Mr U, a 45-year-old picture framer and father of three, went to his GP, Dr F, suffering from severe heartburn. Dr F examined Mr U’s abdomen, finding nil of note, and prescribed lansoprazole.
Two days later, Mr U went back to the surgery. He saw Dr A and gave a history of severe paroxysmal spasms of retrosternal pain radiating to his jaw, occurring one hour after eating. Dr A prescribed ranitidine and an alginate barrier antacid.
A month after this Mr U was back again. He saw Dr F and reported improved epigastric pain. However, over the last three weeks he’d experienced pain in the sternal area when exerting himself, particularly if walking uphill. He’d had pain whilst pushing a wheelbarrow in the garden.
Dr F repeated the prescription for ranitidine and made a note to consider investigation in the form of endoscopy or an exercise ECG. Mr U was given a GTN spray to try.
Three weeks after this Mr U came back to Dr A for a repeat prescription of ranitidine. He told Dr A that he still had epigastric pain after eating. Dr A prescribed more ranitidine, advised Mr U to stop smoking and gave him lifestyle advice. He also arranged an upper gastrointestinal endoscopy.
Six days later, Mr U became acutely unwell and asked for a visit from a deputising on-call GP. Unfortunately, he had died by the time the doctor arrived to see him.
A postmortem examination revealed left ventricular myocardial scarring consistent with previous myocardial infarction and ischaemia. The right ventricle showed changes consistent with a recent infarction. He had marked, extensive, calcified coronary artery atheroma. In many areas the coronary lumen was reduced to the size of a pinhole.
A recent non-occlusive adherent thrombus was present at the origin of the descending branch of the left coronary artery. The right coronary artery contained an extensive, occlusive thrombus.
A claim naming Drs A and F was launched by Mr U’s family. It alleged failure to consider Mr U’s risk factors for ischaemic heart disease, failure to assess him adequately and failure to investigate his condition.
Expert GP opinion was critical of both doctors, particularly Dr A, whose clinical records were felt to be of insufficient detail to give him any defence. As the symptoms progressed, and became more characteristic of ischaemic-myocardial rather than oesophageal pain, the expert felt Dr A should have reviewed the response to antireflux therapy and the GTN, and decided to investigate Mr U’s heart.
Regarding Dr F, it was felt that his assessments were more thorough, but his failure to follow up on his suspicions and arrange an exercise ECG, refer for advice, or start formal treatment for angina, were indefensible.
Cardiological opinion concurred and thought Mr U’s risk of fatal MI would have been reduced if he had been referred and received treatment.
A failure to elucidate fully and document Mr U’s cardiac risk profile was criticised. However, the severity of his disease meant that his long-term life expectancy was severely limited and optimal treatment was unlikely to have extended his life by more than ten years. We settled the claim, taking this fact into account.
See our article in Casebook 2003 (4) on how to avoid pitfalls when assessing chest pain.
Diagnosis can be difficult, particularly when distinguishing between gastrointestinal and cardiac pain. In this case, it appears that the clinicians fell for the common pitfall of assuming that post-prandial symptoms must be related to the gastrointestinal tract. Such pain can be caused by myocardial ischaemia due to splanchnic blood diversion.
It’s useful to bear this in mind, particularly in primary care, and have an appropriate threshold for investigation of potential ischaemic heart disease, especially where the response to therapies for non-cardiac causes is poor.
There is no substitute for a full clinical assessment when a patient presents with epigastric or chest discomfort. A few minutes spent establishing risk factors for ischaemic heart disease, examining the cardiovascular system and documenting this information allows you to gauge your degree of suspicion of cardiac disease accurately and puts you and your patients in a much better position.
Given the difficulty of reaching an accurate diagnosis of the cause of chest pain without further investigation, a willingness to review your initial clinical impression and change tack is essential.
An analysis of 1,000 consecutive GP claims handled by MPS revealed that delayed or failed diagnosis of myocardial infarction/ischaemic heart disease accounted for 5% of all general practice claims.