Pierce v Metro North Hospital and Health Service

[2016] NSWSC 1559

Supreme Court

New South Wales

• Amendment notes

Medium Neutral Citation:

Pierce v Metro North Hospital and Health Service [2016] NSWSC 1559

Hearing dates:

16 –17 November; 19 – 20 November; 23 – 24 November; 26 – 27 November 2015

Date of orders:

03 November 2016

Decision date:

03 November 2016

Jurisdiction:

Common Law

Before:

Campbell J

Decision:

My orders are:
(1) Judgment for the plaintiff in the sum of $1,672,790.75;
(2) The defendant to pay the plaintiff’s costs;
(3) Liberty to apply in respect of interest on past economic loss.

Catchwords:

TORT– medical negligence – plaintiff sufferer of epilepsy – where plaintiff a young person whose condition is by nature changeable – plaintiff underwent voluntary testing to determine whether she was a candidate for surgical intervention–test involved allowed seizure to occur in order to measure and record it – existence of duty of care accepted–breach of that duty of care admitted by Hospital by allowing seizure to continue for extended period of time

 

TORT– medical negligence–causation– circumstantial case –whether plaintiff’s condition worsened following breach – where plaintiff’s condition debilitating prior to breach– where no definitive medical knowledge exists to measure any damage sustained or change in severity or not of condition

 

TORT– medical negligence – damages – where condition of plaintiff poor prior to breach – where manner in which breach argued to have worsened her condition similar to how her condition would otherwise present if its natural progression as a disease was to worsen – evidence of worsening of condition prior to breach– whether plaintiff worse off because of breach

  PRIVATE INTERNATIONAL LAW – federal diversity jurisdiction – choice of law – torts – where action brought in New South Wales for alleged tort which occurred in Queensland – where the lex loci delicti is the law of Queensland– Civil Liability Act 2003 (Qld) applies– no question of principle

Legislation Cited:

Commonwealth of Australia Constitution Act (The Constitution) (Cth) s 75(iv)
Civil Liability Act 2002 (NSW), ss 5(D), 5(E)
Civil Liability Act 2003 (Qld), ss 11, 12
Civil Liability Regulation 2014 (Qld)
Civil Proceedings Act 2011 (QLD)
Hospital and Health Boards Act 2011 (Qld), s 18
Judiciary Act 1903 (Cth), ss 38, 39, 80

Cases Cited:

Adelaide Stevedoring Company Ltd v Forst (1940) 64 CLR 538; [1940] HCA 45
Cardiff Corporation v Hall [1911] 1 KB 1009
EMI (Australia) Ltd v Bes [1970] 2 NSWR 238
Fernandez v Tubemakers of Australia Limited [1975] 2 NSWLR 190
Holloway v McFeeters (1956) 94 CLR 470
John Pfeiffer Pty Ltd v Rogerson (2000) 203 CLR 503; [2000] HCA 36
Jones v Great Western Railway Co (1930) 144 LT 194
Purkess v Crittenden (1965) 114 CLR 164; [1965] HCA 34
Ramsay v Watson (1961) 108 CLR 642; [1961] HCA 65
Seltsam v McGuiness (2000) 49 NSWLR 262; [2000] NSWCA 29
Strong v Woolworths Ltd (2012) 246 CLR 182; [2012] HCA 5
Tabet v Gett (2010) 240 CLR 565; [2010] HCA 12
Tubemakers of Australia Limited v Fernandez (1976) 50 ALJR 720; 10 ALR 303
Wallace v Kam (2013) 250 CLR 375; [2013] HCA 19
Watts v Rake (1960) 108 CLR 158; (1960) HCA 58

Category:

Principal judgment

Parties:

Emily Pierce (Plaintiff)
Metro North Hospital and Health Service (Defendant)

Representation:

Counsel: D Graham SC with S Maybury (Plaintiff)
   J Glissan QC (Defendant)

  Solicitors: Edwards Michael Powell (Plaintiff)
   Corrs Chambers Westgarth (Defendant)

File Number(s):

2012/353698

Judgment

1. Ms Pierce sues Metro North Hospital and Health Service (“the Hospital”) for damages for the harm suffered by her as a result of video telemetry testing conducted at the Royal Brisbane and Women’s Hospital (“RBH”) on 4-5 January 2010.

2. Ms Pierce suffers from epilepsy due to antenatal causes. The purpose of the testing at the RBH was to determine whether the epilepsy she suffered was due to a lesion amenable to neurosurgery. For this reason a seizure was induced by withdrawal of her medication and deprivation of sleep. The video telemetry of the resulting seizure activity consists of recording by video Ms Pierce’s clinical presentation during the seizure with Electroencephalographic monitoring of brain activity (“EEG”) and electrocardiographic monitoring (“ECG”).

3. The seizure commenced early in the early morning of 5 January 2010. The staff of the Hospital did not intervene with appropriate medical treatment as promptly as they should have, allowing Ms Pierce to descend into a more serious, prolonged period of seizure activity, referred to as “complex partial status epilepticus”(“CPSE”). There are various stages of the development of the induced seizure, in ascending order of seriousness, from simple partial seizure; to complex partial seizure; and to CPSE. And it is common ground that the telemetry event included all of these progressions, lasting for 2 hours and 44 minutes (“the telemetry event”).

The proceedings

4. Ms Pierce alleges that the Hospital’s negligence caused a marked and permanent deterioration of her epilepsy involving brain or neuronal injury and consequential psychiatric injury. Her case about the deterioration in her pre-existing condition is that there has been a “change in nature, frequency and character of seizure activity”: (Amended Statement of Particulars, 16 December 2013, [9]). Particularly, Ms Pierce relies on the absence of warnings for, or premonitions of, her seizures and lack of predictability in terms of the usual triggers for her seizures, in comparison to the nature of her illness prior to the 2010 event. She relies on these as key facts demonstrating the occurrence of injury by the January 2010 seizure event: 341.5–40T. This change is particularly relied upon for the claim for damages for loss of future earnings and the cost of future care. It is the Plaintiff’s case that this change has severely impacted on her ability to care for herself and obtain future employment.

Constitution of the proceedings

5. Ms Pierce first initiated proceedings on 13 November 2012 against Dr Cecilie Lander, the treating neurologist who prescribed the test, as first defendant, Dr Alice-Ann Sullivan, the specialist responsible for the test, as second defendant, and the Hospital as third defendant. By consent, verdict and judgment was entered in favour of Dr Lander on 23 April 2015 and Dr Sullivan 9 July 2015. The matter proceeded only against the third, and now single, defendant, the Hospital.

Admissions by the Hospital

6. In its Notice of Defence filed 15 February 2013, the Hospital denied all claims of negligence and breach of contract (at [8]). But by email dated 29 June 2015, the Hospital admitted breach of duty of care by failure to:

“(a) treat the Plaintiff’s seizure event in a timely manner;

(b) properly instruct the staff who were to be monitoring the Plaintiff as to the appropriate care and treatment of the Plaintiff;

(c) treat the Plaintiff’s seizure event appropriately; and

(d) take any or any proper steps to terminate the Plaintiff’s seizure within an appropriate time after it was initially commenced” (Exhibit A)

And on the second day of the hearing, Mr Glissan of Queen’s Counsel, on behalf of the Hospital, admitted liability in the following terms:

“… I am instructed on behalf of the defendant to admit liability in addition to breach of duty to this extent, that the breach of duty of the defendant brought about a seizure episode with simple and complex partial seizures, and complex status epilepticus, the duration of the event being two hours and 44 minutes… It's the nature and extent of that injury and then the secondary consequences of it that are in issue” (49: 40-44T; 50: 4-5T).

From this admission I understand the question for determination to be the nature and extent of the plaintiff’s injury, extending to whether the Hospital’s negligence caused a deterioration in Ms Pierce’s underlying epileptic condition. The Hospital’s case is that by its natural course her condition was likely to worsen, and this is the probable explanation for any deterioration after 5 January 2010.

Choice of applicable law

7. This matter arises in the federal diversity jurisdiction under s 75(iv) of the Constitution because when her cause of action arose, Ms Pierce was (and is) a resident of New South Wales and the hospital was (and is) a manifestation of the State of Queensland under s 18 Hospital and Health Boards Act 2011 (Qld). This federal jurisdiction is invested in the Supreme Court of NSW by s 39 Judiciary Act 1903 (Cth): cf s 38.

8. A question then arises about the identification of the law applicable to the resolution of the parties’ dispute in the exercise of federal jurisdiction. In John Pfeiffer Pty Ltd v Rogerson (2000) 203 CLR 503; [2000] HCA 36, at 544 [101] – [102] the High Court of Australia determined “that the lex loci delicti should be applied by courts in Australia as the law governing all questions of substance to be determined in the proceeding arising from an intranational tort” whether in the exercise of federal, or non-federal jurisdiction. Questions of substance extend to “all questions about kinds of damage or amount of damages that may be recovered” (544 [100]) (my emphasis).

9. It follows that the Civil Liability Act 2003 (Qld) (“CLA”) applies to the extent to which it modifies the law of negligence (see especially ss 11 and 12 concerning causation), and the law of damages for personal injury: Chapter 3 and the provisions of the Civil Liability Regulation 2014(Qld) (“the regulation”).

10. This conclusion follows from the reformulation of the common law choice of law rule for actions in tort having an interstate element wrought by Pfeifer v Rogerson. And the requirements of s 80 of the Judiciary Act that “the common law in Australia,” applies unless modified by the Constitution, New South Wales State laws or laws of the Commonwealth. There are no relevant statutory modifications to the common law choice of law rule applicable here; the common law rule therefore applies in federal jurisdiction.

Amplification of the issues and applicable principles of law

11. 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.

12. 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.

13. 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.)

14. 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.

15. 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.

16. 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.

17. 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.

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

18. 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.

19. 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”

18. 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.

19. “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.

CPSE not CTCS

22. 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.

23. 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”.

24. 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.”

25. 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.

The telemetry event at RBH on 4-5 January 2010

26. 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.

27. 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].

28. 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].

29. 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).

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

30. 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].

31. 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.

32. 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.”

33. 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].

Hospital records of the seizure 4-5 January 2010

34. 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.

35. 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.

36. 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”.

37. 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)

38. 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”.

39. 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.

40. 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.

41. 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.)

42. 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.

43. 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.

Professor Dunne’s expert opinion of progression of 5 January seizure

44. Professor JW Dunne is the expert qualified by the Hospital. To accommodate the professional commitments of the experts, Professor Dunne was interposed in the plaintiff’s case before Dr Fong gave evidence. He is a clinical professor of neurology attached to the Adult Epilepsy Centre and Clinical Neurophysiology laboratory at Royal Perth Hospital.

45. Professor Dunne expressed the opinion that the seizure episode was made up of both simple and complex partial seizures. The CPSE began at 4:03 am and continued for 2 hours and 44 minutes. A simple partial seizure began 50 seconds after the onset of the seizure at 4:03 am, at which time Ms Pierce retained consciousness and the ability to speak but experienced bilateral limb movements. An ongoing simple or complex partial seizure then occurred, with varied degrees of consciousness, followed by a CPSE at some time between 4:45 and 4:57 am. During this period Ms Pierce was conscious, and was able to speak and respond to questions, with occasional eye flickering and left sided twitching. According to Professor Dunne, the seizure activity stopped at 6:47 am, after which Ms Pierce was asleep but able to be wakened (Exhibit 1.2, p 50–57). He concluded with his opinion that at no time did Ms Pierce suffer a GTCS or have generalised convulsive status epilepticus (“GCSE”).

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

46. 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.

47. 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.

48. 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).

Classification of the nature of the 5 January 2010 seizure event

49. It is therefore common ground that throughout the whole of the period Ms Pierce was suffering a CPSE that was more pronounced in the right hemisphere: 261.1–33T. The disagreement between Dr Fong and Professor Dunne is about the significance of the epileptic activity in the left hemisphere which was clarified in the Report of Dr Lander dated 22 September 2015 and Dr Fong’s restated opinion during the course of the trial. In fairness Professor Dunne had been and gone before Dr Fong’s revised opinion emrged. Mr Graham SC, who appeared for the plaintiff with Mr Maybury, in any event, did not put his case higher than that the episode was an incident of CPSE with some secondary generalisation, but not amounting to situation of GCSE or GTCS. To the extent that there is any difference in opinion between Dr Fong and Professor Dunne on this point, it was submitted to not be material to the plaintiff’s case or determinations of issues in contention: 398.1–50T.

49. Given the course of the evidence, I accept that what occurred on 5 January 2010 was a severe incident of CPSE and not a secondary GTCS. However, I accept Dr Fong’s opinion that there was evidence of some epileptic activity in the left hemisphere. This amounted to “some secondary generalisation”, but not a GCSE. Nonetheless I take the degree of generalisation identified by Dr Fong involving a cross-over to the left hemisphere as being a marker of the degree of severity of the particular incident of CPSE suffered by Ms Pierce on 5 January 2010.

Ms Pierce’s epilepsy from 1989-2004

51. 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.

52. 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.

53. 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.

54. 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.

55. 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.

56. 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.

Ms Peirce’s condition 2004-2010

57. The exact nature of the Ms Pierce’s condition in these years was the subject of much debate between the parties. While this period precedes the occurrence of the central events, the inferential reasoning urged by both parties relies upon the state and nature of Ms Pierce’s condition in this period for establishing their competing case theories.

Who carries what onus?

58. 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.

59. 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.

60. 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.

61. 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.

62. 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.

63. 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”.

64. 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.

65. 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.

21 June 1995 event

66. 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).

67. 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).

68. 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).

69. 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.

3 August 2005 event

70. 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)

71. 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.

72. 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.

73. 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.

74. 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”

75. 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.

76. 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.

10 April 2006 event

77. 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.

78. 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.

77. 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.

78. Professor Dunne regards this as “by far the worst seizure event suffered by the plaintiff” (Exhibit 1.1, p 26).

79. 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.

82. 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.”

83. 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.

84. 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).

Medication changes

85. 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).”

86. 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.

87. 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.

88. 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.

89. 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.

Ms Pierce’s experience of “lines” and their significance on the epileptic spectrum

90. 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].

91. 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.

92. 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.

93. 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.

94. 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.

95. 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.

96. 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”.

97. 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).

Seizure diaries

98. 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].

99. 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.

100. 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].

101. 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].

102. 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.

Seizure frequency

103. The diaries and the clinical notes of the hospitals run to very many volumes of evidence. What they show according to the defendant’s submission is summarised in the 131 pages of MFI 10; the plaintiff’s summary is Exhibit U. They otherwise comprise Exhibits E, M, N and O. Professor Dunne and Dr Fong have summarised what they derive from the primary records in tabular form. Professor Dunne attached a detailed summary of their contents in Exhibit 1.4. On page 3 of Exhibit 1.4 he provides a comparison of his conclusions and Dr Fong’s. This table omits or excludes the visual auras. An inspection of it demonstrates, with respect, that there is very little difference between them. And in my view the differences are immaterial with the possible exception of the 2009 year where Professor Dunne’s revised calculation has 16 seizure days and Dr Fong 12. The submissions of plaintiff’s counsel include their own summary which agrees with Dr Fong. Whichever calculation one prefers, my impression is that there is a significant increase in seizure frequency in 2010 and thereafter. I expand on this below.

Summary of the submissions of the parties

104. 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;

Out of pocket expenses

183. Past and future out of pocket expenses, including necessary curative aides and apparatus as assessed by the occupational therapists have been agreed in the sum of $27,500.

Past economic loss

184. 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.

185. 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.

186. Ss 54 and 55 are applicable to both past and future awards of damages for loss of earnings.

187. 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.

188. She commenced work in 2008 as a pharmacy assistant, doing a range of shop work including general inquiries, stocking shelves and working the checkout.

189. 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.

190. 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.

191. 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.

192. 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.

193. 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.

194. 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.

195. 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.

Loss of past superannuation

196. A claim is made for loss of employer’s contributions to superannuation for the past. No claim is made for the future as counsel seek an assessment on a “buffer” basis. S 56 of the CLA is relevant. The allowance is restricted to a percentage of past loss calculated by reference to the minimum percentage required by law to be paid by an employer on an employee’s behalf as the employer’s contribution to superannuation. Conventionally, on net figures (at least in New South Wales), 11 per cent is adopted. I allow $2,213.75.

Future loss of earnings

197. 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.

198. 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.

199. 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.

200. 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]).

201. 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.

202. 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.

203. 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.

Past attendant care

204. 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.

205. 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.

206. 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.

207. 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.

208. 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.

209. 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.

210. 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.

211. 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.

212. 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.

213. 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.

214. 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.

215. 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.

Future care

216. I accept that given the ages of Mr and Mrs Pierce, (the former was born in 1954 and the latter in 1947), it is appropriate to allow future care at commercial rates. It is simply unrealistic to suggest that Ms Pierce’s parents can continue to provide the care they provided in the past. Having said that, however, it has to be acknowledged that there is a degree of artificiality in the provision of commercial care, especially for seizure management when considers the inherently unpredictable nature of Ms Pierce’s seizures. This is especially so when one considers that she no longer experiences premonitory symptoms of a coming seizure. Reasonableness does not require an enrolled nurse to be on standby to provide the Midazolam injections. At the same time adequate allowance must be made bearing in mind what is reasonable between Ms Pierce and the hospital in the application of the compensatory principle to the consequences of the hospital’s negligence.

217. So far as future care is required, it is very important to bear in mind that Ms Pierce’s epilepsy is a naturally deteriorating condition. The likelihood that she would need care at this level in the future even in the absence of the negligence of the Hospital increases as time goes by. This being so, I think it appropriate to discount the agreed rate of 73.5 hours by 75 per cent in calculating for future loss. As I have said, Ms Pierce’s life expectancy according to the median life tables is 61 years. The 5 per cent multiplier for that period is 1,014.9. 73.5 hours by $59.33 produces a weekly rate of $4,360.75. Application of the multiplier produces a total of $4,425,725.18. Applying the discount of 75 per cent, the net figure (discarding cents) is $1,106,431.

Summary of damages

General Damages   $70,580.00

Out of pocket expenses   $27,500.00

Past economic loss    $20,125.00

Past employer superannuation contributions   $2,213.75

Future economic loss   $255,051.00

Past care   $190,890.00

Future care   $1,106,431.00

TOTAL DAMAGES   $1,672,790.75

218. My orders are:

1. Judgment for the plaintiff in the sum of $1,672,790.75;

2. The defendant to pay the plaintiff’s costs;

3. Liberty to apply in respect of interest on past economic loss

**********

Amendments

07 November 2016 - Coversheet change "ss5(e), 5(f)" to "ss 5D,5E;

Paragraph [44] change "attached the Adult Epilepsy Centre" to "attached to the Adult Epilepsy Centre";

Paragraph [46] change "principle" to "principal";

Paragraph [63] change "affects" to "effects";

Paragraph [128] change "13 April 2015" to "2010";

Paragraph [148] change "discreet" to "discrete";

Paragraph [165] change "that it had been" to "than it had been";

Paragraph [170] change "schedules to the Act" to "schedules to the regulation";

Paragraph [173] change "form" to "former;

Paragraph [192] change "unable" to "able";

Paragraph [194] change "2004" to "2014"

Decision last updated: 07 November 2016