There are 2 lessons to be learned from this case: (1) keep your nerve; and (2) exercise extreme caution when settling claims involving brain damage in children, as a child claimant’s full level of disability may not become apparent until after puberty.
LA was born on 20th April 1998 and developed normally, reaching all the appropriate milestones for the first 8 months of her life. In late December 1998 she developed what appeared to be an upper respiratory tract infection and a left otitis media. She was prescribed an antibiotic by her General Practitioner but deteriorated, becoming pale, pyrexial and irritable. On the morning on 4th January 1999 she vomited and became listless, floppy and difficult to rouse. She was admitted to the hospital.
Central to the claim was the dispute as to LA’s clinical condition when she first attended the hospital. It was recorded that she had an abnormally high respiratory rate of 70 breaths per minute, although there was no cyanosis, a high pulse of 185 bpm and a significant fever of 40.2°C. It was further recorded that she looked unwell and lethargic. Possible diagnoses of urinary tract infection and viral upper respiratory tract infection were considered. She was commenced on oral Erythromycin and paracetamol. Her pulse and temperature improved slightly and LA’s mother was advised to take her home. Her mother asked to remain in hospital overnight, as she was concerned about LA’s condition. It is LA’s mother’s recollection that she was unresponsive, floppy and pale from the time of admission to the hospital and did not improve at any stage.
On 5th January 1999, LA remained unwell with a fast pulse and respiratory rate and a blood oxygen saturation in the mid-80s (low). She was sleepy but rouseable with no focal neurological signs. A diagnosis of pneumonia, possibly secondary to either bronchiolitis or mycoplasma infection, was made.
Intravenous Augmentin was added to the oral Erythromycin. At about 13.00 on 5th January 1999 she had a possible seizure. LA’s condition continued to deteriorate and she became less responsive. Blood tests showed a normal white count but raised inflammatory markers. Blood culture revealed infection with Streptococcus pneumoniae and her antibiotic treatment was altered accordingly.
At midnight on 5th January 1999 she had another seizure and a lumbar puncture performed at 02.00 on 6th January 1999, revealed the presence of Streptococcus pneumoniae in the cerebrospinal fluid, confirming that LA was suffering from pneumococcal meningitis. LA had further fits and was transferred to ICU at Great Ormond Street where she required artificial ventilation for some days. Subsequently MRI brain scans showed acute hypoxic brain damage which progressed to mild generalised cerebral atrophy in the deep white matter of both hemispheres. LA developed bilateral sensori-neural deafness, which has been treated with cochlear implants.
The case brought on behalf of LA was that her condition on admission to hospital was consistent with a serious bacterial infection including bacterial meningitis, which should have been investigated. It was unreasonable to have assumed that LA was suffering from a minor infection and subsequently a chest infection without excluding other more serious conditions. It was alleged that LA should have been commenced on intravenous antibiotic therapy within 2-3 hours of her admission on 4th January 1999. At that time the infection was still in the bacteraemic phase (remaining within the blood stream) and had not crossed the blood-brain barrier. Appropriate and timeous treatment with antibiotics would therefore have prevented the bacteraemia from developing into damaging meningitis.
The defendant’s initial position was that it was reasonable practice to have diagnosed a viral infection and subsequently a chest infection and to have treated LA with oral Erythromycin. The defendant also contended that had a lumbar puncture been performed earlier it would have been normal and would not have assisted with the diagnosis.
At the meetings of the experts the defendant’s experts gave some ground. It was agreed that LA’s presentation was consistent with a serious bacterial infection including bacteraemia, with a risk of meningitis and it was a breach of duty to have failed to include this within the differential diagnosis. The breach of duty experts agreed that if LA’s mother’s description of LA was held by the court to be accurate, the defendant was in breach of duty in failing to have commenced appropriate intravenous antibiotics by at the early hours of 5th January 2009. If the medical records were held to present an accurate picture of LA’s clinical condition, then the paediatric experts were polarised, with regard to breach of duty. Thus establishing breach of duty depended entirely upon LA’s mother’s evidence. LA’s mother is a sensible and intelligent woman, whose memory of events is vivid, for obvious reasons. She was aware of the heavy burden of responsibility she would bear at trial. The issue was whether a judge would consider that her memory was more reliable than the medical records.
The Causation experts were largely agreed that had LA been appropriately treated by at latest the early hours of 5th January 2009, she would not have sustained damage.
A RTM was held on 4th September 2012, in view of a trial commencing on 15th November 2012. On the basis of the stark conflict of factual evidence a 50/50 split was briefly discussed but no firm offer made. The defendant’s opening offer was to agree 75% liability in favour of LA, however this was rejected and after some discussion 85% was offered. The outcome of clinical negligence cases is more difficult to predict than personal injury claims, as both breach of duty and causation turn on which expert is the more persuasive on the day. The offer of 85% was considered carefully. Nevertheless, we considered that the claim was a strong one and a counter offer of 90% was made. It was accepted by the defendant.
When the claim was served in 2010 and LA was only 12 years old, (based on earlier medical examinations) it was thought that her main problems were sensorineural deafness and speech and language difficulties, partly attributable to the deafness and partly due to severe oro-motor dyspraxia. Her speech is hardly intelligible to those who do not know her. She was known to have some difficulty with concentration, however her cognitive and intellectual abilities were within the normal range. As time has gone on, LA’s ability to interact with her peers has deteriorated significantly and she has fallen behind both with her education and her social skills. Her behavioural problems are particularly troublesome and there is now considerable doubt as to whether she will be able to live independently as an adult. The value of the claim is now significantly higher than it would have been thought to be if settled when she was say 10 or 11 years old.
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