Chapter 3 - Investigations
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The care provided to Ms J at Halton General Hospital
Complaint against
Halton General Hospital NHS Trust
Complaint as put by Mr J
1. The account of the complaint provided by Mr J was that in July 1996 his sister, Miss J, was diagnosed with Maturity Onset Diabetes in Youth (MODY). Her diabetes was controlled by diet. On 22 April 1997, Miss J attended the diabetic clinic at Halton General Hospital where she saw a consultant (the first consultant) and a diabetes nurse specialist (the nurse specialist). Her blood glucose reading was 10.3mmols. Her treatment was not altered. On 14 July, Miss J tested her blood glucose and recorded that it was 11. During July Miss J felt unwell and consulted three general practitioners on four occasions. On 22 July, Miss J was admitted to Halton General Hospital (the hospital) with diabetic ketoacidosis (an excess of acid and ketones in body tissues and fluids which develops in diabetics when their condition is getting out of control, and may indicate approaching coma). She appeared, initially, to respond to treatment, but at 8.00pm developed a severe headache, which recurred at 3.00am shortly before she collapsed. She had developed cerebral oedema (swelling of the brain within the skull) and lapsed into coma on 23 July. On 29 July, brain stem death was diagnosed and on 31 July, Miss J's ventilator was switched off.
2. On 18 February 1998, an independent panel review was held at the hospital to consider complaints made by Mr J about his sister's care and treatment. The panel subsequently issued a report, which included a statement that the panel considered that Miss J had had 'difficulty in coming to terms with the diagnosis of diabetes' and suggested that she had suffered a 'denial reaction'. Mr J remains dissatisfied and complains that staff at the hospital mismanaged his sister's care and that the panel was wrong to assert that his sister was in denial of her illness.
3. Mr J believes that his sister's death could have been avoided and that it was caused by a combination of misdiagnosis; inadequate education about management of diabetes; poor monitoring of her condition in the Trust's diabetes clinic; the failure of general practitioners to check Miss J's blood sugar when she reported symptoms including vomiting, which he contends indicated the onset of diabetic ketoacidosis (and should, of themselves have triggered testing even if diabetic ketoacidosis had not been suspected); and mismanagement of diabetic ketoacidosis during her admission to hospital, including over-administration of fluids, which he believes caused cerebral oedema and thereby her death.
4. The matters investigated were that:
(a) the care and treatment provided to Miss J by Halton General Hospital NHS Trust was inadequate; and(b) that the report of the independent review inappropriately included a statement that Miss J was in denial of her diabetes.
Investigation
5. The statement of complaint for the investigation was issued on 8 June 1999. Comments were obtained from Halton General Hospital NHS Trust; and relevant documents, including Miss J's clinical and nursing records, were examined. My investigator took evidence from Mr J, Miss J's parents and Trust staff. Clinical advice was provided by five external professional assessors; and their report is at Appendix A. I have not included in this report every detail investigated, but I am satisfied that no matter of significance has been overlooked. This was a detailed and complex investigation; and, for reasons of brevity, the evidence contained within this report is a summary of that considered most pertinent to the case. In addition, my Office has previously investigated two other complaints from Mr J, relating to his sister's diabetic care by a general practitioner and the handling of his complaint by the relevant health authority. The reports of these investigations have been published (W.138/97-98), (W.125/97-98). The actions of the two other general practitioners concerned were considered and criticised by independent review under the provisions of the NHS complaints procedure. I have included information about events which were external to Miss J's involvement with the Trust to set matters in context; and to facilitate a clearer view of the events leading to Miss J's death. I emphasise, however, that in making my findings, I have considered the actions of the Trust staff on the basis of information to which they had access. A glossary of terms is at Appendix B.
(a) The care and treatment provided to Miss J by Halton General Hospital NHS Trust was inadequate
6. I set out the evidence below in chronological sequence.
Background information
7. The notes of Miss J's GP record that on 26 February 1996, Miss J consulted her GP, complaining of feeling faint about one hour after her mid-day meal. Her grandmother had tested her urine which showed glycosuria. The GP diagnosed asymptomatic reactive hypoglycaemia. On 13 March, the GP explained the diagnosis to Miss J and arranged a referral to a consultant endocrinologist (the first consultant). On 29 March, the notes of Miss J's GP record that diabetic diet was discussed, and that she was referred to a chiropodist and advised to see an optician in six months time. At this stage, her diabetes was being monitored by the practice.
Diabetic clinic
8. Miss J's clinical and nursing records show that on 12 July 1996, Miss J was seen by the first consultant at the Trust's diabetes clinic. He entered a diagnosis of MODY in her notes. He wrote to her GP and told him that she 'is a most interesting MODY' and he also thought her thyroid gland was enlarged; that she should manage well on diet; and that he would review her notes with the nurse specialist in two months and see her in the young persons' diabetes clinic in 4 months. She was seen separately by the nurse specialist that day, who recorded that Miss J was 'diet only'; that they had had a 'general chat about diabetes'; that she had taught Miss J how to test her blood; and that 'info.' had been given. Miss J then continued to be monitored at intervals by the nurse specialist, and the first consultant at the young persons diabetes clinic
Miss J's blood result diary
9. Miss J's record card shows that she tested her blood at approximately 3-5 day intervals. There are some extended periods during which she did not record results in her diary, and which appear according to evidence supplied by Mr J to coincide with holiday periods. Her results ranged between 4 and 7. On 26 July 1996, she recorded 9mmols which was noted by the nurse in her records as 'odd one at 9mmols'. Miss J also recorded a reading of 11mmols on 6 September 1996 and ceased testing for a period. The reading was highlighted by a circle, but was otherwise not remarked upon.
Mr J's evidence
10. Mr J contends that the first consultant should not have reached an initial diagnosis of MODY and that his sister did not fit the criteria for such a diagnosis. Mr J believes that the first consultant should have been more cautious and considered whether Miss J might have been a slow onset type 1 - a much more common form of diabetes in the young. If the first consultant had reached a correct diagnosis Miss J would have received education relating to type 1 diabetes; and would have been taught to test her urine for ketones and about the signs to watch for of developing diabetic ketoacidosis. He thought the nurse specialist should have questioned the diagnosis of MODY and taken steps to ensure that she was sufficiently well-informed about the condition to care for his sister appropriately. He also complains that neither the first consultant, nor the nurse specialist gave his sister appropriate education; and that they failed to tell her what to do in the event of illness, what action to take in the event of hyperglycaemia, and how to recognise the symptoms of diabetic ketoacidosis. Mr J maintains that Miss J's blood glucose and HbA1c measurements during the period of monitoring at the clinic clearly indicated declining diabetic control and that action should have been taken to alter his sister's management.
Evidence of Miss J's parents
11. Miss J's mother explained that her daughter saw the first consultant on her own. She then saw the nurse specialist who told her that she need test her blood only every 4-5 days. The nurse specialist taught her how to use a diabetic pen (for testing her blood sugar) and gave her a diary to record the results. She also told her to have her eyes and feet checked regularly, and that she would be referred to a dietician. The first consultant had said to Miss J that 'if she stuck by him and did what he said she would never need insulin', which pleased her. On 22 August 1996, the nurse specialist came to see Miss J at home (she lived with her parents). She asked how she was, and she said she was fine. She again said that Miss J should test every 4-5 days and, when she asked what she should do while on holiday for two weeks, the nurse specialist told her that she should test before she went and again when she returned. Conversation then turned to general matters. Her daughter was not given any literature by the nurse specialist other than a British Diabetic Association membership form, and a price list. Miss J's diabetes clinic card was shown to the investigator. Miss J had written 'I have MODY diet controlled diabetes'.
Evidence of Trust staff
12. The first consultant is a consultant physician in diabetes, endocrinology, and general medicine. He ran two diabetes clinics: an adult clinic and a young persons clinic where he saw young patients (between the ages of 18 and 30) frequently. Miss J was seen for her first appointment in the main (adult) diabetes clinic. The first consultant explained what diabetes was. She had been quite worried, and thought she might have type 1 diabetes. The first consultant explained the difference between type 1 and type 2 diabetes, and told her that he did not think she had type 1 but that he would keep 'a close eye' on her. He thought type 1 was a possibility but, based on the history she had given him and his clinical findings, thought she actually had MODY. Miss J told him that her mother was diabetic and that her grandfather had also been diabetic and had used insulin. The first consultant did not know whether he was type 2 insulin treated or not. The first consultant concluded, therefore, that Miss J was from a family with adiabetic history over three generations; that her onset was at under 25 years of age; and that she was symptomatic, but had not lost weight. The first consultant acknowledged that he had written to Miss J's GP with a diagnosis of MODY, but stressed that he had referred her to the young persons clinic (usually attended by people with type 1 diabetes) where she could be monitored more closely. He saw Miss J four times over the next 9 months. He also explained to her what type of problems she might experience as a result of her diabetes. The consultant was sure that Miss J understood the difference between type 1 and type 2 diabetes and he explained to her the risk of hyperglycaemia. Her HbA1c was under 7.5 at every visit; at the last visit it was 7.3. The first consultant had referred Miss J to the nurse specialist. The guidelines recommended by the British Diabetic Association had been followed - that non-insulin patients should not routinely be taught ketone testing. Miss J was told to contact the clinic if her blood sugar exceeded a reading of 9. The first consultant recognised that there was an increased risk of decompensation with diabetes and autoimmune thyroid disease.
13. The nurse specialist said, when interviewed, that she was employed as a specialist nurse and had held this post for just under two years when she saw Miss J. She was responsible for the young persons clinic. She usually sat in on consultations with patients. However, as Miss J was seen first at the adult clinic she had not been privy to the conversation with the first consultant. Miss J saw the first consultant and then came to see her. The nurse specialist said that her understanding at the time was that MODY would be managed in the same way as for a type 2 diabetic - ie taught to be aware of normal blood sugar levels, about monitoring and the need to be aware of changes. She would not have told Miss J about diabetic ketoacidosis as she would not be using insulin in the short term. She told the investigator that when teaching a patient such as Miss J to test their blood she would tell them what the normal range was; that she would expect their fasting and pre-meal blood sugars to be between 4 and 7; and that random blood sugar should not exceed 9. She would have told Miss J to test 2-3 times a week (Note: this figure varies in the evidence between 2-3, 3-4, 4-5). If patients recorded a high reading, 11 for example, they would be advised to test again the next day if they felt well, or later that day if they felt unwell. They would always be told to consider how they were feeling. She would explain that the reason for testing was to avoid hyperglycaemia. She would not be concerned about one high reading in isolation, but would have been looking for a general change in the pattern of results when reviewing Miss J's self-tested blood results. (Note: it is not possible from the documentary evidence to determine precisely what was or was not said to Miss J in this regard.)
14. The nurse specialist would normally give out two forms of literature: a Balance (diabetes information) magazine and a type 1 or type 2 diabetes leaflet as appropriate; and she thought she had given them to Miss J. The diabetes record card was a 'stand alone' document containing personal details and a record of each visit. Record cards were filled out by the nurse specialist and kept in the clinic office. There was no care plan system at that time. Doctors made entries in the case notes and patients kept diaries to record their blood testing results. The nurse specialist accepted that her standard of documentation had not then been good enough; she had since made improvements. She accepted that if she had at least written 'sick day rules explained' instead of simply 'info. given' or 'all well' she might not now be facing a complaint as she would have been able to draw on documentary evidence as confirmation of the advice which she believed she gave to Miss J.
15. The clinic also now operates a revised educational procedure. There is a mini check list for type 1 young persons which they tick to indicate they have been given an education update. Those with type 2 diabetes are taught about targets for control; their understanding of HbA1c results is checked; and their education review is tailored to their individual needs. Young persons are also subject to an annual education review which is signed off by both patient and nurse. Records are now more detailed and clear. The nurse specialist agreed that she would have told Miss J that she need test only at the beginning and end of a holiday; but she would have added the proviso that she should take her equipment with her and test more frequently if she felt unwell. Miss J was last seen in the clinic on 22 April 1997.
Events in the week before admission
16. On 14 July 1997, Miss J recorded a higher than average blood sugar reading in her record book (11mmol); and on 16 July she saw her GP, complaining of muscle pain and lethargy. The GP recorded that she had limb girdle weakness in her shoulders and thighs, and that her thyroid hormone level was 'borderline'. The GP passed this information to the consultant. (Note: the GP's notes reveal no more than that he contacted the first consultant following this consultation.) The GP did not test Miss J's glucose levels or urine and there is no mention of diabetes in his record of the consultation. On 17 July, Miss J tried to test her blood on two occasions, but was unable to read the result. Her niece, who was present, also tried, at Miss J's request. The niece thought that the reading was between 7 and 9, but could not be certain. Miss J made no entry in her book. On 18 July, Miss J travelled with her fiancé, his cousin and his cousin's wife, to a holiday camp intending to celebrate the cousin's 21st birthday.
17. During the journey Miss J began to feel unwell. The following day she saw a GP at the holiday camp complaining of stomach pain and that she had been vomiting for two days. She told the GP that she was a diet controlled MODY patient, and that she had not tested her blood glucose level. The GP did not test it or her urine: he diagnosed gastritis, and prescribed an anti-nausea medication. On 20 July, Miss J returned home, still feeling unwell, and was visited by a locum GP who noted abdominal tenderness and vomiting 'since last Friday'; that she was a diet controlled diabetic; and that she was not dehydrated. The locum GP also diagnosed gastritis. He did not test her blood sugar or her urine. On 21 July, Miss J was seen at home by her own GP, who recorded that she had been vomiting for 3 days, was being made sick by the anti-nausea medication she had been given, was passing urine normally and was not dehydrated and that her random blood sugar level was around 7. (Note: The GP has said that Miss J's mother told him this, though Miss J's mother denies that she did.) Miss J's GP also diagnosed gastritis and did not test her blood or urine. On the morning of 22 July, Miss J's family called her GP, who recorded that she had been delirious all night and that her 'parents were unable to check her blood sugar'. The GP arranged Miss J's immediate admission to hospital by ambulance.
Hospital admission
Summary of clinical and nursing notes
18. Miss J's notes contain detailed entries specifying tests carried out and the results. My advisers have concluded that the records show that she was diagnosed as having diabetic ketoacidosis; that her sodium level was unusually low on admission to hospital, (hyponatraemia); that the acidosis had not been brought under control; and that her fluid balance was negative, rather than positive. My internal professional adviser has concluded that, judged from the composite evidence of fluid intake, urinary output, likely initial volume deficit, insensible loss from skin and lungs, plasma creatinine and urea concentrations, the absence of leg or back oedema (swelling) and the first CVP measurement (on 23 July), the initial fluid deficit was corrected and there was no evidence of material fluid overload by the time the intravenous fluid intake was reduced on 24 July. All the evidence taken together, accepting inaccuracies in charting, indicates that by the end of 24 July her total fluid volume was effectively in balance. The notes record three episodes of headache at 8.00pm on 22 July and at 2.00am and 3.00am on 23 July. The post mortem report listed the cause of Miss J's death as 1) cerebral oedema, and 2) diabetic ketoacidosis. In view of the volume of technical information, I have included only key points from the notes, but they have been considered in their entirety by my external clinical advisers in conjunction with comments made by Mr J. The notes include the following information:
22 July 1997
At 1.30pm hrs the first consultant wrote the following advice noting high potassium and acidosis: '.... Check potassium again, if high again and pH still 7.1 or less suggest small bolus [bicarbonate] 50mls over Þ hr, this will reduce potassium' .... Following later discussion with the first consultant, the registrar did not administer bicarbonate.
At 3.45pm the first consultant returned. His assessment was that Miss J was better, noting that her potassium and glucose had improved but that she was still acidotic. He wrote, '.... Still vomiting but better .... pH still 7.1 may need small amount of [bicarbonate] 50mls of 8.4% [sodium bicarbonate] over Þhr will probably need to give a small amount of [potassium chloride] at same time to ensure potassium doesn't drop significantly'
At 6.00pm the first consultant reviewed Miss J again and concluded that she was 'better still', nevertheless he suggested switching the intravenous infusion to 10% dextrose and giving a bolus of bicarbonate to correct the acidosis.
At approximately 8.00pm Miss J suffered a headache and became increasingly agitated. Physical examination revealed no objective neurological signs: the SHO noted that her metabolic status was not improving. Following a review of the notes, the SHO in her written statement says, '.... unsure which advice in notes to follow, therefore decided to ask both the [second] Registrar as senior, [the second] Consultant physician as knew case and [the first consultant] as knew case but not on call ....' The second registrar advised giving intravenous bicarbonate 100mls of 8.4%. The second consultant advised the SHO to contact the first consultant for his advice before administering the bicarbonate. The possibility of cerebral oedema was not suspected as a possible cause of headache and agitation.
At 8.55pm the SHO began giving a small amount of 10% dextrose pending the first consultant's advice. The SHO then requested the locum anaesthetic SHO to place an arterial line: this was achieved after three attempts.
At approximately 9.40pm the SHO spoke with the first consultant on the telephone. He advised her to give 50mls of intravenous sodium bicarbonate and supplementary potassium and to discontinue the 10% dextrose. He also gave further instructions regarding a revised insulin sliding scale and how and when to use 10% dextrose if the acidosis should continue.
By 11.30pm Miss J appeared settled: her pH was 7.14.
At midnight, following the bicarbonate, the pH had risen to 7.25.
23 July 1997
At 3.30am the SHO was called urgently to ITU, where she was told that Miss J's condition had suddenly deteriorated. The SHO noted a reduced consciousness level, reduced respiratory rate, and hypotension (low blood pressure) with tachycardia (rapid heart rate). Staff reported that Miss J had been complaining of increased headache since approximately 2.00am.
A CT scan of Miss J's brain was performed approximately four and a half hours after she had become comatose, requiring ventilation. The consultant radiologist's report says, 'Generally the brain appears "tight" and I suspect a degree of cerebral oedema. There is no convincing evidence of a subarachnoid haemorrhage. No mass lesion is demonstrated'.
During the afternoon of 23.7.97 a consultant neurologist reviewed matters and wrote, '.... the CT does not show any focal lesion, haemorrhage etc. There may be some mild symmetrical swelling of the cerebral hemispheres, but in someone of her age the scan may well be normal. In particular I note that the lateral ventricles are easily visible. She has been exceedingly unwell from the metabolic/ electrolyte/acid-base viewpoints, with shifts in solutes and fluids. I think this may have played a role, and certainly myelinolysis may sometimes be more extensive than just the pons ....'.
Thereafter Miss J never regained consciousness, requiring ventilation until her death on 31.7.97.
All possible reasons for her comatose state were sought; but no specific cause was found. Empirical treatment for any reversible condition was given. Cerebral oedema was considered to be the most likely explanation for her sudden deterioration.
Mr J's evidence
19. Mr J contends that staff failed to manage his sister's acidosis adequately; over-infused fluids to a significant extent, failed to keep an accurate fluid chart; did not insert a central venous pressure line (CVP); did not observe his sister's neurological functioning following her headache at 8.00pm on 22 July; and, most significantly in his view, were unaware of the risk of cerebral oedema in relation to diabetic ketoacidosis and did not initiate treatment with mannitol which might have averted the onset of cerebral oedema. He was certain that his sister's headache at 8.00pm, in which she clutched the back of her head, (occipital region) indicated the onset of cerebral oedema. He pointed out that the first consultant's written statement described the same symptoms at 3.00am on 23 July and that the earlier occurrence must, therefore, have been the start. If treatment had commenced at that time Mr J believes that his sister's death could have been prevented.
Evidence from Miss J's parents
20. Miss J was admitted to the hospital's A&E department on 22 July 1997 - her speech was slurred. A doctor [the SHO] put up a drip and a nurse asked how far she wanted it opened. The doctor replied, 'fully because she needs this quickly'. The doctor [SHO] told Miss J's parents that she was very poorly; but that they were 'getting her stabilised'. Miss J's mother told the doctor [SHO] that the GP had asked her to test her daughter's blood just before the ambulance had arrived to take her to hospital, but that Miss J had not wanted her to. At the hospital a doctor told them that Miss J was to be transferred to intensive care overnight to stabilise her condition. Miss J was anxious about this; but a nurse reassured her and said that she was simply going to intensive care overnight as a precaution and would go to an ordinary ward in the morning. Staff wanted to insert a catheter; but Miss J refused to let them. She did not seem to be herself. At about 7.45pm Miss J began to scream 'unmercifully'. She held the back of her head and kicked off her bedding. A staff nurse (the first staff nurse) ran up and asked Miss J what was the matter. Miss J's mother apologised on her behalf, and explained that her daughter was not normally like that. The family were ushered out but could still hear Miss J screaming. Then it suddenly went quiet. They went back in and believed Miss J to have been sedated. She appeared to be asleep, but her face was sweaty and her breathing shallow. Another nurse (the second staff nurse) joined them. The first staff nurse told the family to go home, and that they would 'find a different person in the morning'.
21. At 2.55am on 23 July, Miss J's mother awoke suddenly with a premonition that something was wrong. She telephoned the hospital and was told that something had gone badly wrong, and that they would call her back when the doctor had seen Miss J. About 5.30am Miss J's mother spoke to a doctor (the second consultant) who told her that Miss J had collapsed and had been put on a ventilator. They later met the first consultant at the hospital, who said that he did not think Miss J's collapse was related to her diabetes. He told them the situation was very grave. He also asked why they had not got her to hospital earlier. A nurse also talked to them and told them about diabetic ketoacidosis. They had never heard anything about it before. If they had known it was a risk, they would have been on their guard. (Note: the family was told later that Miss J's brain had swelled a little.)
Evidence of Trust staff
Medical staff
22. The senior house officer (SHO) who first saw Miss J on admission, said when interviewed that she had been employed at the Trust as a locum, and that 22 July had been her second day at the Trust. She had been responsible for one ward, which was for acute admissions through the minor injuries unit and for GP referrals. Responsibility was split after 5.30pm with the medical registrar. The medical staff on duty at the time of Miss J's admission were: consultant on call (the second consultant); the SHO, a house officer; and a staff grade doctor, acting as registrar on duty from 9.00am - 5.00pm (the first registrar), who was replaced from 5.30pm by a locum medical registrar (the second registrar). The SHO had a first day induction to duty. A ward sister took her round the ward and explained the routine. The first registrar explained the SHO's responsibilities. The SHO could not recall having been shown treatment protocols. There was no central figure co-ordinating her induction to duty; and no written package of information was given to her. (Note: Despite these reservations my advisers have complimented the SHO on the exemplary care she gave at this time.)
23. When Miss J was admitted, the SHO saw her and realised that she was very unwell. She had dealt with diabetic ketoacidosis before and was familiar with the standard treatment; and so she commenced investigations and treatment and contacted senior staff. Miss J was more unwell than any patient with diabetic ketoacidosis the SHO had seen before. (Note: personal notes written by the SHO on 4 August 1997 recorded that Miss J was 'intermittently hysterical, screaming "I want a drink"'. She also recorded that Miss J's GP had told the parents that she was not dehydrated, to which the SHO had replied, 'well, she is now'.) The first registrar arrived and carried out her own assessment of the patient; she confirmed the SHO's diagnosis and management. The hospital's own diabetic ketoacidosis treatment protocol was not drawn to the SHO's attention until 11.00pm, when the charge nurse in intensive care did so. The first registrar confirmed her diagnosis, decided to admit Miss J to intensive care overnight, and took over her care until 5.00pm that evening.
24. At 8.00pm the SHO was bleeped by the nurse in charge and was asked to review Miss J urgently because she was very agitated and complaining of headache. She went to see her. Miss J was very panicky and crying, "I'm having a brain haemorrhage, please do something, please help me". The SHO had observed previously that she was a nervous patient and that staff had found it difficult to reassure her. There was no fluctuation in her level of consciousness. The SHO thought Miss J's headache was due to dehydration and gave her Calpol (liquid paracetamol) as she did not like swallowing tablets. That seemed to settle her down. The SHO checked Miss J again at 9.00pm and found that the Calpol seemed to have worked.
25. The SHO said that she was 'vaguely aware' of cerebral oedema from her paediatric training three years before; but it was not mentioned to her by any of the senior doctors or nurses. She contacted the first consultant at 9.30pm who gave her a management plan. She understood that the second consultant, in liaison with the first consultant, was in charge of Miss J's care. The SHO stayed in ITU until 1.30am. She was not informed of any resumption of headache until 3.30am when she was bleeped and told that Miss J had collapsed.
26. The first registrar said that when she saw Miss J in the minor injuries unit she was conscious and talking. A drip had been inserted; and her heart rate and blood pressure were stable. Bloods samples had been sent to the laboratory. She took another sample to test Miss J's electrolytes. She saw and endorsed the SHO's care plan and arranged for Miss J's admission to ITU. She did not refer to the written protocol but to her own knowledge. She attempted to insert a CVP line by the subclavian route; but could not get a vein. Miss J was 'very fed up', her vital signs were satisfactory, and urine output was good. The first registrar did not think Miss J would accept another attempt being made at that time. If she had thought the procedure essential she would have called an anaesthetist. The consultants arrived just before the abortive attempt at insertion. They reviewed the care plan, made no changes to it, and instructed the first registrar to carry on. She spoke to the SHO before she went off duty, but not to the second consultant. She viewed the first consultant as the consultant in charge of Miss J's care at this time. The first registrar was worried about Miss J's condition because her pH had stayed at 7.1; and because she had passed as much fluid as she had been given and attempts were being made to rehydrate her. The first registrar was aware of the risk of cerebral oedema as she had worked previously for a consultant who had an adult patient who had developed diabetic ketoacidosis; but it was not discussed in this case and there was no reason to suspect it might be a factor. The use of Mannitol was not considered.
27. The second consultant said that he was a consultant physician with a special interest in respiratory medicine. He confirmed that the on call consultant arrangements entailed 24 hour shifts. In Miss J's case, he was the on call consultant that day and so she was admitted to his care; but as she had diabetic ketoacidosis and was the first consultant's patient he decided to refer her to him. The first consultant had asked to be informed immediately when diabetic patients were admitted and took a keen interest in them. The second consultant was notified of Miss J's admission by the first registrar who told him that they had a diabetic patient with diabetic ketoacidosis, that she was getting better, but that they intended to transfer her to ITU for monitoring and management. He was told that he was not needed immediately and he said he would see her after a staff meeting. He so informed the first consultant and they both went to ITU. He asked the first consultant to take over Miss J's management and he agreed to do so. The second consultant did not notify staff formally that the first consultant had assumed responsibility for Miss J's care: he did not feel he needed to because it was well known that he would do so in such cases and would make quite clear what the patient's future management plan should be. The Trust's practice was that patients were managed by the consultant specialist relevant to their condition under a 'shared care' arrangement.
28. The SHO and the second consultant had an evening ward round. They discussed Miss J's care, but the second consultant did not formally assess and review her, as responsibility for her care had been accepted by the first consultant. The registrar had updated the SHO and she in turn updated the second consultant. The SHO telephoned the second consultant at 8.46pm to tell him that Miss J had not been well. The SHO was concerned that the diabetic ketoacidosis had not resolved as anticipated and sought advice on how this might be improved. She also mentioned that Miss J had had an episode of headache and agitation, but that this was responding to simple analgesia. She felt that Miss J possibly had a low pain threshold. The second consultant advised the SHO to telephone the first consultant at home for advice. The second consultant telephoned the SHO at 11.30pm to check that all was well. The SHO said that Miss J was getting better and that she (the SHO) had talked to the first consultant. The alteration in treatment had improved Miss J's diabetic ketoacidotic state and at that time her headache was not presenting a problem. The onset of her headache struck the second consultant as unusual; but as it seemed to respond to simple analgesia it did not give rise to concern at that time. He did not know about the association of cerebral oedema with diabetic ketoacidosis. At 3.57am the SHO telephoned the second consultant and said that Miss J had deteriorated suddenly, was unconscious and needed to be ventilated. The second consultant instructed the SHO to ventilate the patient and telephone the consultant anaesthetist. The second consultant then went straight in and after assessing Miss J telephoned the first consultant at 5.15am.
29. The first consultant told the investigator that he saw Miss J on 22 July at 1.30pm in ITU. She was confused, although her mental state had improved since admission. She was not able to give him a history. She was very breathless, lying flat and drowsy. He noticed that her sodium was very low, but it rose quickly. Miss J was under the care of the second consultant, but the first consultant advised him. The first consultant saw Miss J three times during the day: she improved dramatically, and by 5.45pm was a lot better. He thought that her care had been managed appropriately. Clinical management fell within accepted protocols (guidelines for the treatment of particular conditions) for the treatment of diabetic ketoacidosis and was well understood by the staff concerned. The first registrar had followed the protocol, with minor variations. Miss J had persistent acidosis and it was consistently improving. The first consultant would have preferred to have been told about her headache at 8.00pm, but was not telephoned between 5.50pm and 9.45pm. If he had been contacted he might have considered pituitary apoplexy. He would have ordered a CT scan, but would not have considered cerebral oedema. In 15 years as a consultant he had had only three deaths, including Miss J's; and he had never seen cerebral oedema in an adult patient with diabetic ketoacidosis. The protocol has since been amended to add the risk of cerebral oedema and to emphasise the use of 10% dextrose.
Nursing staff
30. The first staff nurse explained that on 22 July she was in charge of the ITU day shift and took charge of Miss J's care. She had no experience of cerebral oedema associated with diabetic ketoacidosis. Protocols were kept on the ward including diabetic ketoacidosis guidelines. They were often referred to, and senior staff were aware of them. The first staff nurse would have had the protocol open by the patient's bedside for reference purposes. Miss J had been quite a difficult patient to manage, as she kept refusing nursing interventions and did not seem to appreciate the seriousness of her condition. Miss J reported a headache at about 8.00pm. She held her head and said, "I'm having a brain haemorrhage". The first staff nurse was unsure of the significance of Miss J's headache and unsure whether she was being 'over dramatic'. However, she contacted the SHO at once. Miss J's conscious level was constant and the first staff nurse did not suspect her neurological functioning. She told the second staff nurse on the night shift that Miss J's mother had asked for her daughter to be nursed by a female member of staff because she was a very private person and had not been an inpatient before. (Note: Miss J's mother disputes this account.) The first staff nurse could not recall writing a care plan. (Note: There is no care plan in the notes.) She commented that it had been a very busy shift and she had not had a break. There were three patients in ITU, and four staff, including one nursing auxiliary.
31. The charge nurse said that the skill mix that night had been inadequate. He was a G grade nurse and was working with two D grades. One was a junior who had worked in ITU for only a few months and had no ITU qualifications; the other an agency nurse who had worked in ITU before. The agency nurse had no formal ITU qualifications, but the charge nurse had a reasonable knowledge of her skills. He was the only qualified nurse on duty and was working with a locum SHO. The charge nurse said in evidence that he had drawn his concerns about the skill mix on that shift to the nurse manager in advance. The charge nurse also commented in his evidence on the absence of senior consultant management in ITU and that there was no clear policy on senior clinical patient ownership. He was told at handover that Miss J did not like to be cared for by male nurses. He observed that that was the case and that she responded better to female staff. He therefore assigned her care to the agency nurse, though he would otherwise have cared for her himself. The charge nurse was satisfied that the agency nurse's experience and ability were sufficient and he oversaw the care of all patients on ITU that night. The admitting (second) consultant technically had patient ownership; but endocrine patients were normally referred immediately to the first consultant. Diabetic ketoacidosis cases were usually handled by the on call registrar who liaised with the on call (second) consultant. He was not present on the ward when, at 8.00pm, Miss J developed a headache, but was informed about it at handover. Miss J complained of a headache persistently during the shift and this indicated to the charge nurse dehydration or toxicity. He drew his concerns about Miss J's persistent acidosis to the attention of the SHO, who contacted the first and second consultants. He tested baseline reflexes a number of times, but there were no changes. Miss J was able cognitively and could count backwards.
32. The second staff nurse was a D grade agency nurse. She usually worked 4 or 5 shifts a week for the Trust, had done so for about a year and worked the night shift on 22 July. She normally cared for coronary patients. She was not aware of any treatment protocols on the ward. She administered fluids on the oral instructions of medical staff. Miss J had refused to be catheterised and had to be coaxed into accepting an arterial line. She talked about her boyfriend and how they were planning to marry. She asked for a commode, appropriately, and showed no evidence that she was confused. Miss J was very tired, but if she fell asleep she woke instantly: there was no change in her level of consciousness. The second staff nurse was not present at 8.00pm, when Miss J developed a headache, but was informed about it at handover. The SHO was in almost constant attendance. At about 2.00am Miss J went to the toilet, and then said that her head was 'awful' and at one point, 'quite out of the blue', said that she thought she was going to die. The second staff nurse said that she did not attach any particular significance to Miss J's headache. She thought it was simply the consequence of her high sugar levels, and it seemed to settle. She did not smell ketones on Miss J's breath until 3.00am. The second staff nurse wrote up the nursing notes and fluid chart after the shift ended. Staff had no break on the night shift.
33. Some of the staff interviewed commented that Miss J had refused some medical and nursing interventions during her admission. Her behaviour was described in evidence to the investigator in terms such as 'demanding', 'immature' and 'difficult'.
Findings
34.Mr J has complained that his sister's death could have been avoided and that mismanagement by the Trust and its staff contributed to the sad outcome. Specifically, he complains that Miss J was misdiagnosed; that she received inadequate education about management of her diabetes and monitoring in the diabetes clinic; and that her final illness was mismanaged in hospital including by over-administration of fluids causing cerebral oedema. My findings address each of these concerns.
Diabetic clinic
35. I consider first the first consultant's diagnosis of MODY. Mr J has complained that the diagnosis was incorrect. The first consultant said that although he entered a firm diagnosis of MODY in his notes, he still had in mind the possibility that Miss J might have slow onset type 1 diabetes. The external professional advisers in this case are clear that the diagnosis of MODY reached by the first consultant was wrong and that Miss J most probably had slow onset type 1 diabetes. They also advise that such a diagnosis can safely be reached only after a significant period of time. The first consultant did not record that he had an alternative diagnosis under consideration; and the diagnosis he did record was unequivocal. It is clear from the evidence, and is wholly unsatisfactory, that Miss J believed that she had MODY and that that was a firm diagnosis rather than a working hypothesis which would need to be kept under review.
36. Mr J also complained that his sister did not receive the education and information she needed: in particular, that she was not told about the difference between type 1 and type 2 diabetes, about hyperglycaemia and about diabetic ketoacidosis. The first consultant is clear, on the other hand, that he covered all but diabetic ketoacidosis. The nurse specialist also maintains that she provided information and education appropriate to type 2 diabetes, but was unable to demonstrate this from her records. At the very least, Miss J understood from what she was told that she had MODY; that she did not require insulin; and how to test her blood sugar. I am unable to determine with any degree of certainty, however, the full extent of the information the first consultant provided to Miss J and, as a consequence, whether important information was not provided. I note with approval that the diabetes clinic now operates a revised educational procedure to ensure that young persons receive the information and instruction they need and that this is documented. I recommend regular audit of the effectiveness of these measures.
37. Following my investigation I am satisfied that, given the diagnosis, the actions of the nurse specialist fell within the accepted standards for a nurse of her experience and I do not consider that she was in a position to challenge the first consultant's diagnosis. However, it is a matter of concern that inadequacies in her records mean that neither I nor she can be certain what information she gave to Miss J. I note with approval that the nurse specialist has now taken steps to improve the standard of her record keeping and I recommend that she should follow the advice given by my advisers (Appendix A - paragraph 41). I also urge the nurse specialist to take note of the advice given at the conclusion of the advisers' report (Appendix A - paragraph 84) and that it is essential that all diabetic patients, regardless of type or severity, are taught to test their blood sugar at least once a day if they are unwell, and that it should be made very clear to them in what circumstances they should contact the diabetes clinic for advice.
38. Mr J also complains that the first consultant and the nurse specialist failed to monitor his sister's condition adequately. He maintains that Miss J's blood glucose and HbA1c measurements clearly indicated declining diabetic control and that, as a result, action should have been taken to alter her management. The first consultant has said that, even had he diagnosed type 1 diabetes at the outset, Miss J's care would not have been managed differently. My advisers agree, and have said that her HbA1c results revealed a slight deterioration in diabetic control, but that this would not have required a change in monitoring procedure. In Miss J's case I am advised that blood glucose monitoring would have been sufficient to reveal the serious metabolic deterioration that occurred after 14 July 1997. I am satisfied, therefore, that Miss J's diabetic monitoring by the first consultant and the diabetes clinic was within acceptable bounds. I do not comment in this report on the actions of the other clinicians who saw Miss J between 14 July 1997 and her eventual admission to hospital.
Inpatient care
39. I turn now to the care provided to Miss J during her admission to hospital. Mr J has complained that hospital staff should have been aware of the risk of cerebral oedema in association with diabetic ketoacidosis; that they failed to treat diabetic ketoacidosis appropriately; and that they administered too much fluid so causing cerebral oedema. He believes that staff should have responded differently to the onset of headache and should have observed his sister more closely.
40. Miss J was admitted with diabetic ketoacidosis; she also had hyponatraemia and was clearly seriously ill. In view of that, a consultant should have taken an active role in planning, managing and evaluating her care. Neither the first nor the second consultant considered himself to be actively directing and monitoring Miss J's care over the first 24 hours. They considered they were sharing care but did not meet together with the SHO to lead the management; they were content with the SHO variously contacting each of them for advice. If the first consultant was unable to be fully involved because he was not on call, consideration should have been given to transferring the patient to another unit. I understand that the ITU management arrangements in place at the time were designed to ensure the involvement of specialists in the care of patients being cared for there. However, one consultant should have had clear over-arching responsibility for coordinating all aspects of Miss J's care. I find it wholly unsatisfactory that that did not happen with the result that there was a degree of confusion, a lack of focus on a care plan, and a lack of clear leadership to doctors who were still in training. I am pleased to learn that ITU management arrangements have now been changed.
41. I acknowledge that Miss J's care was in accordance with the hospital protocol for the management of patients with diabetic ketoacidosis. However, protocols provide no more than guidelines for clinical management, and have to be seen in the context of the patient's developing condition. Miss J was an exceptionally difficult case and her condition did not improve as expected. There is no evidence that she was overloaded with fluid; but it is clear that staff failed to bring the acidosis under control. In such circumstances, a senior member of the medical staff should have considered whether other approaches to treatment were necessary. As it was, it was only after Miss J's condition had deteriorated that the second consultant reviewed her himself. I find this wholly unsatisfactory. I cannot say with any certainty, however, whether regular bedside assessment by an appropriately experienced senior clinician would have altered the outcome in Miss J's case.
42. Mr J has complained that his sister was over-hydrated and that that caused cerebral oedema. I am advised that the state of a patient's hydration, particularly in the absence of a central venous pressure line, is a complex matter to determine. My advisers differed slightly in their views as to whether Miss J's fluid balance was restored or remained in deficit. They agree however, that she was not over-hydrated.
43. I am advised that the insertion of a central venous pressure line is considered a pre-requisite if fluid balance and the rate of fluid infusion are to be monitored effectively, particularly when a patient has, as in this case, both hyponatraemia and diabetic ketoacidosis. I understand that unsuccessful efforts to insert a line caused Miss J distress and that, as a result, the first registrar decided not to proceed. I consider that the absence of a CVP line made it all the more important for an experienced consultant to have been actively directing treatment and personally monitoring progress with the SHO until the patient was out of danger. The first and second consultants did not counter the first registrar's decision: I find that that was unsatisfactory.
44. It is not possible to determine precisely why Miss J developed cerebral oedema. She was clearly severely ill as evidenced by her profound hyponatraemia on admission. I am advised that the reason why cerebral oedema develops in some patients but not others is not clearly understood, but that it is recognised that fluid balance is not the only determining factor. The Trust's staff had little awareness of cerebral oedema in adults with diabetic ketoacidosis, and acknowledge that they did not perceive it as a risk in Miss J's case. I am advised that cerebral oedema is rare but widely recognised as a cardinal danger of diabetic ketoacidosis and it occurs more commonly in children than adults: I accept that advice.
45. When Miss J developed severe headache at 8.00pm on 22 July, I am advised that she probably had early cerebral oedema. Once cerebral oedema develops it usually results in death or severe neurological damage. My advisers have commented that the staff who were involved in Miss J's care in the ITU were generally unaware that cerebral oedema in association with diabetic ketoacidosis is a potentially life threatening problem or what to do if it is suspected. I appreciate that levels of knowledge vary about the relationship between cerebral oedema and diabetic ketoacidosis and my advisers recommend, and I agree, that advice about cerebral oedema should be included in the protocols for the management of diabetic ketoacidosis. I am pleased to note that the Trust has now included this in its protocols. They also advise regular neurological monitoring with the aim of detecting the early signs of cerebral oedema. Again, I agree. My advisers comment that cerebral oedema in association with diabetic ketoacidosis is a rare, but recognised condition in adults. Given that the Trust accepts for care patients with diabetic ketoacidosis and has on its staff a consultant with a special interest in diabetes (the first consultant), I consider that the first consultant at least should have been aware of the risk in relation to diabetic ketoacidosis with hyponatraemia and should have considered it. Had Trust staff made a provisional diagnosis of cerebral oedema appropriate to Miss J's symptoms and treated her accordingly, for example by a trial of Mannitol as my advisers suggest in paragraph 71 of their report, she might possibly have survived. In reaching this conclusion I realise that there are no studies to confirm or refute the value of this intervention. But an opportunity was, I believe, missed, in circumstances where once cerebral oedema developed death or severe neurological damage was the likely outcome.
46. I do have some concerns about the nursing care given to Miss J and I believe that there are important lessons to be learned. First, the standard of documentation was poor. Fluid charts were not completed accurately, yet they are vital when the patient is seriously ill as was Miss J and where restoration of fluid balance is an essential part of a patient's management; and a care plan was not completed. In addition, it was not entirely appropriate to allocate Miss J's care to a nurse without an ITU qualification. At the very least there should have been regular review and supervision by the charge nurse: but there is no evidence of this in the notes. Greater efforts should also have been made to ensure senior clinical review: and the SHO should have been made aware earlier of the treatment protocol. I am also concerned by the general tenor of remarks made about Miss J, whilst she was in intensive care. I do not consider that staff were aware of just how ill she was, nor did they fully understand the effect of severe diabetic ketoacidosis upon a person's mental and emotional functioning. Although I do not think it affected the outcome I do think the views nursing staff expressed about Miss J coloured, to some extent, their responses to her reports of pain and her behaviour. The first staff nurse, despite her personal reservations, responded appropriately by calling the SHO; and the SHO reported the headache to the second consultant. She did not mention it to the first consultant when she called him later, presumably because the second consultant had not considered it especially noteworthy being unaware of the risk of cerebral oedema in association with diabetic ketoacidosis. The second staff nurse did not report the onset of headache at 2.00am. The charge nurse said that Miss J suffered a headache more or less continuously throughout the shift and yet the impression gained by the SHO was that it was settling with paracetamol and, therefore, was not serious. I recommend that the nurse manager should reflect, with his staff, upon this episode of care as part of staff development.
47. I have considered all aspects of Miss J's inpatient care by the Trust. Taken together, the shortcomings I have identified indicate that her inpatient care could and should have been more expertly co-ordinated. However, I do not infer that these shortcomings caused or substantially contributed to her death. I uphold the complaint.
(b) the report of the independent review panel included, inappropriately, a statement that Miss J was in denial of her diabetes.
Documentary evidence
48. The report of the independent review panel that considered Mr J's complaints included the following advice from its clinical assessors:
'The complainant describes his sister as naïve and painfully shy. He said that she was extremely fearful when she attended the clinic for the first time and thought that she might die. He describes her as having a great weight lifted from her after being told that she would not need insulin injections. Information which had not been previously submitted but had been used in an earlier complaint hearing against a general practitioner came to light in the course of the review (Note: this was subsequently proved by Mr J not to have been used at that review). This information was in the form of a letter of 2nd December 1997 from [the SHO] who writes, "Amongst other things, [Miss J's] mother informed me that she (the mother) had attempted to take BM [Stix] measurements in the 2 or 3 days prior to admission however [Miss J] herself had refused to let her mother do this and her mother had not forced [Miss J] to comply". The home blood glucose testing record book shows good values which are very consistent until the last entry of 14th July 1997 which shows a value of 11mmol. Thereafter there are no tests. We were told that [Miss J] did not do her own tests but that all of her tests were done by her mother. We consider that two inferences can reasonably be drawn from this information. Firstly it suggests that the patient had difficulty in coming to terms with diagnosis of diabetes, had realised that control was poor and that a progression of the diabetes had taken place so that insulin treatment was likely to be advised. This kind of anxiety is recognised to cause a reaction of denial of the diabetes in some subjects. Secondly [it] tends to support the view that she did understand the signs and symptoms of deteriorating diabetic control and recognised their significance.'
49. The panel concluded that:
'Miss J's home blood glucose testing record book shows values consistently around 7mmol until the last entry of 14th July 1997 when it shows a value of 11mmol. After this it seems that no further tests were done, and, according to [the SHO's] written statement, Miss J refused to allow her mother to take any blood samples for testing after this date. The Panel considers that it is reasonable to deduce from this that Miss J had difficulty in coming to terms with the diagnosis of diabetes, and had realised (when the blood glucose began to rise) that the disease was progressing and that insulin treatment was likely to be advised. This kind of anxiety is recognised to cause a denial reaction to the diabetes in certain people.'
Evidence of Mr J and his family
50. Mr J believes that the panel's conclusion that his sister was in denial of her diabetes was unjustified and unfair. He said that he had not been shown the SHO's letter, and had therefore not been given an opportunity to refute the assertion upon which it was based. He was annoyed that the consultant appeared to have 'floated' the idea that Miss J was in denial as a mitigating factor and that the panel had quickly latched on to it. Mr J said that his sister did not test her blood sugar more frequently when she was ill, or contact the clinic, not because she was in denial but quite simply because she had not been instructed to do so. He produced a number of signed statements from members of his family testifying that his sister always tested her own blood sugar and that family members had observed her doing so. The signed statements included one from Miss J's niece that her aunt had tried to test her blood twice on 17 July and had asked her to assist with timing and trying to read the result. They had, however, been unable to determine a reading, though the result seemed to lie between 7 and 9. Mr J said in evidence that his mother did not know how to test blood sugar and he supplied a letter from her GP confirming that she was not diabetic but merely had impaired glucose tolerance. His mother confirmed that she tried to test Miss J's blood sugar on only one occasion and that was when her daughter's GP asked her to do so shortly before the ambulance arrived to take her to hospital. She denied having told any of the doctors at the hospital that she tested her daughter's blood sugar; except on that one occasion, when her daughter was clearly feeling very ill and had refused to allow her to do so (see paragraph 20). Mr J thought that the method by which the evidence of denial was produced at the panel was unfair, and that the Trust had fabricated it.
The panel chairman's evidence
51. The panel chairman said that this was only the third panel she had chaired. She had not been provided with any training for her role before hearing this case, which was complex and involved the assimilation of a great deal of information. She and the other panel members tried very hard to deal thoroughly and fairly with the case. The panel chairman commented that, with hindsight, although she would still have included comment about denial she would have used slightly different language and made it very clear that it was just a theory and was not supported by hard evidence. She accepted that, as written, it did seem quite dogmatic and had not been expressed quite as she had intended.
52. The clinical assessors had expressed their very strong opinion that Miss J had been in denial. The chairman accepted, now, that the panel had got 'swept along' with this theory and made assumptions which, in retrospect, they probably should not have done. The panel had heard Miss J described as shy, innocent and naïve. She had been a late arrival to the family and was obviously cherished and 'protected' by her older brothers. It seemed from the letter submitted by [the SHO] that her mother tested her blood sugars for her. Miss J had apparently stopped testing her blood sugar when she became ill, and had been described as fearful of diabetes. She appeared to have refused to let her mother test her blood sugar when she was ill. On that basis, it seemed reasonable to conclude that Miss J was in denial. The panel wanted to try to understand, to explain how this might have happened and to help the family come to terms with events. The panel certainly did not intend to add to the family's anguish.
53. The lay chairman could not recall precisely what evidence the panel had been given. She remembered seeing [the SHO's] letter, but could not recall seeing a written statement from the first registrar which contained similar information. The panel was not told that Miss J's mother did all the tests. The chairman believed that the clinical assessors had assumed that that was so. Denial had been a fundamental tenet of the clinical assessors' view and not one the panel could disregard or overrule. However, the chairman was clear that, in future, she would be more cautious and would ensure that conclusions expressed in panel reports were founded on the evidence.
Evidence of Trust staff
54. On 28 November 1998, the first registrar wrote in a signed statement:
' ... At about 5.15pm I rechecked the blood gases, again with difficulty in obtaining the sample. [Miss J] was very unhappy about having yet another needle. At this stage her relatives were visiting, and while her Mother was present I asked [Miss J] if she had been checking her blood sugars at home in view of the fact that she had been unwell for several days. [Miss J] said that she had not checked her own blood sugar, and [her mother] said that she had been trying to encourage her to do so, but [Miss J] was unwilling to do so as she did not feel well enough, even having returned from a holiday in Wales after only two days as she felt unwell. [Her mother] said that she also is diabetic, and had offered to check the blood for her, but that [Miss J] had refused.'
55. The first registrar said when interviewed that she had gained the impression that Miss J's mother intended to convey that her daughter had refused on more than one occasion. She thought her mother was saying that she had known something was wrong, but that her daughter would not let her test her blood.
56. The SHO explained that the Trust's medical director had asked her to provide a written statement and information about her communication with Miss J's family. She provided a written statement which set out her clinical involvement and, in a covering letter, dated 2 December 1997, her recollection of conversations she had had with the family. The letter included:
On admission I gained information from both [Miss J] and her mother about the preceding illness. Amongst other things, [Miss J's] mother informed me that she ([Miss J's mother) had attempted to take BM Stix measurements in the 2 or 3 days prior to admission however [Miss J] herself had refused to let her mother do this and her mother had not forced [Miss J] to comply.'
57. The SHO told the investigator that she had talked to Miss J's mother when she admitted her and that she had asked questions about Miss J's blood monitoring history in order to establish the pattern prior to her admission to hospital. Her recollection in December, was that Miss J's mother had told her that she had wanted to test her daughter's blood sugar, but that Miss J had become upset and she had not wanted to force her. She understood this situation to have spanned a 2 or 3 day period. She was unable at this distance in time to recall the incident with any greater clarity. She would have needed to establish what Miss J's blood sugar levels had been over the preceding few days to determine whether her condition was a sudden onset or a gradual deterioration. She certainly had the impression that Miss J's refusal to allow her mother to test her blood related to a period of time rather than one specific occasion.
58. The nurse specialist said when interviewed that Miss J had been a shy person and generally came to clinic with her mother. She was co-operative; seemed to take information on board; was happy to receive it and to engage in conversation. She did not observe any behaviour that might indicate to her that Miss J was in denial; she thought she understood her role in the management of her own condition. Miss J answered questions appropriately, accepted her diagnosis, attended clinic regularly and tested her blood. There had been no 'no shows' or excuses not to attend clinic. The diabetes nurse specialist did not notice any changes in Miss J's emotional state over the period that she saw her.
59. The first consultant said when interviewed that he told the panel that he thought Miss J was in denial. He did not think she was in denial of diabetes, but thought she was in denial of transition from type 2 to type 1. She did not test her blood sugars when she was ill and would not let her mother do so. Miss J had told the GP that her blood sugars were '7'ish' when her last reading had been 11. She was vomiting for four days, ill for ten, and yet failed to contact the clinic. She was an educated and compliant woman.
Findings
60. Mr J has complained that the independent review panel's finding on the question of denial was both incorrect and unjust. He and his family had been upset by the implication that Miss J had contributed to her own death. Mr J believes that there were insufficient grounds to support the panel's conclusion and he contends that the panel did not test the evidence. The lay chairman accepts that the panel's conclusion should have been expressed differently: but she felt it important for the panel to reflect the advice it had been given. I do not criticise the panel for doing so. It is important however, that in reaching a conclusion a panel should consider carefully whether it is supported by the evidence and whether all reasonable opportunities have been taken to test that evidence. I have done so in the course of my investigation and have taken account of the views of my adviser in clinical psychology (Appendix A) as denial is a psychological concept, an inference from behaviour. I am advised that it is generally accepted that particular patterns of behaviour can arise for a variety of psychological and other reasons. The first consultant invoked (during the IRP panel), and the panel accepted, a psychological account for Miss J's presumed failure to act. It was, therefore, appropriate for me to seek a psychologist's view on the evidence that a particular psychological process was implicated in Miss J's alleged failure to act. The consultant cited no independent evidence other than the presumed failure to act as the grounds for inferring denial. He did not at the time cite, let alone test, other possible explanations for Miss J's behaviour. I have concluded that Miss J was not in denial. The panel chairman has recognised that the panel's views on this matter were expressed unwisely. I am pleased that this is accepted. I do not believe that there was any deliberate attempt by the Trust to mislead the panel or to fabricate evidence. I uphold the complaint.
Conclusions
61. I have set out my findings in paragraphs 34 - 47 and 60.
62. There is no doubt that type 1 and type 2 diabetes are serious life threatening conditions. Equally, there is no doubt that if they are correctly managed the risk of premature death and complications can be substantially reduced. Yet Miss J died. This investigation needs to be seen in the context of those previously conducted by my office and through the NHS complaints procedure into the entire course of Miss J's treatment and care. From these it is clear that a number of mistakes were made beginning with the initial, unduly definite, diagnosis of type 2 diabetes. Avoiding any one of these mistakes would have improved Miss J's chance of survival. It is not possible for me to say that one or more of these mistakes individually led to her death: but taken together they almost certainly did. If, for example, the diagnosis had been correct or expressed with sufficient caution; if we could be certain that Miss J received the information and education she needed; if any one of the three GPs involved in her care had tested her blood or urine; or if Miss J had had impressed upon her, in no uncertain terms, that she must test daily when unwell, and had done so and reported untoward results, she might have survived.
63. This investigation has revealed that Miss J's inpatient care could have been more expertly co-ordinated and that she had a right to expect better from the Trust and its staff. For example, I have commented on the failure to insert a CVP line, on the failure to keep accurate fluid balance charts and on the lack of clear consultant leadership in ITU. I have also commented on nurse staffing and supervision in ITU and on the nurses inappropriate reaction to Miss J's behaviour. I cannot say with any certainty, what contribution, if any, these failings made to the tragic outcome in this case. It is not understood why some patients develop the rare condition of cerebral oedema and I cannot be certain whether different clinical management would have prevented this condition. I am advised that once Miss J collapsed as a result of cerebral oedema her death, or severe neurological damage was inevitable. I have also commented, however, that, in these circumstances, the diagnosis of cerebral oedema and the use of a trial of Mannitol should have been considered.
64. An important lesson from this case, is the need for all those involved in diabetic care, not least patients themselves, to be aware that it is essential to test blood glucose and urine ketones more frequently during an intercurrent illness, whatever the type or severity of diabetes. This simple measure could have saved Miss J: I hope it will save others.
65. The Trust has advised me that significant developments have taken place in diabetes care and education at the hospital in the last three years. The drivers for these developments have been a combination of the issues highlighted in Mr J's complaint and a wider series of significant service enhancements, which include:
-the appointment of a further consultant physician with a special interest in diabetes working with both secondary and primary care;
-successful primary and secondary care partnerships including for:
- ·diabetic foot clinics
- retinopathy clinics
- specialist nurse clinics
- pre-conception clinics
- ante-natal clinics
- young persons clinics
67. Many changes have also taken place in the delivery of critical care services at the hospital. These range from the introduction of a specific policy on the management of ketoacidosis and the modification and updating of fluid charts and results sheets. A review of nurse staffing levels has also taken place which has resulted in strengthened nurse leadership within the unit and robust plans for further nurse recruitment. This will support the transfer to a purpose built critical care facility with additional bed capacity and the provision of a high quality patient environment including relatives accommodation.
68. The Trust has asked me to offer to Mr J and his family its apology for the shortcomings I have identified. I do so through the medium of this report. The Trust has also agreed to act upon my recommendations in paragraphs 36, 37, 45, 46 and in Appendix A where action has not already been taken, including in the course of the service developments described above. I have also recommended, and am pleased that the Trust has accepted, that a meeting between senior officers of the Trust and Miss J's family would be a helpful way forward in deciding how the Trust might respond to the findings in my report.
M S Buckley
Health Service Ombudsman
August 2000
