, in taking the wrong course of action, the defendant allowed the standard of care of Jake to fall below that of a reasonable obstetric practitioner.

Obstetricians were advised that any forceps delivery should be carried out in such a way that traction was moderate or gentle. The notes referred to a “hard pull” which implied a degree of traction which was greater than moderate or gentle. It was possible to use Wrigley’s forceps with excessive force or traction, the cephalic curves of Wrigley’s forceps being similar in size to the curves of mid-cavity forceps. The only significant difference was the length of the handles. In Wrigley’s forceps they were short. That design feature did not make it impossible to apply too much traction. From the pattern of bleeding on the MRI, from the circumstances which presented at delivery and from the note that the delivery was expedited by a “hard pull” instead of the further enlargement of the uterine incision, it seemed certain, as Mr. Thomas put it in his report, that Jake’s intracranial subdural bleeds were the direct result of a traumatic forceps delivery. Regrettably, in Mr. Thomas’s opinion, the standard of care offered during that delivery fell below the reasonable expected standard.

In his evidence in chief, Mr. Thomas said that usually the forceps were used to lift gently. If it was not possible to lift gently to deliver the head, then the incision should be enlarged to the left, followed by a gentle lift out. It was possible for the forceps to pull on either side of the head: that is where the parietal bones were. Mr. Thomas would say that, from the fact that it was necessary to pull hard, that was the source of the damage. Inside the baby’s head, there were the venous sinuses. If there was a shearing force, that may cause damage to those venous sinuses. The impression gained was of a massive bleed. Mr. Thomas assumed that a large vein bled to cause this rather than a small one. They were the bridging veins. It was possible that they were damaged by shearing force. Mr. Thomas agreed that in the joint report of himself and Professor Bennett it was said that both experts would have expected more soft tissue damage to the face if excessive traction had been used. Mr. Thomas said that he thought that was so, if the forceps were moving up and down. Where there was compression from traction, then there was going to be decompression. If one pulled hard on the forceps one was going to compress the parietal bones. The forceps were often taken off hurriedly, allowing the skull to decompress, resulting in a straightening of the falx. Instead of increasing the strength of the pull, one should enlarge the incision. In a caesarean section, one could increase the space; it was not necessary to increase the traction. No vertical incision appeared to have been made. Mr. Thomas had never seen a “hard pull” at caesarean section. He thought that the nature and extent of the damage was entirely consistent with too much force being applied. He could see no other explanation for the injuries suffered by the claimant. In the addition to the joint report, Mr. Thomas agreed that Mrs. Smith’s subsequent delivery of Max might be relevant, not so much from the ascending infection theory because, after all, no intra-uterine infection was shown, but more from the anomaly point of view. An inverted “T” incision was required for the delivery of Max. The uterine wall was described as inelastic. The delivery took place some seven weeks early; it was likely that the lower segment was poorly formed. As Mr. Thomas added in his evidence, the surgeon there made an inverted “T” incision; there was something about the uterine wall which was ungiving. Mr. Thomas had dismissed DIC arising as a result of infection, as there was no sign of infection. The membranes did not seem to have been ruptured. It seemed to be accepted that there was no DIC pre-delivery, but that DIC was triggered in resuscitation. Comparing the two deliveries (those of Jake and Max), Mr. Thomas said that by not enlarging the incision so as to lift Jake out gently, the defendant fell below an acceptable standard of care. He demonstrated the carrying out of a “T” incision and said that it was normally possible to make such an incision without damaging the baby, by lowering the baby’s body while the incision was carried out. The low platelet count after birth did not trouble Mr. Thomas; he said that where there was DIC, the first thing to look at was the platelets.

Mr. Thomas was cross-examined. Mr. Thomas agreed that elective caesarean section was safer than any form of vaginal delivery. When using forceps in caesarean section, one used gently controlled traction; one was lifting and not pulling. One lifted the baby out by applying a gentle amount of traction. Mr. Thomas agreed that the use of some degree of traction did not imply sub-standard care. He agreed that no expert had heard of massive damage as in this case in elective breech caesarean section. Mr. Thomas said he would know that the risk was always there. By not increasing the space for the baby, the obstetrician was replicating the circumstances of a vaginal breech delivery in which subdural haematoma was common. In the case of caesarean section, one would imagine that the soft tissues would provide less resistance. It was easy to tear the uterus. The incision would usually self extend.

Mr. Thomas agreed that one could have a spontaneous intracranial haemorrhage, including a subdural haemorrhage, with NAIT. Mr. Thomas was referred to “Bennett One”; Mr. Thomas said that related to a slow insidious haemorrhage; it was not so different from “Anslow One” where there was a damaged foetus. That was not the picture which one saw with Jake. Inutero, subdural haemorrhages were slow collections of blood.

In re-examination, Mr. Thomas was referred to “Bennett One”. That was thought to be the first case of a spontaneous subdural haemorrhage. The foetus was short of platelets. The mother was advised about termination but continued. There were spaces in the brain and collections of blood. With Jake, there was nothing of that nature; the ante-natal records of Jake and his mother show that all was well including the platelets. There was no massive or rapid bleed or trauma in “Bennett One”.

Professor Bennett, PhD, FROCG, Professor of Obstetrics and Gynaecology, Imperial College Faculty of Medicine and Consultant in Obstetrics and Gynaecology Hammersmith Hospitals Trust gave evidence. His reports were taken as read. There were no significant complications during Mrs. Smith’s pregnancy (with the possible exception of her fall). Jake was a normally grown baby. The CTG recording made half an hour before Jake’s birth showed an entirely normal and reassuring pattern suggesting that he had normal blood gases at that time. Jake was born in surprisingly poor condition. Intermittent positive pressure ventilation did not lead to resuscitation. It was only after administration of adrenaline and intravenous fluids that his cardiac function began to improve and he began to be “resuscitated”. It was subsequently determined that he had had a large intracranial haemorrhage. That sequence of events suggested to Professor Bennett that the intracranial haemorrhage did occur at or close to the time of Jake’s delivery. In Professor Bennett’s opinion, it was impossible that a Wrigley’s forceps delivery of the type described by the defendant could cause any significant intracranial haemorrhage in an otherwise normal baby. If Jake’s cerebral damage was due solely to the forceps delivery, without any other factors playing a role, it was impossible that there would not have been extensive bruising to his head. Clinically identifiable cranial haemorrhage, secondary to a vaginal forceps delivery, which led to permanent neonatal cerebral damage or death, was extremely rare. Despite extensive electronic searches of medical literature databases, Professor Bennett could not find any case report which described this type of injury at caesarean section. In Jake’s case, he was in obviously poor condition from the moment of birth, and appeared to have had DIC from the outset. That suggested to Professor Bennett some pre-existing problem, with its origins in the time prior to delivery. Professor Bennett would have anticipated that excessive traction on the forceps at caesarean section would have led to damage to Mrs. Smith. The material myometrium (muscle of the womb) would tear readily if an attempt was made to pull the head through an inadequate incision using excess force. That would lead to extension of the incision into the uterine angle. That did not happen which pointed away from the use of excessive force with the forceps. Nevertheless, it was likely, in Professor Bennett’s opinion, that the intracranial haemorrhage did occur during the forceps delivery. To his mind there were two possibilities. The first was that Jake was at risk of intracranial haemorrhage because of pre-existing severe cerebral hypoxia-ischaemia. The second was that he was predisposed to intracranial haemorrhage but had abnormality of blood clotting. In Professor Bennett’s opinion it was highly unlikely that cerebral hypoxia-ischaemia was the primary cause of Jake’s problems. It was unlikely that Jake would have developed sufficient hypoxia since the CTG recording to explain his very poor condition at birth and his substantial intracranial haemorrhage. It seemed to Professor Bennett highly likely that Jake had a pre-existing bleeding abnormality and/or profound thrombocytopenia (lower platelet count) at the time of birth and that it was this which predisposed him to intracranial haemorrhage in association with the forceps delivery. Thrombocytopenia in a neonate may be part of DIC. Professor Bennett considered two possible mechanisms for thrombocytopenia without DIC in a foetus/neonate; these were immune thrombocytopenia (ITP) in the mother and NAIT. In Professor Bennett’s opinion it was highly unlikely that Jake had ITP. As to NAIT, this was the most likely mechanism leading to Jake’s thrombocytopenia, in Professor Bennett’s opinion. However, Jake and his parents had undergone tests to exclude “incompatability” in the major platelet antigens which caused NAIT. Professor Bennett understood that it remained possible that Jake could have developed NAIT through expression of (very rare) private platelet antigens, but that was not within his expertise.

In Professor Bennett’s view, Jake may have had thromocytopenia as part of DIC present at the time of birth, prior to the forceps delivery, which would place him at high risk of intracranial haemorrhage during an otherwise satisfactorily performed forceps delivery. There were no strong clues as to what might have led to Jake having foetal/neonatal DIC, but there were several possible mechanisms. There may have been a viral infection. There may have been a feto-maternal haemorrhage. It was possible that there may have been a foetal membrane rupture on 8^th May 1999.Although the evidence for it was poor, an ascending infection secondary to pre-labour membrane rupture was another possibility for DIC in Jake. Professor Bennett had considered whether the normal CTG recording made prior to the caesarean section excluded the possibility of pre-existing DIC in Jake prior to his birth. Since DIC was not necessarily associated with blood gases, in his opinion, a normal foetal heart pattern did not exclude the possibility of DIC being present prior to Jake’s birth. It seemed to Professor Bennett probable that the likely series of events was that Jake’s primary problem was thrombocytopenia probably as part of a foetal DIC, meaning that, at the time of his delivery, he was at very high risk of intracranial haemorrhage.

There would have been no reason for the defendant to take any particular precautions at the time of delivery with regard to the risk of foetal haemorrhage. It was every obstetrician’s experience that on occasion it could be difficult to deliver the aftercoming head of a breech. Jake’s head was relatively large. The sequence of manoeuvres which the defendant undertook were precisely what Professor Bennett would have expected any competent obstetrician to do. If it was necessary to use forceps, then usually the after coming head could easily be delivered using the light pattern Wrigley’s forceps. If that was unsuccessful in achieving delivery, then the uterine incision should be extended using scissors, as was done by the defendant. It would not be wise to attempt to extend the uterine incision as a primary manoeuvre without first attempting delivery using forceps since there was a significant risk that the incision may tear into the angles of the uterus. Professor Bennett would have anticipated that most obstetricians would, after an initial failure to achieve delivery using Wrigley’s forceps, choose to extend the uterine incision upwards and laterally (the so-called J-extension) rather than as a mid-line vertical incision, (the so-called T-incision). It was probably easier and safer, using scissors, to extend the uterine incision to a J since it would be easier to pass the scissors along the side of the baby’s head rather than making a cut in the mid-line behind the baby’s head. With an assistant holding the baby’s body up, a lateral incision would be an easier and more obvious approach. If it was the case that Jake did have pre-existing DIC, that could not have been identified by the defendant in the ante-natal period. The defendant could not have known that Jake was at increased risk of intracranial haemorrhage. Even had he known this, however, it was difficult to think of any other sequence of events which the defendant might have undertaken to achieve delivery with less risk of intracranial haemorrhage. In Professor Bennett’s opinion, the technique of delivery described by the defendant was competent and, although there was some minor difficulty in delivery of the after coming head, could not have been the sole cause of Jake’s injuries, Although the common causes of NAIT had been excluded in Jake’s case, the other features of his case strongly suggested intracranial haemorrhage secondary to pre-existing abnormality of blood clotting, rather than secondary to the forceps delivery alone.

Professor Bennett said in his evidence in chief that he did not agree with Mr. Thomas as to gentle traction, if Mr. Thomas was saying that the after coming head was falling out or was just lifted out. If Mr. Thomas was right, then the opening would be too big and there would be risk to the mother and her tissues. If the incision was not sufficient so excessive force had to be used, Professor Bennett would expect the incision to self extend, by tearing on both the left and right sides of the incision. The defendant was able to deliver the aftercoming head, so Professor Bennett thought that sufficient space had been made for the delivery. It was Jake’s immediate collapse after delivery that was not the picture of a not-well-done forceps delivery, so Professor Bennett thought there must have been some other factor producing intracranial haemorrhage. He had always held the view that the degree of damage found could not be done by pulling on forceps in a caesarean section. He thought this was a classic case of NAIT. He also thought it was a case of pre-existing DIC and until the trial, he preferred DIC as pre-disposing Jake to intracranial haemorrhage. There was no clinical evidence of DIC until later (the first blood sample was not tested). Professor Bennett now much preferred NAIT to pre-existing DIC. He did not exclude the possibility that there was some other explanation. To exert sufficient force to cause Jake’s injuries, the defendant would have had to perform unusual manoeuvres which would have been noticeable.

As to “Anslow One”, Professor Bennett understood it to be said that the injuries to Jake were consistent with shearing forces from an incompetent forceps delivery. “Anslow One” showed that you could get a similar injury without shearing forces. “Anslow One” was dysmorphic and had an abnormal CTG. Dr. Anslow’s point was that the haemorrhage there was caused by NAIT. As to “Bennett One”, in NAIT it was possible to get any form of intracranial haemorrhage including subdural haemorrhage. It had been suggested that in NAIT there was no tendency for bleeding, but “Bennett One” said there was. It had been suggested that some trauma was needed but “Bennett One” showed that that was not so. In NAIT you could get subdural haemorrhage; you did not need obvious compression/decompression and there was a tendency to bleed spontaneously. Professor Bennett did agree concerning the forceps pressing on the parietal bones but he did not agree that you could have had such pressure as to cause injury or at least, these injuries. It was not possible to apply a degree of traction which would damage the baby without damaging the mother. If this had happened before, it would be in the literature. Professor Bennett would not have expected injury to the baby by the using of more than normal force. He said that he would probably have used more than gentle traction to deliver the baby.

Professor Bennett was cross-examined. He agreed that it was unacceptable to pull too hard until one had used all the options of making the opening larger, so as to prevent serious damage to the mother. He had always felt that it was inconceivable that Jake’s injury could have been caused solely by the use of forceps. NAIT was a very rare condition; 95% of the causes for NAIT had been excluded. This was an exquisitely rare form of NAIT. Max, Jake’s younger brother, was not suffering from NAIT.

Professor Bennett was referred to questions 27 and 28 of the telephone meeting between him and Mr. Thomas:

“27.

If the Court finds that the intracranial haemorrhage was caused by trauma, on the balance of probabilities, was this suffered at the time of the forceps delivery?

Both agreed: Yes.

28.

On the balance of probabilities, did the use of forceps in this case make a material contribution to the injury to the claimant?

Both agreed: Yes

Mr. Thomas, saying “Yes” bases his opinion on the factual evidence of Mr. Smith and the clinical record of a “hard pull”.

Professor Bennett, saying “Yes” reiterates his opinion that there must be another contributory factor ”.

Professor Bennett was also referred to questions 30 and 31 of the same telephone meeting:

“30, Do the experts consider that the nature of the claimant’s injury is, of itself, indicative of sub-standard care in the management of the delivery,

The experts have divided this into two questions.

On the first there is variance between the experts

Professor Bennett says No, intracrancial haemorrhage can occur spontaneously without sub-standard care in the management of the delivery.

Mr. Thomas says Yes, on balance of probabilities ……

and could it have occurred in the absence of a pre-existing clotting disorder, without sub-standard care?

Both agreed: Yes. Intracranial haemorrhage can occur for no apparent reason in normal vaginal delivery.

However, Mr. Thomas will say that in this case, considering the factual evidence of the claimant’s parents, such a postulate is unnecessary.

31.

If the Court finds that there was no pre-existing clotting disorder and that the intracranial haemorrhage was caused by trauma suffered at the time of forceps delivery, does this indicate that excessive traction was applied?

Both experts agreed: Yes. Each expert adds a rider.

Professor Bennett says Yes, but he reminds the Court of his view that such damage as was experienced by Jake is inconceivable without one or more contributory factors.

Mr. Thomas says Yes, but he will reiterate his opinion that it is sudden decompression of the aftercoming head which renders the neonate at risk of an intracranial haemorrhage and that the risk of decompression is likely to rise with the degree of traction.

Both experts feel that whether or not the traction used in this case should be considered excessive will depend upon the Court’s findings of fact”.

As to question 31, Professor Bennett said that there must be some other explanation. And, he said, the mother would be damaged in such a way that the baby would come out. If one pulls so hard as to cause massive intracranial bleeding, that is sub-standard care. Professor Bennett did not completely exclude very early DIC. The NAIT hypothesis was much stronger.

Professor Bennett was re-examined. During labour and delivery, there are shearing forces and compression and decompression; this was the first time a baby was exposed to mechanical forces before coming into the world. Prior to this case, Professor Bennett had never seen or heard of a case like it. Therefore he would not have felt uncomfortable about applying a degree of traction more than the ordinary. That was not out of the way; it was completely within the bounds of normal practice, having first extended the incision.

Mr. John Grace, Q.C., on behalf of the defendant accepted that the claimant’s injury occurred at or about the time of delivery, when the claimant suffered a significant subdural haemorrhage. He also accepted that the subdural haemorrhage involved a disturbance of the integrity of blood vessels, probably small bridging veins or venules. He submitted that that carried the case no further since haemorrhages could occur spontaneously, and subdural haemorrhage could occur without any, or any significant, degree of trauma. The question for the Court was whether there was excessive trauma, and whether the claimant had proved that the injury was caused by negligence on the part of the defendant. Mr. Grace submitted that on the evidence there was no breach of duty by the defendant. The defendant’s actions had to be judged on the basis that the defendant would have been aware that there was no known/reported incidence of brain damage occurring in these circumstances to an apparently healthy foetus. The head fit was not so tight that the forceps could not be applied. It was pleaded that the extension of the original incision by about 2 centimetres with scissors was insufficiently large. As Mr. Grace submitted, it was now understood that the claimant’s real case was that the extended incision should have been further extended or an additional T incision performed. The defendant, having found that his original incision in the uterus could be extended digitally, was entitled to expect that any inadequacy in the size of his extension would be immaterial and would be rectified or compensated for by a spontaneous extension of the incision (by means of a tear). Further, the fact that the defendant delivered the head without tearing the uterus indicated that the incision as extended was of sufficient size (and that no excessive force was used).

As to excessive traction, this was a subtle question of degree and “feel” and of seeking to distinguish between hard and excessive traction. The experts agreed that this was a question of fact for the Court. Mr. Grace relied upon a number of points arising from the evidence of those who witnessed the operation. As he submitted, the factual evidence conveyed no impression, let alone proof, of excessive force. As he submitted, it was inconceivable that experienced professionals observing events would not have noticed or recognised the use of undue or exceptional traction.

As to the expert evidence in relation to the allegation of excessive traction. Mr. Grace made a number of points. First, although this was pleaded as a resipsa loquitur, this was not such a case; if it was, the defendant had exercised reasonable care or a plausible explanation, namely, some pre-existing vulnerability, most likely a clotting disorder, existed. Second, there was almost universal surprise that there were no forceps marks or bruising. Third, it was common ground that the mechanics were such that much less force can be exerted by Wrigley’s forceps in caesarean section than by other forceps vaginally. Fourth, much less force needed to be exerted in the circumstances as compared to a vaginal delivery, the only resistance being maternal soft tissues in a caesarean section. Fifth, the spectrum of traction (the difference between gentle and hard) was much less with Wrigley’s forceps at caesarean section than in other circumstances. Sixth, no adverse inference should be therefore be attached to the defendant’s note “hard pull”. Seventh, the Court should adopt the common sense view of Professor Bennett that hard does not necessarily mean excessive, but simply more traction than is normal or simply harder than the first attempt. Eight, the Court should reject the attempt by Mr. Thomas to suggest that no more than “gentle” traction was ever permissible. Ninth, the absence of any maternal damage was conclusive proof that no excessive degree of force was used. Tenth, the impossibility of using excessive force was evidence by the fact that, despite the frequency with which Wrigley’s forceps or similar were used to deliver the aftercoming head at caesarean section for breech presentation, there was no recorded case of brain damage being caused in those circumstances; as Mr. Grace put it, the claimant’s case was therefore a world first.

As to alternative explanations, Mr. Grace submitted that the defendant did not have to prove any alternative explanation. In the context of a known incidence of unexplained intracerebral haemorrhage, including subdural haemorrhage, in the absence of any trauma or any sub-standard management, the Court would be entitled to conclude that medical science, and therefore the Court, was unable to come to any conclusion as to the cause of the intracerebral haemorrhage. Nevertheless, he submitted that insofar as the Court thought it necessary to consider it, there was a plausible explanation, namely, a pre-existing clotting disorder, most likely NAIT. Mr. Grace made a number of points. First, the claimant’s case had to be that the birth process was worse than a traumatic vaginal delivery, and such as to cause massive damage in the absence of any pre-existing abnormality; this was utterly improbable. Second, the damage was equivalent to that of a battered baby. Third, Dr. Kendall in cross-examination agreed that in this case there had to be “some other factor”. Fourth, the instinctive initial collective reaction of Professors Wyatt and Bennett and Dr. Letsky was that this was a case of a clotting disorder. Fifth, it was no objection to NAIT that the private antigens were very rare (some 3-5 cases a year), when the claimant’s explanation, (excessive traction at breech caesarean leading to major intracranial haemorrhage or subdural haemorrhage) was even rarer i.e. unheard of. Sixth, it was no objection to NAIT to argue that it did not make the veins more friable as any haemorrhage involved loss of integrity of blood vessels, and it was clear from “Bennett One” that spontaneous bleeds, including subdural haemorrhage, could occur with NAIT and it was clear that subdural haemorrhages did not require trauma in any recognisable sense. Seventh, a minor “trauma” of the delivery ruptured bridging veins, but torrential bleeding ensued because of a clotting disorder; thus, the coincidence in time between the onset of the bleeding and the delivery established a causal or relationship that was entirely neutral. Eighth, the subsequent events, on a proper reading of Volpe, were outside the spectrum there described, because the “rapidly lethal” cases showed progression from stupor to coma as the clot became larger, whereas the claimant’s case effectively showed coma within 2 minutes. Ninth, to dispel the plausible explanation of a clotting disorder the claimant has to prove that the platelets were normal at birth, but was unable to do so. Tenth, on Dr. Baglin’s evidence, once the platelets approached 20, spontaneous bruising and minor bleeding could occur, and below 20 bleeding could be severe; in cross-examination he said that with platelets at 19 the patient was vulnerable to minor trauma, and it would not take much to produce severe bleeding. No other explanation for the catastrophic events was necessary. Eleventh, neither “Bennett One” nor “Anslow One” were cases which were directly comparable in clinical terms to the claimants, but they demonstrated importantly that no identifiable trauma was necessary to provoke intracranial haemorrhage, which may include subdural haemorrhage, in NAIT. Twelfth, the recovery of the platelets, if it was within 12 hours, could have been consistent with NAIT (Dr. Letsky’s evidence), but in fact they were not back to normal even at four days after infusions of platelets. Thirteenth, the expert evidence as to when the platelets fall in DIC was contradictory. The Court was entitled to conclude that the picture may be variable, and that on Dr. Letsky’s evidence the platelets fall late but that in any event the very low figure of 19 at less than an hour of age was consistent with a pre-existing clotting abnormality.

Miss Susan Rodway, Q.C., on behalf of the claimant submits that there is sufficient evidence for the Court to be satisfied on a balance of probabilities that the cause of the bleeding and consequential damage was excessive traction at delivery. The claimant relied upon Mr. Thomas who stated that these were delicate structures (the baby’s head was not formed, there was room for movement, the head being malleable and pliable) and that was why it was so important not to use force. He gave a clear explanation of how the claimant’s injuries could have taken place. At the end of the trial there was sufficient extrinsic evidential material, agreed by the experts, to enable the Court to approach the case from a point analogous to an accident reconstruction. In this regard, all the experts accepted that, in the absence of any other plausible explanation, the cause of the claimant’s injuries must have been excessive traction at delivery. Although this was similar to a res ipsa loquitur case, it was in fact a stronger case than that. The claimant had said throughout that there was no plausible explanation other than excessive force. Miss Rodway submitted that the defendant had not produced any plausible alternative explanation for the claimant’s injuries. The only candidate which remained in the defendant’s armoury at the conclusion of the evidence, was NAIT. It was not sufficient to raise a remote possibility of which there was no evidence. It was even less sufficient to raise the hypothesis of “some condition not known to medical science”. The case had to be judged on the evidence now. In any event, NAIT did not assist the Court. Even if NAIT was present, it was not an explanation for the rapid and colossal bleed at delivery. The starting point here was the nature of the damage suffered by the claimant. Apart from Professor Bennett (on some points), there was agreement on the following matters:

On the claimant’s case, as soon as the defendant discovered, as he must have done, that it was not possible to deliver the head with gentle traction, then it was mandatory for him to enlarge the opening still further. This was an operation under anaesthetic. The safety of the baby was paramount. The defendant’s evidence did not support any pre-existing problems of clotting, infection or anything other than a completely normal baby. As Miss Rodway submitted, the defendant provided the explanation for the injuries in his contemporaneous operation note. In the defendant’s own words there was a “hard pull” followed by delivery of a flat baby. In his evidence, the defendant sought to qualify his own words. “Hard pull” became “moderate” but that was untenable on the evidence. The defendant could not recollect ever having to increase an incision before, he had never encountered a head with such a tight fit before and, according to his witness statement he had never needed to use more than gentle traction which was guiding the baby out. When it came to it, the defendant pulled rather than made another incision. Despite all the experts in the case agreeing on the point, the defendant would not accept that, if there was no evidence of a pre-existing clotting disorder, then he must have pulled too hard.

Miss Rodway submitted that, on the evidence, issues of clotting disorders and bleeding did not arise without bleeding have first occurred. The clotting disorder argument did not begin to explain the initial torrential blood loss. The two main candidates for clotting disorders were infection leading to DIC, and NAIT. As to pre-existing DIC from any cause, that was no longer sustainable. There was no evidence of infection in mother or baby, no evidence of rupture of membranes and no evidence of DIC inutero. Dr. Letsky agreed with Dr. Baglin that the DIC (which everyone accepted was established later) was triggered by events after birth and probably around the time of resuscitation. Thus, there was a clotting disorder which was due to the events of delivery and resuscitation and which extended the later bleeding and consequential damage. As to NAIT, Miss Rodway submits that the defendant had failed to prove that NAIT existed. It was a remote theoretical possibility. 95% of the normal variants of NAIT had been excluded. The theory now rested on the existence of a “private” antigen which could not be demonstrated and which did not pass to the claimant’s brother, Max. None of the experts had any knowledge of a case of NAIT presenting with a sudden torrential subdural bleed. NAIT was atypical for a completely well grown and normal baby. NAIT was atypical for the speed with which the clotting derangement corrected. There was, in fact, a very fast correcting of a position deranged by post-delivery DIC. None of the treating clinicians conceded a pre-existing disorder to be a candidate. NAIT remained no more than an extremely remote theoretical possibility. On a balance of probability, the clotting problem which the claimant experienced was due to the massive and rapid blood loss and the subsequent DIC. Not one of the experts, apart from Professor Bennett, suggested that a clotting disorder made the veins more susceptible to tearing. It was agreed in this case that a vein or veins must have torn. Dr. Letsky agreed that a clotting disorder would not cause this. That was also the evidence of Dr. Baglin, Dr. Lyon, Professor Wyatt, Mr. Thomas and Dr. Clarke.

This was a caesarean section and not a vaginal delivery. Thus, as Miss Rodway submits, the argument that there were “normal mechanical stresses” of delivery was not available to the defendant since those were the normal mechanical stresses of a vaginal delivery. In a vaginal delivery there may well be situations where there was no choice but to have to try to deliver the baby’s head through an inadequate opening. That was not this case. This was an operative delivery with an anaesthetised patient. The patient was not in established labour so there was no urgency or emergency in the sense of having to deliver very fast because the baby was, e.g. descending into the birth canal. This was a planned, elective caesarean section which had simply been brought forward. In those circumstances, it was mandatory to make an opening large enough (meaning an opening which did not subject the baby to undue mechanical stresses) to deliver the whole of the baby including the head. Distortion of the baby’s skull sufficient to tear the veins in the tentorium was not acceptable at caesarean section. It was not acceptable in this case as there was more that could have been done to avoid any mechanical distortion at all. That was to make a T incision just as was done with Max and the baby delivered without any trauma. As Miss Rodway submitted, the Court was driven to the conclusion that the defendant had to have exerted mechanical forces which tore the veins in the tentorium and hence such force was excessive. That was the only reasonable interpretation of events.

As to the defendant’s argument that the absence of any report of a similar case in the literature negated the likelihood of the damage being caused by pulling too hard, that was not decisive in itself. Everyone, with the exception of Professor Bennett, accepted that the damage must have been caused by trauma at delivery and, if there was no other explanation, then the trauma must have been due to excessive traction. As Miss Rodway submitted, there was in fact evidence of excessive force in similar situations causing severe damage but those often led to death and were hence consumed in those statistics; the damage here brought the claimant very close to death. It was insufficient to say that an event could not happen merely because there was no medical literature in respect of it. The argument could be turned round to say that if the damage seen here was due to some particular vulnerability of an infant then given the number of deliveries and the statistical chances of more than one infant suffering from such vulnerability, such a condition would by now have become known to medical science.

In all the circumstances, Miss Rodway submitted that the Court can properly reject the evidence of Professor Bennett and rely upon that of Mr. Thomas. He was measured and reasonable and willing to make concessions. He was very clear in his views that the damage in this case was caused by the delivery being due to excessive traction which, with the delicate and tiny structure of a new born baby’s head, would cause movement in the paraietal bones (which had not yet “set” in position and were free to move) and either this movement alone or in conjunction with sudden decompression tore the veins in the brain. That was perfectly feasible with Wrigley’s forceps if too hard a pull was applied.

I have reached the firm conclusion in this obviously difficult case (i) that the defendant did use excessive force in delivering Jake’s aftercoming head, (ii) that such excessive force caused sudden and massive bleeding within Jake’s skull including subdural haemorrhage, (iii) that Jake collapsed as a result and was very seriously ill, (iv) that resuscitation of Jake was thus necessarily difficult and prolonged and resulted in Jake acquiring DIC which exacerbated the bleeding and (v) that all the damage to Jake, as well as the deficits, described by Dr. Clarke were caused by what the defendant did in using such excessive force. I am clear that the defendant fell below the standard of care to be expected of a reasonable obstetric practitioner and was thus negligent in two respects:

I have reached those conclusions for the following principal reasons. As I find, the injuries to Jake were caused at the time of delivery and by trauma, and consisted of the tearing of a vein or veins in the brain around the tentorium cerebelli which led to the primary subdural haemorrhage as a result of distortion of the skull. In the two minutes or so of delivery of Jake’s after coming head, Jake suffered sudden and torrential bleeding leading to a loss of up to a third of his circulating blood volume. The tearing of the vein or veins was not caused by a clotting or bleeding disorder (which, as I find, does not make veins more friable or likely to tear) but, as a result of the difficult and prolonged resuscitation, and in the course of it, Jake acquired DIC which exacerbated the bleeding. I accept Miss Rodway’s submission that the only candidate for the cause of damage to Jake was what happened in the two minutes or so that it took to deliver the after coming head, that some mechanical force must necessarily have been applied which was sufficient to tear the vein or veins and that such force applied in a caesarean section breech delivery was excessive. I also accept that, as soon as the defendant realised, as he plainly did, it was not possible to deliver the after coming head with gentle traction, then it was mandatory for him to enlarge the opening (the uterine incision) further. I accept the evidence of Dr. Anslow, Dr.Kendall, Dr.Lyon and Mr. Thomas that there was probably a distortion of Jake’s head from the use of the Wrigley’s forceps, resulting in shearing forces between the skull and brain which either alone or together with sudden compression led to the tearing of a vein or veins in the brain. That led to the sudden and massive bleeding.

Dr. Anslow suggested that Jake’s brain stem (which controls breathing and heart rate) was damaged. He did say that he would defer to expert opinion that, if there was major damage to the brain stem, that would have resulted in death. Dr. Lyon was entirely clear that Jake had a low circulating blood volume and was hypoxic: if there was brain stem compression as well affecting breathing and heart rate, Jake would have died. That was not challenged and it seems to me that I should accept Dr. Lyon’s evidence. As I find, there was no damage of any significance to the brain stem.

As I find, there is no reasonable possibility that Jake was suffering from pre-existing DIC. I find that, post delivery in the course of resuscitation, Jake did acquire DIC which was triggered by hypoxia and acidosis. I accept the analysis of Dr. Lyon, supported by Dr. Baglin and Dr. Letsky and eventually by Professor Wyatt who deferred to the haematologists, that DIC was not acquired by Jake until after the delivery when he was seriously ill as a result of the sudden and massive bleeding. There was no evidence of infection, all the indicators, such as they were, being against it. I am clear that there was no pre-existing DIC in this case and I reject Professor Bennett’s views to the contrary.

As to NAIT, I am entirely clear that it played no part in this case and I reject the argument that there was a reasonable possibility that Jake had “private” antigen NAIT. The arguments in favour of NAIT as a reasonable possibility are in my judgment, at best tenuous. The arguments in favour of concluding that Jake did not have “private” antigen NAIT I see as overwhelming. NAIT is a very rare condition and 95% of the normal variants of NAIT had been excluded. NAIT now rested on the existence of a “private” antigen which could not be demonstrated and which did not pass to Max there being a 50/50 chance that it would do so, if it had existed. None of the experts had any knowledge of NAIT presenting with a sudden and torrential bleed. NAIT was atypical for a completely well grown and normal baby. NAIT was atypical for the speed with which the clotting derangement corrected.

I am not persuaded that Jake’s low platelet count within about an hour of his birth affects the position. Dr. Letsky accepted that it was certainly possible that Jake’s platelets dropped from a normal level of about 150 down to 19 within about an hour of birth although she said that that was very unlikely. I accept the evidence of Dr. Lyon, supported by Dr. Baglin that Jake’s low platelet count of 19 is accounted for by the sudden and massive haemorrhage he suffered at the time of his birth together with DIC he acquired in the course of resuscitation, his low circulating blood volume and the dilution of it by the treatment he received following his birth. I do not accept that the low platelet count at about an hour after birth is in any way indicative of the existence of NAIT. NAIT remains a remote possibility, which cannot be strictly or completely excluded. It is not, in my judgment, a plausible explanation for what happened to Jake.

The defendant had never had to extend an incision before, he had never before encountered an aftercoming head with such a tight fit and, according to his witness statement which he said in his evidence was true, he said in effect that he had never used more than gentle traction:

“It is impossible to pull hard on these forceps as they are designed to simply ease the lifting of the baby and not as a pulling agent…. I confirm that the head is placed in the widest part of the forceps and then the baby is gently lifted out” (the defendant’s witness statement page 59).

The defendant himself had written the operation note describing a “hard pull” then, in his evidence, the defendant referred to the “hard pull” in the following words:

“I didn’t feel it was excessively hard. I have pulled as hard on many occasions with no ill effect, touch wood”.

As I find, the defendant in his operation note, no doubt with commendable honesty, did provide the explanation for Jake’s injuries, i.e. he pulled hard and, as I find, too hard. The defendant would not accept that, in the absence of a clotting disorder, he must have pulled too hard. Professor Bennett agreed that by pulling hard the defendant made a “major contribution” to Jake’s injuries, adding that there must be another contributory factor. As I have found, there was no pre-existing clotting disorder. The result must be, as I have found, that the defendant pulled too hard, using excessive force to deliver the after coming head.

As to resistance from maternal soft tissues, Mrs. Smith’s uterus was apparently inelastic and ungiving and provided sufficient resistance to require a “hard pull” for it to be overcome. There is no evidence as to whether or not there was tearing of the uterus. It was the effect of Mr. Thomas’s evidence that what gave way was the baby’s head and not the uterus. The uterus in clamping down was replicating the vaginal wall. That the incision did not extend may have been unusual but the defendant would clearly have been aware that he was faced with much more than usual resistance and yet, as I have found wrongly, he continued to pull and in the end pulled too hard. In the case of younger brother Max, he was delivered without the use of forceps (his head apparently being smaller than Jake’s), the surgeon there making an inverted “T” incision, the aftercoming head being trapped in an inelastic uterus. I do not accept either that the defendant could expect the uterine incision to tear before excessive force was used or that the fact that the uterine incision did not tear (if it did not) meant that excessive force was not used.

As to the absence of marks e.g. bruising, on Jake’s skull, it seems to me that this aspect of the case has been over-emphasised by Dr. Anslow and by Professors Wyatt and Bennett. I accept Mr. Thomas’s evidence, supported by Dr. Lyon, that any marks on Jake’s skull would be related to the time during which traction was applied. Here the time was very short, being probably less than 2 minutes, a very considerably shorter time that could be the case when using forceps in a vaginal delivery. Further as Dr. Lyon remarked, it is not uncommon in such cases to have no direct evidence of trauma; here, the mechanism of Jake’s injuries was one of shearing force between brain and skull so, as he put it, “You do not have to have direct evidence, externally, of trauma”. I accept that evidence.

As to the possibility of Wrigley’s forceps being used to pull too hard, I have seen them and I have seen how they are operated in demonstration in Court, during the hearing. I regard it as obvious that they could be used with excessive force; the design of them does not exclude that happening. I accept Mr. Thomas’s evidence on this. It is curious that the defendant says in his witness statement that it is impossible to pull hard on these forceps and yet writes in the operation notes “hard pull” and in his evidence in chief refers to the “hard pull” not being excessively hard. I have already referred to that. I find the defendant’s position to be difficult to understand; it is not one which inspires confidence.

As to there being no report of any similar case in the medical literature despite extensive researches, it seems to me that this can be taken only so far. Clearly, it cannot be decisive. There may be a number of reasons why such a case should not be reported. A case or cases similar to Jake’s may actually have happened resulting in the baby’s death with the case or cases thus being subsumed in statistics of infant mortality. Anyway, as Dr. Clarke said, it is very difficult to get single case reports published. I have obviously considered the rarity of a baby suffering any significant damage in the course of a breech caesarean section, as spoken to particularly by Professors Wyatt and Bennett, and the suggestion that, if this is not a case of NAIT, then there must be some other possible unidentified vulnerability in Jake which led to his problems. I am entirely persuaded that the combination of circumstances here, looking at all the evidence, properly leads, on a balance of probabilities, to the conclusion that it was excessive force during delivery and not NAIT or any other unidentified vulnerability in Jake which led to the sudden and massive bleed which has resulted in all his problems.

I accept Mr. Thomas’s evidence and his approach to the use of forceps in a breech presentation caesarean section, to the effect that there is no need for more than gentle traction as more room can be made for the baby. That was the defendant’s own view in his witness statement when he said that Wrigley’s forceps “are designed to simply ease the lifting of the baby and not as a pulling agent….”. I accept Mr. Thomas’s evidence (supported in this by Professor Bennett in the joint report) that there would have been no particular difficulty in extending the initial transverse incision either to the right or by performing an inverted “T” incision.

I accept the criticisms of Professor Bennett’s evidence. In my judgment, he did surrender his objectivity in his determination to find an alternative explanation to trauma for Jake’s injuries. I have to say that he seemed to become over-enthusiastic. He went on a frolic of his own in carrying out further research and producing “Bennett One” very late in the day after all the experts (with the exception of Mr. Thomas) had completed their evidence and had left. Professor Bennett was apparently determined to show that the other experts were wrong in their views that veins did not become more friable or liable to tear with NAIT. As Miss Rodway put it, it is a moot point as to whether “Bennett One” does support such a thesis- I would say that it does not. However, that thesis was expressly rejected by all the other relevant experts i.e. Dr. Lyon, Professor Wyatt, Dr. Baglin and Dr. Letsky. Nonetheless, incorrectly as I find, Professor Bennett would not allow himself to be shifted from this thesis, in which he persisted, and he ended up by saying that he was correcting the neonatologists and haematologists and that Jake’s veins were so friable as a result of NAIT that they tore apart by reason of minor stress. It seems to me that that was an untenable position to adopt and was one, looking at all the other evidence, in which Professor Bennett should not have persisted. I have to say I was not assisted by Professor Bennett’s evidence that, because he had never seen or heard of a case like Jake’s, he would not have felt uncomfortable about applying a degree of traction more than the ordinary. I reject that because it is not necessary to apply more than usual force in order to discover that there is more than usual resistance from a head stuck in the uterus. There is an undesirable element here, as it seems to me, that the “world first” argument may be used as a licence to use unnecessary force because, so it is said, nothing bad is going to happen. As I see it, that is a recipe for disaster. It is an approach which Mr. Thomas, as I see it, correctly rejected.

In my judgment, the observations of the witnesses, (other than the defendant) who were present at the operation do not assist me in deciding this case. Mr. and Mrs. Smith were clearly not experienced observers and do not help, which is not surprising, on the critical issues in this case. It is impossible, as it seems to me, to say that the two midwives or the anaesthetist sufficiently observed what was going on to say one way or the other whether the defendant used excessive force. Their recollections were in very general terms and, in the end, do not assist in deciding the case.

The fact that subdural haemorrhages can occur spontaneously and without trauma does not assist in this case. Such subdural haemorrhages are asymptomatic bleeds; they originate from very small bleeding points which may then leak or ooze. The fact is that all the experts (with the exception of Professor Bennett) agreed that no amount of clotting disorder could explain the initial tearing of the veins necessary for the bleeding in this case and no clotting disorder could account for the sudden and massive bleed in Jake’s case. I accept the evidence of Dr. Anslow, Dr. Kendall, Dr. Lyon, Professor Wyatt, Dr. Baglin, Dr. Letsky and Mr. Thomas to that effect.

I do not see this as a resipsaloquitur case, because, in my judgment, it is clear that the defendant must have used excessive force in delivering Jake and was thus negligent in the absence of any other explanation. The only other possible non-negligent explanation is NAIT; I regard NAIT as no more than a remote possibility which cannot strictly be excluded and which certainly does not qualify as a plausible explanation. I have been referred to the helpful case of Ratcliffe –v- Plymouth and Torbay Health Authority [1998] Lloyd’s Law Reports: Medical 162. Having regard to the findings I have made, I do not see the point of relying upon resipsa loquitur.

As to Mr. Grace’s point that Jake’s case presents as worse than traumatic vaginal delivery and amounting to a battered baby case, this is an unusual case, but it is a combination of excessive traction causing veins in Jake’s head to tear and DIC acquired in the course of the resulting resuscitation which combined to cause the overall damage to Jake. I am clear that, on all the evidence, normal mechanical forces in caesarean section should not be sufficient to tear the veins in the head of a baby where there is no abnormality. This baby had no abnormality, as I find, and was therefore subjected to more than normal mechanical forces which tore veins in his head. As I have found, that resulted from excessive force and was therefore negligent. The “some other factor”, as it seems to me, spoken of by Dr. Kendall could well be the DIC acquired in the course of resuscitation; it exacerbated the bleeding and obviously increased the damage to Jake.

As to the alleged initial reaction of Professor Wyatt and Bennett and Dr. Letsky that this was a case of a clotting disorder, in fact Professor Wyatt’s evidence was that his initial conclusion was that the explanation was extreme mechanical forces. Dr. Letsky said that she found this to be a classic presentation of NAIT which it was clearly not as NAIT could not account for the sudden and massive bleeding which Jake suffered.

As to the suggestion that there was “minor” trauma rupturing bridging veins with torrential bleeding ensuing because of a clotting disorder (presumably NAIT), that is not the evidence. Both Professors Wyatt and Bennett were clear that more than normal mechanical forces or significant force would be required to tear bridging veins. Further, none of the experts could explain the torrential or massive bleeding in terms of NAIT. It follows that the coincidence in time between the onset of Jake’s bleeding and the delivery establishes a significant causal relationship and not one, in my judgment, that can properly be regarded as neutral.

As to Jake being outside the spectrum set out in Volpe, I accept the evidence of Dr. Lyon which seemed to me to be convincing. It was to the effect that Jake did fall within Volpe’s spectrum. Relying on his clinical experience, Dr. Lyon said that one could not categorise babies into precise areas. There was no reason, he said, why there should not be a picture of the baby being “okay one minute and then moribund the next”, after all, his heart had stopped.

Mr. Grace submitted that, to exclude the explanation of a clotting disorder, the claimant had to prove that the platelets were normal at birth. It seems to me that the true position is that, to make a clotting disorder a plausible explanation, the platelets had to be low at birth. They were, as I find, almost certainly not so. The CTG trace was normal; Jake was in all discernible respects normal and well some two minutes before he was damaged. The low platelet count of 19 at about an hour after birth, as I find, was brought down to that level by the sudden and massive bleed and by a combination of what Dr. Lyon called “raging DIC” acquired in the course of resuscitation, Jake’s low circulating blood volume and the dilution of it. I accept the evidence of Dr. Lyon and Dr. Baglin in relation to those matters. Dr. Letsky never explained why those features could not account for Jake’s low platelet level of 19 at about an hour from delivery; she simply said that it was unlikely.

As to Professor Wyatt’s extrapolation from the first platelets that they were likely to be abnormal at birth, the clear evidence of Dr. Lyon and the overall balance of Dr. Baglin’s evidence was that Jake’s platelets were likely to be normal at birth and had come down to 19 as a result of the factors referred to in the previous paragraph.

Accordingly, for all the reasons I have given, I find the preliminary issues of liability and causation in favour of the claimant.

As it will now be necessary for there to be an assessment of damages, it seems to me to be necessary for there to be a short hearing at which I should give procedural directions in respect of that matter or make provision for a Master to do so. I will also deal with any other consequential matters arising from this judgment.