Dual life-threatening pathologies presenting simultaneously

Abstract

A 70-year-old male presented to hospital with both anterior ST elevation myocardial infarction and spontaneous oesophageal rupture (Boerhaave’s syndrome). He underwent primary angioplasty and stenting for a lesion of the left anterior descending in addition to cardiothoracic surgery for the oesophageal rupture. This combination of pathologies is a rare entity and often difficult to diagnose. To date, only a few cases have been reported.

BACKGROUND

This combination of pathologies is a rare entity and often difficult to diagnose. To date, only a few cases have been reported.

CASE PRESENTATION

A 70-year-old male presented with central chest pain of sudden onset. The pain had begun while he was on a tractor at a golf course. He reported having felt nauseated and a few moments later he vomited copiously.

Apart from diet-controlled diabetes mellitus and hypercholesterolaemia, he did not have any other cardiovascular risk factors. No other past medical history of note was reported.

Physical examination was unremarkable with a heart rate of 78 bpm and a blood pressure reading of 118/70 mmHg.

In the emergency department he was not only having chest pain but also some abdominal pain for which an ultrasound was done; no abdominal aortic aneurysm was found. His electrocardiograph (ECG) showed significant anterior ST elevation. Bedside chest radiography (CXR) revealed a right pneumothorax with no mediastinal shift.

At the emergency department he complained of significant right upper abdominal pain, which became the predominant feature of his presentation. An urgent ultrasound was done; this excluded an abdominal aortic aneurysm.

While awaiting transfer to the cardiac catheterisation laboratory, he had two episodes of ventricular fibrillation both of which were successfully treated with 360 joules of defibrillation shocks.

He was rapidly transferred to the cardiac catheterisation laboratory where coronary angiography revealed a totally occluded mid left anterior descending coronary artery (mid-LAD) (fig 1A); the right coronary artery and circumflex vessels were patent. The LAD lesion was crossed easily with a 0.014 inch balance middleweight wire (BMW) wire. Following pre-dilatation of the mid-LAD lesion, it was found that there was a further 80% narrowing in the distal LAD. Both lesions were stented and thrombolysis in myocardial infarction (TIMI) III flow was obtained within 11 minutes of arrival at the cardiac catheterisation laboratory (fig 1B). The door to balloon time was 64 minutes.

Figure 1.

Coronary angiogram. (A) Illustrates the totally occluded left anterior descending (LAD) artery (black arrow). (B) Final angiogram (arrow showing well patent LAD artery).

Left ventricular assessment showed a left ventricular end diastolic pressure of 27 mmHg with preserved anterior wall motion with an overall ejection fraction approximately 70%. After the coronary intervention, the abdominal discomfort re-developed. A re-study of the LAD revealed patent stents with thrombolysis in myocardial infarction III flow.

A few hours later in the coronary care unit, the patient was noted to be very distressed and cyanotic. He was barely speaking and appeared profoundly drowsy. No focal neurological deficit was evident and he remained in sinus rhythm at a heart rate of 90 bpm. His systolic blood pressure reading was 100 mmHg. There was resolution of the ST elevation on the ECG. In view of his initial CXR an urgent CT scan of the chest was undertaken. This showed a large right hydropneumothorax and pneumomediastinum with an obvious mediastinal shift (fig 2A). Decompression of the pneumothorax with a large-bore needle was undertaken with good relief. A size 28 chest drain was then inserted into the right hemithorax through the fourth intercostal space in the midaxillary line.

Figure 2.

(A) CT chest demonstrating a right hydropneumothorax with mediastinal shift (white arrow). (B) Oesophagography illustrating the extravasation of contrast (black arrow).

The posterior pneumomediastinum raised the possibility of an oesophageal perforation and a barium meal was therefore requested. A focal region of oesophageal wall irregularity was evident just below the carina over the postero-lateral aspect of the mid-oesophagus on the right. This was associated with a pool of contrast (adjacent to the oesophagus), which gradually increased in size throughout the study with ongoing swallowing (fig 2B) consistent with extravasation of contrast through a perforation within the oesophageal wall.

The clinical scenario had, thus, rapidly evolved into a discussion regarding whether it was justifiable to undertake a high-risk operation in a patient who had an oesophageal rupture, recent coronary artery stenting and recent administration of potent anti-platelet medication. Since the situation was dire, and the likelihood of patient demise without intervention was high, the next of kin were involved in the decision making and it was agreed that cardiothoracic surgery should be undertaken.

Oesophagoscopy preceded the surgery; this showed a fluffy, jet black mucosal area with a probable tear in the upper part of the oesophagus. A normal mucosal lining was visualised in the lower oesophagus. The appearance was suggestive of an ischaemic oesophagus and it was decided to isolate it rather than repair it. The lower end of the oesophagus was isolated using blunt dissections and stapled. The azygos vein was cut in the middle and both ends were over-sewn and tied thoroughly; thereafter, the oesophagus was dissected out right up to near the thoracic inlet where it was doubly stapled and cut in the middle.

The patient was transferred to the intensive care unit where his condition remained stable. Aspirin and clopidogrel were continued per rectally. Initial feeding was via total parenteral nutrition; this was weaned off after laparoscopic insertion of a jejunal feeding tube was undertaken.

A few weeks later he underwent a retro-sternal pull-up operation and cervical oesophagogastric anastomosis for reconstruction of his defunctioned oesophagus.

OUTCOME AND FOLLOW-UP

He is now doing well at home and can just about eat anything he wishes. He gets regular review at the surgical and cardiology outpatient clinics.

DISCUSSION

The above case demonstrates an interesting presentation of two life-threatening conditions: anterior ST elevation myocardial infarction and spontaneous oesophageal rupture (Boerhaave’s syndrome).

Pneumothorax is known to present with ST elevation on ECG and relieving it has been associated with resolution of ST changes.^1–3 Despite the current time constraints for coronary reperfusion in the setting of acute myocardial infarction, it is important for clinicians to consider other possible diagnoses in patients presenting with chest pain and ST elevation on ECG.²

In patients presenting with ST elevation and a pneumothorax without mass effect, we feel that undertaking a percutaneous coronary intervention has a lower ongoing risk of complications compared with traditional thrombolysis as these individuals may, as in our patient’s case, subsequently need invasive procedures such as chest drain insertion or even cardiothoracic surgery.

Acute oesophageal necrosis was also considered as a differential diagnosis.⁴ In this entity there is circumferential black discolouration with or without exudates involving the distal oesophagus, which terminates sharply at the gastro-oesophageal junction; however, our patient’s necrotic lesion was limited to the upper part of the oesophagus.

It is likely that our patient sustained an anterior myocardial infarction and thereafter developed Boerhaave’s syndrome from forceful vomiting. In this case, there was no evidence of pneumomediastinum or pleural effusion on initial chest radiography as commonly occurs with Boerhaave’s syndrome. After treating the myocardial infarction there was further deterioration in the patient’s condition that prompted us to look for further thoracic pathology. The combination of myocardial infarction and Boerhaave’s syndrome is a rare entity and often difficult to diagnose and to date only a few cases have been reported.^5,6

LEARNING POINTS

• The case demonstrates a patient presenting with more than one life-threatening condition.

• Acute ST elevation myocardial infarction may be associated with Boerhaave’s syndrome.

• In medicine “common things occur commonly” but it is important to entertain rarer or even multiple diagnoses for cases with atypical presentations, especially if there is further deterioration following appropriate treatment.