The case is presented of a 54 year old man who attended the emergency department with a history of central abdominal pain and electrocardiograpic changes consistent with an anteroseptal myocardial infarction. Myocardial infarction was not confirmed with serial cardiac enzymes and a subsequent laparotomy revealed a gangrenous retrocaecal appendix. This case highlights the rare but recognised association between an acute surgical abdomen and pseudomyocardial infarction. It is, to the authors’ knowledge, the first reported case of pseudomyocardial infarction complicating a retrocaecal appendicitis.
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A 54 year old man self presented to the emergency department with a 12 hour history of central abdominal pain. The pain was described as dull in nature with no radiation; there was associated nausea but no vomiting. The patient denied any previous similar episodes of pain. His only medical history of note was tinnitus and sciatica.
Physical examination revealed a mild fever (37.8°C) with epigastric and central abdominal tenderness; there was no evidence of rebound or guarding. Examination of the cardiovascular and respiratory systems was entirely normal. The patient was normotensive with no clinical evidence of shock. A subsequent electrocardiogram revealed anteroseptal ST segment elevation consistent with an acute myocardial infarction (fig 1). The patient was treated as for an acute myocardial infarction with aspirin and thrombolytic therapy. Initial routine blood tests were normal apart from a mildly increased white blood count of 14.4 and a C reactive protein of 152.
After admission the patient continued to complain of lower abdominal pain. Further examination at this stage revealed tenderness in the right lower quadrant. Over the course of the next 24 hours serial abdominal examinations did not reveal any evidence of rebound or guarding. Serial cardiac enzymes (creatine kinase) and two separate amylase results were normal.
In view of the persistent abdominal tenderness an appendicectomy was performed, which revealed pus in the pelvis and a retrocaecal gangrenous appendix. The patient subsequently made an uneventful recovery and was discharged home nine days after initial admission. A total of four electrocardiograms were performed, three on the day of admission (including one after thrombolysis), all of which showed persistent ST segment elevation as shown in figure 1. The fourth electrocardiogram was performed before discharge, which showed the ST segment elevation to have resolved (fig 2).
Electrocardiogram changes resembling acute myocardial infarction can rarely occur in association with an acute surgical abdomen. Pseudomyocardial infarction has been reported in association with acute pancreatitis,1,2 perforated duodenal ulcer,3 and acute abdominal conditions associated with shock and severe metabolic stress.4 ST segment elevation has also been reported in an episode of variant angina induced by biliary colic.5
It has been postulated that the electrocardiogram changes that occur in acute abdominal conditions are related to episodes of electrical silence in the myocardium. Electrical silence is not synonymous with myocardial death; if the causative abnormality can be corrected the electrocardiogram changes will return to normal.6 Several mechanisms have been postulated for this phenomenon including hypotension leading to decreased coronary perfusion, coronary artery spasm, systemic or local electrolyte disturbance, vagal stimulation, and circulating proteolytic enzymes. Electrolyte abnormalities such as hyponatraemia, hypokalaemia, and hypocalcaemia can modify the repolarisation phase on the electrocardiogram, but ST segment elevation in such cases is rarely seen. Profound hypotension may diminish coronary perfusion and cause ischaemia leading to electrocardiogram changes, especially in patients with coronary artery disease. Vagal reflexes can cause cardiac damage by acting directly on the myocardium, indirectly altering coronary blood flow or through increased secretion of pancreatic proteolytic enzymes. The membrane of the myocyte may be directly damaged by pancreatic proteolytic enzymes with subsequent changes of cell permeability and possible cellular necrosis, as well as secondary electrical disturbance.
Acute myocarditis has been associated with peudomyocardial infarction electrocardiogram changes. This is typically related to viral myocarditis, however there is one reported case of pseudomyocardial infarction occurring in association with staphylococcal myocarditis.7 It is of interest that in the previously documented case of pseudomyocardial infarction complicating a perforated duodenal ulcer, postmortem examination showed necrotic tissue in the lesser sac scattered focal changes of acute myocarditis. It is unlikely that the ST segment changes occurring in our case were related to bacterial myocarditis in view of the normal serial cardiac enzymes.
This particular case emphasises the rare but recognised association between ST segment changes that may mimic acute myocardial infarction and acute surgical pathology. Emergency physicians should be aware of this association and consider this possibility when a patient presents with atypical symptoms or signs.
C Dewar wrote the paper and acts as guarantor. A Siddiqi assisted with the literature search. J Kayani reviewed and edited the manuscript.
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