Brain damage caused by badly managed Insulin Therapy

BACKGROUND TO THE CLAIM

C was born in January 1981 with a congenital heart abnormality in which the left coronary artery originated from the pulmonary artery rather than the aorta - in other words on the wrong side of the heart. The pregnancy had been uncomplicated apart from some maternal gestational diabetes.

C underwent corrective open heart surgery at Royal Liverpool Children's Hospital (RLCH) on December17 1981 and up until the surgery her physical and intellectual development had been normal despite the cardiac abnormality

Post-operatively C was admitted to ICU in a stable condition with a normal potassium level of 4mmol/litre. It was decided that it was in her interests to commence glucose/insulin/potassium (GIK) therapy, a treatment that requires very close biochemical monitoring as insulin lowers both blood sugar and potassium levels. It is well know that very low or very high potassium levels can lead to cardiac arrhythmias and very low blood sugar levels can result in brain damage.

On December 18 1981 C was breathing spontaneously and responding to stimuli. She received her first dose of insulin at 08.00 and also recommenced digoxin, which was continued thereafter. From then on she was infused with dextrose containing insulin and potassium at varying rates.

C's potassium levels on December 18 varied between normal and 2.2mmol/L (very low) and her blood sugar level was 3.8mmol (lower end of normal)

The GIK therapy continued throughout December 19 when the potassium fell as low as 2mmol/L (dangerously low.) Intermittent tachycardia was also noted, which was almost certainly the result of the very low potassium level.

During December 20 C. appeared to be improving although episodes of tachycardia persisted. The GIK therapy continued and the diuretic Lasix was recommenced even though the potassium level remained very low at 2.3mmol/L. At 21.00 the blood sugar level was exceptionally low at 1.6 mmol so the insulin was reduced and the dextrose increased.

On December 21 1981 at 01.05 C suffered an episode of ventricular fibrillation resulting in a cardiac arrest. She was defibrillated and resuscitated although it is not recorded how long this process took. The serum potassium at this time was 2mmol/lL

As a direct result of the cardiac arrest C suffered a sustained period of cerebral anoxia resulting in severe and permanent brain damage.

BREACH OF DUTY

Stress induced hyperglycaemia frequently occurs in critically ill patients, including those undergoing open heart surgery, and can result in increased morbidity and mortality. The aim of GIK therapy is to maintain a normal blood glucose level thereby increasing the chances of recovery.

Insulin therapy with tight glycaemic control has been widely adopted throughout the world, especially in post cardiac surgery patients, but in 1981 it was not standard treatment for infants who had undergone open heart surgery and it does not appear to be listed in standard contemporary texts or literature.

The key therapeutic component of GIK is insulin and the potassium and glucose are given to counteract its biochemical effects - ie lowering both potassium ( hypokalaemia) and blood sugar (hypoglycaemia) The metabolic advantages of insulin can only be enjoyed if these potentially adverse side effects are adequately monitored and maintained at near normal levels.

It is the claimant's case that the management of the GIK therapy in her case was inadequate and substandard for the following reasons -

The dose of insulin was excessive. An appropriate dose would have been between 0.35 to 1.14 units per hour. In fact C received doses varying between 1.8 and 3.5 units per hour.
The balancing of insulin, dextrose and potassium infusions to maintain near normal (and therefore safe) blood chemistry was not achieved.
A careful treatment plan to ensure this biochemical balance was achieved was not implemented.
The persistently low potassium levels were not acted upon.
Digoxin was administered even though it is well recognised that in the presence of hypokalaemia it can cause ventricular fibrillation and cardiac arrest.
Lasix was administered in the presence of already low potassium levels even though it is known to deplete levels even further.
C's blood sugar was allowed to fall to dangerously low levels.

In summary, the claimant's case is that the defendant negligently failed to monitor/manage her GIK therapy. By the administration of excessive amounts of insulin and/or by the insufficient balancing of her dosage of glucose and potassium they so depleted her blood glucose and serum potassium levels as to cause her to develop hypoglycaemia and hypokalaemia. Hypoglycaemia and hypokalaemia together with the administration of digoxin caused the episode of ventricular fibrillation and cardiac arrest suffered on December 21 1981, which in turn resulted in severe and permanent brain damage.

OUTCOME

The consequences of the negligent action of the defendant have been catastrophic for C. and her family. She is severely brain damaged and although she is now 28 years old she has the developmental age of a 7 year old. She has severe learning difficulties and is unable to communicate any more than simple ideas or to manage her own affairs. She has frequent epileptic seizures and requires full-time supervision as she cannot tolerate being left alone for more than a few minutes. She has behavioural problems, particularly anxiety and aggression and often demonstrates obsessive and inappropriate behaviour.

C. will remain incapable of any independent life and will require 24 hour care for the remainder of her life. Hitherto she has relied on the dedicated care of her mother and father, together with other members of her family, to provide for all of her care needs. She will not be able to work in any capacity.

PROCEEDINGS

Following admission of liability made on March 12 2007 the parties investigated quantum issues and entered into an exchange of expert evidence. In the first instance meetings were held between the psychologists to discuss the impact of C's behavioural problems on the need for care. There then followed by a meeting of the care experts. There remained a dispute between the parties as to the number of carers required to provide care at night.

The parties met at a joint settlement meeting on October 16 2008 and agreed a settlement of damages, subject to the approval of the Court on the following terms:-

1. Payment of a lump sum of £2,150,000 less interim payments made of £200,000.
2. Periodical payments in respect of care and case management at the following rates subject to annual increases in accordance with ASHE 6115 80th percentile:

From the present to December 15 2011 at the rate of £ 82,500 p.a.
Thereafter until December 15 2018 at the rate of £115,000 p.a.
Thereafter for life at the rate of £132,500 p.a.

The staged increases in the periodical payments were designed to meet C's immediate and long term needs and were consistent with the likely plans of the family in terms of accommodation and the introduction of a care regime which would need to be gradual having regard to the to C's obsessional routines and behavioural problems.

The settlement was approved in the high Court on November 14 2008.

Experts and counsel Stephen Grime QC

Tim Ryder - counsel.
Maggie Sargent - Care
Julia Ho - Occupational Therapy
Dr David Johnson - Neuropsychologist
Peter Ball - Accommodation
Professor Anthony Schapira - Neurologist
Dr Stuart Green - Paediatric Neurologist

For the claimant

Sue Taylor - fee earner with conduct
JMW Solicitors
Manchester

For the defendant

Tony Gibbons - fee earner with conduct
Hill Dickinson Solicitor