Pierce v Metro North Hospital and Health Service

Pierce v Metro North Hospital and Health Service - [2016] NSWSC 1559 - NSWSC 2015 case summary — Zoe

[8]

Amplification of the issues and applicable principles of law

The key issue between the parties is whether any change in Ms Pierce's epilepsy was caused by the January 2010 event: 339. 9-19T; 402.44-50T. Epilepsy is a disease which is not yet fully understood. Accordingly, its nature, natural progress, factors affecting it and its rate of progress are all subject to degrees of contestation. This being so it is apposite to recall the principle expressed by Hayne and Bell JJ in Tabet v Gett (2010) 240 CLR 565; [2010] HCA 12 at 564 [66]: "For the purposes of the law of negligence, "damage" refers to some difference to the plaintiff. The difference must be detrimental. What must be demonstrated (in the sense that the tribunal of fact must be persuaded that it is more probable than not) is that a difference has been brought about and that the defendant's negligence was a cause of that difference. The comparison invoked by reference to "difference" is between the relevant state of affairs as they existed after the negligent act or omission, and the state of affairs that would have existed had the negligent act or omission not occurred." Given the application of this principle, it is important to bear in mind certain considerations relevant to proof of Ms Pierce's case at the outset. There are no clinical signs or available diagnostic tests that can conclusively demonstrate that the alleged harm occurred; that is, that a difference has been brought about and that the Hospital's negligence caused that difference. It is also the case that no sign or test can prove the negative proposition that there has been no different outcome. It is also important to keep at the front of one's mind that it is not enough for Ms Pierce to prove she is worse than she was. She is required to prove that she is worse than she would have been if the admitted negligence had not occurred.
Sections 11 and 12 CLA govern my decision about these matters. These provisions are to the same legal effect as ss 5 D and 5 E Civil Liability Act 2002 (NSW), the subject of the decisions of the High Court in Strong v Woolworths Ltd (2012) 246 CLR 182; [2012] HCA 5 and Wallace v Kam (2013) 250 CLR 375; [2013] HCA 19. It is sufficient to record that the factual causation limb of s 11(1)(a) CLA requires an inquiry into whether the hospital's breach of duty "was a necessary condition of the occurrence of the harm" suffered; I understand harm in this context to be synonymous with "detrimental difference" as discussed by Hayne and Bell JJ in Tabet v Gett (240) CLR 537; [2010] HCA 12 at [69]. Section 11(1)(a) calls for a decision about factual causation by application of the "but for" test. The parties are agreed that if factual causation is established, no question arises about the scope of liability test raised by s 11(1)(b): Wallace v Kam at 385 [22] and [26]. Section 12 CLA makes clear that the plaintiff always bears the onus of proving on the balance of probabilities any fact relevant to the issue of causation.
Given the uncertainties remaining in this branch of neurology and the absence of a definitive medical investigation to measure whether Miss Pierce's condition is worse than it otherwise would have been after 5 January 2010, and the cause of that worsening, the case falls into the category where the state of medical science may create difficulty for a plaintiff in demonstrating that she or he has discharged the civil onus of proof. As Herron CJ observed in EMI (Australia) Ltd v Bes [1970] 2 NSWLR 238 at 241 the problem is not "new" and the proper approach is "familiar enough". After reviewing various cases until then, starting with Adelaide Stevedoring Co v Forst (1940) 64 CLR 538, the Chief Justice expressed the principle in the following terms at (242): "… it is not incumbent upon [the plaintiff], upon whom the onus rests, to produce evidence from medical witnesses which proves to demonstration that the [plaintiff's] contention is correct. Medical science may say in individual cases that there is no possible connection between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be the touchstone, then the judge cannot act as if there were a connection. But if medical evidence is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical science denies that there is any such connection that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try." (My emphasis.) (See also Asprey JA at 243; Seltsam v McGuiness (2000) 49 NSWLR 262; [2000] NSWCA 29 at [94]; Fernandez v Tubemakers of Australia Limited [1975] 2 NSWLR 190 at 197; affirmed on appeal to the High Court: Tubemakers of Australia Limited v Fernandez (1976) 50 ALJR 720; 10 ALR 303 at 311 - 12.)
In Seltsam v McGuiness at 296 [93] Spigelman CJ said: "With respect to many diseases, medical science is able to give clear and direct evidence of a causal relationship between a particular act or omission and a specific injury or disease. There are, however, fields of inquiry where medical science is not able to give evidence of that character. There are cases in which medical science cannot identify the biological or pathological mechanisms by which disease develops. In some cases medical science cannot determine the existence of a causal relationship. Such a state of affairs is not necessarily determinative of the existence or non-existence of a causal relationship for purposes of attributing legal responsibility." Seltsam v McGuiness concerned the use to which epidemiological evidence could be put in filling an evidential gap on causation in a "dust" case, but the formulation of principle by Spigelman CJ is of more general application.
In Fernandez v Tubemakers at [197] Glass JA said that "the only principle of law" is that "the evidence will be sufficient if, but only if, the materials offered justify an inference of probable connection". In a circumstantial case "you need only circumstances raising a more probable inference in favour of what is alleged": Jones v Great Western Railway Co (1930) 144 LT 194 at 197; Holloway v McFeeters (1956) 94 CLR 470 at 480 - 1. At least in cases where the issue is not concluded one way or the other by settled tenets of medical science, it is permissible for the experts to express their "opinion as [an] inference of probability rather than as a logically established certainty". But it is for the court "to weigh and determine the probabilities". And the question is simply am I "on the whole of the evidence satisfied on a balance of probabilities" that Ms Pierce's condition is worse than it would have been but for the negligence of the hospital in the administration of the telemetry EEG: Ramsay v Watson (1961) 108 CLR 642 at 645.
In this case, the parties advance two competing hypothesises. The Hospital contends that there has not been an appreciable change in Ms Pierce's condition since the telemetry event, and to the extent that there has been an adverse change, this is due to the natural progression of the illness: 403.16-29T. This hypothesis has been colloquially referred to by the parties and experts as the "natural progression hypothesis" or "hypothesis B". The competing hypothesis, referred to again, colloquially, as the "waxing and waning" hypothesis or "hypothesis A", advanced on behalf of the plaintiff, is that prior to the telemetry event, her condition tended to ebb and flow in severity, however a dramatic change in the nature of her seizures occurred following, and because of, the telemetry event: 348.6-12T; 350. 22-28T.
The Hospital also joins issue with Ms Pierce on the quantum of her claim for damages on the same basis. Due to the ongoing nature of the claimed injury, the cost of future care, and future economic loss claimed by Ms Pierce are considerable. The Hospital argues that even if the January 2005 event did cause an injury, Ms Pierce is not appreciably worse compared to her state prior to 2010. Particularly, the Hospital argues that her need for care has not changed, neither has her future prospects of employment. Consequently, should causation be established, no compensatory damages are payable: 405.23T-406.27T. To the extent that there is a finding that she is worse, the Hospital further argues that this is because of the natural progression of the disease, not the 5 January 2010 event: 402.44-50T. The Hospital also challenges the claims on the basis that insufficient evidence has been provided to establish any loss: 429.20-27T.

[9]

Some general concepts relevant to Ms Pierce's epileptic condition established by the evidence

At the heart of the contest is the severity of Ms Pierce's condition at relevant times, particularly whether it could be said to be worse or better than at other times. Various terms were employed by the expert witnesses to classify different progressions of Ms Pierce's condition, and also the diagnostic and clinical significance of Ms Pierce's symptoms in the context of determining the nature of the epileptic activity she was experiencing at a particular time. It is therefore relevant to briefly set out the meaning of some of these terms.
Where the epileptic activity is isolated to only a particular part of the brain, this is referred to as "focal" or, more commonly in the evidence, "partial" epileptic activity; where the whole of the brain is involved, it is classified as "generalised" in nature (Exhibit 1.2, p 58). A seizure may commence as "partial" but progress to become "generalised". Where this occurs the seizure is referred to as a "secondarily tonic-clonic seizure"
The state of a patient's consciousness is also relevant to classification. Where the consciousness of the patient is not impaired, the seizure is referred to as "simple"; where there is some impairment of consciousness, it is classified as "complex": Exhibit 1.2, p58; 272:7T (Dr Fong). A generalised tonic-clonic seizure ("GTCS") whether "secondarily" or not, is characterised by complete loss of consciousness. "Tonic" and "clonic" refer to body movement or posture. The former consists of "unilateral jerks"; the latter to asymmetric posturing, or complex whole body movement. In a simple generalised seizure the patient may suffer no loss of consciousness and yet exhibit tonic or clonic signs.
"Status epilepticus" is a series of seizures or a prolonged seizure "creating a lasting epileptic state" of greater than 30 minutes duration. "Complex partial status epilepticus" ("CPSE") is a series of partial seizures, or a prolonged partial seizure, creating an epileptic state involving altered consciousness, not complete unconsciousness, and continuing for greater than 30 minutes. EEG is required for definitive diagnosis of CPSE. It can last for days, weeks and months: Exhibit 1.2, p60; Exhibit L.1, Appendix 1.

[10]

CPSE not CTCS

There had at one time been an issue about whether the evidence of the telemetry EEG demonstrated that Ms Pierce had suffered a GTCS as a result of the defendant's negligence. GTCS is regarded as a most serious, indeed life-threatening, event. The significance of this would have been that such a development would have clearly shown a definite increment in the progression of Ms Pierce's condition on that date. I record, however, that there is no strong evidence that she never previously suffered such a seizure. As I discuss below, there is much evidence of previous complex partial seizures, some of it suggestive of previous CPSE. There is some suspicion that the event of 10 April 2006, discussed in detail below, may have been a GTCS: see Exhibit 1.2, p 61.
The evidence of a GTCS on 5 January 2010 arises directly out of the hospital's records including a report dated 19 January 2010, apparently completed by Dr Lander (Exhibit E.2; pp H990 - 3). In her conclusion Dr Lander said the following (Exhibit E.2, p H993): "The focal epileptitiform activity arises from the right fronto-temporal region. This resulted in a focal temporal lobe type seizure with secondarily generalised tonic-clonic and then a three hour episode of non-convulsive status epilepticus. It is not possible to know whether the seizure origin arises from the right mesial temporal sclerosis or from around the frontal porencephalic cystic area." I interpolate that the reference to a generalised seizure is a description of a GTCS; the porencephalic cyst is a malformation or defect with which Ms Pierce was born. In Dr Lander's opinion it was due to perinatal ischaemic insult. The better view is that of Professor Dunne that it is specifically ante-natal in origin. This defect is also associated with a right ventricular atrophy and right mesio-temporal sclerosis. Ms Pierce's epilepsy is undoubtedly associated with these matters. There is a consequential associated left hemiplegia which Dr Lander regarded as "of mild to moderate degree".
The opinion about a GTSC also appears on page H992 of the report where it is said to "slowly" subside "over eight to ten minutes". In her report of 22 September 2015 (Exhibit 3), Dr Lander recanted this opinion. She said that she reviewed the telemetry EEG and that her report "is … inaccurate and incorrect in part, and is potentially misleading". Essentially having reviewed the material, Dr Lander states that Ms Pierce did not suffer a total loss of consciousness during the seizure, which as I have said, is a condition of the generalised seizure initially diagnosed. She states that her conclusion should have read: "This resulted in focal, right, predominantly frontal type seizure which began as a simple partial seizure then developed into a complex partial seizure with bilateral limb posturing. The first seizure was followed by a three hour episode of non-convulsive partial status epilepticus."
It is difficult to understand how this error could have been made. However, Dr Lander was not cross-examined and it is apparently, following the evidence in the trial, not controversial that no GTCS occurred. This is probably because, as I explain below when I detail his evidence, Dr Fong, Ms Pierce's principal liability expert, resiled from the opinion expressed in his second report (Exhibit L2, p 4) that there had been such a seizure. As I make clear below, Dr Fong maintained that there was some secondary generalisation of the epileptic activity from the right hemisphere to the left in the frontal region. I have referred to these matters again in what appears below to explain the flow of the evidence.

[11]

The telemetry event at RBH on 4-5 January 2010

I think it appropriate to deal with the evidence concerning the telemetry EEG of January 2010 before dealing with the evidence of Ms Pierce's condition prior to and after that event.
Ms Pierce began seeing Dr Cecile Lander, Neurologist, on 18 November 2008, as she was now an adult and her previous medical specialist, Dr Ingall, is a paediatrician. During their consultations, Dr Lander mentioned a neurosurgeon named Professor Berkovic, who was successfully treating some patients with epilepsy with neurosurgery. Ms Pierce was interesting in exploring this option, and Dr Lander wrote to Professor Berkovic about Ms Pierce's case. Later, Dr Lander told Ms Peirce that Professor Berkovic was not confident that she would be a suitable candidate, but Ms Peirce wanted to investigate the possibility further as she was "very keen to see if [she] could cure" herself: Exhibit F, p 5 [41].
Dr Lander informed Ms Pierce on 26 October 2009 that prior to seeing Professor Berkovic she would need to undergo testing in hospital by way of an Electroencephalograph Telemetry, in order to determine whether the seizure activity was originating from a focal lesion which may be amenable to surgery. This result of this test would enable Professor Berkovic to give advice as to the Ms Pierce's suitability as a candidate for surgery: Exhibit F, p 6 [43].
The test involved inducing a seizure which would be recorded by video; 22 scalp channels or electrodes attached to her head for the EEG and 2 channels or electrodes placed in the region of her heart for the ECG. Hospital records of the event detail that no "provocative procedures" were used to trigger a seizure. Rather, Ms Pierce was to be sleep deprived, and her regular medication withdrawn. At that time, her regular medication included Keppra 1000mg BD, Diamox 250mg OD and Lamotrigine 100mg BD. Her medication would be re-instated the day after the seizure, and a dose of Phenytoin and Clobazam given (Exhibit E, H980).

[12]

Ms Pierce and Mrs Pierce's evidence of the 4-5 January 2010

Ms Pierce was admitted to the Hospital on 4 January 2010, accompanied by her mother Mrs Pierce who stayed with her during the testing, except for the last half an hour or so of Ms Pierce's seizure. At that time Ms Pierce was taking her anti-seizure medication twice daily. On instruction from the Hospital she did not take her evening dose: Exhibit F, p 6 [49]. Dr Ingall had prepared a letter detailing the medication he had prescribed to be given to Ms Piece in the event of a seizure. Mrs Piece provided a copy of this letter to Dr Lander at the last consultation prior to the admission into hospital, and nursing staff on admission to the Hospital on 4 January 2010: Exhibit G, p 8 [43].
Ms Pierce has limited memory of the event. She remembers that the seizure didn't commence until early in the morning on 5 January 2010, and that she pressed the emergency button when the seizure started. She said she fell in and out of consciousness: " I came up out of the seizure but did not quite make it out and then went right back into it again. I thought initially I would be okay because I was at a hospital but when I kept seizing I got very worried and scared" (Exhibit F, p 7 [51]). It is now common ground that there was no complete loss of consciousness.
Ms Pierce gave further evidence on her experience of the seizure: Exhibit F, p 7 [53]-[54]: "53. I felt it was a very intense seizure. It came on in a way that I would describe as full-on. It was very strong. It really wore my body and mind right out. It was one of the worst seizures I have ever had in terms of intensity and also by far the longest seizure I have ever had. 54. I eventually came to in the morning of 5 January 2010. I felt totally exhausted. When I regained consciousness in the morning, I felt like I had been hit by a truck. It is hard to explain. I just felt totally spent physically and mentally."
She further gave evidence that previously when she experienced successive seizures, while she would "still feel a bit unwell" between each event, she would otherwise be "coherent, able to walk and so on". During the morning of 5 January 2010, between the seizure events she 'never really felt 'with it' until after it had completely finished in the morning": Exhibit F, p 7 [52]. Mrs Pierce gave evidence that between seizures she was sometimes able to answer a few questions, but "was very vague or detached" and that she "she did not appear to me to come back to normal": Exhibit G, p 8 [49].

[13]

Hospital records of the seizure 4-5 January 2010

This narrative of the telemetry event is derived from the hospital records of the EEG and ECG as interpreted by the experts and the video recordings. The video was played in court on the laptop of the plaintiff's solicitor and displayed on the AVL screens. That laptop remains in her possession upon the solicitor's undertaking to reproduce it to the court if required.
What is depicted on the DVD is to some extent distressing. From my entirely lay perspective, I formed the impression that the event was very distressing for Ms Pierce and one of some severity not just because of its duration but also due to its intensity bearing in mind medical intervention was delayed.
The seizure event started at 4:00:36 am on the 5 January 2010. Stretching out of her left hand was observed at 4:00:46 am and again at 4:01:53 am. According to the telemetry record, Ms Pierce reported a "funny feeling" in her stomach and vision "fuzziness" of 15 seconds prior to the onset of the seizure: Exhibit E, H982. At 4:04:10 am Ms Pierce's right leg stiffened and her left hand stretched out. She used her right hand to reach for the event button at 4:08:58 am; she then looked up to the monitor and described the sensation of her heart racing (4:09:26 am). She pressed the event button with her left arm at 4:10:12 am. She lifted her right hand to her face, used it to throw off her blanket (4:1014-16 am) and then called out for her mother at 4:10:19 am. The EEG reading for the period from 4:00:50 until 4:09:50 am shows "a build-up of rhythmic fact activity… at the mid frontal and right frontal electrodes", "increasing in amplitude and becoming more sharpened with intermixed spike components" as the time passed: Exhibit E, H981. More sharpened and spiked components were registered at 4:09:50 am and there is an increase in semi rhythmic delta, including "high amplitude and irregular pikes and irregular slowing".
After this point, the EEG readings show: "a marked increase in myogenic artefact…with the sharpened activity becoming widespread over the right side. The left side appears slowed with some rhythmic theta and the spread of the discharge to the left side also. This activity continues on the right side reducing in amplitude slightly on a few occasions but remaining continuous until 06:47:42. At this stage the discharge had developed into rhythmic slowing with intermixed sharp components. The EEG then appears slowed and attenuated bilaterally with postictal slowing prominent on the right side. " (Exhibit E, H981)
Between 4:10-25-28 am, the video record shows the Nurse enter the room and Mrs Pierce confirming her impression that a seizure was taking place. At this time, Ms Pierce's right hand was raised to her face (4:10-14-4:10:30 am), which then moved to hold her left hand (4:10:32 am). At this point, Ms Pierce was conscious, and able to correctly respond when asked where she was, "Royal Brisbane Royal Hospital": 4:10:38 am. Her hands became postured and there was bilateral leg extension at 4:10:42 am. The nurse then rolled Ms Pierce onto her side (4:10:44 am); at this point both legs and right arm are flexed at the joints and Ms Pierce is still conscious and responsive (4:10:49-54 am), but to me, looks "out of it". She is far from entirely "with it".
The nurses began to prepare the oxygen mask, with Ms Piece saying, "quick quick" (4:11:24-28 am) Clonic movement of her left arm was observed at 4:12:06 am and continues until 4:18:36 am. Ms Pierce begins to gag at 4:12:19 am; Intra Muscular Midazolam was administered shortly after at 4:12 54 am. She was still conscious at this point, and able to give her name when asked and to request help and for the nurses to act quickly (4:13:35-4:15:06 am). Rectal Diazepam was administered at 4:15:17 am. Ms Pierce subsequently became more confused (4:15:17-4:16:38 am) and again there was clonic movement of her left hand at 4:17:05 am.
At 4:17:37 am Ms Pierce was feeling better and thought that she emerging from the seizure; the clonic movement stoped at 4:18:36 am. She appeared well, but for her left hand which was still postured and stiff, until 4:21:10 am when Ms Pierce loses her sight, and Mrs Peirce observes her eyes flicking (4:22:53 am). She appears to improve slightly, with her sight returning and reporting feeling more relaxed (4:24:09 am). Her eyes soon after again became blurry at 4:24:58 am; her heart rate was measured to be 166 beats per minute at 4:26:08 AM. The nurses reported Ms Pierce's eyes as flickering and that she was tachycardic at 4:27:09 am.
Ms Pierce reported feeling unwell at 4:32:37 am. She is then administered another dose of intra muscular Midazolam at 4:37:35 am. She is reported to have been staring straight ahead, not interacting with anyone (4:37:43 am). A 12 lead ECG is performed at 4:40:31 am, with a doctor shortly after attending (4:41:45 am.)
Ms Pierce was unresponsive at 5:03:20 am and the event button was pressed four seconds later. She became responsive at 5:03:44 am- 5:04:06 am with slight facial movement. She then vomited at 5:13:34 am, and the event button was pressed again three seconds later. By 5:21:22 am there was well formed spike and slow wave activity, and a build-up of rhythm activity T6 O2 at 5:35:20 am. She began gagging again at 5:50: 52 am, and the event button was pressed twice a minute later. She was not jerking at this time but was vomiting.
At 6:18:22 am there is a record of her left hand jerking; and again at 6:32:13-19 am, a record of left hand jerking and posturing. The event button was pressed at 6:32:24 am. Her left arm continued to jerk, and the event button was pressed again at 6:43:22 am. Her left arm was tonic and jerking at 6:43:51 am. The rhythmic slowing was lessening by 6:47:42 am with the seizure event ended at 6:47:42 am. By this time, the Hospital report records that Ms Pierce was very drowsy, and went to sleep. In total, throughout the night she received 15mg intra-muscular Midazolam and 2 doses of rectal diazepam (Exhibit E, H982). The pressing of the event button in my view was indicative of a heightened level of distress.

[15]

Dr Fong's expert opinion of progression of 5 January seizure

The plaintiff's principal expert is Dr Jason Kaunyeung Fong, a specialist neurologist practising in Hong Kong. He is also a fellow of the Neuroscience Research Centre at Hong Kong University and a former president of the Hong Kong Epilepsy Society. There is no issue about the expertise and indeed, professional eminence of each of Professor Dunne and Dr Fong.
Dr Fong agrees with Professor Dunne that what occurred was a prolonged event of CPSE, and that Ms Pierce did not develop a secondary GTCS: Exhibit L(2), p 4. Initially Dr Fong disagreed with Professor Dunne on this point, writing in his reports that a secondary GTCS had occurred. For this, he relied upon the Hospital notes made by Dr L Wilkinson and the "uncorrected" telemetry report of Dr Lander. Dr Wilkinson recorded: "patient had a further seizure with secondary generalisation and subsequent drop in [Glasgow Coma Scale] to 10, responding to pain only" (Exhibit E.3, p H1024; Exhibit L(1), p 4). Dr Lander noted that: "The focal right frontal discharge spreads bilaterally and she experiences a secondarily generalised tonic-clonic seizure." (Exhibit E 3, p H992). This drop in consciousness followed upon a spread of abnormal EEG from the right to the left hemisphere of the brain, which according to Dr Fong, indicated either the occurrence of a frontal seizure or a secondary GTCS. he considered the distinction academic: Exhibit L(2), p 4.
After considering Dr Lander's revision, and re-examining the EEG print-outs, Dr Fong, in examination-in-chief, altered his previous opinion, instead finding that there had been a degree of secondary generalization of the epileptic activity, spreading from the right hemisphere across to the left in the frontal region, between 4:10:32-4:16:02 am (253.1-37T, 252.21T). Dr Fong agrees that the mere presence of epileptic activity in the left hemisphere does not necessarily imply that there is generalised epileptic activity. It could, for example, be due to some spreading between the two frontal lobes by way of the bridge connections: 263.12-17T. Dr Fong agreed that the extent to which the left hemisphere was involved was comparatively minor; at no time was there GCSE or GTCS (261.1-33T).

[17]

Ms Pierce's epilepsy from 1989-2004

Ms Pierce was born 23 May 1989 to Glenda and Robert Pierce with a proencephalic cyst in the right frontal lobe of her brain, and suffered from some hemiplegia affecting her left side of her body, particularly her limbs: Exhibit F, p 2; Exhibit R(1), p 1. Professor Dunne described these matters as "tantamount to [Ms Pierce] having an ante-natal stroke" (150.5-10T). This pathology has not progressed. The professor said: "In addition [Ms Pierce] not only has this cyst which indicates an injury or disturbance in formation of the brain before birth, in addition to this the whole of the right hemisphere is shrunken somewhat and in particular the right temporal lobe. So it is a hemispheric disturbance that [Ms Pierce] has." I accept Professor Dunne's explanation and description of the pathology affecting Ms Pierce.
She began suffering from epilepsy at an early age, with her first epileptic seizure at age 6 for which she was admitted to Lismore Base Hospital on 21 June 1995. Dr Ingall prescribed anti-seizure medication: Exhibit F, p 3.
Dr Ingall's evidence will be examined in further detail below, as it bears upon the central questions in the case. However no issue is taken with his evidence as to Ms Pierce's early epileptic and general health condition prior to her teenage years, supported as it is by her own evidence which is not challenged by the defendant in this regard: 403. 30-43T.
After the first seizure Ms Pierce commenced to experience, as she puts it, "a small number" of seizures up and until around the year 1999, when she was about ten years old: Exhibit F p 3. Apart from motor seizures, from late 1997 she also reported seeing 'lines' as well as experiencing stomach problems, which prompted Dr Ingall to think that she may also suffer from migrainous tendencies as well as epilepsy. On 24 April 2003 Ms Pierce reported experiencing headaches accompanying some of her seizures as well as the 'lines'. Dr Ingall subsequently commenced her on the migraine medication Sandomigran on 16 March 2004: Exhibit R(2), p 1.
Ms Pierce's mother, Glenda Pierce, gave uncontested evidence that Ms Pierce was relatively seizure free after the initial seizure in 1997 until the onset of puberty when Ms Pierce was about 14: Exhibit G, p 3[9]. Ms Pierce gave evidence, also uncontested, that by 2006 at age 17, her seizures began to follow a more regular pattern, tied to her menstrual cycle: Exhibit F, p 3 [21]. It is the plaintiff's case that this changed after the 2010 event, contributing to the unpredictability and hence manageability of her condition: 341.31T.
Her experience of headaches, abdominal complaints and seeing 'lines' subsequently decreased, but she continued to experience ' lines' around the time of also experiencing small absence seizures; she never experienced 'lines' along with more major epileptic events or seizures: Exhibit R(2), p 1.

[19]

Who carries what onus?

The Hospital points to several seizure events in the years before the telemetry event which they say were cases of CPSE. Particular emphasis was placed upon seizures on 21 June 1995, 3 August 2005, and 10 April 2006. In fact, Professor Dunne, on his examination of the clinical records estimates that there could be as many as 10 or 13 previous CPSE events. However, he accepted that in the absence of continuous EEG data, it was impossible to be certain from the contents of hospital records whether a particular event was, or was not, an incident of CPSE. The hospital's argument about this, is that the telemetry was one incident in a number of incidents of CPSE and it is not therefore possible to be satisfied on the probabilities that the event of 5 January 2010 was of any particular significance.
It is relevant to point out that it is Ms Peirce's case that the telemetry event is the only time she has experienced a CPSE. Counsel for the plaintiff argue that the previous instances, on the evidence, are not shown to have been of the requisite duration and severity: 345.30T. Further, the known difficulties of diagnosis, particularly as no EEG machine was used to record these alleged instances, make any definitive diagnosis after the event difficult if not impossible, particularly in the context of where those attending to Ms Pierce at those times did not make the diagnosis of CPSE: 346.10T. In the alternative, Counsel for Ms Pierce argue that, consistent with their argument that Ms Pierce's illness followed a waxing and waning pattern, it is not fatal to their case that 5 January 2010 not be the only occasion of CPSE: 345.25T.
The principal line of attack taken in the exhaustive cross-examination of Professor Dunne by Mr Graham was, conventionally, to suggest other explanations for the matters recorded in hospital clinical notes, mainly by medical practitioners and other staff who were not specialists neurologists, to suggest explanations other than CPSE. An example of this is questioning to suggest that rather than the record providing evidence of a prolonged seizure, a better understanding may be that Ms Pierce was then postictal or, as I understood it, in the aftermath of a seizure. For the 10 August 2006 event considered below it was suggested that some of the symptoms and signs recorded were really due to an intercurrent illness, said to be glandular fever, rather than epilepsy. Professor Dunne generally, but not always, was prepared to accept other possibilities.
Another line of attack was that, in the absence of continuous EEG material,l at its highest the evidence may be consistent with a possible CPSE. Again, Professor Dunne was generally prepared to accept that description, although he was obviously of the view there was a degree of probability in the evidence suggesting previous CPSEs.
Mr Graham relied upon Watts v Rake (1960) 108 CLR 158; (1960) HCA 58 and Purkess v Crittenden (1965) 114 CLR 164; [1965] HCA 34 to argue that the Hospital bore an evidential onus of establishing that the prior events were instances of CPSE. That is to say, that the Hospital bore the burden of introducing evidence that Ms Pierce's condition was wholly the result of her pre-existing epilepsy.
Mr Graham argued by reference to the plurality judgment in Purkess v Crittenden (at 168) that it was for the hospital to adduce evidence which: "…if accepted would establish with some reasonable measure of precision, what the pre-existing condition was and what its future effects, both as to their nature and their future development and progress, were likely to be." As I understood the thrust of the argument, something that was merely possible did not rise to the required "reasonable measure of precision".
I think, however, this argument, with respect, is misconceived in the circumstances of the present case. This is not a case where a plaintiff suffered from an asymptomatic, perhaps unsuspected pre-existing condition which had been rendered symptomatic by reason of the defendant's negligence. There is no issue that Ms Pierce suffered from pre-existing symptomatic epilepsy. The issue was whether her epilepsy waxed and waned on a more or less constant plane or, overall, it was progressing and deteriorating.
In a case such as the present, the principle in Purkess v Crittenden has no real work to do, especially given the provisions of s 12 CLA. Really, "it is for the plaintiff upon the whole of the evidence to satisfy the tribunal of fact of the extent of the injury caused by the defendant's negligence": at 168. To the extent then that any previous incidents of CPSE may be relevant to the question whether Ms Pierce suffered a detrimental difference by the hospital's negligence it is for Ms Pierce to exclude possible prior events of CPSE from the evaluation of the probabilities, if she could, or otherwise establish that any previous incident was probably no more than incidental, proving nothing about the probable consequences of the events of 5 January 2010. In the end all she was required to prove that probably there was a detrimental difference caused by the Hospital's negligence.

[20]

21 June 1995 event

The 21 June 1995 seizure was the first such event. Ms Peirce was found by her mother around 8 am, on the floor next to her bed. The left side of her body was rigid and twitching. She retained consciousness and the ability to converse. This lasted about an hour; with the symptoms diminishing after 2.5 mg of intramuscular Valium was administered by ambulance officers who collected Ms Pierce at 8:59 am (Exhibit N, H4). On admission to the Lismore Base Hospital, Ms Pierce had a right-sided headache and was vomiting. The nursing notes from the emergency department record a loss of consciousness, but no indication of when specifically this occurred and for how long (Exhibit N, H5). An EEG carried out the day following by Dr Alison Reid, shows "very high voltage right hemisphere slow delta components with focal sharp activity in the right frontal region…The left hemisphere is mild to moderately abnormal for the age. The Right hemisphere is diffusely severely abnormal with an epileptic focus in the Right frontal region" (Exhibit N, H22).
Professor Dunne is of the opinion that on the clinical evidence, this seizure as recorded in the clinical notes is consistent with a classification of CPSE of about 1 hour (Exhibit 1.2, p 6; 198.2T).
There is a note in the hospital records of a respiratory infection, which Professor Dunne agrees could have triggered the seizure, or rather, could be the cause of Ms Pierce's fever, rather than it being consequential on, or related to, the seizure activity (198.10-19T). Professor Dunne also concedes that it is not possible to be exact about the length of the seizure activity due to the lack of specific notes about this in the records. But he maintained his opinion of the length of this seizure by reference to the timing of the ambulance call at 8: 41 am, 41 minutes after Ms Pierce was found by her mother, although admitting that this involves a degree of speculation (199.1-4T).
I think it important to bear in mind in relation to this matter, that this was the first event, when Ms Pierce was just 6 years old, which lead to the diagnosis of epilepsy. Professor Dunne's opinion is wholly based upon an assumption that Ms Pierce had a prolonged seizure during the period between 8 am when she was discovered by her parents and 8:41am when the ambulance was called (198.45-199.5T). By the time she arrived at the hospital and was examined by a doctor at about 9:30 am the seizure, as I understand his evidence, had long settled (198.30-40T). Professor Dunne agreed that "it is speculative to assert that there was (CPSE) of about an hour" because the records are not clear (199.10T). It seems to me that notwithstanding the record of an improvement after an injection given by the ambulance officers, there is just too much uncertainty about this incident to have any confidence that it may even possibly had been CPSE and I am satisfied that the plaintiff has excluded this as an incident of CPSE. It was undoubtedly a significant complex partial seizure.

[21]

3 August 2005 event

Ms Pierce was again admitted to Lismore Base Hospital on 3 August 2005 following a seizure at her aunt's house, commencing at 2:30 pm. An ambulance was called, with Ms Pierce experiencing a second seizure while en route to hospital; 3 mg of midazolam was administered by the ambulance staff. Each seizure was approximately ten minutes in duration. She was said to be unconscious on arrival at 3:19 pm, but was rousable; further notes were made of muscle twitching and nystagmus and a Glasgow coma Scale of 3. She received five doses of intravenous midazolam between 3:50 pm and 4:15 pm. She received 500 mg of phenytoin at 9 am the following day, improving after this medication was administered. (Exhibit N, H169-1722). Later that day she underwent an EEG, which according to Dr Alison Reid, neurologist, showed : "The left hemisphere is essentially normal. The right hemisphere is diffusely moderately abnormal being dominated by slow unstable high voltage activity. The right hemisphere looks potentially epileptogenic, although there are no actual spike wave discharges present" (Exhibit N, H185)
Professor Dunne expressed the opinion that this record was consistent with Ms Pierce being postictal, and that the hospital notes suggest that what had occurred was a seizure event of at least 2 hours, perhaps longer, with the symptoms suggesting that it was consistent with CPSE; that is, that this is the probable diagnosis: Exhibit 1.2, p 10; 199.28T.
Under cross-examination, Professor Dunne accepts that the hospital and ambulance notes are such that no definitive diagnosis is possible. For example, it unclear whether only one, or two seizure events of ten minutes occurred prior to the seizure in the ambulance; and her state in between the seizures is unclear: 205.7T; 205.14-18T. He relies on the fact that she arrived at the hospital in an unconscious state; and that the successive administration of 5 doses of midazolam within a 25 minute period on arrival in hospital, and prior en route in the ambulance, to suggest that there was no improved state of consciousness or improvement to the twitching and nystagmus, and hence an ongoing uncontrolled seizure state: 208.14T. CPSE is defined as "either a prolonged or recurrent seizure state in the absence of recovery over a period greater than 30 minutes": 207.5-16T. Further, the noted ongoing confusion and subsequent improvement after the administration of phenytoin the following morning is further consistent with this diagnosis: 208.36T.
Mr Graham took issue with Professor Dunne's conclusions on several grounds. Underpinning his argument is the point agreed to by Professor Dunne, that is, that his conclusions cannot be positively and definitively established without a more complete history and EEG recording of the seizure activity; postictal recordings are insufficient: 208.41T. He further argued that Professor Dunne failed to appreciate the confounding factor of Ms Pierce's glandular fever at the time, both as a trigger for the seizure event and as a possible explanation for her vagueness and confusion, rather than the epileptic activity: 209.36-40T. He further criticises Professor Dunne's "intuitive synthesis" of the information in the formation of his opinion. He argued that he did not adequately set out what specifically he relied upon when coming to his conclusion, which makes his opinion difficult to scrutinise: 371.28-39T. Further, Professor Dunne failed to contextualise this seizure event in his report, namely, that Ms Pierce had otherwise been seizure free since April 2004, and had over the last three weeks been suffering from glandular fever: 205.44T.
Professor Dunne did agree that it was "supposition [on] supposition" to rely on the clinical notes "to say this is ongoing seizure activity indicative of status epilepticus" (205.30T). He agreed that Ms Pierce's unwellness, due to suspected glandular fever or some other viral illness, may account for some of the clinical signs and be a confounding factor. However he said he "synthesised" the information available to him and formed the opinion that "this is an episode of status epileptucus"
In accordance with Ramsay v Watson, there are occasions when an expert can form an opinion by the process of inference. But I accept the force of the argument advanced by Mr Graham that generally the hospital records treat Ms Pierce as being postictal. Rather than ongoing seizures, there seems to be two seizures, each of ten minutes, the second in the ambulance when Ms Pierce was being brought into hospital and perhaps a third between 3:50 pm and 4:15 pm when she was treated with a series of Midazolam shots. This is a period of 25 minutes. None of these three discreet events, if that's the better view, was of greater than 30 minutes necessary to satisfy the accepted definition of status epilepticus. An earlier shot had been given 3:05 pm upon arrival at the hospital, but as I have said, the clinical notes then said Ms Pierce was postictal. Professor Dunne seems to have treated the whole episode commencing at about 2:30 pm until at least 4:15 pm as an ongoing episode (207.5T). Dr Fong was not cross-examined about each of these incidents on the basis that there was no dispute about the underlying principles, only about whether the evidence engaged them.
I think it appropriate to take the records at their face value. On this approach, I am satisfied that the period of seizure activity for each seizure suffered on this day demonstrates that Ms Pierce did not suffer an episode of CPSE. Arriving at this conclusion I have given respect to Professor Dunne's intuition as an eminent highly experienced neurologist. But I am satisfied on the balance of probabilities that although there were a series of seizures on this particular day they did not individually or together amount to an episode of CPSE.

[22]

10 April 2006 event

Ms Pierce experienced what Professor Dunne considered was a status epilepticus, at 5.30 pm on 10 April 2006. An ambulance was called and while still at home, her father administered rectal diazepam. While in the ambulance en route to Ballina District Hospital, ambulance notes record that Ms Pierce suffered a focal seizure, which lessened in severity after the administration of 5 mg intramuscular midazolam. She arrived at Ballina District Hospital in a postictal state at 6:47pm, where she remained until 9:30 pm when she was transferred to Lismore Base Hospital: Exhibit N, H281-282. The notes from Ballina record that Ms Pierce vomited five times while in attendance there. While en route to Lismore Base Hospital she experienced a left sided seizure at 10 pm, characterised by left arm and leg shaking; 10 mg of midazolam and an intravenous phenytoin infusion were administered. The notes also record that there has been a change in Ms Pierce's medication from Topomax to Keppra on the previous Saturday: Exhibit N, H281.
Ms Pierce is said to have regained consciousness between seizure activity. She was seizing on arrival to Lismore at 11:30 pm, when further 10 mg of rectal diazepam and intravenous phenyotin infusion were administered; she was conscious during these seizures. Ms Pierce was then transferred to the intensive care unit at 11:45 pm as her seizure activity was not responsive to medication. There she was given another course of intravenous midazolam and a midalzolam infusion. There was at that time ongoing "small seizure activity", sinus tachycardia and fever. The activity settled following the midazolam injection, eventually ended at 2 pm on 11 April; however there is further record at 4:15 am of the Plaintiff being unresponsive, not obeying commands, being agitated and uncooperative and having a temperature of 38.9 degrees Celcius although the records report her having been seizure free since 2:00 am: Exhibit N, H242-43, 248, 249. She was transferred from ICU to the wards at 1:40 pm on 11 April: Exhibit N, H250.
Professor Dunne was of the opinion this episode was one of CPSE of at least 8 and one hours duration. The discharge summary (Exhibit N, p H243) proffered a diagnosis of "status epilepticus unresponsive to Benzodiazepine and Midazolam". Notes suggest that having been taken to Ballina Hospital suffering from an earlier seizure she was transferred to Lismore Base Hospital where she was said to be postictal. At about 10:35 pm she started having a seizure; she appeared to be still fitting when examined by the paediatric registrar Dr Baxter at about 11:30 pm and he formed the impression that Ms Pierce was suffering an acute left focal seizure. A nursing note recorded at 11:50 pm records that she continued to fit which may have "halted" (Exhibit N, p H243) when she was admitted to ICU at about 11:45 pm after receiving further treatment. The notes suggest that the last seizure activity was observed at around 2 am.
Professor Dunne regards this as "by far the worst seizure event suffered by the plaintiff" (Exhibit 1.1, p 26).
Dr Fong thought the narrative of the events of 10 April 2006 were suggestive of CPSE (280.15-35T), but he explained (at 281.10-15T): "… without an EEG it would not be possible to determine the duration of the CPSE because she might have clusters of seizures and intermittent postictal period after each seizure which we don't know whether it's the postictal phase or ongoing CPSE." He also agreed that if it could be established that there was a period of status epilepticus lasting 8 and a half hours, it would be against his theory of the case that the January 2010 incident is the most significant matter.
It is convenient to also record here that he said of the 2006 event (282.30T): "If it were fair to say that she had previous CPSE of similar or longer duration, I would expect they would have some effect on her subsequent seizure frequency, but taking the admission in 2006 during which she was admitted to ICU this was not followed by a dramatic increase in seizure frequency, so at that rate, some doubt as to whether that admission is a long or prolonged CPS. That could be a short CPSE with some prolonged postictal period which we are not too sure about the duration."
I am not satisfied that Ms Pierce, on all of the evidence relevant to it, has excluded this event as a previous CPSE. But for the reasons Dr Fong gives I am satisfied that it should not be regarded as a continuous CPSE event of 8 and one half hours duration. Giving full faith to the clinical records, I am satisfied that the plaintiff has proved that the duration of that event did not exceed about 1 hour and 25 minutes between 10:35 pm and around the time of her admission to ICU at about 11:50 pm when effective medication was administered. The earlier seizure which caused her presentation to Ballina Hospital and the later seizure noted around 2 am by nursing staff were probably isolated complex partial seizures of less than 30 minutes duration.
When one reviews the primary seizure diaries, clinical records and histories recorded by treating specialists over the years, it's difficult to be satisfied that there were no other instances of status epilepticus in the years leading up to 5 January 2010. The records of Ballina District Hospital for 5 December 2009 contain the following record: Has had an episode of status epilepticus, vomiting with aspiration and admission to ICU with ventilator support in the last 12 months. I have been unable to locate records of such an admission and it's probable that this is a reference to the admission of 10 April 2006. There appear to have been ten attendances, or admissions, to Ballina Hospital in 2009. On my review of that material, I have not located any admission involving treatment in the intensive care unit. Even so, as I have said, there may well have been other events properly fitting the definition of status epilepticus. I am satisfied, however, that none of these events were of the same long duration and intensity as the telemetry event of January 2005. I accept the evidence of Dr Fong that generally speaking, a medically induced, or "activated seizure tends to be much more severe and also more prolonged and more likely to result in a status condition" (273.5T).

[23]

Medication changes

It's quite clear from the history and the opinions of the specialists (see for example Exhibit 1.2, p 27) that Ms Pierce's epilepsy is drug-resistant or medically refractory in that she has continued to have seizures (before and after January 2010) despite trials of various anti-epileptic drugs. Professor Dunne is of the view (Exhibit 1.2, p 28): "[Ms Pierce's] young age at seizure onset, known structural cause of the epilepsy, focal seizures (simple or complex partial seizures), neurodevelopmental delay, epileptic EEG abnormalities seen on her first EEG in 1995, and the failure of initial AEDs are all predictive of seizure intractability. [Ms Pierce's] structural lesions (porencephanic cyst and hippocampal sclerosis) strongly predicted drug-resistant epilepsy. [A 1985 study] study found seizure control was achieved in only 11% of those epilepsy associated with hippocampal sclerosis, and only 1 patient in 44 with dual pathology (hippocampal sclerosis and another lesion)."
This medical opinion appears to be borne out by Ms Pierce's evidence (Exhibit G, p 7[34]) that from 2008 it had become apparent that Ms Pierce's medications were regulating her seizures (but not ridding her of them). In her statement (Exhibit F, p 6 [29]) Ms Pierce said she was taking AEDs twice per day, but still suffering seizures "around every four to six weeks" (p 5 [39]). Nor did I understand Dr Fong to disagree that Ms Pierce's epilepsy was drug resistant, in fact, quite the contrary.
A review of the clinical material in general terms bears out Professor Dunne's diagnosis. I was left with the clear impression that Ms Pierce's medication was frequently changed in the years between about March 2003, when seizures seem to have recommenced, and January 2010. These changes were principally related to what I would describe as a spike in seizure frequency from time to time over the years. I did not have the impression that seizures were entirely regular, although I accept that Ms Pierce and Mrs Pierce frequently reported that seizures were related to Ms Pierce's menstrual cycle. The impression I have formed is that a number of seizures occurred within a relatively short space of time. There would be a modification in the medication prescribed which would help for a period of time during which Ms Pierce would be relatively seizure free or at least her seizures were reasonably controlled. In this context I am speaking of the focal seizures and leaving to one side entirely the lines or simple partial seizures. Sometimes a change in medication might itself be provocative of seizures. Sometimes medication would be changed because Ms Pierce suffered unpleasant side-effects. Whatever was tried was not successful for very long. In this sense therefore it could be said that the activity of her significant seizures waxed and waned, but there did seem to be something of an increase in significant seizure activity during 2009. This may have been related to a number of different factors including as she matured and Ms Pierce sought greater independence, her social activities away from the watchful eye of Mrs Pierce were provocative of further seizures.
It is worthwhile here recording that notwithstanding the vigilance of Ms Pierce and Mrs Pierce and their strict compliance with the prescribed medical regime, the best recovery from significant seizures was obtained by intramuscular injections of Midazolam. I am satisfied that Mrs Pierce was not trained in administering these until after the telemetry event and probably sometime in 2011. For this reason when a significant seizure occurred notwithstanding treatment with oral and suppository medication, an ambulance was called and the paramedics, generally, administered intramuscular Midazolam. Even if Ms Pierce recovered fairly quickly following the injection this generally involved a trip to hospital. Hospital attendance therefore is not necessarily an indicium of the severity of the event. Their decline since Mrs Pierce became adept at administering the injections is not a marker of a general improvement in Ms Pierce's condition.
In her statement (Exhibit F, p 6 [29]) Ms Pierce said she was taking AEDs twice per day, but still suffering seizures "around every four to six weeks" (p 5 [39]). I did not understand Dr Fong to disagree that Ms Pierce's epilepsy was drug resistant and I will proceed on this basis.

[24]

Ms Pierce's experience of "lines" and their significance on the epileptic spectrum

Ms Pierce has experienced seeing "lines" from 1997. This involves her vision becoming affected by "wriggly lines", accompanied by a sense of "feeling detached, quiet, vague, but otherwise totally conscious". Such experiences are transitory, lasting only several seconds without any lingering side effects, and would not be observable to another person: Exhibit F, p 3. For a period prior to puberty, they would occur on an almost daily basis, while at other times she would not experience them for periods of weeks or months: Exhibit F, p 3. Mrs Pierce gave evidence that her daughter did not exhibit externally observable signs of the lines; there may be a brief pause in conversation, but not to the extent that Ms Pierce lost track of a conversation: "it was just like she had missed a beat": Exhibit G, p 7 [39].
Dr Ingall agrees that this description of the lines is consistent with the history he recorded: 314.12T. When Ms Pierce first reported experiencing lines in 2004, Dr Ingall thought they were associated with a possible migrainous condition as discussed above. He considered that the concurrent onset of abdominal discomfort and visual disturbance were key symptoms of a migraine condition in children: Exhibit R(2), p 1. After the commencement of her migraine medication in 2004, Dr Ingall recognised a decrease in Ms Pierce's experience of headaches, abdominal and visual symptoms (315.21T) although she would still experience lines around the time of what he then regarded (wrongly) as absence seizures. Ms Pierce gave evidence that, more generally, her experience of lines changed following on from changes in medication: Exhibit F, p 3. Dr Ingall considered that there was possibly an overlap between the experience of lines related to her migraines and those related to her epilepsy. Her improvement with migraine medication indicated that this was likely, as that medication would not be effective against epilepsy symptoms: 315.14-24T.
Ms Pierce never reported to Dr Ingall experiencing these lines immediately prior to the onset of her major seizures and hence he concluded that, in comparison with her more serious seizure events, they had relatively little impact on her quality of life and function: Exhibit R(2), p 1-2. In treating her epilepsy, Dr Ingall drew a distinction between those symptoms that had a major impact on her life, and those that only affected her in a minor way. He classified major events as involving some "large motor component of some description, whether its focal or generalised and loss of consciousness, or a large considerable change in consciousness and then taking some time, hours to days, to recover from", with the minor events having a relatively little effect on her functionality, such that she is able to rapidly continue on at her task or activity, after their brief occurrence: 314.33-44T.
In his report of November 27 2014 (Exhibit R(2)) Dr Ingall refers to the occurrence of lines about the time of small absence seizures: p 1. In examination in chief he clarified his use of this language, saying that it would be more accurate to refer to them as minor seizures, as they were associated at the time with "short changes in levels of consciousness" (315.3-11T) or simply partial seizures under the contemporary nomenclature: 314: 19T. He ascribes this slight change in classification as being a consequence of the usual difficulty of diagnosis in the situation of imperfect knowledge (315.5-7T), alongside the consideration that such instances were not otherwise impacting on Ms Peirce's functionality and so of less clinical importance at the time: Exhibit R(2), p 2.
In a slight difference from Dr Ingall's evidence, Ms Pierce gave evidence that, prior to January 2010, she would experience lines prior to a seizure, which functioned as a warning for a more serious epileptic event. There was otherwise little change between her experience of lines prior and post the 5 January 2010 incident: Exhibit F, p 3.
Counsel for the plaintiff found her case on the change in "the frequency and character of the complex partial seizures". Hence to the extent that there is any evidence of a change in Ms Pierce's simple partial seizure, or "lines" , it is not relied upon in the plaintiff's case to establish a change in severity or frequency of her seizures: 341: 6-11T. However , the plaintiff does say, to the extent that a change in the presence of the lines prior to a complex partial deprives her of a warning of the onset of such an event, it goes towards demonstrating a negative impact on her functionality, with this lack of warning attending after the telemetry event making her complex partial seizures more difficult to manage: 341.12-19T.
Dr Ingall's description of the "lines" as absence seizures is with respect clearly incorrect. This is perhaps not surprising given that notwithstanding his involvement as the primary care giver for Ms Pierce's epilepsy for so many years, he is a paediatrician, not a neurologist. As I understand the evidence absence seizures involve a brief loss of consciousness. Ms Pierce's description of her "lines" does not include this difficulty. It is quite clear, as I have said in the previous paragraph that the lines are simple partial seizures. There is some debate between Professor Dunne and Dr Fong about the significance of these matters as a marker of the severity of Ms Pierce's condition. Dr Fong referred to the lines as "visual auras" and pointed out, like Dr Ingall, that one needs to distinguish between migrainous auras and epileptic auras (Exhibit L, 2 [6]). Dr Fong was of the view that these auras "are often mild and non-debilitating" they may not be epileptic in nature. He was of the view they "should be excluded [from] the evaluation of her overall seizure frequency and severity".
Professor Dunne regards the "lines" as simple partial seizures (169.1-7T). Whether or not the visual symptoms were counted in a calculation of seizure frequency prior to January 2010 and thereafter, Professor Dunne regarded them as epileptic, sometimes associated with other symptoms including an inability to speak or epileptic left focal motor activity (Exhibit 1.4, p 4 - 5).

[25]

Seizure diaries

Mrs Glenda Pierce began keeping a seizure diary for Ms Pierce's seizures from 2003, on the recommendation of a member of the Epilepsy Society. Ms Pierce's seizures were written into the general "Kitchen Diary" in which all members of the family would write their appointments. Mrs Pierce then transcribed these entries into a diary provided by the Epilepsy Society, which she took to Ms Pierce's medical appointments. When she wasn't present for the seizures, Ms Pierce would inform her of them and they would similarly be duly recorded: Exhibit G, p 5 [25].
The intended purpose of the diary was to make a record of Ms Pierce's epilepsy as an aid for best managing her condition. From this, patterns, triggers and reactions to medications could be observed, and the management of her illness managed accordingly: Exhibit G, p 5 [26]. But the diaries are a family record, not a clinical record. They sometimes contain entries relating to other family members. And meticulous as Mrs Pierce sought to be they probably are affected by errors and omissions.
Mrs Pierce gave evidence that entries were made usually as soon after the seizure as possible, and all attempts were made to ensure they were as accurate as possible. She acknowledges however that she did not always record when there were a series of seizures in quick succession. In recording such instances, Mrs Pierce was more concerned with the day of the seizure activity, and its start and end time in terms of the whole of the seizure activity, rather than individual episodes: Exhibit G, p 5 [32].
She remembers sometimes taking note of successive seizures in the period prior to 2010 when it involved trialling new medication. For example, sometimes administering oral midazolam would mean that Ms Pierce would be quite well for a time, before later experiencing a further seizure. Mrs Pierce gave evidence that she was therefore more likely to make a record of this. She would also more likely record individual seizures in succession where there was a time lapse between the seizures: Exhibit G, p 5 [32]. She was further asked by Dr Lander during their first consultation on 18 November 2008 to keep very detailed records of Ms Pierce's condition, including such things as side-effects, their nature and severity, frequency and her experience of "lines". This was because Dr Lander was in the process of making some changes to Ms Pierce's medication regime, and this information would be useful in monitoring their effect. After this consultation Mrs Pierce began a separate diary for the purposes of Dr Lander, recording both the seizures and episodes of lines: Exhibit G, p 7 [35]-[37].
The seizure diaries were relied upon significantly by both parties during proceedings. The Hospital does not challenge the truthfulness of any of the evidence of Ms Pierce and Mrs Pierce, including the diaries. Rather what is in contention is what these records can be taken to mean, and what inferences and conclusions can be drawn from them. Seizure diaries provide an important primary record in conjunction with the clinical notes of medical practitioners, in particular hospital records, as to the frequency of seizures. These provide an important part of the before and after picture for assessing the existence, and extent, of any detrimental difference in Ms Pierce's condition because of the negligence of the defendant.

[27]

Summary of the submissions of the parties

To make her case that her epilepsy changed for the worse because of the negligence of the defendant, Ms Pierce relies upon the following circumstances: 1. Her unchallenged evidence and that of her mother as to the temporal connection between the telemetry event and an increase in the incidence, and change in the nature, of her seizures; 2. The contemporaneous evidence from the primary records provided by clinical notes and seizure diaries of the number of seizures before and after 5 January 2010; 3. The opinion of Dr Fong as to the temporal connection and the scientific possibility of a connection existing; 4. The concessions by Professor Dunne that a connection is possible; 5. The evidence of Dr Rowe as to the particular nature of Ms Pierce's cognitive deficits and the timing of the onset; and 6. The evidence of Dr Ingall as to the change in Ms Pierce's condition following the telemetry event.
The Hospital relies upon the opinion of Professor Dunne that any worsening evident after the telemetry event is entirely consistent with what one would expect of the natural progression of the condition. It points to what it submits is an absence of objective evidence of change in Ms Pierce's functioning in the activities of daily life. The Hospital challenges the reliability of the diary entries as a basis for comparison of Ms Pierce's condition before and after January 2010, particularly in light of what it submits is the incomplete nature of the record: 403.30-43T. As mentioned above, what was recorded varied over time. As the record was that of lay people it lacked clinical focus, even accepting that Mrs Pierce, the principal record-keeper, was diligent and astute with the closest interest in Ms Pierce's wellbeing, she is not a medical expert. If the record is accurate, the Hospital argues that the seizure diaries show that while there was some apparent worsening during recovery from the January 2010 event this was temporary: Ms Pierce soon resumed a regular work routine (407.32-408.12T; 409.12-31T; 411.1-31T); retained the "advantage" of recognisable triggers for her seizures (409.13T; 410.11-17T; 411.35-37T; 412.36-50T; 412.18-24T); was able to return to work on the day following a seizure (410.36-50T; 412.34-39T); her new medication regimes of intra-muscular injections of Midazolam and Frisium had reduced the severity of her seizures and their recovery time (413.6-12T); and her seizures still occur mainly at night (414.6-12T).
Mr Graham joins issue with the interpretation of the seizure diaries by Mr Glissan. Specifically, in respect of the conclusions he draws from them in respect of Ms Pierce's capacity to continue to work in the period after the telemetry event, her travel and social activities and the perceptibility of triggers: 433.3-39T.

[28]

Assessment of the lay evidence

Ms Pierce's case is that there was an abrupt change following the telemetry event. This manifested itself in a number of ways: the seizures became more frequent; they were of more sudden onset, without warning; the apparent connection with the menstrual cycle was broken; they occurred more frequently during the day, rather than mostly at night; they are less regular, often separated by only a few days; the "lines" are experienced more randomly rather than being related to changes in medication or as a warning of a seizure; and the period of recovery is longer: Exhibit F, [59] - [72]. This evidence is largely corroborated by that of Mrs Pierce: Exhibit G, [12], [21], [63] - [65]. Moreover the primary records indicate that Ms Pierce suffered seven seizures between the telemetry event and her consultation with Dr Ingall on 15 April 2010. On four of these occasions she was taken to hospital. According to the seizure diaries and hospital notes the dates are 15 January, 24 January, 12 February, 2 March, 21 March, 5 April and 13 April 2010. Moreover, as the increased frequency of Ms Pierce's significant seizures after January 2010 shows (see below) she continues to suffer from far more significant seizures each year than formerly.
The difficulty is, as the hospital submissions demonstrate, there are few other objective markers of a significant worsening of Ms Pierce's epilepsy. There are more, in my view many more, significant seizures after January 2010, but no real change in the pattern of them, whether day or night, or identifiable precipitants.
Ms Pierce and Mrs Pierce's description of the change in the nature and quality of the seizures, leaving aside frequency, is largely subjective. As was put, their evidence was largely unchallenged, and I do not doubt for a moment their sincerity as witnesses, but not all of the changes they describe are borne out by the primary contemporaneous records.
It would be wrong and contrary to the evidence to conclude that Ms Pierce's epilepsy was not a very debilitating condition prior to 5 January 2010. It is well to remember that the epilepsy is part and parcel of an ante-natal brain injury leading to malformation of aspects of the right side of the brain and a degree of left sided hemiplegia which latter condition itself required treatment. Although Ms Pierce, very much to her credit, strove to lead a "normal" life, there were significant difficulties, mainly due to her epilepsy. She was naturally bright but needed the assistance and encouragement of her devoted parents to complete her school work. Dr Ingall at different times sought extra consideration for her in assessments due to the effects of her epilepsy, including some cognitive difficulties. He recommended that she did not sit her school certificate examinations because of the difficulties she was then having. She did, however, obtain her school certificate. She left school and undertook a course at TAFE, again with the assistance of her parents and in particular her father. She was able to hold down, more or less, a full time job, but it must be said only with understanding employers. And she did from time to time during the day suffer seizures at work, which I suspect may have strained the employment relationship with a less than understanding employer. She was able to gain entry as an undergraduate to a Bachelor of Arts course at Southern Cross University, but again by limiting her endeavours to one or two subjects per semester. Her father devoted time to encouraging and assisting her with her course.
She was anxious to get her licence and by importuning Dr Ingall persuaded him that she was a suitable candidate at least for a daylight-hours licence. I interpolate its clear on the whole of the evidence, including that of Dr Ingall that she never really was eligible for such a licence because of her condition. But it was important to Ms Pierce that she makes the attempt as part of her normal life. As has been pointed out by the Hospital, she persisted in this after January 2010 and again prevailed upon Dr Ingall to certify her as suitable, and again against his better judgment. She did not obtain a licence.
Like any young person her age, she went out at night, and away for weekends (including to Melbourne) with friends. After the telemetry event, to better accommodate her work she moved out of home for a time to shared accommodation with friends in Byron Bay. Each of these endeavours, which took her outside her normal protective zone, was provocative of seizures.
All of these circumstances demonstrate the real limitations upon her activities of daily life to which Ms Pierce was subject by her epilepsy before January 2010. This is referred to in the evidence sometimes as "the burden of epilepsy".
From these matters it is quite clear that even before the telemetry event Ms Pierce had not achieved that level of independence in life for which she so admirably and assiduously strove.
As it is necessary for me in assessing whether there has been a detrimental difference caused by the negligence of the Hospital to compare the outcome obtained with that which would have been but for that negligence, it is relevant to consider what her prospects were for succeeding in her endeavours in the future, adjudged from the date of the telemetry event. In my judgment it is unlikely that Ms Pierce would have managed to do better in the future. I say this because of the intractable nature of her disease. There is simply no evidence that her condition was likely to improve but for the hospital's negligence. Rather the expert evidence suggests that at best her condition would have continued to wax and wane, probably deteriorating slowly over the years. It is at least highly possible that Professor Dunne's more pessimistic prognosis is correct. That is to say that Ms Pierce's condition, given its resistance to medical treatment was, and would continue, progressively worsening.
In making this finding, I have taken into account that when Dr Lander was first consulted on 18 November 2008 Ms Pierce was seeking "treatment to be "normal" to be free of epilepsy, to be able to drive and live a normal life." (Exhibit M, p TDR310). In his letter dated 28 November 2008, (Exhibit 4.1, p I44) Dr Ingall recorded that Ms Pierce expressed frustration with her then "life situation". Dr Lander had ordered a MRI scan of Ms Pierce's brain. During their second consultation Dr Lander mentioned Professor Sam Berkovic of Melbourne "who is having success treating patients with epilepsy through neurosurgery" (Exhibit F, p 5 [41]). Ms Pierce was interested in exploring this "as [she] was very keen to see if [she] could cure [herself] of [her] epilepsy so [she] could live a more normal life." Dr Lander agreed to write to Dr Berkovic. In her letter to Dr Ingall on 10 March 2009, Dr Lander referred to the porencephalic cyst and mesiotemporal sclerosis shown on the MRI scan. As I have said previously I infer from her report (Exhibit 4.1, p I143-I144]) that the latter feature had not been detected previously. I mention it again for the sake of the narrative. Dr Lander said "it's difficult on this picture to say exactly where her epilepsy arises". Dr Lander also thought an apparent increase in significant seizures during the early part of 2009 may have been due to the fact that Ms Pierce had been able to increase her working hours to 40 hours per week and was finding it very tiring. Dr Lander commented that 40 hours "sounds like rather a lot for her with her burden of illness". She thought Ms Pierce's hours should be reduced if the employer would agree. Ms Pierce, in her determined way, persevered.
In response to Dr Lander's inquiry, Professor Berkovic replied, after weighing the pros and cons of surgery in Ms Pierce's case (Exhibit 4.1, p B13): "Thus she is not a particularly good surgical candidate, but if the motor attacks are quite disruptive then it may be worth doing a pre-surgical evaluation to see whether a simple solution could be found that would have a low risk of worsening her motor defect." It was this suggestion which eventually lead to the telemetry EEG at the hospital.
Ms Pierce consulted Dr Lander for the third time on 20 July 2009. In her statement (Exhibit F, p 5 [42]) she says that while Dr Lander informed her that Professor Berkovic thought she may not be a suitable candidate for neurosurgery, Ms Pierce remained anxious to see him. This account is somewhat amplified by Dr Lander's letter to Dr Betts who had re-referred Ms Pierce to the former. Dr Lander reported to Dr Betts that Ms Pierce "has not been well in the last few months". Indeed she received a history of five seizures in four months, the last two of which occurred one week apart. I interpolate, this was why Ms Pierce was re-referred. Dr Lander reported that Ms Pierce "is getting a bit desperate and would like to consider surgical options". She stated that she agreed that Ms Pierce was "not a particularly good surgical candidate". Her own view was that the chance of a surgical cure was "unlikely, but [Ms Pierce] is keen to at least have a consultation with Professor Berkovic and discuss this option further".
2009 continued to be a bad year with more frequent significant seizures than previously, bearing in mind what I have said about hospital attendance as a marker of severity. When Ms Pierce saw Dr Lander again on 26 October 2009, the prospect of surgery was again raised (Exhibit F, p 6 [43]). Dr Lander suggested the telemetry EEG to "see if we can decide whether the epileptic events all come from the same focus" (Exhibit 4.2, p LH 93).
Ms Pierce saw Dr Lander after the telemetry event, on 15 February 2010, for a follow-up. The latter records that the telemetry EEG "was a quite a difficult time and [Mrs Pierce] was unhappy with the management at Royal Brisbane." Dr Lander thought that the focus of the seizure came from the right-temporal region where Ms Pierce's obvious defects are situated, but added that for much of the prolonged seizure "the whole right hemisphere is involved". This consideration made her "hesitant" about the prospect of a good outcome from surgery, but she would follow-up with Professor Berkovic. There was again some adjustment of the medication prescribed for Ms Pierce.
Dr Lander sent the telemetry results to Professor Berkovic and expressed her pessimism about the prospect of surgery. Professor Berkovic agreed "that it is a nasty focal seizure". Like a good surgeon perhaps, he expressed optimism about "successful seizure surgery" and suggested a consultation in person in Melbourne. I think it a fair inference that Dr Lander passed this information onto the GP for what it was worth but without any particular enthusiasm for the idea (Exhibit 4.1, p LH 79).
The greater frequency of seizures continued throughout 2010. There is certainly some evidence that not only were they more frequent than formerly, but more intense and longer lasting. For example, on 7 June 2010 a seizure which commenced at home at 8:30 pm, is recorded in the notes of Ballina Hospital as initially lasting 15 minutes. There seems to have been a further seizure on arrival at the hospital and the notes are suggestive of continuing seizure activity for a number of hours (MFI 10, p 90; Exhibit U p61-2). On 2 July 2010 Ms Pierce told her GP that the seizure activity was worse in recent months and described an episode lasting 6 hours which was probably that of 7 June 2010. Another example is an episode occurring on 29 September 2010 when she was in Townsville which persisted for one and one-quarter hours until she was treated with intravenous Midazolam.
This was the context in which she saw Professor Berkovic at the end of September, or start of October, 2010, soon after the Townsville incident. I interpolate that in her description of her condition to Professor Berkovic, Ms Pierce did report a vague premonition of the onset of seizure with an aura and some jerking which enables her to lower herself to the floor. The attacks continue unless they are "aborted with Benzodiazepine (and) sublingual Midazolam". Ms Pierce told Professor Berkovic that most of the seizures occur in the evening; sometimes they occur during the day. Menstruation was a precipitating factor or occasionally if she has a late night with friends.
Notwithstanding his somewhat bullish attitude in the correspondence with Dr Lander, Professor Berkovic explained that no surgical cure could be offered. He advised that before any surgical treatment could be offered, further intracranial monitoring with subdural strips was required involving "a minimum of two operations, a long period in hospital and no guarantee that surgical treatment would be offered". Ms Pierce was not prepared to take the risk of worsening her left hemiplegia. Professor Berkovic explained to Dr Lander that any surgery would probably involve a large resection entailing "significant risks of a worsening neurological deficit".
From Professor Berkovic's opinion, it seems quite clear that the prospects of surgery were at the very best, very doubtful, if not bleak, and that Ms Pierce was unlikely to achieve better independence and a more "normal" life.
The contemporaneous documents I have just surveyed make it clear that there was no real change at least by October 2010 in Ms Pierce's understanding of the pattern of her symptoms at the time based upon her experience over many years. She was certainly very aware of an increase in their frequency. At a simple level, given their increased frequency, they could not then have been directly precipitated by her menstrual cycle especially as that was regulated by oral contraceptive drugs.
The increase in the frequency of the seizures is not only dealt with in the seizure diaries and other primary records, but is consistent with the history recounted by Ms Pierce and her mother in the months after the telemetry event. I have already recounted that there were seven seizures between the telemetry event and the consultation with Dr Ingall on 15 April 2010 (which followed an admission to hospital on 13 April 2010). He received a history of the increase in seizure frequency and was told they still occurred in the evening and night. I interpolate that one had occurred during the day at work on 5 April 2010 when she was taken to Byron bay hospital. Dr Ingall was also told that Ms Pierce had suffered two seizures in the last eight days and that tachycardia had become more prominent. A seizure on Easter Monday had lasted half an hour. This seems longer than most typical seizures.
When Ms Pierce had attended the Ballina Hospital on 13 April 2010, Mrs Pierce said that the pattern of seizures had changed and the seizures had become more frequent. A full history recorded at the hospital was: "Had a video EEG test in Brisbane in January 2010 … since the pattern of her seizures has changed - they are more frequent (every 2 - 3 weeks), with less warning" (Exhibit O, p H 813).
As I have already recorded, Dr Francesca O'Neil of the Lennox Head Medical Practice recorded at a consultation on 2 July 2010 that "seizure activity worse of recent months".
I acknowledge the force of the Hospital's argument that during 2010, Ms Pierce continued to work; continued her limited socialising with friends, and occasional holidays away; continued to complain that her seizures were related to her menstrual cycle, mostly came at night and only occasionally during the day; and these factors suggest that her seizures continued on more or less the same pattern after the telemetry event. However, it is significant, I think, that they were much more frequent, apparently more severe, and associated for example with prominent tachycardia. I accept the evidence of Ms Pierce and Mrs Pierce, at least to the extent to which there was a noticeable change in the frequency, severity and nature of the symptoms after the telemetry event and that this change has a close temporal connection to its occurrence. I regard this as an important circumstance to be considered with the other circumstances in deciding whether there is a detrimental difference.

[31]

Naturally, the raw numbers on their own say little about the nature and severity of each seizure and therefore its significance. But I regard them as a relevant matter to consider in conjunction with the other factors. Two things are clear, 2009 was "a bad year" for Miss Pierce. That may be significant given that on any understanding of her epilepsy, it was likely to be, at the very least, slowly progressive. And that has some significance. I accept there are other explanations for an increase in the frequency of seizures for that year. She was then around 20 and, as I have said already, was seeking more independence, socialising with friends, going away for the weekend and by pushing her previous boundaries she engaged unfamiliar activities which were provocative of seizures, as she herself says in her statement (Exhibit F, p 4- 5[32] - [33]). I accept that for that reason, the apparent spike in 2009 was not entirely related to a deterioration in Ms Pierce's condition. Some of the extra seizures that year are consistent with her engaging in unusual provocative activities. But part of increased numbers may well be due to a deterioration, especially given the treatment resistant nature of her epilepsy.
There is no doubt, however, that since the telemetry event there has been a large and consistent increase in the frequency of her seizures, and not just in the weeks and months following the event. This increase in frequency is marked. At least in general terms it has also been consistently maintained rather than increasing suggesting something of a plateau.
Moreover, as the more significant seizures are coming at about the rate of about two a month, it supports the argument, whatever her perception, that in 2010 and 2011 any nexus between seizures and Ms Pierce's menstrual cycle has been broken. And this probably supports the argument that her seizures have been less predictable.
While the seizure events have markedly increased, hospital attendances have greatly declined. This led to a submission that the increased number of seizures does not evince a worsening of Ms Pierce's condition. Implicit in this argument is, of course, the idea that the individual events are not as severe as they were formerly, even if there number has increased. There is another, I think better, explanation. As I have already pointed out, since 2011, Mrs Pierce has been able to give Ms Pierce the intra-muscular injections of Midazolam which generally has been the most effective way of treating Ms Pierce's seizures.
There is a note in the Lennox Head Medical Centre file dated 25 January 2012 which records Mrs Pierce stating that she had been giving intra muscular injections to her daughter without difficulty for 7 years. This is inconsistent with other clinical material upon which I have drawn to make the finding on this topic. This point about Mrs Pierce giving injections, albeit one of some importance, was not explored with Mrs Pierce in evidence and is not dealt with in her statement (Exhibit G). It is referred to only in passing in Ms Pierce's statement (p 9 [76] - [77]). Probably the entry in the Lennox Head Medical Practice notes is a conflation of circumstances. When it was written Mrs Pierce had certainly been treating Ms Pierce's seizures by various means for about seven years, given the recrudescence of Ms Pierce's symptomatic epilepsy in the early part of 2004. I accept Mrs Pierce did not commence administering intra-muscular injections until 2011.

[32]

The opinion of Dr Fong

In his second report of 18 December 2014, (Exhibit L2, [5]), Dr Fong expressed the following views: "Taking into consideration of the medical records and the seizure diaries, showing the number of motor seizures from 2008 to 2011, it is apparent that she had 9 seizures in 2008 and 12 seizures in 2009 (excluding the lines and visual auras). Following and including the prolonged CPSE in Jan 2010, she had 23 seizures in 2010 and 19 seizures in 2011. This represents an average increase in seizure frequency from 10.5/year to 21/year i.e. a two fold increase. There are two possible explanations for her seizure exacerbation following her video-EEG testing in early 2010. A. Her prolonged CPSE has caused a subtle brain damage including reorganizations, enhanced excitability and loss of normal seizure inhibitory mechanisms especially affecting her right hippocampus. As such, she has experienced a doubling in her motor seizure frequency with other associated consequences. B. It is apparent that the plaintiff has drug resistant epilepsy and previous episodes of CPSE, which may escalate in seizure frequency as abnormal electrical firing causes further excitotoxic damage to surrounding neurons, i.e. her seizure severity deteriorates according the natural history of drug resistant epilepsy. In my opinion, I am in favor of hypothesis A which is consistent with her abrupt change in seizure frequency from 2009 to 2010 and after. However, if we accept that her epilepsy deteriorates naturally at about the same time, it would then be difficult to differentiate how much is contributed by her CPSE in early 2010 and the accumulative effect of her previous seizures. My estimation would be her CPSE in early 2010 would have been responsible for at least 50% of such deterioration."
As I have said, in cross-examination (as he had in chief) Dr Fong agreed with Professor Dunne's analysis that the telemetry event was one of CPSE. There was no GCSE (or GTCS for that matter) (261.15-30T). From Dr Fong's interpretation there was a degree of secondary generalisation, for five minutes, where both hemispheres were similarly affected (261.35T). Dr Fong explained he thought the difference between he and Professor Dunne about this five minutes "is more of academic interest because in practical terms we are not seeing this making a huge difference in outcome" (282.45T).
As I have said elsewhere, Dr Fong expressed the view that an activated seizure tends to be more severe, more prolonged and more likely to result in a status condition (273.5T).
Dr Fong did not think the reduction in hospital admissions was indicative of a less severe condition. He said at 281.30T: "A. I think it all depends on how best she applied those emergency rescue medications when she experienced prolonged or recurrent seizures. If she had applied those treatments effectively that would significantly reduce her hospital admissions. Q. After May 2011, she's been able to be treated by [intra muscular Midazolam? A. That turns out to be a more effective rescue medication."
I asked some questions of Dr Fong at the end of the cross-examination (282.15-283.15T): "Q. If there was established in the evidence a previous occurrence of CPSE would that of itself make any difference to your preference for hypothesis A? A. Well, I would say if she'd had previous episodes of CPSE of long duration that would have an inference on the probability of hypothesis A versus hypothesis B, but unfortunately reviewing the medical records do not allow us to give an accurate estimate of the duration of her previous so called CPSE, so that leaves us some uncertainty as to how much contribution is related to a previous CPSE. Q. When you're talking of one of long duration, the CPSE of 5 January 2010 qualified as one of long duration because it went on for about two hours and 45 minutes? A. Yes. Q. Would you be looking for something like that in the past if it was to affect the probabilities as you see them? A. If it were fair to say that she had previous CPSE of similar or longer duration, I would expect they would have some effect on her subsequent seizure frequency, but taking the admission in 2006 during which she was admitted to ICU this was not followed by a dramatic increase in seizure frequency, so at that rate, some doubt as to whether that admission is a long or prolonged CPSE. That could be a short CPSE with some prolonged postictal period which we are not too sure about the exact duration. ….. Q. I just wanted to ask you finally about hypothesis A and hypothesis B and if you look at the top of the next page where you say it would be difficult to differentiate how much is contributed to by her CPSE and the accumulative effects of her previous seizures, that made me wonder whether there was a mid ground, that there was a possible combination of hypothesis A and B? A. Well you can say that assuming she does have previous episodes of CPSE, which may be of shorter duration, that she might have a number of such CPSE which can have an accumulative effect and how would you compare this effect to that particular CPSE in January 2010 and which is more important or severe, we don't have scientific data to suggest which is causing more damage to your brain or worsen her seizure subsequently so this is just based on my personal opinion that I think the one properly documented in 2010 is of a sufficient severity and coinciding with the change in seizure frequency and characteristics which shortly following that episode would allow me to say that this is more important than all her previous so called episodes of CPSE in worsening her seizure outcome."
There are two things in particular which impressed me about Dr Fong's reasoning. The first is his emphasis on the consideration that the telemetry event was properly documented, I infer so that it is known that it was of sufficient severity to cause a change, and its occurrence did coincide with a change in seizure frequency and characteristics. I am of the view all of those things are well established by the evidence. It is for these cogent reasons that he concludes that the telemetry event "is more important than all her previous so-called episodes of CPSE in worsening her seizure outcome." (283.15T).
The second matter is that even if one prefers hypothesis B, he remains of the view that the telemetry event is contributing to her worsened condition by a factor of at least 50 per cent. In anyone's language this is a material contribution. On either basis, Dr Fong provides cogent evidence of a detrimental difference caused by the negligence of the defendant.

[33]

Concessions made by Professor Dunne

As I have attempted to demonstrate, Professor Dunne is strongly of the view that Ms Pierce's condition was a naturally deteriorating one and that the telemetry event is not of itself causative of any increment in its deterioration. Professor Dunne's considered opinion is well encapsulated in the following evidence from cross-examination (222.50 - 223.13T): "Q. Apart from the episode of complex partial status epilepticus, you have found no other medical explanation for that other than the fact that it's mere coincidence as a matter of her underlying epilepsy, that's correct, isn't it? A. That's not correct. A medical explanation for the exacerbation of epilepsy that is increasing seizure frequency and severity, a valid medical explanation, does not require a specific trigger, because the natural history of epilepsy, unfortunately, in a fair proportionate of people with epilepsy, is in the absence of specific triggers and increased intensity, an inexplicable increase in intensity and frequency of seizures over years, including doubling or tripling of seizures without a specific trigger or explanation. This is very common. Q. Just trying to understand that, apart from the complex partial status epilepticus that occurred on 5 January 2010, the only other explanation that you say can explain the change in character and frequency of her seizures from 5 January 2010 is this natural progression of her underlying epilepsy? A. That's correct". I interpolate that Professor Dunne regards natural progression of the disease as one possible explanation for the deterioration in Ms Pierce's condition. That at least since Mrs Pierce started giving intra muscular Midazolam, which he dates to about May 2011, the "acute as needed medication" is now more satisfactorily resulting in a decrease in the number of presentations to hospitals (143.30-35T). But it is not just the intra muscular Midazolam which is important, it's the combination of drugs that counts. He accepts that notwithstanding better acute care at home "two seizures on average per month" is "too many" (142.35T). (See also 139.40 - 141.40T).
In Professor Dunne's opinion, scientific literature did not support the hypothesis that CPSE of less than three days duration causes discrete brain or neuronal damage. On the other hand, chronic epilepsy sufferers suffer cognitive dysfunction. The causes are complex and included in a case like Ms Pierce's is the pathology affecting her right hemisphere, the burden of epilepsy including "ongoing sporadic seizures" and the side-effects of anti-epileptic drugs. Professor Dunne also added that "how seizures cause cognitive dysfunction is another vexed mystery". The electrical disturbance of epilepsy, even if insufficient to trigger a seizure "can and does degrade cognitive function". The mesial-temporal sclerosis shown on Ms Pierce's MRI scan is also relevant to this (151.35T). The changes brought by epilepsy are insusceptible even to modern imaging techniques (152.20T).
Although Professor Dunne favoured the natural progression hypothesis (221.5T) he agreed that for there to be a change "in frequency and character … there must be a change in some way in the electrical activity of the relevant neurons within the brain" (221.15T). He agreed that there was no scientific reason why the electrical activity of CPSE "cannot cause neuronal damage" (224.15T).
Professor Dunne also explained in his first report (Exhibit 1.2) that there are shortcomings in the epidemiology. Many of the studies that dealt with the effects of status epilepticus dealt also with patients whose status epilepticus was due to illnesses other than epilepsy, or with other cerebral accidents. I did not form the view that the epidemiology provided a sure or certain guide to the "capacity, or not" of an induced event like the telemetry event to produce the type of change, or electrical disturbance, in the brain that could have itself lead to a definite progression, acceleration or aggravation of epilepsy.

[34]

The evidence of Dr Rowe

Dr Donald Rowe is Consultant Neuropsychologist, Neurophysiologist and clinical psychologist. His PHD is in clinical neuropsychology. He is associated with the Brain Mind and Research Institute and the Department of Psychological Medicine and Psychiatry at the University of Sydney. His report of 10 July 2012 was admitted after extensive objections as Exhibit P1. Dr Rowe administered a number of psychological and neuropsychological tests on Ms Pierce. He also reviewed literature in relation to the neurophysiological effects of CPSE. His testing results showed deficits consistent with cognitive impairment especially of Ms Pierce's executive functions. He also documented results of psychological testing which were consistent with aspects of post-traumatic stress disorder (PTSD). He explained that the literature indicated that the occurrence of CPSE had the potential to cause brain damage by way of neuronal injury. Animal studies suggested that neuronal damage had a relationship with the duration of continuous seizure activity. Although the studies were not directly transferrable to outcomes in humans, these studies suggest that a threshold of 30 minutes. But this could not be precisely determined. Research in CPSE induced neuronal injury has shown hippocampal cell loss and neuronal atrophy in focal areas of intense seizure activity. He said that the hippocampus is particularly susceptible to abnormal electro-neurophysiological activity. Neuronal damage can leave the brain susceptible to further instability with a resulting increase in seizure frequency.
One may accept this hypothesis which does not seem inconsistent with Professor Dunne's understanding of the mechanism of subtle brain damage in epileptic patients. At the same time, as I have said at the outset, there is no way of measuring whether this mechanism has occurred in Ms Pierce's case or the extent of it. Nonetheless the epidemiological evidence provides a circumstance which may be taken into account with all the other circumstances proved by the evidence in the case to determine whether a causal connection has been established.
A difficulty however with Dr Rowe's evidence is that no neuropsychological testing had been carried out on Ms Pierce prior to the telemetry event. This made comparisons impossible. Moreover, it was possible that the anti-epileptic drugs Ms Pierce was taking could have had an effect on her test-performance. He acknowledged that Ms Pierce's academic transcripts during and after 2010 continued to demonstrate a commendably high level of achievement, although she was not undertaking a normal work load for a full-time student.
Given the chronicity of Ms Pierce's epilepsy it is not surprising that her neuropsychological test results would show cognitive impairment. From the evidence of Professor Dunne, I have recounted above, this was only to be expected. It is at best a neutral factor for determining the issue of causation.
I accept that the tests confirm some features of PTSD. However, notwithstanding his impressive qualifications, Dr Rowe is not a Consultant Psychiatrist and, in my view, is not in a position to proffer that diagnosis. Once again, the evidence firmly establishes that psychological symptoms are a concomitant of chronic epilepsy. Again given Ms Pierce's condition, it is to be expected she would suffer such symptoms. I am prepared to infer that if her condition has been worsened by the telemetry event, that worsening will include an aggravation of her psychological symptoms.

[35]

Dr Ingall's evidence

Dr Ingall has been treating Ms Pierce since she was nine months old. Although a paediatrician he has been the principal person treating her epilepsy for most of her life. He is particularly well placed, as an experienced physician, in my opinion, to cast light on whether there was a relevant change in Ms Pierce's condition following the telemetry event.
Dr Ingall saw Ms Pierce in consultation on 15 April 2010. In his report of the same day Dr Ingall recorded the history of an increase in seizure frequency suffered by Ms Pierce and thought her condition "is certainly showing acceleration in frequency". His findings on examination, however, were virtually unchanged.
He saw her again on 29 November 2010 at which time he was told that Ms Pierce had moved in with two friends in Byron Bay. At that time, it seemed a matter of comment that she had been seizure free "for 32 days" since there had been a change in her medication. However, on 12 May 2011 he recorded the following: [Ms Pierce] has struggled since I last saw her, with unpredictable seizure control ever since the prolonged seizures she suffered in Brisbane whilst having her telemetry.
On 5 October 2012, he wrote: Presently, [Ms Pierce] is having fortnightly focal seizures, some of which progress to grand mal, which is obviously unacceptable. They start down her left side and then become generalised with loss of consciousness. They can last for up to half an hour and often require an ambulance to be called. Her parents have trialled giving Buccal or intra muscular Midazolam, but this on occasion she still needs to go to hospital for intravenous loading of Dilantim. He also recorded Ms Pierce was anxious about the increased frequency and severity of her seizures. I should say Dr Ingall's description of the seizures is probably not correct. There is no evidence that Ms Pierce suffers GTCS.
In his report of 30 May 2013 (Exhibit R1), Dr Ingall expressed the view that it is "highly likely … that the video telemetry status epilepticus event was the cause of [Ms Pierce's] increased seizures". He also observed that, at least on occasions I infer, that she appeared of flat effect and he was concerned about the possibility of depression.
The thrust of Mr Glissan's cross-examination, with respect, was that properly understood many different types of medication had been tried without lasting success, but "the natural history of [Ms Pierce's] epilepsy was one of progressively more frequent seizures" (319.45T). Dr Ingall said "over the entire 20 years, yes".
He agreed that there were elements of "reactive depression" because of the burden of Ms Pierce's epilepsy going back to letters he had written in February, May and November of 2008 (320.15 - .40T).
He also agreed that Ms Pierce had exhibited cognitive difficulties well before 2010. On 26 November 2004, he had written to the Department of Education saying that Ms Pierce was "doing well in all areas except mental processing" (322.40T). He agreed that Ms Pierce's "processing speed in particularly would have affected her marks, even though she may have had all the information in her head". I asked the following questions at the end of the cross-examination: Q. You have expressed in your reports, what have been referred to your medico/legal reports, your strong impression that there was a, let me put it this way as the reader, a definite worsening of her condition after January 2010 in general terms? A. Yes. Q. Having been asked the questions you have been asked today by reference to your contemporaneous records, has anything caused you to review that impression? A. No, I think the questions are, if I may, the questions I wasn't asked were about burden. You can have epilepsy and be mildly burdened if at all, you can have epilepsy and be seriously burdened and for Emily we can talk about the frequency, the type and so forth and all that's important, but they added up to a burden I believe from what I've seen pre and post that event, a considerable increase in that burden on her life because not only did the seizures become more frequent but they became much more unpredictable and that was the predictability that allowed me to initially particularly say, look, because they are predictable you can be safe driving, okay and with that increase in burden, there has been a significant increase in burden because it's not much more intrusive,, the seizures last and their total effect lasts for longer and in truth when I saw Emily a month or so ago, I felt that her left arm for example was not working as well as it had been in the past and that the unpredictability of the seizures was weighing heavily on her and again it's the frequency, the unpredictability and the fact that they were mainly occurring around the times of her period, menstrual just in the week prior to, so that's why we tried using various hormonal or other treatments which were somewhat successful. That is no longer the case, so there's no way for her to predict either in time or severity what's going to happen next and that has increased her burden significantly I feel. Q. It could be said to me that given the nature of her condition from birth and the comparatively early onset of epilepsy from when she was a young child, I think the first seizure was around the age of six? A. Yes. Q. (It might be submitted to me) That what we are seeing now in terms of increased burden might be better explained just by the natural progress of her epileptic disease; do you have a view about that? A. That's possible. That is possible. The reason I guess to answer that that I have come down on the negative to that one is that the nature of the seizures has changed, not the minor ones, they have remained pretty steady. On the times I have spoken to her on the nature of the seizures, that seems to be much more intrusive and to have a much longer time for her to recover from them which you wouldn't expect. People do run their course with epilepsy generally. You have clusters and then you have times when you are not but over a five or ten year period you will see the trajectory. That usually runs reasonably true. Here it just seemed like to have there has been a jump in frequency and also the nature, the severity of the seizure and therefore the burden.
These answers impressed me as very thoughtful. Dr Ingall, as I have said more than once, is not a neurologist, but he is a specialist medical practitioner who has had a long and close relationship with Ms Pierce as his patient. His impressions struck me as being entitled to great weight. He acknowledged that the increased burden he identified might be due to the natural progress of Ms Pierce's epileptic disease. His references to "a considerable increase" in the burden of her epilepsy, and his reference to "a jump" in the burden struck me as very telling evidence.

[36]

Finding as to causation

I accept that the plaintiff has proved on the balance of probabilities from the circumstances relied upon that the telemetry event on 5 January 2010 caused a significant increase in the burden of her epilepsy, especially in relation to her motor seizure activity. I accept that she has established a detrimental difference in her condition due to the negligence of the defendant. I accept that generally her pre-existing epilepsy was a progressive disease. I accept that absent the telemetry event it would have been worse now than it had been at the end of 2009 in any event. Making the comparison called for in the judgment of Hayne and Bell JJ in Tabet v Gett, I am satisfied that there is a detrimental difference even comparing her condition now to "the state of affairs that would have existed had the negligent act or omission [of the Hospital] not occurred'.
The difference is difficult to quantify. Rather it seems it can be best described only by reference to the concept of the burden of her epilepsy. Perhaps Dr Fong's general assessment that the telemetry event has contributed about 50 per cent to her worsened condition is about as accurate as one can be. Even on that score, accepting Ms Pierce would have been worse now than then, the detrimental difference remains very significant.
In coming to this conclusion, I do bear in mind, as I have said, the progressive nature of the condition and the objective factors which suggest she continues to cope, more or less, as well as she has done previously. I am referring to her ability to continue working albeit now at reduced hours because of the occurrence of a seizure at work and I accept that she has graduated with her BA. This must be regarded as a very singular achievement for a young woman who has laboured under the burden of this disease. I also bear in mind that she was able to take a holiday to New Caledonia at the end of 2014 travelling unaccompanied by her parents. That trip was a success and in the event was virtually seizure free (only one occurred which was successfully treated with sublingual medication). However it may be that these objective factors provide only a semblance of "normality" for her due to Ms Pierce's great determination to live as normal a life as possible and in some measure, as I have already said to the devotion of her parents. These factors whilst significant do not detract, in my judgment from the other factors I have referred to, which to my satisfaction prove Ms Pierce's case on the balance of probabilities.

[37]

Damages

As I stated at [10] above, the common law of damages for personal injury has been relevantly modified by the provisions of Chapter 3 CLA. By Section 61, if general damages are to be awarded, the court is to assess an injury scale value (ISV). This requires assignation of a numerical value on a scale from zero to one hundred. The scale reflects equal gradations of general damages "from a case in which an injury is not severe enough to justify any award of general damages to a case in which an injury is of the gravest conceivable kind" (s 61(1)(b)). In assessing the ISV, the court is to apply the regulation and have regard to ISV's assessed in similar previous cases. I have not been provided with any comparative verdicts. Departure from an ISV attributed to a particular injury by the regulation requires a statement of "the factors on which the assessment is based that justify the assessed injury scale value" (s 61(2)). S 62 requires general damages to be calculated by reference to the provisions applying to the period within which the injury arose.
Personal injury is defined as extending to psychological or psychiatric injury; and to disease (s 8, schedule 2 CLA). "General damages" is defined by s 51, generally speaking, by reference to its meaning at common law.
The regulation prescribes various rules and principles relating to the assessment of the ISV (s 7 of the regulation). S 7 of the regulation directs attention to the various schedules to the regulation which apply in particular circumstances. It is not necessary for me to set out the whole of s 7 for present purposes. By s 7(2) schedule 4 applies to provide the range of ISVs for particular injuries. In assessing an ISV for an injury not mentioned in schedule 4 "the court may have regard to the ranges prescribed in schedule 4 for other injuries". Schedule 3 "provides matters to which a court may or must have regard in applying schedule 4": s 7(4).
S 8 of the Regulation deals with the method of calculation of the amount of general damages to be awarded for an injury. It is in the following terms: 1) For each period stated in a table in schedule 7, this section and that table are the general damages calculation provisions for the period. (2) For an injury within the injury scale value stated in an item of a table, the general damages are the sum of - (a) the base amount for the item (if any); and (b) the variable amount for the item. (3) In this section - variable amount means the amount worked out in the way stated in the column of a table with the heading 'variable amount'.
S 2(2) of schedule 3 provides that the "range of ISVs for the injury reflects the level of adverse impact of the injury on the injured person". Where the injury, as here, consists of the aggravation of a pre-existing condition "the court may have regard only to the extent to which the pre-existing condition has been made worse by the injury": Sch 3, s 7. In assessing the ISV, the court may have regard to other relevant matters: Schedule 3, s 9. Examples given include age, life expectancy, the effects of a pre-existing condition, difficulties in life likely to have emerged whether or not the injury happened. Where available, an assessment of whole person impairment "is an important consideration": Schedule 3 s 10. No such assessment is available to me.
Schedule 4 provides a range of ISVs for particular injuries in tabular form. Counsel agree that Part 1 concerning the central nervous system and head injuries is, generally speaking, applicable. The dispute between them crystallised as whether the present case is more aptly covered by item 7 concerned with moderate brain injury, or item 8 concerned with minor brain injury. The former provides a range of 21 to 55 and the latter of 6 to 20. I reproduce items 7 and 8 below. 7 Moderate brain injury 21 - 55 Comment The injured person will be seriously disabled, but the degree of the injured person's dependence on others, although still present, is lower than for an item 6 injury. Examples of factors affecting ISV assessment . degree of insight . life expectancy . extent of physical limitations . extent of cognitive limitations . extent of sensory limitations, for example, limitation of hearing or sense of taste or smell . level of function and pre-existing function. . degree of independence . ability to communicate . behavioural or psychological changes . epilepsy or a high risk of epilepsy . presence of, and extent of, secondary medical complications. Comment about appropriate level of ISV . an ISV OF 21 TO 25 will be appropriate if there is reduced concentration and memory, or reduced mood control, and either or both - . reduced capacity for employment . a noticeable inference with lifestyle and leisure. . an ISV of 26 to 40 will be appropriate if there is an increased risk of epilepsy and either or both - . a moderate cognitive impairment . loss of or greatly reduced capacity for, employment. . An ISV of 41 to 55 will be appropriate if there is no capacity for employment, and 1 or more of the following - . moderate to severe cognitive impairment . marked personality change . dramatic effect on speech, sight or other senses . epilepsy or a high risk of epilepsy 8 Minor brain injury 6 - 20 Comment The injured person will make a good recovery and be able to take part in normal social life and to return to work. There may be minor problems persisting that prevent a restoration of normal function. Examples of factors affecting ISV assessment . severity of any physical injury causing the brain damage, having regard to - (a) any medical assessment made immediately after the injury was caused, for example, CT or MRI scans, an ambulance officer's assessment or hospital emergency unit assessment; and (b) any post-traumatic amnesia. . extent of any ongoing, and possibly permanent, disability . extent of any personality change . depression . degree of insight . life expectancy . extent of physical limitations . extent of cognitive limitations . extent of sensory limitation, for example, limitation of hearing or sense of . taste or smell . level of function and pre-existing function . ability to communicate . behavioural or psychological changes . epilepsy or a high risk of epilepsy . presence of, and extent of, secondary medical complications Comment about appropriate level of ISV An ISV at or near the top of the range will be appropriate if the injured person has - (a) an increased risk of epilepsy; and (b)ongoing reduced concentration and memory, or reduced mood control, that does not significantly interfere with the person's ability to take part in normal social life or return to work
In detailed written submissions, Counsel for the plaintiff argued that I should conclude that the range of 41 to 55 was appropriate, and I should assess an ISV of 50. Defendant's Counsel argued if I was persuaded of an ongoing aggravation, item 8, Minor brain injury with a range of 6 to 20 was appropriate (421.25T; 422.40T).
As I have found, Ms Pierce's injury is an aggravation of a pre-existing condition, namely epilepsy. In reality it is only, at best, similar to the types of brain injury directly dealt with by the table. Without attempting to be exhaustive, the types of brain injury dealt with from item 5 to 9 are concerned with what might be referred to as acquired or traumatic brain injury. This is perhaps best illustrated by the comment which accompanies Item 5, extreme brain injury, which is in the following terms: The injury will involve major trauma to the brain with severe permanent impairment. The various sub-categories of item 5 are then described, which are generally consonant with matters one sees in cases of severe traumatic brain injury. It may be said that the malformation of Ms Pierce's brain is an acquired brain injury on the evidence I have accepted. But that is not the injury to be assessed. Rather the ISV relates to an aggravation of the epilepsy which is a consequence of the ante-natal injury.
As Professor Dunne described it, the processes of epilepsy certainly involve injury to the brain but they are, or may be, of great subtlety and generally speaking are opaque or non-detectable, by even sophisticated modern computerised scanning techniques. Except for measuring the severity of seizure activity, and its general location, by EEG, cases of epilepsy do not show up obvious focal damage like those one may see in cases of traumatic brain injury. This does not mean, however, that the seriousness of the condition and the degree of suffering of the patient are necessarily less, or to be categorised as minor. From Professor Dunne's evidence, I am satisfied that epilepsy is a very serious disease, which at least in some cases may lead to sudden death and, in others, a general reduction of life expectancy. (Exhibit 1.2).
Ms Pierce's epilepsy involves significant cognitive limitations and the aggravation of the telemetry event made them, in my judgment, significantly worse. Despite her determination, her independence had been significantly compromised by her epilepsy and it has been made much worse by the aggravation. As counsel for the plaintiff pointed out, examples of factors affecting the ISV assessment for moderate brain injury included "epilepsy or a high risk of epilepsy". Ms Pierce has epilepsy and it has been made much worse. This factor makes her injury more analogous to item 7 than item 8.
She has continued in employment with some reduction in hours due to experiencing a seizure at work. However, as I will develop further below and have said already, her pre-existing epilepsy was such that she needed to work in a very sheltered environment. That is not to suggest that she was not performing useful, remunerative work. But at the same time she falls into that category where there are very limited options indeed available for open employment in the labour market.
It is also to be borne in mind that she suffers significant psychological symptoms, made worse, by the telemetry event.
As I understand the operation of the provisions I have been discussing it is not necessary for me, in any way, to arrive at an ISV which is a proportion of "an injury [which] is of the gravest conceivable kind".
Bearing all of these factors in mind, in my judgment Ms Pierce really falls into that broad range covered by an ISV of 26 to 40, at one end, and 41 to 55 at the other. Looking at the effects of her aggravation alone, leaving out of account the pre-existing condition and the degree to which it has deteriorated as a natural progression since January 2010, I assess the appropriate ISV as 41.
Ms Pierce's injury is covered by table 1 to schedule 7. The base amount for the purpose of s 8 of the regulation is $68,000. The variable amount is to be calculated by deducting 40 from the ISV of 41, producing a factor of 1 which is multiplied by $2,580. I assess general damages therefore in the sum of $70,580. By s 60 CLA interest is not payable on an award of general damages.

[39]

Past economic loss

Section 54 CLA limits the amount that may be awarded for damages for loss of earnings to an amount equal to the present value of 3 times average weekly earnings per week for each week of the period of loss of earnings. Average weekly earnings is a phrase defined in the dictionary as "the amount of Queensland full-time adult person ordinary time earnings" as declared and published by the Australian Bureau of Statistics.
S 55 makes provisions which may be applicable to this case. Where the loss of earnings "are unable to be precisely calculated by reference to a defined weekly loss", s 54 continues to apply and s 55(2) imposes the following condition: The court may only award damages if it is satisfied that the person has suffered or will suffer loss having regard to the persons age, work history, actual loss of earnings, any permanent impairment and any other relevant matters. The Section requires a statement of the assumptions upon which the award is based and the methodology used to arrive at it.
Ss 54 and 55 are applicable to both past and future awards of damages for loss of earnings.
Ms Pierce's evidence about her employment history is not challenged. Given the burden of her epilepsy, her ability to maintain herself in the workforce is a testament to her remarkable determination and drive to lead as normal a life as possible and also to the devotion of her parents.
She commenced work in 2008 as a pharmacy assistant, doing a range of shop work including general inquiries, stocking shelves and working the checkout.
At about the beginning of 2009 she changed her employment to that of a receptionist at a caravan park in Byron Bay. She mostly caught the bus to and from work on her own. She changed again, commencing at a second caravan park in September 2009. Initially she was employed as a casual to work in reception. However, she was generally given 40 hours per week and her shifts would vary so that sometimes she would work alone, opening the office at 7 a.m.. As there was no available bus, her mother would drop her off when she was allocated an early shift.
Ms Pierce appears to have been able to maintain herself in this employment until 16 August 2014 when she had "a bad seizure at work" (Exhibit F [105]). Fortunately a colleague was nearby and able to give her oral Midazolam, but she had to be taken home.
Since this seizure, her hours at work have been reduced and she is working 20 hours per week. She is no longer permitted by her employer to work alone. She is concerned about the security of her employment as a new employee has been taken on and trained to perform some of the duties she was accustomed to perform. Ms Pierce has from time to time asked for additional shifts, but she feels excuses have been made for refusing her request.
I have no doubt that having regard to the nature of Ms Pierce's pre-existing epilepsy that she fell into that category of employment formerly known in the workers' compensation jurisdiction as the "odd lot". That is to say, that she was fit for the work she was doing, but if that work came to an end it was very unlikely that she would be able to find any similar work in the open labour market: Cardiff Corporation v Hall [1911] 1 KB 1009 at 1020-1.
There are difficulties in assessing damages under this head as seizures, often requiring hospitalisation, were a feature of Ms Pierce's pre-existing condition and notwithstanding what I have found to be the material aggravation of her condition, her epilepsy would have worsened, in any event, again according to the findings I have already made. I am satisfied however, that the aggravation by the telemetry event has materially contributed, to a significant degree, to the impairment of her earning capacity; and I am satisfied that she has suffered, and will in the future suffer, financial loss, having regard to the matters set out in s 55(2) CLA. Nonetheless, given the other factors at play in a causal sense, in assessing economic loss for the past and the future, I am satisfied that the principles discussed in Malec v Hutton (1990) 169 CLR 638, as expounded in Seltsam Pty Ltd v Galeb [2005] NSWCA 208 at [103] - [107] and Ridolfi v Hammond [2012] NSWCA 3 at [86] - [88], are engaged. And it is appropriate for me to assess Ms Pierce's economic loss in accordance with them.
Ms Pierce's pre-existing condition and its natural deterioration are possible "causes entirely unrelated to the defendant's negligent act [which] might have contributed" not only to her ultimate condition but also to the losses she has suffered which otherwise sound in damages. "Appropriate allowances must be made for these contingencies": Seltsam v Galeb at [106] - [108]. Given these principles, and my findings, it is not appropriate for me to award the arithmetical difference between Ms Pierce probable earnings after 16 August 2014 and her actual earnings since then to calculate the amount appropriate for past economic loss. An adjustment has to be made to that difference to take account of the contingencies I have identified. In my view, the appropriate discount is 50 per cent.
I accept the calculations of plaintiff's counsel that the net loss is in the order $350 per week. It will have been about 115 weeks from 16 August 2014 until the date of judgment. This produces a figure of $40,250, 50 per cent of which is $20,125. This is the amount I will allow.

[41]

Future loss of earnings

As I have said, s 55 also applies to future economic loss particularly in circumstances where the approach contended for by plaintiff's counsel is for the allowance of a buffer. I accept that this is an appropriate approach in this case given the great uncertainty which surrounds Ms Pierce's future employment prospects but for the telemetry event. I also bear in mind what I have said about the odd-lot category. It seems to me from Ms Pierce's evidence, and by application of common sense, having regard to the medical evidence about the severity of her condition before and after the telemetry event, notwithstanding her remarkable and commendable determination, that there is a very high degree of probability that: 1. she will lose her current job; and 2. she will be unable to find other suitable work, because of the totality of current impairment due to her epilepsy resulting from all causes. The aggravation by the telemetry event is one, concurrent cause.
In making this finding I have borne in mind her evidence that she has an ambition to be a writer either as a freelance journalist or as a novelist (57.10T). Notwithstanding her cognitive difficulties, Ms Pierce struck me as a very intelligent young woman. Her drive, I think, speaks for itself. Notwithstanding these obvious attributes, I also bear in mind that the wonderful achievement of her BA was obtained at a measured pace with the assistance of her father. It will not be easy for her to obtain work as a freelance journalist at a sufficient level to support herself and, at least proverbially, there are very, very many more novelists who go unpublished than published; of those who are published, the great majority struggle financially.
Ms Pierce also spoke about the possibility of going back to university to obtain a Diploma in Education and teaching English (57.35T). From her previous academic experience that is likely to take time and require assistance. It is notorious that teaching jobs are hard to come by and there may be difficulties in finding a placement in circumstances where Ms Pierce continues to live in regional New South Wales and cannot obtain a driver's licence. Teaching placements in seaside towns are likely to be in very great demand from established, experienced teachers.
Bearing all these factors in mind, I think it appropriate to at least start with the figure propounded by the plaintiff's counsel of $750 net per week, being the rough equivalent of her pre-16 August 2014 earnings (written submissions [98]).
At age 27 Ms Pierce has a life expectancy according to the medium life tables of about 61 years. Even assuming her life expectancy is affected by her epilepsy in its aggravated state, it is reasonable to assume a remaining working life of 40 years as a starting point. Under s 57 CLA the discount rate for future losses is that prescribed by s 61 Civil Proceedings Act 2011 (QLD), or 5 per cent. The multiplier for 50 years is 976.2. Multiplying $750 per week net by that figure, the figure of $732,150 is produced. This, of course, is the maximum that could be awarded on an assumption Ms Pierce was totally incapacitated today with no prospect of finding other work and without the usual discount for the vicissitudes; and that impairment was solely due to the Hospital's negligence.
I accept the submission that "she is unlikely to be able to obtain and maintain … full time employment and possibly any really meaningful employment, for most of the future period" (written submissions [102]). The difficulty is applying the Malec principle to future loss in this case. There are many imponderables. Factors additional to those relevant to past economic loss come into play including the reality that the underlying epilepsy will continue to deteriorate into the future. Moreover, it is difficult to forecast in any meaningful way how long it is likely Ms Pierce will continue in her present employment. As I have said, if she loses that job it is unlikely she will find another. Moreover, her other ambitions strike me, on the material available to me, as falling into the speculative category at this time and therefore should be put to one side.
Doing the best I can to weigh and assess the competing and conflicting probabilities, I think the appropriate approach is to discount the figure of $732,150 by 66 per cent. 34 per cent of my starting figure is $255,051 which is the amount I allow.

[42]

Past attendant care

Damages for gratuitous services provided to an injured person are governed by the provisions of s 59 CLA. Damages are not to be awarded unless the services are necessary, which need arises solely out of the injury; and the services are provided, or to be provided, for at least six hours per week and for at least six months. Reinforcing that the need for services must arise solely out of the injury, damages are not to be awarded if gratuitous services of the same kind were being provided for the injured person before the breach of duty happened (s 59(2) CLA). In assessing damages, the Court must take into account any offsetting benefit to the service provider and periods during which the injured person has been or is likely to be cared for in a hospital.
I do not understand s 59(2) to be an absolute prohibition against the award of damages for gratuitous services if there is an increased need for services of the same kind which increment arises solely out of the injury in relation to which damages are awarded. That is, s 59 permits recovery of damages for the increased services provided, assuming that the other conditions of the application of the section are satisfied.
As I was reminded by the plaintiff's counsel, the lay evidence of Ms Pierce, Mrs Pierce and Mr Pierce as to the services actually provided to Ms Pierce, and the increase in those services, is unchallenged.
The claim is formulated by reference to the joint report of the occupational therapists, Ms Belinda Moylan, and Ms Ellen Wood dated 27 October 2015 and admitted as Exhibit T.
The joint report is based upon very detailed assumptions about the nature of Ms Pierce's condition, its symptoms, their frequency and care provided before the telemetry event, and after the telemetry event. These assumptions run for some three pages and it may be said break the plaintiff's case down in great detail. If, and on if, the assumptions made by the experts sufficiently accord with the facts as I find them to be, the hospital and Ms Pierce have agreed that for the past, there was a need for an additional 63 hours of gratuitous care per week at a rate of $30 per hour, totalling $1,890 net per week. For the future the additional need is agreed in the amount of 73.5 hours per week. It is accepted that this should be allowed at the commercial rate of $59.33 per hour because an enrolled nurse would be required to provide the intramuscular injections of Midazolam in the event of a seizure.
In Exhibit 10, the experts also allowed additional amounts for the care that Ms Pierce would have provided but for the injury to any children she gave birth to in the future. Given the content of the agreement of the parties, I assume that this claim is not pursued and in any event it would not meet the conditions set out in detail by ss 59A to 59D CLA.
I do not regard it as necessary for me to set out the very detailed assumptions that the experts were asked to make for the purpose of their joint report. I am not satisfied that those assumptions accord sufficiently with the findings I have made about the change in Ms Pierce's condition due to the aggravation of the telemetry event alone to validate the opinion expressed in the joint report: see Paric v John Holland (Constructions) Pty Ltd [1985] HCA 58; 59 ALJR 844.
I think this is illustrated clearly by an overview provided by the experts at page 10 of Exhibit T in answer to the question, "Please provide your assessment of the reasonable need for future care and assistance referrable to the plaintiff's seizure activity". Naturally the claim for care extends well beyond care and assistance for seizure activity. There are consequential matters including, for instance, the assistance Mr Pierce has given for completion of Ms Pierce's university work. But focusing on that question for the moment, Ms Wood assessed care prior to the telemetry event for seizure activity on average as 16 hours per day, five days for one week in every month. That is 80 hours per month. There is some ambiguity in how Ms Wood has expressed her answer to this question. On my reading of it, she seems to be saying that either the additional need is 351 hours per month, or total need is 351 hours per month with the additional need totalling 271 hours per month. Assuming the lessor of those figures, Ms Wood is saying that Ms Pierce's condition is more than three times worse than it was before the telemetry event. I simply do not accept that. I am not satisfied that an aggravation of that severity has been made out on the evidence I have accepted.
Likewise, there is some ambiguity with Ms Moylan's opinion, but at page 14 of the report she "states on the basis of the assumptions provided for the purpose of the expert conclave, she is in agreeance with Ms Wood" (sic). In her answer to question 2 starting on page 10 she assesses, as a starting point, with other needs to be factored in, a need of 53.2 hours per week, itself exceeding 200 hours per month. Again, I cannot accept that this amount of care is solely due to the degree of aggravation caused by the telemetry event.
In dealing with this issue, I record that I am satisfied that additional services are necessary solely because of the consequences of the telemetry event and that those services have been provided and will be provided for at least 6 hours per week and for at least 6 months. That is to say, I am satisfied on the balance of probabilities that the conditions of s 59 have been satisfied. However, it seems to me in assessing damages for past care, that the principles I have discussed deriving from Malec have application to this head of damage.
In my judgment before the telemetry event, Ms Pierce was much less independent and in much greater need of parental care and support than the assumptions made by the experts reflect. Moreover, as I have said the aggravation by the telemetry event is only part of the reason for the deterioration in her condition to its present level. Natural progression of the disease accounts for the other part of that deterioration. Doing the best I can to make some allowance for these matters reflected in the contingency that her level of care would have increased to the extent suggested by the occupational therapists in any event, I consider that the appropriate course is to apply a discount in percentage terms to the agreed figures. Given the seriousness of the pre-existing condition giving rise to a significant need for care, and bearing in mind the natural deterioration, for the past, I think it appropriate to allow one-third of the 63 additional hours agreed at the agreed rate of $30 per hour. That is an amount of about 21 hours per week on average at $30 per hour. I am conscious that I have accepted that motor seizure activity has about doubled since the telemetry event, but as I have said repeatedly, not all of that worsening is due to the Hospital's negligence.
It is approximately 303 weeks since 5 January 2010. At 21 hours per week, this is 6,363 hours. Allowing $30 per hour, I allow $190,890.

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